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The person charging this material is re-
sponsible for its return to the library from
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UNIVERSITY OF ILLINOIS LIBRARY AT URBANA-CHAMPAIGN
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THE
CircuLatTory DisturBaNces
©) DTS
EXTREMITIES
INCLUDING GANGRENE, VASOMOTOR AND
TROPHIC DISORDERS
BY
EE OSBWERGHReE MEAS M.D:
NEW YORK CITY
WITH 192 ILLUSTRATIONS
FIVE IN COLORS
PHILADELPHIA AND LONDON
W. B. SAUNDERS COMPANY
1924
B
t és
hn
y
x
TO
DR. WILLIAM J. MAYO
whose masterly surgery has stimulated
and to
DR. EMANUEL LIBMAN
whose unusual medical insight has inculcated
a spirit of research
THIS VOLUME IS RESPECTFULLY INSCRIBED
“\
3
4)
y?
pi
: 551198
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i
PREFACE
PERHAPS in no other department of medicine has clinical diagnosis offered
greater difficulties to the practitioner than in the domain of circulatory, vaso-
motor, and trophic disturbances of the extremities. When the author began
his pathological studies of the vessels of the extremities in gangrene from
whatever cause some eighteen years ago, he was not a little surprised to note
what confused notions regarding clinical classification existed in the minds of
some of the best internists, neurologists, and surgeons. Chronic rubor
associated with obstructive arterial disease was reported as evidencing an
identity of pathogenesis in such diverse clinical entities as erythromelalgia,
Raynaud’s disease, and thrombo-angiitis obliterans; and these three essenti-
ally different maladies were even described as of similar origin.
Whilst the recognition of thrombo-angiitis obliterans with its kaleido-
scopic manifestations has had a clarifying influence, and whilst descriptions
of its varied symptomatology may have contributed to a better insight into
what phenomena are of neurogenic and what are of purely mechanical and
hydrostatic motivation, the subject seems for many to be still enshrouded
in much mystery. For, it is not only the practitioner who often fails to
clearly segregate the circulatory, vasomotor, and trophic phenomena, but
even in recent contributions of special investigators no dearth of misconcep-
tions can be found.
Perhaps it is the intricacy of the physiological, anatomical, and patho-
logical data on the one hand, and the misconstruction or misinterpretation of
the perplexing objective signs on the other, that account for the lack of
general comprehension.
It seemed appropriate at this juncture, therefore, to assemble, analyze,
and critically interpret the maze and multitude of facts bearing on these
subjects, and now at our disposal. And this with a view to establishing a
correct approach and a clearer insight into both diagnosis and modes of
therapy in the fields under consideration.
But the usual text-book treatment of the subject matter would, it appears
to the author, hardly suffice to give that fundamental knowledge upon which
an understanding of the many varied manifestations can be built up. And
so, to accomplish the purpose in view, it seemed not unwise to leave the
beaten paths and to diverge and intrude with intent at considerable length
into allied departments of anatomy and physiology. If, by conducting the
reader through all those related, basic, and essential facts that only extensive
research into many fields of the literature can disclose, the work of personal
investigation be minimized and confined to the perusal of but one volume; and
if, by a well chosen and well directed series of discussions the burden of com-
prehension be facilitated, the work herein incorporated will not have been in
vain.
Although the greatest importance has been accorded the pathology and
clinical manifestations of the organic vascular affections—in which domain
the author’s experience has been ample to elucidate many of the mooted
points—it was deemed wise to give more extensive consideration to the
conclusions of others in some of the fields. And so, for the exposition of
the normal circulation of the extremities, of thrombosis, of the vegetative
Vv
vi PREFACE
nervous system, and of the vasomotor neuroses, the views of a number
of excellent authors have been more thoroughly incorporated. To the
important researches of such investigators as Beneke, Aschoff, Cassirer,
Hering, Miiller, Dresel, Langley and others must be given credit for much
that is of fundamental importance. Since their works may be inaccessible
to many American readers, their essential deductions and conclusions have
occasionaily been given in extenso.
It is a pleasure to give acknowledgement to Miss Caroline Kleppner and
Mrs. Harry Friedman for their excellent assistance in the researches on
thrombo-angiitis obliterans; and to accord credit to my secretaries, Miss
Ida Lipnitz and Miss Natalie Wood for help in the preparation of the manu-
script. Thanks are due to the W. B. Saunders Company for their valuable
codperation in the publication of this volume.
Leo BUERGER.
1000 PARK AVENUE, NEw YorkK City,
May, 1924.
CONTENTS
GHAP TERS
MANTRODUCTION, » . . . » .
CHAPTER II
ANATOMICAL CONSIDERATIONS. ... .
CHAPTER III
THE MINUTE STRUCTURE OF THE VESSELS . .
fEnesCapillaries ; «< . ..
The Arterioles and Venules.
The Arteries . .
GHAPTER CIV
ae VASOMOTOR NERVOUS SYSTEM. . .. s/s %. 4.
CHAPTER V
FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM ......
CHAPTER VI
PHYSIOLOGY OF THE PERIPHERAL CIRCULATION... .
CHAPTER VII
PHYSIOLOGY OF THE CAPILLARIES .
CHAPTER VIII
METHODS OF INVESTIGATING CAPILLARY CIRCULATION .....
CHAPTER IX
GENERAL CIRCULATION UNDER PATHOLOGICAL CONDITIONS.
CHAPTERUX
Pree ae CIRCULATION... «40. «on is:
Local Anemia or Ischemia .
a CPCI IA tim ora) ce se
CHAPTER
FUNCTIONAL DISTURBANCES OF PERIPHERAL CIRCULATION . . ak
The Superficial Circulation in Obstructive Vascular Diseases . . .
GHAPTERS SIT
COLLATERAL CIRCULATION .. .
GHAP TER TXIIT
CIRCULATION IN THE EXTREMITIES UNDER PATHOLOGICAL CONDITIONS
CHAPTER XIV
THE TROPHIC FUNCTIONS OF THE NERVOUS SYSTEM .
CHAPTER XV
TROPHIC DISORDERS OF ,THE SKIN.......
CHAPTER XVI
GENERAL CONSIDERATIONS OF THROMBOSIS.
Ni eet er eK
PAGE
Vat
1a E
12
13
22
36
48
57
63
69
yi
ve
73
76
80
82
87
go
96
= LOO
vill CONTENTS
CHAP TEREX ME
THE Forces ENGAGED IN THROMBUS FORMATION. . .
GHA P LEREX VILL
PHYSICAL EXPLANATIONS OF THROMBOSIS.
CHAPTER XIX
MECHANICAL TYPES OF THROMBOSIS. .
CHAPTER XX
THROMBOSIS OF CHEMICAL ORIGIN. .
CHAPTER XXI
GENERAL CAUSES OF THROMBOSIS.
CHAPTER XXII
GANGRENE—GENERAL CONSIDERATIONS . . .
GHA PDEREX OCI
METHODS OF INVESTIGATION OF GANGRENE.
CHAPTER XXIV
DIAGNOSTIC SYMPTOMS—ARTERIAL PULSATION .
CHARPTEREOcy
DIAGNOSTIC SYMPTOMS—PAIN. . .
CHAPTER XXVI
DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION.
Symptoms . ag
Historical.
Clinical Types. ;
Dysbasia Angiosclerotica Intermittens . . .
Functional Vasomotor Type (Oppenheim) .
Intermittent Claudication i in Other Territories
‘““Acute Forms” of Intermittent Claudication
Apokamnosis (Goldflam) or Artificial Intermittent Claudication.
Pathology . nag
Critical Summary . . .
Explanation of Phenomena.
Differential Diagnosis .
CHAPTER XXVII
FORMS OF GANGRENE .
CHAPTERS evVill
CLASSIFICATION OF GANGRENE .
GHAPTERSXX TX
CLINICAL EXAMINATION IN GANGRENE .
CHAP TE Rexx
TRAUMATIC GANGRENE.
CHAPTER XXXI
THERMIC GANGRENE. . . rere any ee oat
CHAP TERSXSXSCLT
GANGRENE DUE TO CHEMICALS AND DRUGS.
CHAPTER XXXIII
MICROBIC GANGRENE .
PAGE
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- 155
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. 162
. 168
,
A OLOE
Tae
CONTENTS
CHAPTER XXXIV
MIcROBIC GANGRENE (CONTINUED) .
Gas Gangrene. .......
CHAPTER XXXV
GANGRENE COMPLICATING INFECTIOUS DISEASES. . . . .
CHAPTER XXXVI
INJURIES TO THE BLOOD VESSELS AND GANGRENE .......
CHAPTER XXXVII
ANEURYSMS. .. .
CAP EIN exo. VILL
TREATMENT OF INJURIES TO THE BLOOD VESSELS . . .
CHAPTER XXXIX
THROMBO-ANGIITIS OBLITERANS—INTRODUCTION. . .
CHAPTER XL
THROMBO-ANGIITIS OBLITERANS—GENERAL CLINICAL CONCEPT . .
GHA PTE REXEL
THROMBO-ANGIITIS OBLITERANS—ACUTE STAGE . .
CHAPTER XLII
THROMBO-ANGIITIS OBLITERANS—CHRONIC STAGE
CHAPTER XLIII
THROMBO-ANGIITIS OBLITERANS—CLINICAL PICTURE . .
CHAPTER XLIV
THROMBO-ANGIITIS OBLITERANS—APPEARANCE OF THE LIMB . .
CHAPTER XLV
THROMBO-ANGIITIS OBLITERANS—ISCHEMIA.
Mechanical or Hydrostatic Ischemia.
Vasomotor Ischemia in Thrombo-angiitis Obliterans.
CHAPTER XLVI
ERYTHROMELIA .
CHAPTER XEVII
THROMBO-ANGIITIS OBLITERANS—CYANOSIS.
CHAPTER XLVIII
THROMBO-ANGIITIS OBLITERANS—EDEMA .
CHAPTER XLIX
THROMBO-ANGIITIS OBLITERANS
THROMBO-ANGIITIS OBLITERANS—INTERMITTENT CLAUDICATION .
CHAPTER L
THROMBO-ANGIITIS OBLITERANS—PAIN.
CHAP EER EL
THROMBO-ANGIITIS OBLITERANS—COLDNESS.
CHAPTER LII
THROMBO-ANGIITIS OBLITERANS—ARTERIAL PULSATION.
PAGE
+ Aiefe)
. 190
204
we 204
. 208
200
eos
SG2EA
mes)
237
. 240
204
x CONTENTS
PAGE
CHAPTER LIII
THROMBO-ANGIITIS OBLITERANS—MENTAL SYMPTOMS. ..... . . i se ee
CHAPTER LIV
THROMBO-ANGIITIS OBLITERANS—VASOMOTOR SYMPTOMS. ..... . . «a & Soke
CHAPTER LV
THROMBO-ANGIITIS OBLITERANS—OSSEOUS CHANGES. . ............ . 2975
CHAPTER LVI
THROMBO-ANGIITIS OBLITERANS—OTATISTICAL DATA .°.. 5 = = = = 3)p eure
CHAPTER LVII .
THROMBO-ANGIITIS OBLITERANS—ETIOLOGY. 2, 2...) = ee oe) eee
CHAPTER LVIII
THROMBO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS ............ +. 2979
Thrombo-phlebitis without Symptoms. . +. a oe Sees
Thrombo-phlebitis with Symptoms of Limited Vein Involvement ..... . . 280
Migrating Phlebitis Causing the Patient to Seek Treatment. ...... 281
Both Migrating Phlebitis and Thrombo-angiitis Play Equally Important Réles
in the Symptom-complex . . 284
Migrating Phlebitis or Thrombo- phlebitis Involving Both Upper and Lower
Extremities. . . : 286
Extensive Fulminating Migrating Phlebitis. . 291
Cases in Which Absolute Evidences of eeP a Arterial Involvement Are Lacking . 291
Conclusions from Vein Lesions .. . . Pee ate a 4262
CHAPTER LIX
THROMBO-ANGIITIS OBLITERANS INVOLVEMENT OF THE UPPER EXTREMITIES. ... . 294
CHAPTER LX
THROMBO-ANGIITIS OBLITERANS—ASSOCIATED ARTERIOSCLEROSIS . ...... . . 306
CHAPTER LXI
THROMBO-ANGIITIS OBLITERANS—PATHOLOGY . . . . .... . «= 4) 5 eee
CHAPTERSLAII
THROMBO-ANGIITIS OBLITERANS—MorE DETAILED HISTOPATHOLOGY. . .... . . 321
CHAPTER LXIII
THROMBO-ANGIITIS OBLITERANS—PATHOLOGY IN LETHAL CASES ........ . . 368
CHAPTER LXIV
‘THROMBO-ANGIITIS OBLITERANS—DIAGNOSIS 2 3 27% 4. | we)
CHAP TERIUAV
THROMBO-ANGIITIS OBLITERANS—TREATMENT, . 2: . .°. «=. « © + © =) eg
Prophylactic Treatment . . ).. . i 2 ae
Conservative Treatment . . >... ). 3 6 2s 3 4 5
Operative Treatment. . . Joes s «4. 5° Se
The Selection of Therapeutic Procédures. o.: si) sn nie uct >. 384
CHAPTER LXVI
ATHERO- OR ARTERIOSCLEROTIC DISEASE—CLINICAL MANIFESTATIONS . . . . . . . 385
CHAPTER LXVIL
ARTERIOSCLEROSIS—=PATHOLOGY «© ic” © he ips eo ere ee) een
CHAPTER, LXVIII
ARTERIOSCLEROSIS—MINUTE PATHOLOGY. | . . 4%. 2s 2s > » 2 ee eee
CONTENTS
CHAPTER LXIX
ARTERIOSCLEROSIS WITH THROMBOSIS—CLINICAL COURSE .
CHAPTER LXX
ARTERIOSCLEROTIC GANGRENE WITH DIABETES ......
CHAPTER LXXI
ARTERIOSCLEROSIS—DIAGNOSIS .......
ARTERIOSCLEROSIS—PROGNOSIS ........
CHAPTER LXXIII
ARTERIOSCLEROSIS—TREATMENT. .......
CHAP TERS EXECLV
MISCELLANEOUS AFFECTIONS OF THE ARTERIES. . .
CHAPTER LXXV
HYPERTROPHY OF I1HE ARTERIES... .
CHAPTER LXXVI
ACUTE ARTERITIS .
CHAPTER LXXVII
TUBERCULOSIS OF THE ARTERIES .... .
CHAPTER LXXVIII
SYPHILITIC ARTERITIS AND GANGRENE ...... .
CHAPTER LXXIX
PERIARTERITIS NODOSA. ......
CHAPTER EXecky
- SYPHILITIC DISEASE OF THE VEINS .
CHAPTEROLXXXE
MIGRATING PHLEBITIS—MISCELLANEOUS VARIETIES .
CHAPTER LXXXII
VASCULAR OCCLUSION OF DOUBTFUL ORIGIN. .......
CHAPTER EXCITE
MAL PERFORANT .
CHAPTER LXXXIV
EMBOLISM AND THROMBOSIS. .. . . ’
Arterial Obturation without Immediate Symptoms .
Embolic and Thrombotic Gangrene after Infectious Diseases
CHAPTER LXXXV
EMBoLic GANGRENE—(CONTINUED) ......
Embolic Gangrene with Cardiac Disease. ae
Post-operative Embolic or Thrombotic Gangrene . .
Thrombotic Gangrene in Healthy or but Slightly Diseased Vessels
CHAPTER LXXXVI
THE VASOMOTOR AND TROPHIC NEUROSES—GENERAL CONSIDERATIONS
Xl
PAGE
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. 456
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. 470
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. 481
. 485
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. 489
. 490
- 499
xll CONTENTS
CHAPTER LXXXVII
THE SKIN AND THE VEGETATIVE NERVOUS SYSTEM .
CHAPTER LXXXVIII
DIAGNOSIS AND LOCALIZATION OF VEGETATIVE NERVE LESIONS .
CHAPTER LXXXIX
VASOMOTOR AND TROPHIC DISTURBANCES IN LESIONS OF THE CENTRAL NERVOUS
3.) 2) 3 Lee eee Seis
SYSTR Maa ee Cee
GHAP TER XG
NEUROTROPHIC DISORDERS IN SPINA BIFIDA. ........
CHAP BE RA OOCl
VASOMOTOR AND TROPHIC DISORDERS IN PERIPHERAL NERVE LESIONS
CHAPTER XCII
NEUROSES AND THE PERIARTERIAL SYMPATHETIC NERVES
CHAPTER XCIII
TRAUMATIC VASOMOTOR SPASM . .
CHAPTER XCIV
LOCAL SSHOCK aes a eee
CHAPTER XGV
CHRONIC ACROASPHYXIA . ee eee a est |!
CHAPTER XCVI
ERYTHROMELALGIA. . i... .
CHAP EE Rex Cyt
THE vACROPARESTHESL® Ga 8e ee ;
CHAPTER XCVIII
GANGRENE WITHOUT ORGANIC VASCULAR DISEASE. ... .
CHABTER XCIX
RAYNAUD St DISRASI etme unr elem i SAE es
CHAPTER ’C
SCLERODERMA. . . hs oe ae oh Pe
CHAPTER? CI
MUvLTIPLE NEUROTIC GANGRENE . ee: «.
CHAPTER CI
VASOMOTOR INSTABILITY ...... Abe Se ate, ORs gee
CHAPTER Cit
ATYPICAL VASOMOTOR NEUROSES . . . Shan me
CHAP TE RRG Ly
CLINICALLY BORDERLINE CASES. . Ft ae
CHAPTERIGY,
TREATMENT OF VASOMOTOR NEUROSES.
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0 wel 5 tr ie: | ane ae
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CONTENTS xii
PAGE
CHAPTER CVI
CAPILLARY MICROSCOPY . SE Lata te ae 584
CHAP DER: GVIE
PeariLeaRy MICROSCOPY IN:THE VASOMOTOR NEUROSES . ... .*: . = « «+ « 590
CHAPTER CVIII
CAPILLARY MICROSCOPY IN SPECIAL FORMS OF VASOMOTOR DISEASE ..... . . 5098
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PME SUBJECTS ; . ... « .« eee ae een eer, Se De epee et ae. +38". OOO
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THE CIRCULATORY AFFECTIONS OF THE
EXTREMITIES INCLUDING GANGRENE,
VASOMOTOR AND TROPHIC
DISORDERS
CHAPTER I
INTRODUCTION
The subject of the vascular affections and gangrene of the extremities
will receive consideration together, because of the intimate and inseparable
clinical bonds that link these affections together. It is by virtue of the multi-
plicity of causal modalities that may bring forth similar or identical phe-
nomena, and through the overlapping of manifestations of varied origin, that
intricate clinical complexes are produced. We know that gangrene may be
the issue of wholly different pathologic processes resulting from the action of
direct or indirect mechanical, thermal, and chemical agencies, and a variety
of organic vascular disorders as well as through almost inexplicable neuro-
genic derangements. Many of the prodromal phenomena of diseases of
wholly diverse genesis may so closely resemble each other as to produce
perplexing and clinically confusing pictures. It is because of these facts,
that a discussion of the ultimate and most destructive lesions of
- varied motivation must needs be considered in connection with, and in rela-
tion to all others that may, even though only occasionally, bring about a
similar issue. Only through such a grouping and comparative study
can the clinician obtain a correct appreciation, either of the origin of the
phenomena themselves, or of the proper classification and recognition of the
diseases in question.
We need but pause for a moment to reflect on the intricacy of that maze
of factors upon which the clinical features of vascular disturbances depend, to
realize that not only is a knowledge of the modus operandi of each and of
every one of them essential, but a critical balanced judgment is necessary for
purposes of clinical diagnosis. Whilst for the recognition of a valvular
lesion or an area of pulmonary consolidation, relatively few fundamental
anatomic, acoustic and pathologic facts are necessary, the conditions upon
which the manifestations of organic vascular and vasomotor disease of the
extremities depend, are exceedingly complex. Even with a thorough knowl-
edge of the distribution of the vessels, their gross and minute morphology,
their réles as dispensers of blood, their means of substituting by-paths
through existing anastomoses; and even with a thorough acquaintance with
the pumping mechanism, we are not thoroughly equipped for a compre-
hensive, critical and analytical approach to the subject. Although the
1
a
2 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
physiologists of the past have given us an abundance of conclusions, these
have been modified and amplified by recent investigators, yielding a multi-
tude of facts. A thorough comprehension of these is a prerequisite for cor-
rect explanation of the many varied clinical manifestations.
Whilst it is relatively easy to arrive at a clear concept of the objective
effects of mechanical and hydrostatic forces, the heart action, the patency of
the vascular channels, and the abridgement or intensification of these forces
through gravity action, there are still others of imponderable nature that are
clinically known to be at work, and that have been experimentally proven
capable of exerting an influence. Let us recall merely a few of these. The
vasomotor mechanism with its reflex play of function, its dependency on
external circumstances and even on emotional states, is capable of evoking
clinical pictures of obscure nature; even more so when the two diverse factors,
the mechanical or hydrostatic and the neurogenic are acting in conjunction,
independently, associated or related, as the case may be. In the light of
recent investigations of inherent capillary activities, a new vascular domain
has loomed up as capable of participating in the clinical vascular complexes.
For not only is the neuromuscular mechanism governing the arterioles and
venules recognized, but to the capillaries is relegated a function of their own
and one susceptible to varied impressions. Whilst the mechanical and hydro-
static factors may find a response in dilatation or constriction of capillaries
when there is pressure, a plenum, or a void; and whilst a certain control
(usually constrictive) of the vegetative system is not denied, local metabolic or
chemical influences may bring forth a functional reply in the form of dilata-
tion of corresponding capillary areas.
We have then in the mechanical, hydrostatic, nervous and autonomic
capillary forces, a combination of patrly passive, partly actively function-
ating links, that may intrude upon the clinical picture and make it complex
and hard to interpret.
The author has, therefore, included in his treatise, not only the vascular
affections that may evoke trophic and destructive tissue changes, but also
those nerve or vasomotor maladies that occasionally or often call forth similar
clinical symptoms.
To properly comprehend all phases of this subject, we believe that our
preparatory knowledge should include a study of the following:
1. The anatomy and histology of the normal vascular apparatus of the
extremities;
2. The anatomy and physiology of the nervous mechanism that controls
the vessels;
3. A consideration of normal and pathological local circulation;
4. A comprehension of the origin and action of thrombosis, of mechanical
and of thermal agencies on the tissues;
5. The subject of gangrene in relation to its clinical diagnostic and patho-
logical aspects; and
6. An exposition of the clinical course of all those diseases of either
organic vascular, neurovascular or vasomotor causation, that have, and still
do give the physician much difficulty in clinical differentiation.
Although all of these topics will be discussed, their clinical, pathological
and diagnostic phases will receive the more comprehensive consideration.
ANATOMICAL CONSIDERATIONS 3
CHAP EERe LI
ANATOMICAL CONSIDERATIONS
In applying anatomical data to the interpretation of the circulatory affec-
tions of the extremities, the course, distribution, and anastomoses of the
vessels interest us from certain special angles. What may be germane to the
fundamental hypotheses and observations of the anatomist and embryologist,
is of importance only in an elementary way. For a clarification of our con-
cepts of the organic and neurogenic vascular maladies, we are more particu-
larly concerned with the following phases of the anatomy.
1. The topographical relations of the vessels to the body surface; and
2. The normal anastomoses, and therewith the foundation for collateral
blood supply.
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Fic. 1.—Course of the axillary artery and its branches. (Sobotia)
Diagnosis of the circulatory affections of the arteries of the extremities
will be greatly facilitated through an accurate knowledge of the surface
topography of the important arterial trunks supplying the peripheral parts.
In order to refresh the student’s memory, the essential facts necessary for
the recognition of obliterated peripheral pulses will be given here. Whilst
it may be easy to diagnosticate the exact points of blockage of the axillary or
brachial artery by palpation alone, the patency of the larger arteries of the
4 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
lower extremities may be indeterminable by reason of their inaccessibility to
the examining finger.
The Axillary Artery (A. Avxillaris) (Fig. 1).—This is a continuation of
the subclavian in its course through the axillary space. Beginning at the
lower border of the first rib, in the apex of the axillary space, it courses along
the outer wall of the space to the lower border of the teres major, where it
is known as the brachial artery.
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Fic. 2.—Course of the brachial artery. (Sobotta)
A line drawn from the middle of the clavicle to a point mid-way between
the two condyles at the humerus with the arm abducted at right angles indi-
cates its course. It may be digitally compressed in its lower or third portion
(below the pectoralis minor) against the humerus just within the edge of the
ANATOMICAL CONSIDERATIONS 5
coraco-brachialis and biceps. The pulsation of the axillary artery is not
usually visible. In very thin individuals and in some persons after exertion
especially if arteriosclerotic, the pulse may become evident with the arm lifted
vertically. Palpation along the coraco-brachialis muscle in the lower part of
its course just under the pectoralis minor will usually reveal the pulsation.
The axillary vein occupies a more superficial position and is situated toward the ulnar
(posterior) side, being neither visible nor palpable under normal conditions.
The brachial artery (Fig. 2) is a prolongation of the axillary, beginning
at the lower border of the teres major, and terminating just below the bend
of the elbow where it divides into the radial and ulnar arteries. Above,
the vessel passes along the inner side of the arm, but lower down it is deflected
somewhat outward, so that in its lower part it is on the anterior surface of
the brachium.
A line drawn from the junction of the outer and middle thirds of the folds
of the axilla when continued to a point mid-way between the condyles of
the humerus, indicates its course. In its upper two-thirds it can be felt easily
and compressed against the inner side of the humerus in an outward and
slightly internal direction along the internal border of the coraco-brachialis
and biceps. It may pass either just along the border of this muscle or be
overlapped by the inner edge of the biceps. At the middle of the arm it
is also easily palpated and compressed. In the lowest third if pressure is
applied backwards, it will direct it against the brachialis anticus as the latter
lies over (in front of) the humerus.
For diagnostic purposes it should be remembered that the palpating
finger should be directed laterally against the humerus, along the inner border
of the biceps, whilst above the elbow the palpating finger must be directed
backward.
With the forearm flexed at right angles and with the biceps relaxed the
brachial pulse can be traced downward to within a short distance above the
bend of the elbow, where compression backwards against the brachialis
anticus will usually allow the plantar aspect of the fingers to detect the artery.
In finding it, slight lateral displacement of the mesial border of the biceps
with the tips of the palpating fingers may be necessary.
The Radial and Ulnar Arteries.—The point of bifurcation of the radial
and ulnar arteries is usually so deeply situated that it is difficult to palpate
the pulses in this situation, and therefore an imperceptible beat is of little
clinical value.
The ulnar artery arises just below the bend of the elbow and passes first distally and
inward beneath the muscles which arise from the internal condyle of the humerus and at
the junction of the upper and middle thirds of the forearm, taking a more vertical direction.
At the wrist it passes over the anterior annular ligament to the radial side of the pisiform
bone and then courses across the palmar surface of the hand forming the superficial palmar
arch. Three parts have been described, an antibrachial portion extending to the upper
border of the anterior annular ligament; a carpal portion resting on the annular ligament;
and lastly, the palmar portion.
The lowermost portion of the antibrachial course of the ulnar artery as it
lies on the flexor profundus digitorum with the tendon of the flexor sublimus
digitorum toward the radial side is usually the site of an ulnar pulsation.
Anomalies, however, occur that account for absence of pulsation in this region, such as
those instances in which the ulnar artery is represented only by muscular branches, the
vessel being substituted by a persistent median or interosseous artery. On the other
hand the ulnar artery may be more superficial, passing down the forearm over, instead of
under, the muscles arising from the internal condyle. Such a course may also be followed
6 CIRCULATORY \AFFEGTIONS OF THE EXTREMITIES
when the artery has a normal origin, and occasionally it passes to the ulnar border of the
forearm between the palmaris longus and the flexor sublimus digitorum (Cunningham).
The radial artery is also only palpable in its lower part between the tendon
of the brachio-radialis and that of the flexor carpi radialis. Here it is very
superficial, and on dissection is brought into view as soon as the fascia is
divided.
The usual radial pulse may be absent when the artery passes to the dorsal
surface of the arm much higher up than usual, and in such cases the super-
Lp revesis SEH Lend 29.5918
ES ULES
Biceps LEHIOGITS
Fic. 3.—The popliteal space, with the popliteal vessels. (Sobotia)
ficial volar branch also has its origin at a higher level, and passes downward
to the usual situation of the radial. In such instances it is represented by a
very slender vessel, may give a very small pulse and be erroneously inter-
preted as indicating diminished pulsation in a radial artery.
The femoral artery is best felt just below the interior edge of Poupart’s
ligament, where the vessel can be compressed against the brim of the pelvis,
just outside of the ilio-pectineal eminence. Somewhat below this it is
separated from the femur by more muscle. At the apex of Scarpa’s triangle
it is more difficult to palpate, and the direction of pressure must be outward
and somewhat backward in order to displace it against the femur. In the
most accessible portion of its course just below Poupart’s ligament, only slight
ANATOMICAL CONSIDERATIONS fs
pressure of the finger is necessary to elicit a femoral pulse. As the pulse is
traced downward, however, when a point 3 or 4 finger breadths lower is
reached, more pressure is required for its detection. The normal femoral
vein is neither palpable nor visible.
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Fics. 4 and 5.—Popliteal vessels and their branches at the knee posteriorly and in the leg
(Sobotta)
The popliteal artery (Fig. 3) should be palpated with the patient lying in
a prone position,! and with the leg flexed, but relaxed at right angles. Its
UDG pels se
8 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
course through the popliteal space must be remembered; its relations being
internal to the internal popliteal nerve, and with the vein external and behind
(that is, nearer the surface of the popliteal space). The popliteal artery is a
continuation of the femoral, extending from the termination of the latter
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Fics. 6 and 7.—On the left the popliteal artery dividing into the anterior and the; pos-
terior tibials, giving off peroneal artery, on the right the course of the anterior tibial
artery. (Sobotta)
at the adductor magnus, to the lower border of the popliteus muscle, divid-
ing there into the anterior and posterior tibial arteries.
Where it is not possible to palpate the arteries in stout individuals, a
popliteal pulsation can be occasionally demonstrated as follows: the limb on
ANATOMICAL CONSIDERATIONS 9
the side to be examined is allowed to hang over the other in such a manner
that the popliteal space is supported by the patella of the other leg. Then
the tip of the foot of the superimposed limb may show a transmitted motion
synchronous with the beat of the compressed artery.
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Fic. 8.—Course of the dorsalis pedis artery and its branches. (Sobotta)
A reference to Fig. 3 will demonstrate the relation of the popliteal artery
as it takes an almost vertical direction through the popliteal space, the vein
and nerve. It should be palpated just as it emerges from under the semi-
membranosus muscle in the upper part of the rhomboid.
The posterior tibial artery (Figs. 4, 5 and 6) is a continuation of the
popliteal, beginning at the bifurcation of the latter at the lower border of
10 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
the popliteus muscle and coursing downward to the groove between the
internal malleolus and os calcis, where it divides into the internal and external
plantar arteries.
Except for that small portion that lies immediately above the ankle, it
lies very deep, being separated from the tibia by the muscles of the calf.
Pulsation is perceptible only in its lower portion at the inner side of the ankle,
where it lies under the deep fascia between the flexor longus digitorum and
tibialis posticus tendon behind the internal malleolus. The artery can often
be seen to beat between the internal malleolus of the tibia, and the mesial
margin of the Achilles tendon.
The anterior tibial artery (Fig. 7) constitutes the other branch of the
popliteal, beginning at the lower border of the popliteus muscle, passing
directly forward between the tibia and fibula, over the upper border of the
interosseous membrane. Thenit liesin front of the latter, coursing downward
to the ankle joint where it becomes the dorsalis pedis artery.
It is inaccessible to palpation except in its lowermost portion, where
occasionally pulsation can be felt. Just lateral to the external border of
the extensor propreus hallucis as the latter crosses the vessel obliquely, and
between this and the extensor longus digitorum it becomes more superficial.
Here and below this point, with the foot flexed and the extensors relaxed,
some 2 inches or more of the artery frequently give a distinctly perceptible
pulsation. This pulse, however, is not a constant phenomenon and for clini-
cal purposes the beat inthe dorsalis pedis is of much greater diagnostic
significance.
The dorsalis pedis artery is a continuation of the anterior tibial artery
downward to the proximal portion of the first intermetatarsal space (Fig. 8).
The artery lies just lateral to the extensor longus hallucis tendon between the latter and
the mesial portion of the extensor digitorum, but closer to the former. ‘The artery is best
palpated in the region of the proximal portion of the first intermetatarsal space just lateral
to the tendon of the extensor longus hallucis. If we employ the plantar aspect of the
tips of 3 or 4 fingers and allow these to palpate along a line projected vertically upwards
from the interspace between the great and second toes along the lateral margin of the
extensor longus hallucis tendon, the normal pulsating artery will rarely escape the finger
as it lies over the middle cuneiform bone. Not infrequently, particularly in moderately
arteriosclerotic individuals, a visible pulse can be detected.
The Normal Anastomoses.—From a study of these, conclusions may be
drawn as to the possible functional responses through existing channels,
whenever one of the following modes of impediment obtain; namely, limited
vascular blockage (embolic), ascending or centrally directed obturation,
embolic closure with ascending and descending blockage (progressive throm-
boses), and localized or diffuse coarctation of the vascular lumina (athero-
sclerosis, endarteritis obliterans).
A more complete exposition of this subject will be found in the chapter
dealing with Collateral Circulation (Chap. XII) and the diagnostic signifi-
cance of the anastomoses will be dealt with in the discussions of the various
arterial diseases.
THE MINUTE STRUCTURE OF THE VESSELS 11
CHAPTER III
THE MINUTE STRUCTURE OF THE VESSELS
THE CAPILLARIES
Simple endothelial tubes or capillaries consist of cells or elongated lanceo-
late plates with oval nuclei united by narrow lines of cement substance.
Traced from the arteriole there is a gradual transition, the beginning of the
capillaries being recognized by the final disappearance of nuclei cells. By
virtue of a network of such channels distributed throughout the tissues,
there is provided an excellent mode of insuring the passage of the blood in
intimate contact with the tissue elements.
A nerve distribution along and surrounding them has been recognized; and
while contacts between these fiber-endings and the endothelial cells have not
as yet been brought to light, it is fair to assume that such junctions do indeed
occur. A direct nerve supply can, therefore, be predicated for the vascular
capillaries.
The endothelial layer of cells which constitutes the capillary when con-
tinued into the arteries and veins, forms the innermost layer of the intima
lining these vessels. Tissue structures which differentiate the vascular areas
are laid down upon this endothelium. The essential difference between the
larger arteries and veins is found in the relative thickness of their walls. In
the arteries smooth muscle predominates. In the veins, although a suff-
ciency of smooth muscle exists, there is a preponderance of white and yellow
elastic tissue and the walls are not as thick.
Recent researches by Vimtrup (1922) have confirmed the existence of
the contractile cells first found by Rouget (1873) in the walls of the capil-
laries. Mayer had described similar cells subsequently (1902), although
his observations were accorded little credence.
Investigations of the activity of the capillaries of the frog’s tongue (Vim-
trup) led to the histologic demonstration of a meshwork of contractile cells.
With suitable fixation and staining methods certain nuclei distinctly differ-
ent from ordinary endothelial nuclei were discovered.
Krogh states that the form of these nuclei varies with the state of contraction of the
capillary. Ona dilated capillary they are broad and very thin; by contraction they become
narrower and thicker, their cross-section approaching the form of a circle. The proto-
plasm belonging to these nuclei can be made visible by suitable staining, but even then it
requires high-power immersion. lenses and—especially on dilated capillaries—a good
light, preferably excentric, to see it in its entirety.
On a dilated capillary the protoplasm surrounds the nucleus as a continuous layer
on the capillary wall, but it diminishes in thickness towards the periphery, which is very
irregular and sends out a number of very fine branches along and especially around the
capillary wall. The branches show at their base a definitely triangular cross-section, but
soon become flat. Sometimes they become broader and divide, but the ends are always
very thin and pointed. Most of the branches lie athwart the capillary and are of such
length that they reach those from the other side. Some of the branches, however, run
along the capillary, and both the protoplasm and the nucleus are, as a rule, stretched in
this direction.
There can be no doubt that the richly ramified muscle cells on the capillary wall are
the same as those originally found by Rouget in the hyaloid membrane.
The above data warrant the conclusion (Krogh) that the capillary walls,
too, consist of an endothelial tube and external muscular coat; and that
the essential difference between capillaries and larger vessels is to be found
in the arrangement of the muscle. In the former the musculature is repre-
12 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
sented by a wide-meshed network through which the greater part of the
endothelium is free to transfer substances with a minimum of resistance;
whereas in the larger arteries and veins a continuous layer of muscle is
present. Even the muscular coat of the capillaries has a definite tonus
subject to nervous, hormonal and other influences.
THE ARTERIOLES AND VENULES
The arterioles are situated between the arteries proper and the capillaries,
and between the capillaries and the veins proper lie the venules. Some
authors distinguish between an arterial and a venous capillary. Although
structurally alike, one may differentiate these on a functional basis. Capil-
laries vary in size, but they are structurally uniform in character. The terms
“arterial” and “‘venous”’ in this connection imply a change in character of
the contained blood. No distinct point in the capillary net can be recognized
at which such a change occurs.
SMOOTH MUSCLE CELLS
VENULE 7
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Fic. 9.—Schematic representation of the relation of the muscle cells and connective tissue
about the arterioles and venules. (Hooker and Sabin)
Towards the periphery and along the arteries, there is a gradual decrease
in the size of the lumen and in the thickness of the vessel wall. This attenu-
ation goes hand in hand with the diminution in connective tissue elements.
The smallest arteries are composed of an endothelial lining (intima), a layer
of connective tissue fibers and a layer of muscle fibers. In the arteriole
there occurs an elimination of the connective tissue layer between the endo-
thelium and the muscle fibers. The arteriole is, therefore, made up of muscle
and endothelium alone. ‘Towards the periphery, the arterioles subdivide and
become diminutive; with this, the muscular layer is attenuated gradually
until but the simple endothelial capillary tube is left.
The capillaries in their turn give way to the venules, a transition that is
accomplished by the addition of a connective tissue layer. This antedates
the inclusion of muscle fibers. Thus there is a sharp structural contrast
between the arteriole and the venule. The arteriole is characterized by the
muscle substance intimately overlying the endothelial tube, while the venule
exhibits connective tissue in the same situation (Sabin).
This morphologic distinction is depicted in Fig. 9 where the differential
structural disposition of muscle cells about the arterioles, and of connective
tissue on the venules is evident.
THE MINUTE STRUCTURE OF THE VESSELS 13
THE ARTERIES
Arteries of medium size offer rather typical pictures in exemplification of
the muscular variety and may be briefly described here.
In cross section the intima has a folded appearance directly applied to the
plication of the internal elastic membrane. The latter presents a striking
corrugated line marking the external limit of the inner coat. The endothelial
cells are so thin that they are recognizable mainly as projecting nuclei. But
between the endothelium and the elastic membrane there is a fine layer of
connective tissue and elastic fibrils.
The media is composed of circularly distributed muscle fibers interspersed
with elastic tissue plates, whose presence can be intensified and brought to
view by appropriate elastic tissue stains. The external elastic membrane,
the middle and external tunics, are separated by a distinct layer.
The adventitia is of varying thickness and is relatively larger in
the medium sized arteries than in the larger ones. It is composed of fibrous
tissue and elastic fibers, contains the vaso-vasorum, and main lymph channels
of the vessel wall.
The Structure of the Arteries in Embryonal Development.—Two types of
arteries have been distinguished, the elastic and the muscular types. Of the
| Med.
End.
Fic. 10.—Transverse section of the aorta of an embryo (about the middle of embryonal
life); numerous elastic fibers in the media; none in the adventitia. (Aschoff)
former the aorta is an example, of the latter, the arteries of the extremities—
such as the brachial. For a correct understanding of what is normal and
what constitutes atherosclerotic or arteriosclerotic change, the normal alter-
ations in the arteries through embryonal life and during the first 2 or 3 months
of extrauterine life must be borne in mind.
About the fourth month in both types of vessels differentiation in the
intima, media and adventitia occurs, with simultaneous development of
muscle fibers, elastic tissue and fibrillar connective tissue.
The Elastic Type—The aorta (Fig. 10) as an example, in the fourth
month of the embryo presents an intima made up of endothelium, a rela-
tively broad elastica interna with rather regular folds. ‘The media includes
about ten rows of nuclei, containing numerous elastic lamellae interspersed
14 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
between these. ‘Towards the adventitia these are absent, although no
distinct membrane demarcating the boundary can be discerned. Here the
adventitia is broader than the media, and made up of connective tissue.
SELint
Fic. 11.—Transverse section of the aorta of an embryo taken at the end of embryonal life,
(Aschoff)
Fic. 12.—Section of the brachial artery of an embryo taken at the end of embryonal life.
(A schoff )
The muscular type of artery, as the brachial at 6 months, has a well
developed endothelial layer and elastica interna. The media contains
muscle cells arranged in a more orderly fashion with a very few interspersed
~~
THE MINUTE STRUCTURE OF THE VESSELS 15
elastic fibers. The adventitia and the media are distinctly separated
through an elastic membrane. The adventitia is different being char-
acterized by the appearance of two laminae, the inner one disposed longi-
tudinally, the external more or less circularly and irregularly. Further-
more, longitudinally coursing elastic fibers in the inner portion of the adventi-
tia appear at this stage in a rather characteristic fashion, for such a layer is
absent in the elastic type of vessel.
_ The Arteries Shortly before Birth.—Late in the embryonal stage the
differences between the muscular and elastic types are more striking. In
the aorta, besides the general enlargement, the absence of plication is a
feature. In the media the marked development of the elastic membrane is
prominent, the muscle cells being relatively few in number. The elastica
externa is here also absent. The adventitia becomes relatively narrow,
being made up of connective tissue without elastic elements (Fig. 11).
In the brachial artery (muscular type) the internal elastic membrane
becomes thicker, being regularly folded on section (Fig. 12). In the media
the muscle cells are prominent in number and spindle shaped, particularly in
the outer layers. The elastic fibers have multiplied in the media, although not
so intensively as in the musculature. In the adventitia, however, the elastic
fibers have hypertrophied and are disposed in a longitudinal direction, being
in far greater abundance here than in the media. The separation from the
media through the elastica externa here, too, is noteworthy.
In short, the differences in and during the embryonal development of the
two types of vessels are: The appearance here and there of connective tissue
layers in the intima of the vessels of the elastic type with marked development
of the elastic membrane; in the arteries of the muscular type, the media and
musculature are prominent, as are also the elastica externa and the longi-
tudinal elastic fibers of the adventitia. |
The Arteries in Extrauterine Development. The Elastic Type—Three
layers in the intima have been described in the elastic arteries of children!
(Fig. 13). On cross section the elastica interna is seen to be split into two
or three lamellae, that frequently reunite. Here and there, are interrup-
tions that probably indicate openings in the lamellae. Adjacent and on
the inner side are numerous longitudinal elastic fibers, including a similar
distribution of cells. Then there is a circular layer of elastic fibers and
finally an innermost delicate layer of connective tissue, upon which the
endothelial cells are deposited. Jores has called that layer, which lies
against the elastica interna, an elastic muscular layer, the next one of hyper-
plastic thickening of the intima, and the innermost, the connective tissue
layer.
The growth and development of the musculo-elastic (as well as the hyper-
plastic layers) attain their maximum at the climax of bodily development,
namely between the twenty-fifth and thirtieth years. The connective tissue
coat develops more tardily, possibly after the thirtieth year. These three
layers may attain considerable thickness at an age when morbid changes in
the vascular system are not as yet to be expected. It is only when the hyper-
plasia becomes extensive (especially of the connective tissue coat) that the
so-called sclerotic process is said to begin.
For our studies of the peripheral circulation we are concerned especially
with the following type.
The Muscular Type.—Characteristic for these arteries in their further
development, is the relative marked hypertrophy of the muscular layer
1 Aschoff, Description given as applying to ages of 1-4 years.
16 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fic. 13.—Cross section of the aorta of a child 3 years of age; in the intima three layers;
the external cut transversely being a musculo-elastic longitudinal layer; the middle portion
a hypertrophic elastic layer; the innermost one of very delicate connective tissue belonging
to the normal period of growth. (Aschoff)
Fic. 14.—Cross section of the radial artery at the climax of its development (third
decade); slight development of a hypertrophic elastic coat in the intima, belonging to the
normal period of growth. (Aschoff)
THE MINUTE STRUCTURE OF THE VESSELS 17
Fic. 15.—Normal posterior tibial artery and vein in cross section. Here there is but the
slightest degree of thickening of the intima in places.
oe
Fic. 16.—Normal posterior tibial artery; muscular type (high power). _
18 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
(Fig. 14). As far as the adventitia is concerned, it is believed that the longi-
tudinal elastic fibers undergo a marked increase during the early years.. On
the other hand the inner elastic layers do not develop that marked differen-
tiation and increase that are noticeable in the larger arteries of the elastic
type (the aorta and carotid). The hyperplastic intimal layer may be slight
in extent, but the musculo-elastic longitudinal layer is absent or but little
marked. In the adventitia, on the other hand, the elastic fibers are
exceedingly prominent.
Fic. 17.—A, Elastic tissue stain of a normal (posterior tibial) artery showing early
thickening of the intima (possibly early arteriosclerotic thickening) with reduplication
of the intimal elastic fibers; IEL, internal elastic lamina; M, muscular coat (media);
A, adventitia; P, perivascular fatty connective tissue.
Figs. 15 and 16 illustrate a “normal” posterior tibial artery and vein.
For purposes of orientation and comparison with the lesions to be described
in later chapters, it may be well to point out the following characteristics;
the adventitia is narrow and loosely bound with the surrounding connective
tissue as well as with accompanying veins; the circular muscular layer is
relatively well developed (media) and evidences great dearth of vascular
elements; the intima is narrow except in those zones of slight thickening that
may be regarded as within the normal, or insufficient to be designated as
arteriosclerotic. Thickening of the intima within the physiological limits is
depicted in Fig. 17.
A somewhat more marked example of the effects of hydrostatic and
mechanical (perhaps also toxic) stresses on the development of the periph-
eral arteries is depicted in the sections taken from the dorsalis pedis artery
of an adult. In Fig. 18 we have an excellent illustration of the relation of
the artery to the veins, the absence of vascularization of adventitia and media
so characteristic of the normal. In the discussion of the inflammatory
THE MINUTE STRUCTURE OF THE VESSELS 19
diseases of the arteries (arteritis, periarteritis and thrombo-angiitis, etc.) and
of the intravascular thrombotic processes, it will be seen how penetration of
these coats with new formed vessels may occur; and how in some of them, the
Eee and the relation of the artery to its accompanying veins becomes
altered
In the section of the artery, too, when seen under greater magnification
(Fi ig. 19), the hypertrophy of the middle coat is in evidence. Slight prolifer-
ative changes in the intima, also, mark the transition of a normal artery into
the early stages of arteriosclerosis.
Fic. 18.—Low power transverse section of almost normal dorsalis pedis artery and veins,
showing slight hypertrophy of the media and beginning thickening of the intima; the avas-
cular condition of the media and adventitia are well shown, and the loose connection
’ between artery and veins.
The Senile Changes in the Arteries.—Aschoff, Marchand, Jores and
others point out that the first senile changes are the hypertrophy of the
musculo-elastic longitudinal layers of the intima (Fig. 20). There is no
sharp differentiation between the antecedent normal development and the
subsequent pathological thickening. It is only the proliferating connective
tissue that signalizes a distinct senile change. This connective tissue is
deposited between the elastic fibers of the hyperplastic layer, occupying
there a dominant position. Besides, it is laid down as a strong connective
tissue lamella upon the old intima. It is often difficult to differentiate
between normal physiological thickening and senile sclerosis. In the aorta
20 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
and larger vessels there is usually associated fatty degeneration. Jores
believes that this process begins in the outermost layers of the intima, that
is, in the musculo-elastic longitudinal coat (Fig. 21). Later fatty degenera-
tion and calcification may take place; and coincidentally or subsequently
reactive and degenerative processes in the new-formed intimal layers, with
thrombotic deposits in the lumen and organization.
fa eae
Fic. 19.—Cross section of slightly hypertrophic dorsalis pedis artery showing slight
intima hypertrophy. The intima is somewhat thicker than normal, but avascular; adven-
titia normal (higher magnification of Fig. 18).
In the elastic type of arteries (aorta) the changes in the media are less
intensive. Atrophy does occur and elastic lamellae and muscle fibers dis-
appear. Although microscopically evidenced, the macroscopic destruction
of the media is relatively slight. Streak-like areas of fatty degeneration in
the middle coat and very fine lime deposits do appear.
In the arteries of the extremities (muscular type) the change in the media
and the calcification are noteworthy, and preponderate over the initimal
changes. When the arteries of this type in the extremities undergo calcific
THE MINUTE STRUCTURE OF THE VESSELS 21
alterations, the earlier manifestations thereof will be represented by fatty
degeneration especially pronounced in the media; the lime deposits follow
(Fig. 22). Bone formation as a sequel is not uncommon.
Fic. 20.—Cross section of the aorta at the time of complete development (third decade) ;
in the intima still distinct division into three layers, but with hypertrophy of the connective
tissue. (Aschoff)
The intimal lesions in the peripheral vessels are also of importance and
are essentially represented by the endarterial thickening through connective
tissue proliferation. Fatty degeneration is not so characteristic here.
According to Ménckeberg the changes in the media of the arteries of the
extremities preponderate numerically over those in the intima.
Fic. 21.—Transverse section of the aorta with beginning atherosclerosis at the end of
the fourth decade; marked connective tissue hypertrophy and fatty degeneration of all
three parts of the intima. White areas are those of fatty degeneration. (Aschoff)
The Development of the Arteries and Their Subsequent Pathological
Changes.—It is rather interesting to observe that those elements of the
arteries that exhibit their most profound development late in embryonal
life, and in the early years of extrauterine growth, also suffer the greatest
pathologic alterations in atherosclerosis. If the latter be regarded as a
disease of deterioration, functional stresses (or overactivity) must’partici-
22 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
pate in the resultant lesions. So in the larger arteries of the elastic type, by
virtue of the arterial pressure and its constant variations and the pulsative
forces, extensive and distensive stresses must needs exert longitudinal and
lateral tension on the elastic element of the intimal tubes. With this comes a
tendency to tearing in the longitudinal, as well as in the circular direction.
Such factors have been regarded as playing an important réle in the conse-
quent pathologic alterations.
Fic. 22.—Transverse section of the femoral artery with beginning arteriosclerosis at the
end of the fourth decade; in the media areas of calcification. (Aschoff)
In explanation of the precocious development of atherosclerosis the ques-
tion has been raised as to what influence toxic elements (e.g. alcohol,
nicotin) may have upon the elastic elements of the arteries; or what rdle
an acquired predisposition on the part of the elastic elements through pre-
vious infectious diseases may play. In the muscular type of vessels the
muscle fibers would necessarily suffer greater strain through the arterial
pulsations and excessive dilatation and contraction. Changes in blood
pressure and in the blood stream too, have been regarded as of importance.
The special demands of overacting musculatures of the extremities; the
functional demands of the peripheral arteries; the increased tension result-
ing from difficulties in the capillary flow; the modifications due to vasomotor
influences—all these are believed to be motivating elements.
CHAPTER IV
THE VASOMOTOR NERVOUS SYSTEM
It is a perplexing but nevertheless an interesting clinical fact that many
of the objective symptoms resulting from organic closure of the larger
arteries and veins of the extremities can be easily confused with manifesta-
tions of altogether different etiologic significance. These are in the main
nutritive and trophic derangements on the one hand, and circulatory and
vasomotor on the other hand. And, therefore, it behooves the clinical
observer to be able to discriminate between atrophies or lesions of the skin,
and other tissues that result from circulatory impairment (purely trophic or
nutritive), and similar alterations due altogether to nerve influences (aes
trophic). And so, too, disturbances in the vasomotor mechanism may cause
THE VASOMOTOR NERVOUS SYSTEM 23
phenomena simulating closely those of hydrostatic and mechanical vascular
origin.
A loose concept obtained by a cursory reading of text books on neurology
concerning neurotic trophic lesions should be supplanted by a systematic and
detailed study of the anatomy and physiology of the sympathetic system,
and what is known concerning the neurotrophic, and neurosecretory paths.
For the sake of completeness, therefore, the salient features of the anatomy
and physiology of this portion of the nervous system are described
in detail.
Course of Vegetative Nerve Fibers.—The cerebrospinal motor fibers that
enter the sympathetic system end in branches about the sympathetic cells,
but never directly in vessel walls or other peripheral localities. Their course
is of varied length, some terminating in the nearest ganglion cells- in the cor-
responding ganglion of the ganglionic cord, others traversing several ganglia;
still others continuing until they reach the most peripherally situated ganglia.
It is most probable that all sympathetic cells are influenced through motor
fibers emanating from the cord; on the other hand, the motor ganglionic
fibers of the sympathetic, never act upon other ganglionic cells. Even
these fibers are of different length ending at points near or far from their
source.
Medullated fibers originate in the central nervous system with their cells
in the gray substance, travel in a cerebral or spinal nerve, or with several of
these in a cord to a sympathetic ganglion. This preganglionic cerebro-
spinal fiber ends in a ganglion in that its dendrites surround the sympathetic
cell in a dense network or in sparser distributions. The sympathetic cell
in many instances sends a non-medullated axis cylinder to the peripheral
tissues (the postganglionic fibers of Langley) where this terminates without
cellular interposition. The central precellular fibers never come into contact
with the peripheral tissues, but influence only the cells of the sympathetic system.
So also, a sympathetic, post-cellular fiber does not connect directly with a
ganglion cell, but is in immediate communication with peripheral tissues,
muscles, glands or intestine. A precellular fiber may traverse one or several
ganglia before terminating.
The vegetative system may be subdivided into subordinate portions
whose origins lie in various segments of the cerebrospinal axis. Five
territories are recognized; first, centers in the corpus striatum; second, in the
mid-brain; third, in the medulla; fourth, in the dorsal region up to the second
and third lumbar segments; and fifth, in the region from the second to the
fourth sacral segments (Fig. 23). The centers in the corpus striatum
more recently recognized are shown in Fig. 24.
The mid-brain, bulbar and sacral systems are not infrequently spoken of
as belonging to the autonomic or parasympathetic system, in contradistinction
to the dorso-lumbar portion, called the sympathetic system.
It has been found that nicotin has a selective action on those ganglion cells in which an
anatomical interruption of continuity takes place, with functional relaying of nerve impulses.
Intravenous injection of nicotin as well as local application on a ganglionic node, cause
transitory excitation followed by paralysis of the ganglion cells that lie in the relay station.
Before nicotinization, stimulation of a fiber of the vegetative system produces a certain
irritative effect, irrespective of whether this excitation takes place before or beyond its
entrance into the ganglion. Nicotin paralyzes the interpolated cell only, as that irrita-
tion of the preganglionic fibers is without effect; but the post-ganglionic fibers will respond
as usual. This action of nicotin is confined to the vegetative system. ‘The nicotin method,
therefore, has been employed experimentally to indentify impulses that belong in the
CIRCULATORY AFFECTIONS OF THE EXTREMITIES
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THE VA SOMOTOR NERVOUS SYSTEM 29
vegetative nervous system. It also permits us to decide as to whether a certain ganglionic
node is an interrupting station for certain nerve fibers.
The sympathetic system, is composed of those spinal centers that lie in
the lateral horns of the spinal cord, of the anterior roots emanating from these
and leading to the ganglionic cord through the rami communicantes albi
(hig. 720).
Certain cells at the point of transition between anterior and posterior horns, sometimes
designated lateral horns or intermedio-lateral tract have been regarded as the site of
origin of the fibers leading to the gangliated cord. Jacobsohn! distinguishes a nucleus
sympatheticus lateralis superior extending from the eighth cervical to the third lumbar seg-
ment, and providing all the sources of the rami communicantes of the gangliated cord. In
the parasympathetic system he describes a nucleus sympatheticus lateralis inferior from the
second sacral segment to the coccygeal; also a nucleus sympatheticus medialis inferior located
in the fourth lumbar segment and fusing with the above in the coccygeal region. All of
these nuclei show interruptions in continuity throughout the various segments.
These rami-are split up about the ganglia lying alongside the vertebral
column. Here, the ganglia and their communicating fibers constitute the
gangliated cord. The gray rami have their source in these ganglia, whence
they course either independently (as in the case of the splanchnic nerve), or
join the spinal nerve. The sympathetic system in a narrow sense is
composed, therefore, of the spinal centers, the rami communicantes, the
vertebral ganglia, the gangliated cord of the sympathetic and the peripheral
sympathetic nerves. The upper limit of this system is the first thoracic nerve,
and, in man, it extends downward, to the second or third lumbar segment.
It is noteworthy that there are no sympathetic fibers arising from the cervical
portion of the cord. In the cervical region, the gangliated cord has 3 ganglia;
in the thoracic 11 to 12; in the lumbar 4 to 5, and in the pelvic 4 to 5 sacral
and a coccygeal ganglion. The afferent fibers passing through the rami
albi to the gangliated cord, arise from widely separated spinalsegments. The
efferent fibers, that is, the post cellular fibers are in rather close proximity,
since in their further course they follow closely the spinal nerves in the imme-
diate vicinity.
The superior cervical ganglion supplies the vessels and part of the
glandular apparatus of the head, and part of the vessels of the brain, the
dilator of the iris and Miiller’s muscle of the orbit. The stellate ganglion sends
fibers to the thoracic viscera, and accelerating fibers to the heart. The rest
of the gangliated cord supplies the muscles of the vessels of the extremities of
the trunk, the muscles and glands of the skin, and the blood vessel muscles
of the intestinal tract, of the lungs and intestines.
The anterior extremities receive their vasomotor fibers through
the anterior roots from the 4th to the 1toth dorsal nerves. According to
Bayliss the vasoconstrictor nerves of the upper extremities leave the spinal
cord in the anterior roots from the ard to the 11th thoracic nerves, whilst
those for the posterior extremities are found in the rith, rath and 13th
thoracic, and rst to 3rd lumbar roots, in animals. The skin of the trunk in
man derives its vasomotor nerves from the anterior roots of the dorsal and
lumbar nerves. The lower extremities receive supply from the anterior roots
of the last three thoracic and upper three lumbar nerves. It was formerly
believed that only arteries received vasomotor fibers. It has been shown
more recently, however, that the veins are also thus supplied.
1 Jacobsohn, Abhandl. d. k. preuss. Akad. d. Wissensch., 1908.
26 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
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Fic. 24.—Reflex connections in the vegetative nervous system. Transference of an
impulse at I into Auerbach’s plexus; II, to the postganglionic sympathetic cell in the para-
vertebral ganglion; III, to the preganglionic sympathetic cell in the cord; IV, to the pre-
ganglionic parasympathetic cell in the medulla; V, to the vegetative cell in the corpus
striatum. (Modified after Dresel)
THE VASOMOTOR NERVOUS SYSTEM 27
Septum pellacidun.
Faber crmen:
Fic. 25.—Schematic drawing of the sympathetic nervous system. The dotted lines
indicate the bulbar and spinal paths.
The preganglionic fibers are seen joining the gray
matter of the cord and the ganglia. The solid lines (to subclavian artery and piloerectors)
indicate postganglionic fibers. (Miiller)
28 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Parasympathetic System.—We need merely to refer to this in a general way
here, and point out to what extent this part of the vegetative nervous
system deals with vasomotor impulses. The parasympathetic system is
composed of the cranial and the sacral autonomic systems. Over the
posterior roots of all of the dorsal and the upper lumbar segments there
travel impulses, which serve to bring about vasodilatation and inhibition of
perspiration in the territory of the trunk and the extremities.
That portion of this system, which is called the cranial autonomic system, does not
concern us here, for its main portions constitute the oculomotor nerve, and ganglion ciliare,
and the vagus. The sacral autonomic system is not involved in the innervation of the
vessels of the extremity, but communicates with the pelvic plexuses, the nervi pelvici, and
innervates the genitals and bladder (nervi erigentes).
But there is one portion of the parasympathetic system, which is said to
furnish vasodilator fibers, and sweat inhibiting paths for the trunks and the
extremities. The dorsal and upper lumbar spinal segments (Miiller) not
only give origin to sympathetic fibers for the vasoconstrictors, for the secre-
tion of sweat and the pilomotors, but antagonistic impulses also travel
herein. The parasympathetic system is included in the posterior roots and
not in the anterior. Our knowledge of its functions, however, is not based
upon morphologic data; relevant histologic imformation is not at hand, nor
has the point of origin of these paths in the gray matter of the spinal cord
been discovered.
Cerebral Vasomotor Centers.—Daily observations teach us that blood
vessels are influenced by psychic states and therefore, by way of the cerebrum.
The pallor of the face after fright, the blush after joy or erotic ideas are
examples.
Cortical cerebral vasomotor centers for the various peripheral nerves were
experimentally sought but without convincing results. Even the vasomotor
disturbances after cerebral lesions, such as hemorrhage and tumors, and the
vasomotor manifestations after cerebral injury are too little characteristic and
uniform to allow of binding conclusions as to localization. ‘There are no
certain data at hand to prove the existence of special vasomotor centers in
the cortex. Ina search for such centers elsewhere in the brain, physiological
experiments have brought to light that vegetative functions may indeed be
influenced from a very small cerebral territory. It is believed that the cere-
bral vasomotor center resides in the mid-brain, in the optic thalamus and in
the gray matter of the third ventricle.
The removal of the cerebrum in a dog is not followed by any permanent functional
vascular derangement. There are, however, localities in other portions of the brain that
may be shown to affect the vasomotor nerves. Studies on hyperthermia have demon-
strated that special modes of stimulating the corpus striatum lead to elevation of tempera-
ture (“‘heat puncture”’ of the German authors). So also, ablation of the anterior and
mid-brain of rabbits destroys the function of heat regulation, while exclusion of the anterior
brain alone is not followed by this result.!_ Karplus and Kreidl demonstrated that a center
for vasomotor innervation lies in the mid-brain, especially in the gray matter of the third
ventricle. Not only are vasomotor phenomena dependent upon psychic changes and
emotion, as manifested by external cutaneous phenomena, but distribution of blood in the
organs of the chest and abdomen is affected thereby. Different parts of the body are not
equally influenced by emotional states. The blood in the extremities seems to be dimin-
ished during intellectual work, with simultaneous increase of the blood content in the brain
and abdominal organs.
! Isensch-Krehl, Arch. f. exper. Path. u. Pharmakol., Bd. 7o.
THE VASOMOTOR NERVOUS SYSTEM 29
Although the general tone of the vessels may be influenced through a
circumscribed area in the third ventricle, it is a mooted question as to whether
all vessel innervation has the same origin. Fluctuations in the tonus are not
dependent on impulses traveling from the spinal cord or cerebral nerves in a
centripetal direction alone. Activities in the neencephalon and excitation
of the ganglion cells of the mid-brain following irritant effects of the blood
itself, may also be effective.
In short, the region of the mid-brain, the optic thalamus, and the gray
matter of the third ventricle, contain a center or centers from which sensory
impulses are transferred to the vasomotor paths. This center admittedly
controls the general tone of vegetative innervation and also the special reac-
tions of the vessels. ‘The fluctuations in tone of the centers are subject to
and related to stimuli from three sources; firstly, through the spinal cord and
centripetal cerebral paths; secondly, through psychic mutations in the cere-
brum; and thirdly, by direct excitation of the ganglion cells in the mid-brain
through special irritants in the blood.
According to Starling there is a small region of the medulla oblongata on each side of the
mid-line in the neighborhood of the facial nuclues, that sends impulses. The normal
impulses travel down the cord as far as the dorsal region, and then pass outward by the
dorsal and upper lumbar nerves. These facts have been adduced from experimental
section of the cord at various levels. A marked fall in blood pressure follows division on
a level with the origin of the rst dorsal nerve. Destruction of the above mentioned area
in the medulla also causes immediate lowering of the blood pressure. These conclusions
are further confirmed by the fact that, whereas stimulation of the anterior roots of the
cervical and lower lumbar and sacral nerves has no influence on blood pressure, a rise of
the latter can be obtained by stimulating any of the anterior roots from the first or second
dorsal to the second or third lumbar.t That portion of the medulla concerned with the
sending out of the tonic vasoconstrictor impulses, is spoken of as the vasomotor center.
Here it is subject to and receives stimuli from all portions of the body, from the higher
centers of the brain and especially from the viscera of the chest and abdomen through the
vagi. And so, the sum of the impulses arriving at the center produces a state of average
continued activity which is responsible for the maintenance of arterial tone and for the
regulation of the arterial blood pressure.
Furthermore, paralysis of the vasomotors of the body, as manifested by dilatation of all
the vessels of the trunk and extremities, follows section through the medulla oblongata or
cervical cord, while this does not occur with an interruption made above the medulla and
just below the corpora quadrigemina. Glaser rather doubts the existence of such a vaso-
motor center; but he is in accord with the view, that the vasomotor innervation travels
through paths from the mid-brain through the medulla. Centers of limited function—
local vasomotor centers—controlling the vessels of the brain, the salivary glands or the
dilators of the facial skin territory, may according to this author reside in the medulla.
A few clinical observations corroborate the physiological deductions
regarding the existence of chief vasomotor centers. A beautiful example of
vasomotor disturbances induced by central lesions is the case of Rossolimo.?
A man 38 years of age had manifestations pointing to a growth in the right motor zone;
namely, clonic contractions of the left side of the body and headaches; the left hand was
cyanotic, edematous, and his temperature diminished. Operation disclosed a cyst, which
was followed by a disappearance of the vasomotor manifestations. From this it was
concluded by the author that the cortical vasomotor center lies near the motor area.
Oppenheim distinguishes a vasomotor form of Jacksonian epilepsy, and a
vasomotor monoplegia, in which there are attacks of vasomotor disturbances
in the arm and face of one side, with or without loss of consciousness, and
1 Starling, E. H., Principles of Human Physiology, Phila., rors.
2 Rossolimo, Deutsch. Ztschr. f. Nervenh., 6, 1895, p. 76.
30 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
persistent vasomotor symptoms in the same territory, with only slight
paresis and atrophy.
So also vasomotor changes with cyanosis are observed with the common
forms of hemiplegia, with edema of the paralyzed side, symptoms that are
not altogether to be explained by lack of function.
Subcortical vasomotor centers have been referred to the optic thalamus.
Little is known regarding vasodilator centers in the human. ‘The cere-
brum doubtless has an activating influence on the dilators, as evidenced in the
vascular changes in the integument of the face.
From the center in the medulla oblongata the conducting paths of the
vasomotor system pass to the lateral tract of the cord. Kocher in his study
of vasomotor palsy after traumatic lesions of the vertebral column and cord,
observed dilatation of the vessels and elevation of temperature of the
paralyzed extremities. Such vasomotor phenomona, however, usually
disappeared. In some cases pallor and diminution in temperature initiated
the symptoms, these being irritative symptoms or evidences of incomplete
paralysis of the vasomotors. Compression of the cord by tumors has been
observed with vasomotor symptoms.
Recent Views on Anatomy.—While the descriptions that have preceded
represent the accepted views prevailing for the last 10 years, a school of
Continental investigators (Kraus, Brugsch and Dresel) has arisen that voices
somewhat different anatomic as well as physiologic concepts.
According to Dresel there is a superior center of the vegetative nervous
system in the corpus striatum. Subordinate to this there is a subthalamic
center in the mid-brain which is in communication with the corpus striatum
through the bundle of Forell and through the tinea lenticularis (‘‘Linsenkern-
schlinge’”’). Nerves pass from the mid-brain to all points of origin of sympa-
thetic and parasympathetic fibers in the mid-brain, medulla, thoraco-lumbar
and sacral segments of the spinal cord. Whilst, according to Langley, only
the thoraco-lumbar cord contains sources of origin for the sympathethic,
and whilst parasympathetic fibers emanate from the other parts of the cord
and medulla, it has been shown more recently that at least in the case of the
dorsal vagus nucleus, both parasympathetic and sympathetic ganglion cells
coexist (Brugsch, Dresel and F. H. Lewy). Furthermore, such a combina-
tion is believed to be possible in other parts of the central nervous system.
These parasympathetic and sympathetic nerves arising from the central nervous system,
course in the following structures; in the ocular motor nerve, the corda tympani, the vagus,
the white rami communicates, the gangliated cord, and in the nervus pelvicus, in the form of
preganglionic, mostly medullated fibers. They pass to a second group of ganglion cells,
namely the ganglion ciliare, ganglion submaxillare, the ganglia of the gangliated cord, the
paravertebral ganglia and in the so-called enteric system. In the latter groups of cells, the
interruption of all vegetative peripheral fibers takes place.
Parasympathetic and sympathetic fibers course as postganglionic fibers to their termi-
nations. Most organs contain both parasympathetic as well as sympathetic fibers.
According to Dresel the so-called enteric system! of Langley (which the latter regarded as
an independent plexus, especially in the heart and in the intestinal tract) should more
properly be included in the total mass of post-ganglionic cells; and this because it has been
shown that these cells signify for the vagus (both anatomically and functionally) the very
same thing that the cells of the ganglionic cord do for the sympathetic. Therefore, the
following scheme has been suggested by this author.?
1 Ganglion cell groups in the walls of viscera.
* This scheme has been obtained through the kindness of K. Dresel (Berlin) in a personal
communication; to be published in Handbuch d. Med. Kraus u. Brugsch., 1922.
THE VASOMOTOR NERVOUS SYSTEM ol
NUCLEI IN CORPUS STRIATUM (VEGETATIVE)
Mid-brain Ue (Vegetative)
|
Parasympathetic nuclei Sympathetic nuclei
qa | |
cranial bulba sacral para- bulb. sympa- thoraco-
parasympathetic sympathetic thetic nucleus lumbar
apcist nuclei symp. nuclei
| | |
|
Preganglionic parasympathetic Preganglionic sympathetic
ers fibers
|
“he Ay 2 | | ;
Ganglionic cells of the post-ganglionic Gangliated cord Paravert. ganglia
parasympathetic fibers (ganglia ciliare
submaxillary, etc., plexus parasympa-
thetic, post-ganglionic myenteric,
enteric pens):
eet
OBESE fibers
|
End-organs
Spinal Vasomotor Centers.—There is no doubt but that there are seg-
mentary centers for vessel innervation in the spinal cord. After a transverse
lesion of the spinal cord, vasomotor responses are possible in the anaesthetic
lower parts of the body. Reflex patchy rubor follows in the cutaneous area
that is irritated with mechanical stimuli, such as needle pricks, provided that
the corresponding spinal cord segment is intact.
Stimuli arising by way of the blood may also excite the spinal vascular
centers. In asphyxia, even after section of the cord, an active vasocon-
striction in the paralyzed part of the body is noted. This response is not
obtainable if the spinal cord is destroyed.
The lateral horns are believed to contain the ganglion cell groups for
vegetative function; and more correctly, in the intermediary zones between
the anterior and posterior horns, where pyramidal or comma shaped ganglion
cells control these functions. The cervical cord contains no such cells up to
its lowermost portion. From the eighth cervical segment up to the lumbar,
we find the lateral sympathetic nucleus. From this region emanate the vaso-
constrictors for the face, the upper extremities, the trunk and the lower
extremities. From the lateral and inferior mesial sympathetic nucleus
that extends from the lowermost part of the lumbar cord into the sacral,
the vascular nerves for the lower part of the intestines and for the inner and
outer genitalia have their origin. The ganglion cells of the intermedio-
lateral tract are aggregated into large groups in the middle and lower sacral
cord. These completely fill the transitional zone between the anterior and
posterior horns. Since the vasomotor nerves for the genitals, namely the
nervus erigens or pelvic nerve arise from this segment, the conclusion is
warranted that these cell groups are related to the vascular innervation of the
sexual organs. It is impossible to differentiate, however, the cells that
influence vascular innervation, and those which control the musculature of
the pilo-erectors or the sweat glands. In syringomyelia and poliomyelitis
vasomotor disturbances occur, such as vascular palsy, and lividity attri-
butable to disease of the gray substance.
32 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Vasomotor Paths in the Spinal Cord.—We still lack proof of the existence
of special paths of conduction for the excitation of the vegetative functions.
Clinical and experimental experiences warrant the conclusion that vasomotor
impulses traversing each half of the spinal cord may arrive at both parts of
the body. This explains the relative paucity of the vasmotor paralytic
symptoms in the Brown-Séquard lesions. It has not as yet been proven that
vasomotor paths course in the lateral tracts. The dominating vasomotor
center in the mid-brain seems to conserve and regulate the general vascular
tone. Perhaps qualitative alterations occur in the centers as the result of
varied influences, and through these manifold reactions of the spinal centers
ensue. It is not even definitely shown that the tonus is dependent upon
the existence of certain paths, and the substantia gelatinosa or even the gray
substance has been suggested as possible vehicle for the impulses. Some
suggest that emotions may cause certain changes in the biotonus or in the
general nervous excitability, because of the varied responses in depressive
and sanguine states.
This tonus which controls the spinal cord is under the influence not only
of the emotions, but also of sensory impulses. Various reflexes in the vegeta-
tive system, such as dilatation of the pupils or contraction of the tunica dartos
follow severe pain impulses. In explanation of these phenomena it has been
pointed out that all sensory paths cannot be in direct communication with all
the vegetative centers in the spinal cord, or the medulla and mid-brain.
Therefore, it may be accepted that impulses of sensory or of other nature
may cause an alteration in the excitability of the gray substance of the spinal
cord, with changes in its tonus. The latter in its turn influences the vaso-
motor cell groups.
In all probability the dominant tone of the spinal vasomotor centers is not transmitted
through isolated paths, but propagated through the whole gray matter, and is modified
through a multiplicity of influences, pain, temperature and the like.
The importance of the dominating vascular center in the brain and of the tonus influ-
ences that emanate therefrom, is shown in the experimental work on the effect of section of
the cord on the heat regulating center. The latter is disturbed in proportion to the heighth of
the spinal cord section, and depending upon the number of spinal centers that are thereby
excluded from the influences of the cranial vasomotor center. High section of the cord in
animals makes heat regulation impossible, and the animals die. Therefore, above the
cervical cord there is a regulating center (vasomotor) that controls the tone of the inferior
centers, but the manner of conduction has not as yet been discovered.
Relations of Spinal and Sympathetic Systems.—It must be remembered that
all the paths between the spinal cord, ganglionic cord and peripheral nerves
have not been definitely established. A reference to Fig. 26 will show the
course of the known fibers in continuous lines, of the hypothetical fibers, in
dotted lines.
The medullated fibers crossing from the cord into the sympathetic system arrive in the
lateral horns; from here they pass through the anterior roots, into the peripheral nerves,
making a sharp curve through the rami communicantes. Here they are medullated and
constitute the ramus communicans albus. When the fibers arrive in the proximally situ-
ated ganglion of the sympathetic cord, they come into contact with the ganglion cells in
parts, but their greatest portion continues cephalad and caudad in the internodal portion
either to communicate with ganglia at other levels, or to enter the cervical sympathetic
or splanchnic.
The non-medullated fibers course through the gray ramus to the peripheral spinal
nerves where they supply the skin, vessels, sweat glands and piloerector muscles. How-
ever, there is also a communication between the gray ramus and the spinal cord (shown in
the diagram in a dotted line) although their course has not been definitely established.
Some fibers also pass to the thoracic and abdominal organs.
THE VASOMOTOR NERVOUS SYSTEM 30
| Nerves sympathicus
Hi tfarnus internodaless
% the Prevertebral
Foon glia
Fic. 26.—Scheme of the ganglionic and spinal communications of the sympathetic.
Solid lines indicate definitely known paths; dotted lines still hypothetical. (Miiller)
Fic. 26a.—Reflex paths in the cord. White, receptor neurones; black, connector
neurones; dotted, excitor neurones; A, voluntary system; B, involuntary system; P.R.G.,
dorsal root ganglion; D.H., dorsal horn; L.H., lateral horn; V.H., ventral horn; Sy.G.,
sympathetic ganglion. (Gaskell and Bayliss)
3
34 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
The schematic drawing given by Gaskell and Bayliss (Fig. 26a) shows
the centers of the sympathetic system in the spinal cord, and the relative
disposition of the voluntary and involuntary systems. The cells of origin
in the lateral horn are indicated at LH in Fig. 26a.
Antagonistic Innervation of the Vessels.—Although the finding of antago-
nistic innervation in the visceral territory offers no particular difficulties,
the relations that obtain in the case of the vessels of the extremities are
somewhat more difficult to interpret. The rami communicantes emanating
from the anterior roots appear to contain only the vasoconstrictor fibers.
Clinical facts speak for the probability that vasodilator influences travel from
the posterior horn through the posterior root, and then by way of the spinal
ganglia into the periphery. So we can explain the active hyperemia in the
irritated cutaneous territory, when sensory nerves undergo excitation. An
irritative reflex erythema! takes place, one that is absent when the reflex arc
is broken by section of the nerve. The vasodilator impulses appear to have
their own fibers, and they leave the spinal cord through the posterior
roots, and then course with the sensory fibers through the spinal ganglia to
the periphery.
And so it has been accepted by many that the vessels of the trunk and
extremities are supplied by an antagonistic double innervation in which
constrictor and dilator impulses functionate.
Some time after electrical stimulation of the sciatic stump after section vasodilator
changes are noted, while stimulation immediately after section results in vasoconstriction.
From this the conclusion has been drawn, that the dilator fibers are preserved longer than
those of vasoconstrictor function.
According to Starling, Bayliss and others, besides the main vasomotor center in the
medulla there is a series of subsidiary centers in the gray matter of the lateral horns of the
cord, giving origin to the fibers that go to make up the white rami communicantes. These
centers make possible a certain degree of adaptation between the blood supply of the various
parts of the trunk. If the spinal cord of an animal be destroyed, the blood pressure sinks
almost to zero, and the circulation comes to an end. The spinal centers, like the chief
motor center, are susceptible to changes in the composition of the blood delivered to them.
But these centers may gradually take on an automatic function, replacing that of the higher
chief center, after the medullary center has been excluded by division of the cord just below
the medulla, and after the blood pressure has fallen.
Clinical observations seem to warrant the conclusion that each half of
the spinal cord sends vasomotor impulses to both sides of the body. This
fact explains the occurrence of such minimal vasomotor deficiency symptoms
in the Brown-Séquard lesions.
The Peripheral Course of the Vascular Nerves.—The vasoconstrictor
paths are interrupted by ganglia outside of the spinal cord, just as are all the
nerves of the vegetative system, and they leave the spinal cord through the
anterior roots. We are interested here only with the course of the vaso-
motor fibers of the extremities, which are similar in their paths to those of
the trunk (Fig. 25).
After union of the anterior roots with the nerve bundles emanating from
the spinal ganglion, the fibers of the vegetative function of vessel innervation
leave the spinal nerve through the ramus communicans albus. In the gangli-
ated cord they make contact with multipolar cells, that give rise to the post-
ganglionic or postcellular nerves. The postganglionic fibers pass through
the rami communicantes grisei (gray rami). In their course they accom-
pany the spinal sensory nerve, and particularly the sensory paths. With
these they enter the subcutaneous tissues and the vessels of the latter. This
1 See Chap. XLVI (Dermatographia).
THE VASOMOTOR NERVOUS SYSTEM 30
course applies only to the vasomotor paths of the extremities and to the skin
of the trunk.
In some of the larger vessels (internal carotid, aorta, and renal arteries)
nerve bundles and ganglion cells have been found in the adventitia. Such
nerve elements have not as yet been discovered in the vessels of the
extremities. In view of these facts, some physiologists have concluded that
peripheral vasomotor centers may lie in the immediate vicinity of the vessels,
giving these an independent tone. We would then have three different
centers, the cerebral, the spinal, and the peripheral. Possibly this third
type plays a réle in the responses due to direct excitation.
According to some investigators nerve fibers are present in the blood vessel walls.
Glaser speaks of a reticulum of nerve fibrils in the adventitia, demonstrable with special
vital staining methods. In the deeper layers a network is imbedded between the adven-
titia and media. Between the muscle bundles there are also fine fibrils with nodes. Such
have only been found in the larger arteries and veins.
In the case of the smallest vessels fine fibrils can be traced about the external walls, and
an intraparietal network also has been recognized.
As for the capillaries they are said to be surrounded by a fine network, there being two
accompaning nerves with numerous anastomoses.
According to Sabin, 2 types of nerves are found, forming plexiform nets on and in the
walls of the larger vessels. The motor type appears to be distributed so that contact is
made with each muscular element. This set of fibers undoubtedly evokes functional vaso-
motor responses. Dogiel believes that the other type is distributed to the 3 tunic layers of
the vessel wall, terminating in flattened end-plates or specialized structure. Such fibers
would be of sensory variety.
Miller and Glaser! describe fine nerve filaments coursing along the capillaries and
encircling these through anastomoses.
Since true ganglion cells of the sympathetic type have not been found in
the deeper layers of the vessels, and none at all in the peripheral arteries, the
assumption is warranted that vascular response may occur through direct
action upon the musculature. Indeed, the tonus of this musculature may be
preserved after nerve section. Inasmuch as degenerative changes after the
exclusion of nerves have not been found in the smooth muscle, Glaser takes
exception to the view of those who would postulate a degenerative response
in a fashion analogous to that occurring after section of a vasomotor nerve.
Much discussion has arisen as to the course of the reflexes in these territories. Some
investigators believe that vascular reflexes originating in the sensory nerves must pass
through an arc of which the spinal cord forms a link. The view of Langley, that axon
reflexes may account for the responses, is not universally accepted. According to the latter
author, an irritation of the skin would pass through the centripetal sensory fibers, only up
to that point where the vasomotor paths and sensory diverge, from which the impulse
would lead through the vasomotor fibers to the blood vessels. Such would be a peripheral
reflex arc without interposed ganglionic cells.?
Some of the more recent authors lean to the supposition that the vasocon-
strictor impulses travel by way of the spinal cord; the vasodilator paths,
however, may lead to the vessels without passing through the ganglia of the
sympathetic gangliated cord.
Dissections made by Potts have demonstrated that, as in the arm, the
distribution of vascular nerves in the leg is much more extensive than that
laid down in the text-books; further, that the sympathetic supply for the
vessels of the lower extremities reaches the main vessels at intervals along
their course. Potts also states that the small vessels differ from the large
ones, as a rule, in not having special nerve supply, but in obtaining their
nerve plexuses direct from the sympathetic plexus on the parent artery.
1 Miiller, Das Vegetative Nervensystem, 1920, p. 100.
2 See Chap. V and Kroh’s substantiation of the theory of Langley, Fig. 27a.
36 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Distribution about the Common Femoral Artery. The branches of the superficial and deep
femoral arteries, and the medial and lateral circumflex vessels all derive their nerve supply
directly or indirectly from the femoral nerve. The popliteal artery derives its supply in
part directly from the N. tibialis, and in addition receives a branch in many cases from the
azygos nerve, The same author states that both the main trunk of the vessel as well as
larger arterial branches receive supply direct from the nerve trunks and not through the
medium of a continuation of nerve plexuses from the parent arterial stem. From these
findings it would be difficult to understand the rationale of the operation of periarterial
sympathectomy (Leriche, Chap. CV), to be described later on.
Summary.—The vasomotor system, therefore, is made up of a structure
of superimposed parts, all more or less interdependent. Whilst we note in
the nerves supplying the voluntary muscles but two divisions, we must count
upon four or more in the vasomotor system. (Some even believe that there
may be a vasomotor center in the cerebrum.) Vasomotor paths travel from
here with the motor and sensory conducting system through the internal
capsule through the subcortical large ganglia. Perhaps in the optic thalamus
or in the caudate nucleus, interruption in their continuity takes place through
the interposition of new cell groups. From there they are believed to pass
further through the pons to the large vasomotor centers of the medulla ob-
longata. Thence fibers pass through the lateral portion of the spinal cord to
various levels in the latter to break up about cell groups in the middle portion
of the gray substance, the latter being the spinal vasomotor centers. From
these cell groups, fibers again appear that lead to the sympathetic by way of
the rami communicantes, and from there pass further into the periphery.
At this point in the course, namely, at the gangliated cord or somewhat
nearer the periphery, or even in the vessel wall, further interpolation of gang-
lionic cells may take place. These cells may be regarded as the most distal
vasomotor centers. Some authors believe that an additional autonomic func-
tion or capacity must be ascribed to the smooth muscle of the vessel
musculature.
CHAP TE RIM
FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM
The Vasoconstrictor Nerves.—Experimental data corroborate the view
oft expressed that the vasoconstrictor nerves leave the spinal cord by the
anterior roots of the spinal nerves from the first dorsal to the third or fourth
lumbar inclusive. The white rami communicantes conduct them from the
roots to the ganglia of the sympathetic chain situated along the front of the
vertebral column, from which point they take varied courses according to their
destination.
On leaving the cord (Starling), the vascular nerve fibers carrying vasoconstrictor
impulses come to an end in a collection of ganglion cells that either belong to the main
chain of the sympathetic or are situated more peripherally belonging to a group of collateral
or peripheral ganglia. The fibers leaving the central nervous system are small medullated
nerves that end in the ganglion by arborescing around ganglion cells from which a fresh
relay of fibers carries the impulses to the muscle fibers of the blood vessels.
The splanchnic nerve is regarded as the most important vasomotor nerve of the body.
It receives most of the fibers from the lower seven dorsal and upper two or three lumbar
roots, the latter fibers often taking a separate course as the lesser splanchnics. Experi-
mental section of the splanchnic in herbivorous animals, in which the alimentary canal is
very much developed, causes a marked fall in general blood pressure.
FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 37
Vasodilator Nerves.—Whilst at first it was believed that dilatation of
arteries is produced only by inhibition of the normal constrictor impulses,
another nerve supply antagonistic in function to the vasoconstrictors has been
detected in many parts of the body.
Genuine inhibitory nerves to the arterioles are assumed to exist, through
which vascular dilatation is produced. This is to be expected and con-
forms to the rule; for, smooth muscle not subject to voluntary control is
usually supplied with two kinds of nerves, excitatory and inhibitory.
Stimulation of the peripheral end of the chorda tympani nerve to the submaxillary
gland, causes such marked vascular dilatation, that six to eight times the previous amount
of blood is made to circulate. Amongst other vasodilator nerves we may mention, the
lingual nerve to the blood vessels of the tongue, the small petrosal to the parotid gland, and
the nervi erigentes to those of the penis.
It is a mooted question as to whether vasodilator fibers are present in
the nerves of the limbs. In experimental stimulation the vasoconstriction
produced more than counterbalances any results obtainable through the
simultaneous excitation of possible dilator fibers. The dilators apparently
do not conduct any tonic influences to the blood vessels, so that the only
effect of section of a mixed nerve is that due to the removal of the tonic
constrictor impulses, and the vessels in the area of nerve distribution become
dilated.
Physiological researches have shown that vasodilator fibers course in the sciatic nerve.
The dilator fibers, however, cannot be traced back through the sympathetic system. The
observation of Stricker and Morat that dilatation of the vessels of the hind limb can be
produced by stimulating the posterior roots of the nerves going to the limb, was confirmed
by Bayliss. According to Starling ‘‘Stimulation of the posterior roots, either before or
after they have passed through the ganglia, causes dilatation of the vessels in the area of
the supply of the roots, whatever be the nature of the stimulus employed, whether electrical,
chemical, or mechanical. This effect is not destroyed by previous section of the posterior
roots on the proximal side of the ganglia, showing that the fibers by means of which the
dilatation is produced have the same origin and course as the ordinary sensory nerves to the
limbs. Since the vasodilator impulses pass along these nerves in a direction opposite to
that taken by the normal sensory impulses, Bayliss has designated them as antidromic
impulses. So far this phenomenon of a nerve fiber functioning (not merely conducting)
in both directions, is almost without analogy in our knowledge of the other nerve functions
-of the body. There is no doubt, however, that similar antidromic impulses are involved in
the production of the so-called trophic changes, such as localized erythema or the formation
of vesicles (as in herpes zoster), which may occur in the course of distribution of a sensory
nerve, and is always found to be associated with changes, inflammatory or otherwise, in the
corresponding root ganglia. Moreover evidence has been brought forward that these
fibres may take part in ordinary vascular reflexes of the body, that in fact they are normally
traversed by impulses in either direction.”’
In the antidromic vasodilatation, and in the reddening and inflammatory changes
consequent upon local excitation, Meyer and Bruce believe that impulses course by way of
axon reflexes, these being the remains of local reflexes of a primitive peripheral subcutaneous
nervous system. All the signs of a loca] inflammation can be produced by the application
of croton oil to the skin or conjunctiva. Nor will destruction of the central nervous system
or section of the sensory nerve roots (posterior spinal root or trigeminus) on the central
side of the ganglion alter the reactions. If, however, a division peripherally of the gan-
glion be produced and time be allowed for complete degeneration of the nerve fibers to their
peripheral terminations, the application of croton or mustard oil, even to the delicate
conjunctiva, is without effect. Similar results follow when the peripheral terminations
of the nerves are paralysed by the subcutaneous injection of local anesthetics. Starling says
that we must assume that the axons of the peripheral sensory nerves branch, some branches
going to the surface, others to the muscle-cells of the cutaneous arterioles.
While Bayliss expounded the theory of antidromic conductivity in the sensory nerve
fibers, some of the more recent Continental observers reject this view. According to
Bayliss both centripetal sensory impulses course in the sensory fibers to the posterior nerve
roots, as well as coincidental centrifugal vasodilator impulses. Continental observers
regard this as artificial explanation, all the more so, since existing well-known nerves have
38 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
been demonstrated to conduct both centripetal sensory and centripetal vegetative functions.
As an example may be mentioned the vagus nerve and the chorda tympani, composed of
sensory and parasympathetic nerves. By analogy it could be assumed, therefore, that
other nerves in communication with the spinal cord could be similarly constituted.
Recent Views.—Recently the Continental school of investigators have
made contributions somewhat at variance with the findings of the English
physiologists who were largely responsible for the foregoing facts.
Embryologically the heart forms a part of the total vascular system from
whence it would appear probable that both heart and peripheral vessels
receive parasympathetic and sympathetic innervation. It is believed that
heat regulation depends for the most part upon changes in the transverse
section of the blood vessels; that cooling produces an irritation of the para-
sympathetic and heating a similar response in the sympathetic paths. Up
to the present time, however, double vascular innervation has been dis-
covered for but a small portion of the vascular tree.
It is known that the parasympathetic dilator fibers of the chorda tympani pass through
the vessels of the salivary glands; and that vasoconstrictor fibers from the cervical sym-
pathetics pass to the same vessels. The double innervation of the vessels of the penis is
even more significant. Here vasodilator impulses pass through the N. erigens from the
sacral cord (containing parasympathetic fibers of erection), while vasoconstrictor sympa-
thetic fibers (from the lumbar cord) occasion relaxation.
In spite of the warrantable conclusion, concerning a double antagonistic
peripheral innervation of the vessels acceptable through analogy and physio-
logical considerations, no definite anatomical corroborative evidence is yet
at hand to prove that the vascular nerves of the skin of the trunk and extrem-
ities contain parasympathetic fibers. Langley is largely responsible for the
view that the points of origin of the thoracic and lumbar vegetative fibers
contain only sympathetic fibers. Dresel, Brugsch, Kraus and others express
the conviction, however, that this is no longer in accord with modern evidence.
Basing their deductions upon the well-known double vegetative inner-
vation of the striated muscles; upon the course of the nerve fibers of the sweat
glands; and finally, upon the essential requisite for a parasympathetic vaso-
dilator fiber supply to the vessels of the trunk and extremities:—they believe
that such combinations of sympathetic and parasympathetic cells of origin must
reside in the thoracicandlumbarcord. Forsucha coincidence is accepted for
the dorsal vagus nuclei. Of late, Miiller extends the hypothesis of Bayliss,
regarding the existence of vasodilator fibers in the posterior roots, into the
theory that such paths are constituted of parasympathetic nerves. In
short, enough data are at hand to allow of the assumption that preganglionic
parasympathetic ganglion cells may exist in the thoracic and lumbar cord,
from which the striated musculature, sweat glands, and vessels receive addi-
tional innervation. Dresel agrees with Miiller that we must reject the old
view that a dominant vasomotor center exists in the medulla oblongata.
As for the vasomotor reflexes, an arc is thought to exist, one of whose
limbs is constituted by centripetal sensory fibers, with a relay station in the
cord, through which the impulses then travel through the centrifugal vegeta-
tive paths. Such reflexes can be demonstrated after section of the cord, 7
even in the anesthetic territory.
Nerve Influences in Capillary Motility—Whilst admitting that chemical
or humoral factors are capable of influencing the caliber of the capillaries,
Krogh has recently rejected his original view that the nervous system does
not play an important rdle in capillary activity. In his latest investigation
on the submucous capillaries in the tongue of the frog this author has shown
FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 39
that the capillary dilatation following local trauma is brought about by nerve
action. A reflex is established in the sensory nerves; and its course would
follow an antidromic direction (axon reflex) directly opposed to that of the
sensory impulses (Fig. 27).
Fic. 27.—Scheme of vasomotor innervation in the responses of capillaries to local
mechanical irritants. A, arterioles; S, nerve sectioned. I, A stimulus at X travels over
sensory filaments in the direction of the arrow and in antidromic direction back so as to:
innervate the capillaries; II, shows that the capillary response is maintained even after
nerve section; III, shows that the capillary reaction is absent when secondary nerve degen-
eration has taken place. (Krogh)
These conclusions are based upon the following findings: A puncture trauma brings
about capillary dilatation (except when the wall of an arteriole is injured, when contrac-
tion is induced). Immediately after section of the motor and sensory nerve of the region
under experimentation, no change in the capillary response after puncture follows. Such
a result would seem to be independent of the nervous system. But, if the experiment is
repeated after degeneration of the nerve has taken place, the dilating response of the capil-
laries is absent. Similarly, local cocainization suppresses the reaction.
Experimental work has shown that section of the spinal cord in animals
is followed by an immediate dilatation of all the vessels below the level
of the section in the territory supplied by nerves arising below the level of
section. Afterwards, however, the vessels contract again, an evidence of
functional control in the spinal cord. ‘These facts would tend to corroborate
the assumption that the higher centers only motivate the vessel activities.
Moreover, destruction even of these portions of the spinal cord is not fol-
lowed by complete loss of all vasomotor innervation. Although there is
temporary vascular paralysis, this gives way to normal vascular constriction
after a time. A normal tone of vessels may persist in animals even after
the central nervous system has been excluded as a factor in the regulating
mechanism. From this it has been deduced that a peripheral nervous appara-
tus or local vascular center must exist. This is represented by the ganglion
cells and plexuses that surround the vessels.
Although total loss of the cerebrospinal system is followed by a reduction
in the total responsive capacity of the vessels (in animals), nevertheless
Lewaschew! was able to show that vessels whose vasomotors were paralyzed
still gave the well known reaction of contraction and dilatation to changes in
temperature. ‘The usual vessel activities or responses to direct mechanical,
thermic, chemical and electrical irritation of the periphery are said by
Landois to take the circuit of the peripheral vessel ganglia. In such func-
tions the paths would be axon reflexes (Langley?), that is, within sympathetic
neurons. ‘True reflexes, however are not confined within the sympathetic
system, but usually go through the cerebrospinal paths.
1Lewaschew, Virchow’s Arch. f. path. Anat., 92, p. 152.
2 Langley, Ergebn. d. Physiol., II, 2, p. 818.
40 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Even the veins may contract upon external irritation. Constrict or
phenomena are attributed to the venules in some forms of acroasphyxia.!
Although there is no accord amongst authors regarding the certainty of the
presence of vessel centers, it may be accepted as proven that a certain auto-
matism of peripheral action is a characteristic of the sympathetic system.
The Vasodilator Function.—The action of the vasodilators is demonstra-
ble when, after section of a nerve, irritation of its peripheral end is followed by
dilatation of the innervated vessel, whilst the mere interruption of continuity
produces no constriction of the lumen. The vasodilators do not appear to
have influence upon the normal tone. Up to the present time no center has
been found for these, although one is said to exist in the medulla oblongata.
The course of the vasodilator nerves is still uncertain. In some organs they
course as special nerves; in other parts of the body they are mixed with the
vasoconstrictors. According to Stricker and Gartner? the plexus sacralis
contains vasodilator nerves for the lower extremities.
In the case of the vasodilators, also, subordinate centers are assumed to
reside in the spinal column. Just how the vasodilators work, has not been
discovered. Some believe that their action is direct upon certain longitudi-
nal muscles in the vessels. ‘The view that they act in an inhibiting fashion
on the peripheral ganglia is more acceptable. Others (Lewandowsky) assume
that the vasodilators act directly upon the circular muscles of the vessels
without intervention of peripheral ganglia, making these yield their tone.
Excitation of the vasodilator center may be brought about directly or
reflexly. When venous blood or a poison, such as-chloral hydrate is given in
small doses, a direct effect is produced; or, reflexly, as in erection, through
sensory stimuli. Even the body temperature may be influenced through irri-
tation of these centers. :
Antagonistic Innervation of the Vessels.—According to Miiller® it is
believed that the regulation of the size of the vessel lumina is also under the
control of two separate systems of antagonistic action, namely, from the
gangliated cord of the sympathetic and from the parasympathetic autonomic
system. Such is the case in the other visceromotor functions.
The relations that obtain in innervation of the vessels of the trunk and
extremities are somewhat difficult of interpretation. The rami communi-
cantes from the anterior roots appear to contain only vasoconstrictor fibers.
Clinical facts point to the possibility of the transmission of vasodilator influ-
ences from the posterior horns through the posterior roots, whence they attain
the periphery through the spinal ganglia. Strong irritation of sensory nerves
leads to active hyperemia in the irritated territory. ‘This is a reflex pheno-
menon, for after section of the nerve with interruption of the reflex arc, the
hyperemia is absent.
Whether the vasodilators are also in communication with ganglia of the
gangliated cord, is doubtful. Bayliss was able to produce vascular dilatation
in the lower extremity after irritation of the posterior roots, even when the
abdominal sympathetic was removed.
Not only ts it accepted to-day that there are antagonistic double innervating
paths for contrictor and dilator impulses, but it would seem that the conductivity
of the dilator fibers persists longer than that of the constrictor paths (Miiller).
Still it is not necessary to assume that two separate centers must
be present in the brain for vasodilatation and vasoconstriction. Indeed,
1 Briscoe, see Chap. VII.
Stricker & Gartner, Wien. klin. Wchnschr., 1889, p. 980.
§ Miller, Das Vegetative Nervensystem, 1920.
FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 4]
the sudden blush of the face could hypothetically be brought about through
paralysis of the vasoconstrictor center. It is more plausible that from a
single vasomotor center influences emanate that simultaneously are of an
inhibiting nature, and others of an exciting or vasoconstricting quality.
Physiology of the Large Vasomotor Centers.— Physiologists believe that
the vasomotor centers are ordinarily in a state of mid-tonic excitation. From
them impulses are constantly flowing that induce a middle grade of contrac-
tion of the vessel musculature, thereby producing the normal vascular tone.
Fluctuations in the state of activity of the centers run parallel with the
respiratory movements. According to Simon the function of internal secre-
tions expresses itself in the production of hyper- or hypotension. These
effects are in a state of equilibrium under physiological conditions.
The vasomotor centers may be directly or reflexly stimulated. Direct
excitation results from the action of the gas content of the blood circulating
in the medulla oblongata. A marked venous admixture causes correspond-
ingly strong stimulation of the center leading to contraction of the arteries.
Irritation of certain centripetal nerves can produce contrary reflex effects
either exciting or depressing the centers (pressor and depressor nerve fibers).
Some authors believe such fibers are present in all sensory nerves. According
to Lovén irritation of sensory nerves causes firstly pressor effects; but con-
tinued and intensive stimuli lead to depressor effects and vascular dilatation.
Weak electrical or tactile stimulation of the skin, or thermic influences call
forth depressor effects.
According to certain authors, pressor effects can be obtained in a reflex
way through the action of weak electrical irritation or through the applica-
tion of cold or warmth to the skin. Hallion and Comte! produced vasocon-
striction in a reflex way through various sensory irritants. Experimental
investigation has shown that most of the irritants produced vascular constric-
tion. Some authors have tried to show that sensory regulating fibers are
present in the vessels themselves.
The nerve control of the vessels differs somewhat from that of other organs
whose activities are influenced by the vegetative nervous system. In the
organs, peripherally situated ganglionic cells (such as the Auerbach plexus)
take up impulses that modify the activity of the organs themselves. They
are regarded as peripheral reflex or automatic centers, and have been com-
pared to differentiated anterior horn cells. As such, motivating and inhibit-
ing extracentrally situated sympathetic and parasympathetic nerves con-
stitute the path for nerve control. But these reflex and automatic centers
of ganglionic nature appear to be absent wherever the function is an uncom-
plicated one as in the case of the vessels.
Edinger believes that sensory impressions are produced on sympathetic
cells lying directly in the vessels; and from these cells reflex contractions may
take place in the arterial wall through other fibers.
It is well known that section of the cervical region of the sympathetic
brings about reddening and warmth of the ear of the corresponding side in
experimental animals. The vessels dilate and the blood stream in the
affected partisretarded. The blood pressure is increased, the arteries pulsating
actively, the pulse even being noticeable in the veins. Irritation of a periph-
eral vasomotor nerve itself brings about pallor of the corresponding part,
coolness, reduction of temperature, and constriction of the vessel. In the
case of smaller arteries such constriction can be so marked as to completely
.1 Hallion & Comte, Arch. f. Physiol., 1894, p. 381; 1895, p. 90.
42 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
occlude the lumen. Continued excitation, however, finally brings about
exhaustion of the nerve with the manifestations of paralysis. These
observations are of exceedingly great clinical interest in that they give us a
clue as to the pathogenesis of many of the vasomotor affections, such as erythro-
melalgia, Raynaud’s disease and the cases of vasomtor instability.
It is an important observation that the effect of irritation or paralysis of vasomotor
nerves varies considerably in intensity in different vascular territories. For instance, the
vessels of the ears, nose, fingers and toes are most easily influenced, other regions being less
intensively acted upon. ‘These varying effects may depend to a certain extent upon the
architecture of the arteries.
The Vasomotor Tonus.—It is not necessary to assume that there are
cirsumscribed areas controlling vegetative innervation of vasomotor func-
tion. The dominating vasomotor center in the brain appears to functionate
in conserving and regulating the general vascular tonus. Various emotional
states are believed to cause qualitative alterations in the cranial vasomotor
centers, from whence fluctuations in tonus are produced through activation
of vasomotor centers in the cord. We do not know whether the tonic
influences from the mid-brain are necessarily intimately connected with
nerve fibers, or whether they are conducted through the gray substance, or
through the substantia gelatinosa. For, as in electricity, special conducting
paths are not essential. Miller designates the status of the general nerve
excitability as a biotonus which may suffer alterations under various con-
ditions. Particularly in the spinal cord are such changes possible, as mani-
fested by increased intensity of reflexes during emotional states. This
tonus may also be susceptible to sensory impulses. And, therefore, the
theory has been proposed that pain impulses, or other tactile sensory impulses,
may cause a generalized change in excitability of the gray substance of the spinal
cord. Such modification in the onus of the spinal cord would in turn react
on the function of the spinal vegetative centers, such as the vasomotor cell
group. ‘This theory is supported by the belief that it is quite impossible
for all sensory paths to be in immediate connection with all vegetative centers
in the spinal cord, medulla oblongata and mid-brain. Clinically, note-
worthy is the great vasolability manifested in the lower extremities of
thrombo-angiitis obliterans and to a less degree in the extremities affected by
atherosclerotic and other arterial disease. In the former malady it not infre-
quently follows persistent pain. It is more than likely, that just such a ¢onus
alteration in the spinal cord, in consonance with the above hypothesis, may
obtain in thrombo-angiitis obliterans, and account for the vasomotor lability
of many of the cases.
The tonus that dominates the spinal vasomotor centers appears to be reestablished in
the distal portions of the spinal cord shortly after experimental section of the spinal cord.
It fluctuates according to the sensory impressions that arise in the detached portion of the
spinal cord. After total section, irritation of the sciatic nerve produces increase in blood
pressure. When the feet in a paraplegic are exposed to cold impulses, the subsequent
vasoconstricting effect is limited to the lower part of the body. ‘This observation seems
to speak for the view that the dominating tonus in the spinal vasomotor centers is conducted
not through long isolated paths, but rather controls the whole of the gray substance and
varies or is changed through numerous sensory influences. Of these latter, pain and tem-
perature are the most important. Such impulses do not necessarily come to our conscious-
ness, nor reach the cranial vasomotor centers, as is exemplified by the paraplegic. It
would appear that the alteration in tonus occupies the total transverse area of the cord,
since on the action of cold, not only vasoconstriction but simultaneous pilo-erections, con-
traction of the scrotum and the skin of the penis, as well as contractions of the striated
1 Compare with explanations of erythromelia in Chap. XLI.
FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 43
muscles are observed. It is also noteworthy that heat elicits dilatation of the vessels,
sweat and relaxation of the scrotum.
Histologically the cells resemble the ganglion cells in the sinus nodes and in the auricular
septum of the heart. The small ganglion cell group and the single cells that are sometimes
found in small nerve bundles are found in loose connective tissue of the adventitia. Although
such cells have been found in the vessels leading to the viscera cells and in the aorta, they
have not been demonstrated thus far in the vessels of the extremities.
It is not unlikely that in the neighborhood of the vessels, or in the vessel
walls, peripheral vasomotor centers capable of an automatic tonic function
exist. These have been called vasomotor centers of the third class in contra-
distinction to the first (cerebral) and second (spinal) category. It is be-
lieved that the vessel activities resulting from direct irritation take place
through the intervention of these centers. Indeed, by means of special
tinctorial methods, nerve elements have been demonstrated in the vessel
walls.
According to Glaser! it is possible to demonstrate a network of fibers in the adventitia
of the veins if we employ vital stains and young subjects. A further network of nerves is
seen between adventitia and media; also between the muscle bundles of the media, a branch-
ing network of finest fibrils with knobbed nerve filaments has been found. Some of these
travel the whole media and penetrate into the intima. These appearances have been
demonstrated for all of the larger arteries and veins. Even the capillaries are enmeshed
with nerve filaments that show numerous anastomoses.
In the deeper layers of the vessels ganglionic cells have not been found.
Inasmuch as ganglionic cells have not as yet been demonstrated in the
peripheral arteries, we cannot exclude the possibility of direct muscular ves-
sel reactions to mechanical or thermic stimuli.
As for the distal constrictors and vasodilators very little is known. Indeed, the old
concept that the vasoconstrictors lead to the annular musculature and the vasodilators to
the longitudinal muscle fibers has not been conclusively proven, all the more so, since the
smallest vessels contain no distinct longitudinal muscle bundles.
Recent Views on Physiology.»~—The peripheral parasympathetic and
sympathetic fibers have an antagonistic influence upon the single vegetative
organs. Dresel believes that alterations in the functional condition of the
cells (muscle or glandular cells) may be brought about through nerve impulses
coursing through this system; and that the modus operandi is one in which the
surface tension or potential undergoes a change. Such deviations may be
produced in the electrolytic equilibrium of calcium and potassium, with the
balance in favor of one or the other Ion. ‘This with other biochemical altera-
tions would effect functional derangements in the cells (such as muscle and
gland cells).
A coordination of the antagonistic effects of the parasympathetic and
sympathetic nerve impulses is realized through the central vegetative nerve
stations. The view until recently widely accepted, to wit, that irritation of
one system induces a diminution of tonus in the other system (Eppinger
and Hess), seems to be controverted by recent investigations. Thus it has
been shown (Dresel) that every parasympathetic excitation is followed by
one of the sympathetic and conversely. ‘The mechanism responsible there-
for is one that tends to conserve the dominant equilibrium. This is accom-
plished through a regulating mechanism in the subthalamic center, which
responds to every change of temperature, of blood pressure, or of blood
sugar content, by influencing the subordinate parasympathetic and sympa-
1 Miiller, Joc. cit.
2 Personal communication from Kurt Dresel of Berlin.
44 CIRCULATORY ‘AFFECTIONS OF THE EXTREMITIES
thetic cell origins. For example, if the blood pressure increases by virtue
of irritation of the sympathetic (adrenalin) a parallel stimulation of the para-
sympathetic paths follows through this regulating mechanism, with the pur-
pose of limiting an inordinate increase of pressure and of restricting it to a
certain threshold. ‘These phenomena may be compared with the well-known
manifestation of successive induction (Sherrington) occurring in the animal
nervous system. According to this view, coincidently with every reflex,
agonistic as well as antagonistic impulses are evoked to check excessive
motion.
The above-described regulation may be motivated through the direct
action of chemical and physical blood changes upon the subthalamic centers
(of temperature, sugar content, Ion content, blood pressure, etc.). The sub-
thalamic center takes a subordinate position to that in the corpus striatum,
for the latter is in control of the vegetative function. Indeed, it is believed
that the impulses emanating therefrom determine the threshold. This
threshold (for temperature, blood sugar, Ion concentration and blood sugar)
may be attuned to different levels, through alterations in excitability and
state of excitation of the striate body.
Dresel compares the activity of the vegetative centers with a thermostat in which the
above functions may be symbolized. The mechanism for regulating heat can be set for
varying degrees such as 42° C., 37° C., or 26° C., through the action of the center in the
corpus striatum. Just as the regulatory mechanism of a thermostat reacts to changes of
external temperature, so also do the subthalamic centers, whose function it is to conserve an
equal temperature; and this is effected in that the subordinate centers (points of origin of
the parasympathetic and sympathetic in the mid-brain, medulla and cord) are made to
respond accordingly. Similarly for all other vegetative functions there is a very accurately
and delicately attuned mechanism for the conservation of proper equilibria. It is then
easily understood how very slight alterations may bring about very severe symptoms.
The Vascular Nerve Centers.—It has already been previously mentioned
that the cellular points of origin for the peripheral vegetative vascular nerves
are to be found in the medulla and in the spinal cord, where they receive
their impulses from the superior vascular centers in the subthalamic regions
and corpus striatum. Karplus and Kreidl had already demonstrated the
existence of nerve communications between the subthalamic region and cord
(since irritation of the mid-brain failed to produce typical effects on the vessels
after section of the cervical cord). Dresel obtained anatomical proof in
the finding of retrograde degeneration in the cells of the subthalamic region
after section through various levels of the spinal cord. Furthermore, this
author showed that certain ganglionic cells in the subthalamus undergo
variation in excitory state, through fluctuations of blood pressure.
It is well known that clamping or ligation of the carotid leads to increased blood pressure
in the arteries (with the brain excepted). Such hypertonia results through regulatory
impulses emanating upon the mid-brain. That such must be the case was proven by the
absence of such an eventuality after section through the corpora quadrigemina. So it has
been assumed that the regulatory impulses leading to increased blood pressure are evoked
through the diminished blood supply in the brain, and have their source in the mid-brain.
Analogous phenomena are to be found in the so-called ‘‘vagus pulse.’? ‘This follows
injection of adrenalin, and has been said to be due to direct action of adrenalin or increased
blood pressure upon the vagus center. Perhaps, however, this vagus effect is nothing but a
manifestation of regulatory impulses from the mid-brain, in response to the increased blood
pressure. ‘This conclusion is warranted on the basis of the observation, that the vagus pulse
can be prevented by preliminary separation of the medulla and corpora quadrigemina
through section (whence adrenalin injection will be ineffective in spite of the continuity of
the peripheral nervous system). Although Karplus and Kreidl had already noted the
vasoconstrictor effect that follows direct electrical irritation of the hypothalamus, no
functional conclusions were drawn by these authors concerning blood pressure phenomena
in general.
FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 45
The corpus striatum is said to have a distinct influence upon the vascular
nerves and upon blood pressure (Dresel).
If a point in the nucleus lentiformis (globus pallidus) is accurately stimulated with a
double electrode, the introduction of faradic current brings about considerable fall in blood
pressure, which continues for a time after cessation of the electric irritation and then
gradually disappears.
Here we see then that there is a distinct relationship between blood pres-
sure level and the excitatory condition of the corpus striatum (just as is the
case with the thresholds of other blood components).
The psychic and sensory influences upon the whole vegetative nervous
centers probably take place by way of the center in subthalamic and striated
centers. Here, then, there is disparity between animal and vegetative
nerve functions. Jn the former, actual areas of projection in the cortex of the
brain exist, while the absence of such for the vegetative system would seem to have
been confirmed by researches. For, dogs without cerebral cortex may be
wholly devoid of any vasomotor disturbance.
In the vegetative system, changes of vascular girth run parallel with changes in total
metabolism. With such vascular alterations there is usually a generalized reversal,
inversion or modification in the vegetative system.
Then again the question has been ventilated as to whether delimited vascular territories
are represented in the circumscribed vegetative centers. Indeed, experimental and clinical
experiences would seem to point to the possibility that certain ganglionic cells do control
the regulation of certain vascular territories. It has been even suggested that excitatory
changes in the centers of the striatum and hypothalamus may be induced so as to bring
about limited vascular alteration in an extremity. Emotional impulses are said to evoke
such phenomena. Since cortical centers are absent, the separation of vascular territories
in central stations must needs take place at a higher level than at the points of origin of the
peripheral vasomotor nerves (medulla and cord).
Viscero-vasomotor Reflexes or Vaso-vasomotor Reflexes.—Clinical observa-
tions have suggested that not only do viscero-sensory reflexes exist as exem-
plified by the Head zones, and visceromotor reflexes as in the so-called
‘défense musculaire,’’ but that there may be viscero-vasomotor responses
or even vasomotor responses secondary to irritations of vascular origin.
Zak+ describes hyperemic or erythematous zones below the fossa jugularis,
and just under the mesial half of the clavicle in cases of aortic disease. These
areas are roughly of semilunar shape, and the skin in this region responds
with abnormal activity to mechanical irritation. In some cases the vaso-
motor centers are hyperirritable through impulses sent from the diseased
aorta; in others, the centers themselves are primarily in a state of increased
irritability.
Other visceral affections such as pulmonary diseases may give similar vasomotor zones.
Zak states that in about one-third of the cases of aortic disease distinctly demonstrable
semi-lunar erythematous manifestations are present; and that these are evidences of local
vasomotor hyperexcitability with corresponding segmental alterations in the spinal centers.
There is a certain degree of parallelism between the vasomotor and sensory hyperexcitability.
Miiller? describes a clinical method based in all probability upon reflexes through the
spinal segment corresponding to that irritated. A ring is pressed against the skin, and
the included cutaneous area rubbed energetically with the end of a match-stick, so as to
produce a somewhat painful sensation for a period of 10 seconds. Thirty to 60 seconds
later and after the cessation of the painful irritation there will arise in addition to the
hyperemia within the boundary of the ring, a second hyperemic zone extending for a
considerable distance beyond, the direction of this rubor being in accordance with the
cutaneous segments, that is, more or less vertically over the arm, horizontally over the
trunk.
1 Zak, Wien. klin. Wchnschr., 25, 1920, also Wien. Arch. f. klin. Med., IV, p. 209, 1922.
2 Miller, Ztschr. f. Nervenh., 47, 48, 1913.
46 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Goldscheider,! in some clinical experiments applied a clamp to pinch the skin for r or
114 minutes. Besides the manifestation of pain and a cutaneous areola of rubor, an addi-
tional girdle-like hyperalgesic zone appeared over the trunk, or a longitudinal vertical
streak over the extremities. Similarly a hyperemic zone developed presumably through
reflexes passing by way of the spinal segments.
Therefore, just as a cutaneous zone of hyperalgesia corresponds to a state of irritability
of the sensory fibers and ganglionic cells of the corresponding segments, so also, it is now
believed that an increased excitability of the vasodilator centers may take place. There-
fore, in addition to so-called viscero-sensory reflexes and visceromotor reflexes, a viscero-
vasomotor reflex may occur (Mackenzie).
These observations give further foundation in analogy to the warrantable
assumption that through disease of the arteries, as in thrombo-angiitis
obliterans, and partly by reason of the pain impulses often or continuously
traveling in such cases, vasomotor reflexes establish themselves, and are
responsible for the increased vasolability (vasomotor neurosis) observed in
such cases; and perhaps also for the rubor under certain conditions.?
Pain and the Sympathetic—The exact réle of the sympathetic system in
the production of pain is not known. ‘There seems to be no doubt but that
centripetal impulses occur in the sympathetic system, and further, that
stimulation of these fibers may occasion pain. ‘The origin of a pain of sympa-
thetic causation probably depends upon the quality of the irritant. Num-
erous theories have been advanced to explain vascular pain. We know that
pressure upon arteries produces painful impulses. Stimulation of the centri-
petal nerve fibers of the blood vessels, even though unproductive of pain
sensation under ordinary circumstances, may produce such in exceptional
conditions. Dogiel asserts that the perivascular tissue usually contains
medullated nerve fibers, and Vater-Pacini bodies occur in the adventitia.
Cassirer believes that direct irritation of the vessel wall through its sensory ele-
ments accounts for the pain in erythromelalgia; for, the vasomotor and sensory
irritative symptoms roughly correspond in their distribution. In the acro-
paraesthesiae irritative conditions of the vasosensory fibers may also be
responsible for the symptoms.
Summary of the Vasomotor Mechanism.—A reference to Fig. 27 will tend to clarify the
concept of the mechanism of vasomotility. Through the four neurones, (@) cerebro-
bulbar, (6) bulbospinal, (c) spinosympathetic, and (d) sympatheticomuscular, the brain
and the three relays are brought into communication with each other and with the peri-
phery. Since vasodilator fibers have only been found in certain special regions, they are
not represented in this schematic drawing. Generally speaking, we regard loss of vascular
tone as due to vasoconstrictor paralysis, and vasoconstriction as the result of vasomotor
stimulation.
It is comprehensible then, that a lesion of the ventral horn is followed by vasomotor
paralysis if a discontinuity between the third set of neurones (¢cinFig. 27a) and the central ©
cell group is effected. So also, breaks in the connections of the bulbar and spinal centers
(6) through lesions of the lateral columns may have the same result.
According to Bing,’ spinal vasomotor paralysis, whether produced by destruction of the
vasomotor centres in the ventral horn, or by interruption of the vasomotor fibers in the
lateral columns, seldom reveals itself, and then only in its earliest stages by redness and
heat of the skin. The skin in the territory innervated by the affected regions of the cord,
becomes cold and cyanotic, a condition that may ensue forthwith after the occurrence of
the lesion, or may replace a transitory hyperemia.
A glance at the vasomotor paths will demonstrate at once that central lesions inter-
rupting paths in the spinal cord would have an action over extensive circulatory territory.
The local manifestations of vasomotor derangement seen in the diseases described here, are
limited to such an extent as to warrant the supposition that either more peripheral disorders
of innervation are responsible, or isolated ganglion or horn cells only partake in the neurotic
1 Goldscheider, Ztschr. f. klin. Med., 85, 1918.
2 See Chapters XLVI and L (Erythromelia and Pain in Thrombo-angiitis).
’ Bing, R., Regional Diagnosis in Affections of the Brain and Spinal Cord, Transl.
Rebman, New York, 10913.
FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 47
disturbances. A more detailed discussion will be found under the chapter on the “Vaso-
motor and Trophic Neuroses.”’
In forming a correct concept of the vegetative functions we should not
confine their paths to the gangliated cord, but include as important elements
the higher centers in the spinal cord and brain. Although exact localization
of lesions that could evoke certain vasomotor neuroses is as yet not feasible,
enough data are at hand to make us suspect that the intermedio-lateral region
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(pm ARTERIA
LI
Fic. 27a.—Scheme of vasomotor mechanism. (Bing)
of the posterior gray substance may be the seat of some of the causal lesions
in certain of the vasomotor and trophic disorders. But derangements in
the reflex arcs, too, can be regarded as etiologic factors.
Cassirer expresses the view that a disturbance in the reflex mechanism
between sensory and vasomotor systems could account for many of the cases
of vasomotor and trophic neuroses and their trophic lesions of the skin.
_ Various hypotheses have been offered as to the course of the reflex arc,
alterations in which may lead to vasomotor and trophic manifestations.
Vasosensory fibers may exist and make a portion of the afferent elements of
the sympathetic. Excitation of these is believed to account for the extent
and quality of the peculiar pains of which cases of vasomotor and trophic
neurosis complain. So, too, in thrombo-angiitis obliterans it is not unlikelv
that some of the varied forms of pain, particularly those associated with a
state of marked vasomotor instability may owe their origin to the excitation
of vasosensory nerves (Chap. L).
48 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
In further support of the reflex theory of vasomotor innervation, is the
circumstance that irritation of sensory nerves has a greater influence on
vasomotor tone (especially vasodilatation) than mere section of the sympa-
thetic. The reflexes need, however, not be confined to the sympathetic
system, a territory within which such phenomena do not seem to take place,
but may take place through the intervention of additional spinal sensory
paths.
CHAR LER Va
PHYSIOLOGY OF THE PERIPHERAL CIRCULATION
Elementary Principles.—It may not be amiss to summarize some of those
fundamental facts concerning the general circulation that have a direct
bearing on the blood flow in the extremities.
Although the laws governing a constant flow of fluids through rigid
tubes apply to those with elastic walls (as arteries and veins), a distinct differ-
ence exists when fluid is forced into these intermittently and rhythmically.
Fluid thus driven into rigid tubes is evacuated interruptedly; in elastic
tubes, however, an intermittent pulsatile stream may be converted into a con-
tinuous one. The distended elastic walls of the tube exerts such pressure
on the contents when the inflow ceases, that the current becomes continuous
even during the pause in the main propelling force.
With the heart as the pump, the elastic arterial walls act in this way,
and, during the diastole the current in the capillaries is continuous. ‘The
arterial elasticity, therefore, is of considerable moment in its influence on
the cardiac work. In view of the participation of the arterial walls in the
propulsive mechanism, the total cardiac work is under normal circumstances
commensurately lessened.
The circulation of the blood conforms, then, to these principles and is
modified by the vasomotor innervating mechanism.
Let us briefly discuss here some of the hydraulic principles that govern
the blood flow, in so far as they may clarify our concepts of the criculatory
affections of the extremities; the nerve control and its influences shall be given
consideration elsewhere.
The volumetric increase of the arterial tree is proportionate up to a cer-
tain limit to the internal pressure, only to diminish over this point. Fur-
thermore, the more peripheral the arteries the greater the dilatation with
equal increase in blood pressure. As the arteries become less elastic with age
and disease, the nearer does their function approach the qualities of the rigid
tubes.
The pressure in, and the volume of blood delivered by the arteries are
dependent on a number of factors; namely, (1) the supply to the heart; (2)
the frequency and force of the heart beat; (3) the resistance in the arteries;
(4) the viscosity of the blood; (5) the quantity of blood; (6) the changes in
the flow under special circumstances; and (7), the changes in cardiac work.
t. It is clear that the quantity of blood delivered by the cardiac pump must be related
to that quantity which is emptied into the heart through the large veins. Many experi-
ments have demonstrated that with other conditions unaltered the volume of blood deliv-
ered per minute increases in proportion to that supplied to the heart.
Ha eSLOLUG TOF FH BAPERIPHERAL CLROCULATION. 49
2. If a sufficient quantity of blood enters the heart through the veins to fill it during
diastole, the volume of blood delivered by the heart per minute is directly proportionate to
the frequency of the heart beat. This is true up to a certain limit only; for as the diastole
becomes shorter its duration may be insufficient to permit of adequate filling of the heart.
And so from this point on the amount of blood that is ejected during the systole becomes
smaller and smaller until finally the volume per minute is less than that which the heart
would deliver during periods of diminished activity. Whilst these facts are based on phys-
ical laws, under ordinary circumstances it is maintained that the volume of blood delivered
per minute, as well as the pressure, does not vary with the frequency of the heart beat within
certain limits, when ever the resistance to the vessels remains unchanged.
3. Increased resistance offered by the arteries may cause a rise in blood pressure.
Contraction of the vessels in a large territory (or ligation of a large vessel as the abdominal
aorta) increases the pressure. With moderate increase of the resistance the heart may
either deliver an equal amount of blood during a unit of time, or a greater amount. Inthe
latter case, rise of pressure follows. Should a marked increase of resistance take place,
the quantity of blood delivered becomes smaller and finally stasis of blood in the heart may
result. Nature has provided a reflex mechanism, which, under certain circumstances,
brings about dilatation of the arteries with commensurate relief to the heart (through the
depressor! nerve, irritation of whose central end brings about fall of blood pressure).
The autonomic action of the capillaries” is now recognized as capable of playing a dis-
tinctive réle. Krogh showed that most of the blood capillaries in a muscle when at rest
are to be found in a state of contraction, their lumina not being too small for the passage
of red blood corpuscles. ‘This functional exclusion of the capillaries goes hand in hand
with a reduction in the activity of the muscle fibers and with the diminution in the need
of oxygen, glucose, etc. As soon as the circulatory demand becomes more active by virtue
of enhanced muscular function, the caliber of the capillaries becomes greater, they dilate,
and the flow of blood in the muscles becomes accelerated. In reality the contracted capil-
laries are never completely closed, but allow the blood plasma to circulate.
Besides this functional response on the part of the capillaries, alternate dilatations and
contractions in certain of their territories may occur spontaneously from time to time by
reason of chemical influences.
4. Changes in the viscosity of the blood are said to alter the resistance offered to the
circulation independently of alterations in the vascular patency. It has been shown that
the internal friction of the blood in certain animals is 3/4 times as great as that of distilled
water. The non-defibrinated blood of animals and of the human is believed to possess an
internal friction of 4 to 5 times that of distilled water. After blood letting this friction
diminishes; after feeding animals it increases. The viscosity of the blood also has been
reported as being increased by multiplication of the red blood cells, and reduced by admin-
istration of salt solution. With diminished viscosity, the heart may, in a unit of time
deliver larger quantities of blood than normal without appreciable increase in the blood
pressure. Perhaps this phenomenon explains the apparent improvement in the general
condition and in the circulation of some cases of thrombo-angiitis obliterans after the
administration of large quantities of Ringer’s solution subcutaneously or through the
duodenal tube (Chap. LXV).
5. The total quantity of blood is of no mean importance in determining the volume of
blood delivered into the vessels. Increase of blood pressure may be obtained by inhibition
of fluid through the intestinal tract, under the skin, and by transfusion, with consequent
delivery of larger quantities of blood into the vessels.
6. Exercises and physical work increase the frequency of the heart beat with consequent
increased demands upon the circulation in the arteries. Increased blood pressure may
follow and the volume of blood delivered per minute may increase from 3 to 7 times the
normal. Other external influences (such as obtain with baths), influence the circulation.
The hydrostatic pressure bath is known to exert a distinct effect on the circulation.
7. The response on the part of the heart muscle to changes in the circulation must also
be taken into consideration in an estimation of the quantity of the blood delivered. And
so it is not always the greatest arterial pressure that evokes a corresponding cardiac activ-
ity, but moderate demands or moderate increases of pressure.
Measure of Blood Flow in Extremities.—Perhaps we could obtain a better
appraisal of the adequacy of circulation in the peripheral part of a limb by a
knowledge of the so-called mass movement of blood. It is conceded that
arterial pressure is not in itself an index of the measure of the flow.
1 This nerve crosses into the cardiac plexus, arises in two routes, one from the vagus,
the other from the inferior laryngeal.
2 See Chap. on Physiology of the Capillaries.
ft
50 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Stewart! has suggested an ingenious method of measuring the blood flow,
which he regards as simple and accurate enough for clinical purposes. The
method is based upon the fact that the amount of heat produced by a part,
like the hand during rest, is negligible in comparison with the heat conveyed
to it by the arterial blood. Determination of the amount of heat given off to
a calorimeter in a given time in its relation to the temperature of the arterial
and the venous blood, permits of calculation as to how much blood must
have passed through the part.
Perhaps the wider adoption of methods such as these will prove of some
value in the circulatory affections of the extremities.
Some of the results obtained by the calorimetric measurement of blood
flow through the extremities may be thus summarized (Stewart).
In arteriosclerosis the blood flow in the hands is smaller, and the contra-
lateral vasomotor reflexes are less pronounced than normal.
In cases where there were inequalities in the blood flow of two hands
(through mechanical causes, ligation, embolism, compression) the stability
of the ratio of the flow in successive measurements was found characterisic.
Tests made at long intervals demonstrated the development of collateral
circulation by changes in the ratio of the blood flow in the normal and affected
parts. A feature diagnostic of the organic impairment of the circulation was
found to be the impossibility of abolishing or greatly altering the flow by the
artificial production of vasomotor changes (through external temperature).
In other words, temporary vasomotor instability could be made to give differ-
ent readings in an artificial way.
Inequalities of blood flow in two hands or feet of the nature varying in
degree from day to day, and such as could be abolished, produced, increased
or reversed, by changing the external conditions, were interpreted as due to
unequal activity of the vasomotor mechanism on the two sides.
In 3 cases of Raynaud’s disease the hand flow was subnormal; in the more
advanced cases very much below the normal.
Stewart summarizes the application of his method as follows:
“The arterial pressure is not in itself a measure of the flow. With a high pressure the
flow may be small, with a relatively low arterial pressure it may be large. Indeed, in cases
of marked arterial hypertension the blood flow in the extremities has been found subnormal,
the high blood pressure being associated with constriction of peripheral vessels and under-
irrigation of peripheral parts. If the brachial or femoral artery were obstructed by a clot
(or a ligature) the pressure in the artery central to the block would be at least normal.
But this would be of no consequence to the patient and would not give the physician any
information in regard to the important question, how much blood was passing through the
endangered part below the block. The same is true of more limited lesions involving one
or both hands or feet, or portions of them. In a considerable group of pathological condi-
tions in which the blood vessels of one or more extremities are involved either primarily
or secondarily (thrombo-angiitis obliterans, Raynaud’s disease, thrombosis associated with
the puerperal state, embolism, etc.) measurements of the blood flow from time to time may
yield information of importance, not otherwise obtainable.
In this way the physician may learn: (@) Whether the blood flow is so small that gan-
grene is probably imminent, although it may not yet have declared itself. A blood flow
around the critical level would, of course, emphasize the importance of sedulously protect-
ing the part against mechanical injury or cooling. (b) Whether the vascular condition
is stationary, improving or growing worse. (c) The effect, if any, of therapeutic meas-
ures (vasodilator drugs, baths, Bier’s bandage). In certain cases the diagnosis between a
functional vasomotor affection and a mechanical block, due to embolism, thrombosis or
anatomical narrowing of the vascular lumen, can be made by testing the effects of vaso-
dilator drugs or changes of external temperature upon the blood flow. A mechanical
block will obviously resist such measures, and the blood flow will remain small, while a
1 Stewart, Harvey Lectures, 1912, p. 86 (Lippincott).
PHYSIOLOGY OF THE PERIPHERAL CIRCULATION 51
functional (vasomotor) block may open up. In cases where it is proposed to tie an artery,
information as to the probable adequacy of the collateral circulation immediately after
ligation could sometimes be obtained with advantage before the operation by blood flow
measurements with the artery compressed and open (Matas). In several cases in which the
innominate and right carotid were tied for subclavian aneurism (Hamann) comparison of
the flow in the two hands enabled the gradual establishment of the collateral circulation
to be followed till it was adequate for the normal functioning of the right arm. In cases of
injury to the nerves of a limb, especially unilateral injury, information of value in the
diagnosis can sometimes be obtained by blood flow measurements, paralysis of the vaso-
motors in the injured nerve trunks leading to definite changes. In early brachial neuritis,
e.g., the flow in the corresponding hand is likely to be increased. Such measurements
have aided in discriminating between pressure on the subclavian artery and injury to the
brachial plexus as the cause of certain symptoms in the arm and hand.”’
“In the study of pathological conditions of the circulation in the extremi-
ties it is sometimes useful not only to determine the rate of the blood flow,
but also the degree in which it is affected reflexly through the vasomotor
system. It is perhaps not too much to say that the proper application of
reflex tests is as important in the investigation of diseased conditions of
the vasomotor system as in the investigation of diseased conditions affect-
ing the skeletal affections of the extremities. For, one of the most char-
acteristic properties of the cutaneous circulation (and the circulation of
the hands and feet is essentially cutaneous), is the variation inits rate accord-
ing to the intensity of the metabolism and the temperature of the environ-
ment. And this adjustment is brought about largely through vasomotor
reflexes.
The intensity of the vasomotor reflexes elicited by heat and cold can be
estimated by immersing one hand or foot in cold or warm water, while the
blood flow in the other is being measured. (A reflex vasoconstriction is
associated with a diminished flow, a reflex vasodilatation with an increased
flow. The reflex vasoconstriction to cold has been found intensified in
cases of Raynaud’s disease and allied conditions, feeble or absent in tabes,
in well marked arteriosclerosis, the in long-standing hemiplegia, etc.) It is
obvious that where anatomical changes have occurred which constitute a
block on the vasomotor reflex arcs, even without obstruction of the vascular
path, or a block, on the vascular path, even without interference with the
vasomotors, vascular reflexes must fail to affect the blood flow through the
part.”
The Blood Vessels and the Blood Movement.—Two views regarding the
role of the vascular system in the circulatory activity have found adherents in
the literature. According to one of these the blood vessels take an active
part in the propulsion of the blood. This presumes that the vessels pulsate
actively, and propel the blood forward in a peristaltic wave, and this power
is attributed not only to the arteries, but also to the veins.
According to Hasebroek! the pulse wave occasioned by the heart stimu-
lates first the vasodilators, so that an active dilatation of the arteries ensues.
When the pulse waves have reached the maximum, a vasoconstricting effect
is aroused, and an active constriction takes place. Inasmuch as the pulse
wave is transmitted from place to place towards the periphery, this stimula-
tion and motion of the arteries is believed to take the form of a peristaltic
wave, so that the blood is, as it were, aspirated during the diastole of the
arteries and transmitted onward during the systole.
This view has not been acceptable to all investigators. Indeed, another
school insists that the passive dilatation of vessels and the consequent re-
1 Hasebroek, Pfliiger’s Arch. Bd. 168, 1917, p. 247.
52 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
bound, gives rise to the mistaken impression of spontaneous activity. These
investigators, therefore, hold that the vessels play a passive role only.
There seems to be no doubt, however, that the vessels are active so far as
certain variations in their caliber do .depend upon nervous influences.
Through the vasomotor system the vessels conserve a certain degree of ten-
sion or so-called tonus.
Capillary Circulation and Blood Movement.—The capillaries are prone to
show ryhthmic contractility following nerve stimulation. This observation
is of importance for its bearing on the existence of an extracardiac force
in the propulsion of blood. Fleisch! contends that the rhythmic contractions
exhibited by the excised arterial strip does not prove that an independent
extracardiac propulsive force exists.
This author calls attention to the fact that the rate of contraction of isolated arterial
preparations at body temperature is less than the heart rate. If, therefore, such vascular
movements occurred in the normal intact animal, they would be as likely to impede as to
facilitate the force of the heart beat since they are neither synchronous with it, nor can they
travel with the same rapidity over the vascular tube. He rejects the view, therefore, that
the arteries furnish an extracardiac circulatory force. Whether the veins contribute
circulatory power is still a mooted question. Since cinematographic records show no rhyth-
mic change of caliber in the capillaries, the latter are probably also impotent as circulatory
adjuvants.
Hooker takes exception to these views in the light of recent investigations. He states
that the mammalian capillaries and venules have been shown to undergo post-mortem
changes in that they are almost completely emptied of blood shortly after death. Later
they fill again and subsequently and finally empty themselves. Since no extraneous forces
are at work, this phenomenon cannot be passive in character both as to emptying and filling.
In other words, the capillaries under these circumstances exhibit a functional response
which might be of distinct moment in moving the blood under normal conditions.
In accordance with more modern investigations, it does not appear unwarranted to
entertain the view that the capillaries and venules may offer an extracardiac force of very
considerable significance to the circulation.
Hooker says that “up to the present, no one has attempted to show, except in the case of
the bat’s wing, that the veins proper facilitate blood movement by contractile activity
There is abundant evidence that the tone of the veins is an important factor in circulatory
regulation and we know that respiratory, joint and muscular movements facilitate, by a
massage effect, the movement from valve segment to valve segment of the blood in the large
veins. The sole indication, however, that the veins may move the blood by a kind of
peristaltic activity is found in analogous observations that the large lymphatic trunks in
situ may exhibit spontaneous rhythmicity of a peristaltic character.”
Vasomotor Function and Circulation.—To understand better the action of
the vasomotor nerves, let us quote the example given by Starling? of the
effect of vasoconstriction and dilatation of the arterioles of a part or organ of
the body.
“Tf the arterioles A in the organ B dilate (Fig. 28), the first effect is a diminution of the
resistance to the flow of blood into the capillaries beyond. Supposing that the arterial
pressure in the trunk C remains constant, a local diminution of resistance in A will at once
determine an increased flow of blood through the arterioles, and the fall of pressure from A
to the capillaries will be less than when the arteriole was constricted. If the organ is
distensible and elastic, the increased pressure in the arterioles and capillaries will cause
dilatation of these vessels, and a consequent dilatation of the whole organ. The same
effect on intracapillary pressure, and therefore on the volume of the part, may be caused
by obstruction to the flow of blood from the veins. Provided that there is no obstruction to
the flow of blood through the veins, and that the general blood pressure in Cremains constant,
dilatation of an organ may be taken as an expression of vasodilatation in the arteries with
which it is supplied. The diminution of the resistance in A may also increase the velocity
of the flow through the part, since the amount of blood flowing in a given period of time
through any vessel varies directly as the difference of pressure, and inversely as the resist-
ance in the vessel.’’
1 Fleisch, Schweiz. med. Wchnschr., June 10, 1920, 323.
? Starling, loc. cit., p. 989.
PHYSIOLOGY OF THE PERIPHERAL CIRCULATION 53
Vasodilatation, therefore, leads to increased circulatory conditions and
a heightened velocity of blood through the parts involved. Wherever, an
increased demand for local blood supply occurs, a nervous mechanism is set
into action with a view to enhancing the circulation. So also an increased
blood pressure will cause vasodilatation.
Fic. 28.— Diagrammatic illustration of physiological action of constriction and dilatation
of the arteries. (Starling)
If we compare these physiological observations with the phenomenon of
erythromelia described under thrombo-angiitis obliterans and arteriosclerosis,
we will appreciate how an increase of blood pressure or greater demand for
capacity 1s made on the superficial arterioles. For with so many of the deep
circulatory avenues occluded and with the diminished influx to the muscles and
profound parts, the tendency to fill the superficial arterioles and capillaries by
way of collaterals or paths still uninvolved, must be increased. And with the
rise in local pressure, an inducement to arterial expansion is at hand. To
what extent neurogenic vasodilatation is responsible is not known.
The Vasomotor and Autonomic Responses.—A large number of observa-
tions tend to show that after a transitory contraction, the capillaries are prone
to dilate upon the action of cold. Nagelsbach! observed that when the hand
is put into snow, reactive dilatation of the capillaries can be observed with the
Weiss”? method. ‘This author found the capillaries dilated and the circulation
retarded as a result of the action of the snow compress, the color of the fingers
becoming bluish, continuing so during a five minute period of observation.
After the removal of the snow and drying of the fingers, the altered color and
the dilatory circulation persisted about five minutes before the return to
normal took place.
The dilatation of the capillaries following the action of the cold is regarded
as a reactive process similar to that seen in acute inflammation and in the
hyperemic reactions after the applications of a tourniquet. A similar
phenomenon, elsewhere described as a reactive or reactionary or induced
hyperemia or erythromelia, is noteworthy in organic vascular diseases, espe-
cially in thrombo-angiitis obliterans. Some believe that the dilatation of the
capillaries may, however, be due to the direct action of the cold upon the
vessel muscle.
1 Nagelsbach, Deutsch. Ztschr. f. Chir., 160, 1920, p. 221.
2 Weiss, Ztschr. f. exper. Path. u. Therap., 1918, Bd. 19, p. 390. Described in Chap.
VIII.
54 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Such reactionary conditions may occur without participation of the spinal
nerves. Bier has shown that they manifest themselves in an extremity
that has been wholly cut off from the trunk experimentally, a glass tube
bridging the gap and providing for continuity of arterial circulation.
That the vessel nerves are not essential is deducible from the experiments
of Lewarchew! who was able to obtain reactions in the vessels even after the
electrical irritability of the cut nerve had been exhausted. It is hardly
extraordinary that such independent function of the muscle fibers of the
vessels exists, since the embryonic parts of certain animals are seen to contract
before nerves have been developed. We may concede, therefore, that the
reaction of the vessels through cold does not necessarily take place by way of
nerve paths. ‘This response in the vessels can be strengthened by adaptation
to climatic conditions. The reactionary rubor in thrombo-angiitis obliterans
is another beautiful example of adaptation of circulatory conditions to a new
status, and also can be observed to develop as it were, under our eyes, namely,
during the period of clinical observation.
The secondary vasodilatation after preliminary vasoconstriction that
results from the action of cold, seems to be of teleological significance, since
nourishment of the affected part is furthered by the increased flow of blood.
These phenomena seem to occur most rapidly and most intensively in the
exposed portions of the body. The dilatation of the capillaries diminishes
the resistance in the affected territories, whilst the dilatation of the afferent
arteries makes possible the delivery of a larger quantity of blood. Thus,
the enhancement of the circulation adds calories to the parts, whilst the
flowing of the capillary stream by virtue of their dilatation enables a larger
distribution of calories to take place in the tissues. The added warmth thus
acquired can be so intensive that a limb dipped in ice water may lose no more
than .2° C. after almost an hour’s exposure.
In anemic individuals the reaction is deficient. In keeping with this
observation is the fact that anemic individuals are more apt to suffer from
frost-bite. Bier has observed that in such individuals it is difficult to produce
the typical red form of stasis (hyperemia) or congestion upon the application
of the elastic bandage.
The changes in the tonicity of the vessels is partly of reflex origin, and so
remote actions may be produced. When one arm is plunged into cold water,
the cutaneous vessels of the other arm may undergo constriction; and indeed,
with even a similar but less marked reaction over other parts. This phe-
nomenon has been employed by physiologists (Stewart) in studies of blood
movement in the extremities, and is often invoked as an index of the sus-
ceptibility of the vascular system to vasomotor reflexes.
The Chemical Regulation of the Blood Vessels.—Substances called meta-
bolites produced incident to katabolic activity, may chemically stimulate
the vessels themselves and increase the blood flow. Krogh believes that there
is normally a hormone, possibly derived from pituitary function, that brings
about a certain degree of tone in the capillaries. Here we are concerned,
however, with the larger vessels.
The great enhancement of the flow through the muscles associated with
muscular exercise is brought about largely by overactivity. The experi-
mental introduction of carbon dioxide or lactic acid into the blood causes
marked dilatation of the blood vessels of a limb. Carbon dioxide then,
regarded as a universal hormone liberated in the circulation on general
1 Lewarchew, Pfliiger’s Arch., 1881, Bd. 26, p. 60.
PHYSIOLOGY OF THE PERIPHERAL CIRCULATION 59
increase of body activity, seems to have not only a central effect through
excitation of the medullary and spinal centers (causing contraction of the
blood vessels), but also a local peripheral effect bringing about vascular
dilatation. The total result therefore, according to Starling would be “to
cause dilatation of the blood vessels of the part when carbon dioxide is pro-
duced, and where it is present in greatest concentration, and vascular con-
striction elsewhere under the influence of the sensitive nervous system.”’
How such physiological processes are deranged, can be exemplified by the
ischemia that is often noted after exertion in the foot and legs of cases of
arteriosclerotic disease and thrombo-angiitis obliterans. Such blanching
is diametrically opposed to the functional regional demands and to the modus
above described. Whether we are to presuppose a heightened irritability of
the vasoconstrictor centers whose actions nullify the local tendency to arte-
rial expansion produced by the carbon dioxide, or whether by reason of
impoverished local circulation, other chemical agents counteract the expected
and usual phenomena, are questions that have not as yet been solved or
satisfactorily answered.
The products of tissue activity are also believed to exercise an influence
on the caliber of the arterioles. Gaskell demonstrated that acids (especially
lactic) may have a direct action on the arterioles, causing these to relax.
Bayliss found that carbon dioxide produces a like effect. Both the latter
and lactic acid result from processes of oxidation, carbon dioxide in all cellu-
lar activity, lactic acid usually in muscle. Bayliss concludes that carbon
dioxide may be one of the chief chemical agents capable of bringing about
increased blood supply to active tissues. However, the action of ‘“‘metabo-
lites”’ is in all probability aided by vasodilator nervous reflexes.
The Internal Secretions and the Circulation.—The endocrine glands have
a double relation to the vegetative nervous system; and the regulation of
their secretory activity is believed to be dominated by the vegetative paths
in spite of the fact that the glands may functionate when all afferent nerves
have been divided. Then, too, the hormones delivered into the blood paths
may modify the excitability of the vegetative nervous system.
For example, the adrenals receive secretory fibers from the splanchnic; and adrenalin on
the other hand, may stimulate, the sympathetic nerve endings, and in turn enhance the
secretory activity of these glands.
Authors are not in accord regarding the influence of the thyroid secretion
on the vegetative nerves. It probably exercises a stimulating effect upon the
sympathetic and parasympathetic fibers.
It may suffice here to refer briefly to the latest theories regarding the
action of adrenalin, the hypophysts and the pituitary bodies.
Adrenalin.—The constrictor effect of adrenalin on the small arteries,
arterioles, capillaries and portal veins with the consequent increase in
arterial blood pressure is well-known. This contraction has been observed
after section of the cervical cord, and destruction of the spinal cord, and
therefore has been interpreted as an influence acting directly upon the
vascular musculature. The vasomotor centers, however, are regarded as
playing a réle by some. Although physiological observations would indi-
cate that the normal vessel tone is dependent upon the direct action of ,
adrenalin, this view is not in accord with the circumstance that the adrenalin
action disappears rapidly; nor is it in consonance with the failure of the
blood pressure to fall after bilateral exclusion of the adrenal bodies. And
so others take the view that adrenalin under normal conditions conserves
56 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
the receptivity of the vessel musculature to stimuli brought to it from the
central nervous system. Still others believe that under excessive demands,
an abnormal amount of adrenalin is given off, and the vessel muscle is directly
irritated by this internal secretion. Under such circumstances the adrenal
bodies play an important réle in the regulation of the vascular tone.
The question as to whether adrenin contributes under normal condi-
tions, in the maintenance of the blood vessel tonus has given rise to much
discussion. Although many believe that this substance is continually
present in the blood and is a factor in the maintenance of the tonus of the
blood vessels, Hoskins,! Vincent,” and Stewart? are not in accord with this
view.
These investigators have been unable to find adrenin in the blood stream.
Furthermore, under normal physiological conditions, they believe that it has
no effect on the physiologic processes. Under special strain, however, when
the sympathetics are stimulated, the chromophil cells of the medulla of the
adrenals are stimulated and adrenin is thrown into the blood steam. Under
these conditions it may intensify and prolong the sympathetic action.
Adrenin may not always produce vasoconstriction as is generally believed.
Its effect depends upon its concentration and dosage; and it may produce
vasoconstriction in one set of vessels and compensatory vasodilatation in
others.
Hartman‘ states that the mechanism causing vasodilatation in the intestine, when
adrenalin is injected into the general circulation, is located in the collateral sympathetic
ganglia, probably in the superior mesenteric ganglion. He further believes that ‘‘in the
adult, adrenalin poured into the blood in small quantities, causes by its peripheral effects,
constriction of the vessels in the skin, mucous membranes, and abdominal organs, driving
the blood into the vessels supplying the skeletal muscles which are actively dilated for its
reception through the effect on the sympathetic and dorsal root ganglia mechanism. But
as the quantity of adrenalin liberated increases, the peripheral effect begins to overcome the
gangliar effect in skeletal muscles, the intestinal vessels by action on the sympathetic ganglia
begin to dilate and the blood is reversed in its path.”’
The role of adrenalin with respect to its influence on the regulatory vegeta-
tive mechanism in the corpus striatum and mid-brain (Dresel-Brugsch) is
given more detailed consideration elsewhere (Chapter on Vasomotor Neuroses).
The hypophysts cerebri is also believed to have an influence on the circula-
tion. A colloid substance is formed in its middle portion, which is said
to extend and permeate through the infundibulum into the third ventricle.
According to Schaffer two substances can be extracted out of the hypophysis,
and these differ chemically. One of these produces a transitory fall of
arterial pressure. The other substance is pztuztrin, which can be extracted
from the human hypophysis, and which causes retardation of the heart
action. All vessels of the body, even those of the lungs and the heart may be
caused to contract by the action of pituitrin. Only the vessels of the kidney
are an exception, for these may even dilate. The action of pituitrin as a
vasoconstrictor is more durable than that of adrenalin; but after repeated
injections its effect diminishes, and may at times bring about a reduction in
the blood pressure. Inasmuch as the action of pituitrin continues even
after destruction of the higher vasomotor centers, it probably has a direct
influence upon the peripheral vascular mechanism.
It has been recently suggested that the blood contains a substance
essential for the maintenance of the contractility of the Rouget cells—those
1 Hoskins, Endocrinology, 1, 292. 3 Stewart, Endocrinology, 1, 151.
* Vincent, Endocrinology, 1, 140. 4 Hartman, Endocrinology, 1918, 2, p. tr.
PHYSIOLOGY OF THE CAPILLARIES oO”
elsewhere described as responsible for inherent capillary activity. Experi-
ments (Krogh and Rehberg) have sought to identify this substance with
the pituitary hormone. Indeed, preponderating evidence is in favor of
the existence of such a hormone that may act in a dilution equal to 1:100,000,
Or 1:1,000,000 of commercial pituitrin.! When circulating in the blood, a
physiological effect is doubtless exercised on the capillaries. In view of
the discrepancies in the action of pituitrin on various vessels of animals,
much clarification of our present knowledge on the mechanism of capillary
tonus is still desirable.
CHAP TIGR y If
PHYSIOLOGY OF THE CAPILLARIES?
General Considerations.—For an understanding of the visible mani-
festations of changes in arterioles and capillaries in deranged circulation
of the extremities, it is well to review certain elementary facts regarding
capillary circulation.
1. The total number and volume of the capillaries is enormous as com-
pared to that of the arterioles.
2. The rate of flow is greater in the arterioles than in the capillaries.
3. Pressure on the arterial side must needs be markedly increased when-
ever the caliber of the arterioles becomes diminished; for here the flow is
rapid and friction is proportionate to velocity.
4. The importance of variations in size of the capillaries can be well
understood if we consider that but slight dilatation over a large area may
cause accumulation of a large amount of blood.
Recent observations in the normal state of the capillaries and their
responses to various stimuli are illuminating and open a new vista of thought
in explanation of signs of obstructed peripheral circulation.
Normally, a relatively small number of capillaries in the muscles is filled
with blood (Krogh). Muscular activity alone suffices for the dilatation of
the collapsed capillaries. Nature would not adequately play her rdéle did
not the arterioles, too, enlarge commensurately. For, with dilatation of
capillaries alone, the total blood supply would be hardly augmented, and
stasis in the dilated capillaries with defective oxygenation occurs. With
contracted arterioles the stagnation would be intensified.
From these physiological facts we would infer that a disharmony in the
reciprocal functional activities of arterioles and capillaries may be responsible
for some of the clinical evidences of disturbed cutaneous circulation.
But an independent activity of the capillaries plays an important part
both under normal and pathological conditions. Whilst the arterioles may
contract synchronously with the capillaries as upon the action of cold,
they may manifest opposite motility.
When the skin is hyperemic, red and warm, the flow through the capil-
laries is enhanced and the arterioles are simultaneously dilated. This is a
defense mechanism of nature against cold and other insults.
When the skin is cyanotic or bluish, it is usually cold, the supply of
blood impaired, oxygenation diminished and the current of blood retarded.
1 Parke, Davis & Co., pituitrin from the posterior portion of the pituitary.
? For deductions based on capillary microscopy the reader is referred to Chap. CVI.
58 CIRCULATORY APFECTIONS OF THEE AT REMIT ES
Here we must assume opposed activities—the arterioles constricted, the
capillaries open or dilated. It is conceded to-day that these structures are
capable of active alterations in caliber.
The fact that capillaries consist of but a single layer of protoplasmic
cells and are devoid of a muscular coat does not preclude active changes in
their caliber, since we know that cells other than muscle can undergo altera-
tions in form under stimulation. More recently, however, powers of con-
tractility have been relegated to certain other elements in the capillary
walls (Vimtrup and Krogh). Rouget in 1873 described strongly branched
contractile cells lying on the outside of the endothelial walls, sometimes
almost completely encircling the capillaries. Latterly it has been shown
that the contraction of capillaries begins at one or more of these cells. Their
function is believed to be that of altering the lumina.
The Autonomic Action of the Capillaries.—Clinical observations on the
variations in color tints that may occur in many of the neurogenic forms of
the vascular maladies have often aroused the doubt that pathologic nerve
impulses alone could explain the phenomena. Let us recall the evanescent
mottling of red, white and bluish black that may come and go in certain
cases of thrombo-angiitis obliterans, particularly when the affected part is
unclothed in a warm room after exposure to the cold; and let us call attention
to the play of colors and the variegated mottling in patches of indeterminate
shape and size that are characteristic manifestations in some of the cases of
vasomotor instability and Raynaud’s disease. Such multiform evidences
of capillary activity or passivity, corresponding to no known areas of vascular
or even nerve distribution, have oft awakened the thought that neither purely
mechanical, obstructive or neurogenic influences offer adequate explanation.
Leaving out of consideration the réle of the pumping mechanism, and
reviewing the peripheral factors in the blood vessels themselves, we have
been taught that vasomotor influences are for the most part responsible for
the alteration in peripheral resistance, and the quantitative distribution of the
blood into the tissues. Physiologists have relegated the functional vessel
control to the vasoconstrictor and vasodilator nerves that are said to act in
the arteriole walls. It has been conceded, too, that because of a certain
sensitiveness on the part of the vessels and the products of cellular activity,
and possibly exogenous toxins too, local vascular changes in volume might be |
the result of the action of metabolites and hence not be altogether dependent
on nerve control. Hooker,! believes that capillaries can dilate or contract ©
independently of the larger vessels with which they are continuous. The
capillaries and venules are thus regarded as able to furnish peripheral resis-
tance as well as the arterioles. Hooker concedes the réle of chemical factors
as influencing the peripheral circulation. He thinks that, as a rule, there is a
harmonious interrelation of the activity of the higher nervous control and
the primordial autonomic (possibly chemical) regulated forces possessed by
the smallest vessels.
For an understanding of this more modern view regarding the activities
of the capillaries and their responses to both nerve and local chemical influ-
ences, some of the observations and researches that have led up to the
acceptance of autonomic activity may be worthy of mention.
The facts that have been experimentally adduced may be summarized as
relative to:
t. Nerve control of capillaries and venules; and
1 Hooker, Am. Jour. Physiol., 54, 30, Nov. 1, 1920.
PHYSIOLOGY OF THE CAPILLARIES a9
2. Direct influences on capillaries, arterioles and venules. This second
group of possible motivating agents is again divisible into
(a) Direct mechanical stimuli; and
(6) Direct chemical (metabolic, katabolic) stim uli.
The clinical data in support of the newer concepts will be discussed
separately wherever the diseases or manifestations of deranged peripheral
vascular function seem to have a bearing on the hypotheses here expressed.
1. The Nerve Control of the Capillary Circulation.—In the theory of
capillary function, the effect produced by nerve stimulation is the cardinal
factor. Sectioning and stimulating the cervical sympathetic in the cat
produce at first a cessation of corpuscular flow, due in all probability to
arteriolar constriction. The corpuscles then begin to clump and move for-
ward in an irregular fashion, so that in the relatively brief time that the
electrical stimulus is continued, the corpuscles disappear from the field of
observation. Immediately after cessation of the stimulus, however, the
appearance of corpuscles from the arterial side is again noted in more profuse
flow than before. This phenomenon can be obtained successively on the
same preparation without any indication of fatigue, evincing conclusively
that the capillaries and venules are subject to nervous control.
Still other experiments (Krogh) on the capillary responses to punctiform
trauma of the frog’s tongue have demonstrated that stimulation of sensory
nerve filaments may result in capillary dilatation; and this by way ofa
sensory vasomotor nerve reflex in an antidromic direction.
It is generally conceded to-day that epinephrin acts only on tissues with
sympathetic innervation. If 3 cc. of a 1:50,000 adrenalin solution be injected
intravenously, the action of the capillary bed is similar to that in nerve
stimulation, in that there is a cessation of the corpuscles, clumping, with
gradual and irregular movement out of the field. It may be accepted then
that the observations here described are directly dependent upon a functional
response of the endothelium.
Recent observations also point to a regulatory nerve mechanism in the
case of the veins.
Peripheral Venopressor Mechanism.—Venous pressure may be caused to rise! in the
sigmoidal area of the large intestines in dogs, isolated except for its nervous connections
via the inferior mesenteric ganglion. After washing out the blood by perfusion, the artery
was left open and the drainage vein connected with a water manometer. A rise of pressure
of 7.5 cm. of water followed direct electrical stimulation of the nerve to the part;
indirect stimulation (asphyxiation) acting by way of the medulla gave a rise of 4.5 cm. of
water. For the latest views on Capillary Microscopy in this disease see Chaps. CVI et seq.
FUNCTIONAL DISTURBANCES OF PERIPHERAL CIRCULATION fii
erythromelalgia, scleroderma, and the passive hyperemias of cardiac or
vascular origin. In general we may say that increased pressure in an artery
of supply due to narrowing of the latter, causes retardation of the capillary
stream.
The changes in capillary flow result in corresponding alterations in capil-
lary blood pressure. This endocapillary pressure is increased both in active
as well as in passive hyperemia, whilst it is diminished in ischemic conditions.
With too great a diminution of endocapillary tension the nutrition of the
part must suffer; some injury, too, ensues upon too intensive an increase
of pressure.
As a consequence of a rise in endocapillary tension, diapedesis of the red
blood cells is a common occurrence, particularly with passive, but also with
active hyperemia. ‘The character of the capillary wall, however, also plays a
role in this filtration. A predisposition or hyperpermeability may be
acquired by the capillaries through the induction of artificial ischemia (post-
anemic diapedesis). A predisposing factor, therefore, is artificial ischemia,
which may be observed after the use of an Esmarch bandage. Old people
are especially susceptible. Diseases, too, that alter the constitution of the
vessels (scarlet, grippe, etc.) may also increase the susceptibility to diapedesis.
These observations are of some clinical importance in that they teach
the lesson that the production of too intensive ischemia through whatever
means should be avoided whenever marked obstructive disease of the arteries
of an extremity is at hand. The application of an Esmarch or Martin
bandage for purposes of making functional tests is not without danger, for
irrespective of the perils of thrombotic sequels, the extravasation of red blood
cells may predispose to local necroses and gangrene. So, too, the application
of the author’s postural treatment: for enhancing the circulation and nutri-
tion of the part, must be so carried out that the period of induced blanching
is minimal.
Through the same action a migration of leucocytes, too, may take place
(leucodiapedesis). Because of the spontaneous activity of these cells, we
usually substitute the word emigration for diapedesis. With retardation of
flow the white cells approach and are heaped against the vessel wall. Their
transmigration goes on, both through filtration and their own motility.
Arterial spasm, when it involves larger vessels as in Traumatic Angto-
spasm, gives clinical pictures quite different from those following con-
traction of the arterioles. When the latter contract strongly, the blood
still seeks the veins through the force of the vis a tergo, the capillaries becom-
ing emptied. With this the part blanches and its volume may become
lessened. As the veins fill and the pressure therein overbalances that in
the capillaries, the part may become cyanotic, and even regurgitation of
venous blood may take place. This condition becomes accentuated when
the affected part is in a dependent position.
If we test for return of color after digital expression (compression test)
in asphyctic skin in which the arterioles are constricted and the capillary
circulation poor or nil, the reappearance of cyanotic color must not be
mistaken for evidence of circulation, for it is but the venous blood com-
ing into view.
Spasm of venules is said to be possible, but without arteriolar contraction
the immediate blanching is absent. Lividity is produced through stagna-
tion of the blood in the capillaries. A generalized spasm of arterioles and
1See treatment of arteriosclerotic vascular disease and thrombo-angiitis.
78 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
venules is said to occur, and this is followed by ischemia of the part (anemia).
Associated is a reduction in volume of the part.
2. Disturbances Due to Impaired Exchange of Fluids.—As far as we
know, the capillary walls have partial permeability, not allowing all substances
to pass equally well from both sides. The chemical bodies of the absorption
stream (from the blood into the tissues) are also different from those of the
excretion or outflowing stream (from the tissues into the blood). These
functional elective powers disappear as the tissues lose their vitality. For all
the phenomena are not explicable on the basis of filtration, diffusion and osmo-
sis, but a capillary secretory activity may play a réle. The locality of the
interchange is probably the intercellular spaces. Alterations in the fluid
stream may be of quantitative and qualitative nature.
The changes in capillary pressure also modify the fluid exchange. If we
accept the theory that diapedesis may be a sequence of the above, we must
also be ready to believe that analogous alterations in the fluid waves may
ensue. Indeed, in the occurrence of postanemic edema, we have an example.
After artificial hyperemia, an intensified lymph current has been noted as
an accompaniment of the increased absorption stream. A diminished capil-
lary pressure can evoke an increase in the excretory or outflowing stream.
An excess of capillary pressure may cause fluids to percolate outwards
from these channels; and the increased intercapillary tension may follow
local arteriolar dilatation, venular contraction or venous obstruction, edema
resulting from obstruction to venous flow. It is not certain as to what rdéle
forces other than mere filtration, play in this abnormal fluid exchange.
The theories set forth are that the sluggishness of the capillary flow increases
the permeability of the capillary walls; or, that certain alterations in the
metabolism of the tissues outside of the capillaries make for increased fluid
imbibition from the blood.
For an understanding of some of the trophedemas and conditions of neuro-
trophic nature that are dependent on deranged capillary function, it may be
well to point out that although intracapillary pressure is often responsible for
pathologic phenomena in the tissue currents, the condition of the capillaries
themselves may be the more important. So we have on the one hand, the
nutritive disturbances of the capillaries due to anemia and passive hyperemia;
but, on the other hand, the alterations that certain substances may produce.
Many bodies may increase the activity of the absorption stream. Some are
specifically vessel poisons such as the toxin of diphtheria, tuberculin, pneu-
mococcus serum, etc. But even for the action of these substances a certain
predisposition or idiosyncrasy is necessary. (This is seen in the abnormal
susceptibility of certain individuals to strawberries and shell food.)
Some authors believe that the tissue stream may be modified through nerve
influences. ‘These may be manifested in the production of a neurotic hypere-
mia as well as in an altered permeability of the capillaries. The urticaria
following mechanical irritation of the skin is an evidence in favor of such
a function. Whether a preceding or coexisting reflexly evoked hypere-
mia is responsible wholly or in part, is still a mooted question. In the
evanescent edemas without hyperemia, a direct neurogenic basis is probably
present.
The administration of calcium chloride tends to reduce the permeability of the capillaries
and is therefore of value in circumscribed edemas. Increased density of the cellular mem-
brane through increase of calcium content as well as the opposite effect on intensified
permeability in the deficiency of calcium salts, are well known biochemical and physiological
observations.
FUNCTIONAL DISTURBANCES OF PERIPHERAL CIRCULATION 79
To digress for a moment, it may be well to call attention to the theories
of some of the more recent investigators on the vegetative system regarding
the rdle of the calcium salts in spasmophilic tendency. According to these,
defective calcium metabolism with diminution of this salt, may be an impor-
tant factor in the production of hyperirritability of the vasoconstrictor
centers.
Functional Derangement of the Lymphatic System.—Although it is
known that the intercellular spaces communicate with the lymphatics, it is
still doubtful as to whether they are separated by a thin membrane or not.
Tissue juices or fluids must not be confused with lymph. All cells are not in
direct communication with the lymphatics through the tissue fluids, since
some cells are directly apposed upon the blood capillaries.
Here, too, quantitative and qualitative changes in function occur.
Abnormal acceleration or retardation of the lymphatic flow represents the
former. ‘These may be the result of variations in the production of lymph
and in its outward flow.
Mechanical factors, such as pressure, tumor growth, collections of fluid and thrombosis
may diminish the outflow of lymph. Diseases of the lymphatics and lymph nodes may
interfere with the lymph flow. When there is increased pressure in the venous system, the
discharge of lymph into the veins may be impaired.
Cessation or diminution of lymph flow may set in when the production of lymph is
correspondingly defective as in arterial ischemia. There are a number of substances that
increase the lymph flow. Amongst these are hypertonic salt and sugar solutions injected
into the veins.
Disturbances of the Lymphatic Stream of Capillary Origin.—Since derangements of flow
in the capillaries are transferred to the lymph stream, accumulations of fluid in certain
parts of the body may result. Collections in the tissue spaces are known as edema.
When a large venous trunk of an extremity is ligated in an animal, there usually follows
an increased lymph flow without any edema. If we simultaneously interfere with the
lymphatic flow, or if the blood be hydremic and the vasoconstrictors paralyzed, then edema
may ensue. In general venous stasis, however, edema appears since by reason of the
increased venous pressure the lymphatic outflow from the thoracic duct into the subclavian
vein is impeded.
Edema usually follows derangement of the capillary walls. It can, however, result
from alterations in the cells by virtue of which these give off larger amounts of fluid. As
corollaries, we may mention that transudates seem to indicate an origin through capillary
lesion, whilst the edemas, because of their salt content, may be more correctly explained on
the basis of disturbances in the cell function.
Local fugitive edemas (edema fugax) warrant the supposition that both a local predisposi-
tion of the capillaries as well as neurogenic factors or blood composition, may be at fault.
Inflammatory edema has several causes including lesions of the capillaries and tissues.
Disturbances in Continuity of the Vessel Constituents —Pathologists
(Hering) speak of solution of continuity in respect to the cells of a vessel
and a more gross variety in which the cells themselves are broken up. Whilst
the latter may occur in any vessel, the former applies only to the capillaries
in which varying degrees of separation of the cells from each other may
take place. Solutions of continuity may be produced by a large number
of causes. Mechanical or external agencies, increased pressure from within,
degenerative processes (atherosclerosis, arrosion) infection with suppura-
tion and necrosis, neoplasms and ferment action—all these are amongst the
agencies observable.
In vicarious menstruation, hemorrhages have been attributed to the action of the
internal secretion of the ovaries as also to neurogenic factors.
Diapedesis (or the escape of the red blood cells through separated endothelial elements)
may be altogether due to increased endocapillary pressure into a certain predisposition of
the vessels themselves. The hyperemias are the exerting moments. In the anemias, the
factor of susceptibility may be extraordinarily prominent (so also in hemophilias, purpura,
SO CIRCULATORY AFFECTIONS OF THE EXTREMITIES
etc.). Various poisons alter the fragility of the vessels. We can gain a rough clinical idea
of the degree of individual susceptibility to diapedesis by comparing the tendency to hemor-
rhages after artificial stasis over a given period with the normal. The usual disposition
has been characterized as the “‘endothelial symptom.’
THE SUPERFICIAL CIRCULATION IN OBSTRUCTIVE VASCULAR DISEASES
If we were to enumerate the agents through which objectively visible
alterations in the superficial circulation are modified, we would include:
(1) The diminished force of the stream (vis a tergo).
(2) The hydrostatic and gravity forces.
(3) The changes in the vasomotor mechanism.
(4) The local forces, that directly influence the autonomic capillary
activities.
These all should be taken into-account in explanation of the phenomena
of asphyxia! and rubor,? so often characteristic signs of the obstructive arterial
diseases of the extremities.
1. The Diminished Circulation.—To go into a detailed discussion of the
altered dynamics that are entailed through the exclusion of existing and
important vascular channels, would be a work of supererogation, For, on
the one hand, the thesis requires neither emphasis nor explanation for com-
prehension; and on the other hand, an exact measure of the diminution of
volume and celerity of the blood stream is beyond the pale of our applied
physiological and clinical methods. We must be content, then, to assume
the existence of impaired flow, for, we have no accurate means of estimat-
ing the degree of circulatory impoverishment in a given case, beyond that
knowledge which the rough clinical methods to be described may furnish
us.* Certain it is, that a sufficient reduction of this flow is often obvious in
those significant pallid feet and legs that are cold and blanched even in the
horizontal position. ‘That a reduction in the fullness, or even a collapse of
arterioles and capillaries of peripheral skin and subcutaneous vessels must
obtain through this mechanical cause alone, may be accepted without hesita-
tion. We have elsewhere called attention to the vasoconstriction occurring ~
in arterioles and capillaries as a secondary response.
2. The Forces of Hydrostatic Nature and the Role of Gravity may require
but passing mention, since their more detailed workings and manifestations
will receive attention in other chapters. Through the unnatural imbalance
between the strength of the pumping mechanism and the increased local
resistance through the exclusion of larger avenues, and the prominence of
devious and smaller pathways, conditions are given for an enhancement of
the effects of gravity and hydrostatic forces. Indeed, the latter are influen-
tial, inversely with the patency of the natural vascular lumina; or they
modify the objective circulatory phenomena more and more, the greater the
obturation in the affected vascular territory.
Whereas the normal limb when elevated above the horizontal, presents
a pinkish integument even over the most peripheral parts, gravity and hydro-
static pressure may make for complete blanching when larger vessels are
occluded. And so, the position of the part must be taken into due consider-
1 Vide, Chap. XLVII, Cyanosis in Thrombo-angiitis.
? Vide, Chap. XLVI, Erythromelia.
3 Except perhaps the method of Stewart (Chap. VI) which has not been extensively
used.
FUNCTIONAL DISTURBANCES OF PERIPHERAL CIRCULATION 81
ation when the fullness of arterioles, capillaries or venules is being investi-
gated or discussed. Whilst elevation may deplete the venules (when the
veins are adequate for return), depression may make for stasis and asphyxia
when the propulsive forces are inadequate to force the blood through
arterioles, capillaries and venules with sufficient celerity.
3. The Changes in the Vasomotor Mechanism.—Many of the basic
facts that physiologic researches have brought to light have already been
summarized in the chapter on anatomy and physiology of the vasomotor
paths. Here we wish to allude merely to those special circumstances in
local disease that bring about alterations in the normal mechanism. Such
occur both in the neurogenic and organic obstructive vascular affections.
Concerning the former, a more detailed discussion will be relegated to the
chapters that are concerned with the special classes of vasomotor neurosis.
The deviations of nerve function in the latter, however, may properly be
referred to here.
Nerve malfunction may result from the following causes.
1. Organic intrinsic lesions of the vessels and perivascular tissues impli-
cating the terminal nerve distribution.
2. Perivascular inflammatory and secondary fibrotic processes (thrombo-
angiitis obliterans) influencing the adjacent nerves.
3. Reflex alterations.
4. Exhaustive states.
5. Altered local metabolism and abnormal chemical products in the
tissues.
In thrombo-angiitis obliterans the perivascular fibrosis and the inflamma-
tory products of the acute stage may exert an influence on the surrounding
sensory and motor nerves. Through the former, both pain impulses and
reflexes with vasomotor responses may travel. That pain alone may evoke
neurovascular phenomena has been elsewhere mentioned.
We need only emphasize here the great importance of reflexes on the
vasomotor functions, for these have been already described. In addition
to the multitude of impulses that are constantly received from within and
throughout the body, local changes, metabolic, nutritional and patho-
logic (especially trophic ulcers, etc.) as also external causes (thermal and
mechanical) may play a réle in engendering abnormalities of vasomotor
function.
4. Exhaustion.—To what extent an exhaustion of the vasomotor impulses
of constrictor type can be produced through overactivity, cannot be
accurately determined. That a recoil into a paralytic state or a passive
vasodilatation is possible after continued angiospasm, cannot be denied.
Investigators have shown that certain chemicals may initiate a condition of
constriction that yields to a palsy with chronic dilatation. So, too, may
nervous mechanism finally fail, be it through continued and over-excitability
or be it through reflexes evoked through intense and constant pain.
5. Chemical Action.—If we base our conclusions upon the data furnished
by physiologists regarding the effects of chemical alterations in the tissues on
arterioles and capillaries, and the observations of clinicians, we must assume
that an abnormal vasomotor mechanism can be induced when pathological
nutritional conditions obtain. In this way a reversal of a normal vaso-
dilating response into an abnormal vasoconstricting reaction may occur when-
ever an unusual stress (exercise) develops an inordinate amount of poisonous
constituents in poorly nourished tissues. It has been assumed that the symp-
6
82 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
toms of intermittent claudication (page 156) may be brought about in
this way.
In arteriosclerosis and thrombo-angiitis obliterans, where circulation is inadequate,
exercise produces an accumulation of CO: and lactic acid and a deficiency of O. These
chemicals are believed to be able to cause a reversal of the vasodilating into vasoconstricting
reflexes. The cramp-like pains that succeed, have been interpreted as the subjective
manifestations of this altered physiology. According to Hopkins the normal cycle of
events in muscular activity consists of two phases separated in time: the first anaerobic
during which lactic acid is formed; the second aerobic during which it is removed. Only
with conditions of inadequate oxygenation will this acid accumulate. Perhaps it is this
chemical that calls forth the reflex.
CHAPTER XII
COLLATERAL CIRCULATION
By the term collateral hyperemia we may designate that arterial flow which
occurs in the territory adjoining one whose main artery has become occluded.
The origin of such hyperemia depends upon the nature of the arterial distribu-
tion. Whenever adequate arterial anastomoses are present, as in the case of
the arteries of the hand or the foot, obturation of one large trunk is imme-
diately followed by deflection of the current into other adequate paths. If
the arterial connections, however, are insufficient ,an anemic focus surrounded
by a peripheral zone of collateral hyperemia develops.
The term collateral hyperemia has also been defined as that increased influx of blood
which may occur into one of a pair of important sister organs, such as the kidneys, when
the artery of one is occluded or the organ itself has been removed. Certain conclusions
concerning the physiologic hyperemia occurring in such organs may be extended to the
peripheral vascular system. Increased blood pressure consequent upon the occlusion of
a large vessel leading to such an organ would not account for the vicarious hypertrophy of
the remaining organ; and a reflex irritation of vasodilator nerves has been suggested as a
more plausible explanation.?
Another similar manifestation is the secondary or postanemic hyperemia
that occurs after transitory arrest of the circulation in an extremity.
Collateral hyperemia is the prelude to, or preliminary stage of an elabor-
ation of a new collateral arterial circulation after occlusion of an important
arterial trunk. Its development takes considerable time. Whenever a
large artery is ligated, collateral flow occurs in reverse direction and usually
with great rapidity. The development of such a current is proportionate to
the dilatability of the arteries. In the development of collateral circulation,
either small arterial anastomoses participate or new ones must be formed.
As a rule, the anastomosis formation is well marked in a few days.
In collateral circulation, as well as in that of collateral hyperemia, the
mechanical factor of increased pressure does not sufficiently explain its origin.
Continuous dilatation of the arteries presupposes diminution of the tonus to
nerve influence; and we would suppose an iucreased tonus after increased
pressure. The genesis of collateral hyperemia after closure of a large arterial
trunk, therefore, must be regarded rather in the light of a product of altered
innervation, possibly of irritation of the vasodilators. Pari passu with the
dilatation of the small vessels, increased growth takes place, so that large
thick walled vessels may result from small thin ones.
1 Hopkins, Harvey Lectures, 1920-1921, p. 210.
2 See Chapter XLVI on Erythromelia and the explanation of rubor.
COLLATERAL CIRCULATION 83
The collateral avenues are preexisting channels whose total capacity bears
a relationship to their size (caliber), number, patency and dilatability. Any-
thing which interferes with the accommodative enlargement of these, such as
sclerosis and congenital hypoplasia, may correspondingly limit their func-
tional value under special stress. The local increase of pressure above the
point of arterial obstruction is important in the development of the collaterals.
Its degree is proportionate to the size of the closed vessel, and also influenced
by the general blood pressure. How delicate the mechanism causing circu-
latory disturbances is, may be concluded from the observation that hyper-
tension may be produced also through reflex causes as well as mechanical.
It is even believed that the chemical alterations in the anemic territory may
bring about a rise in tension. So also, dilatation of the collaterals may be
evoked by reflex as well as mechanical forces. Since the general pressure
depends on the heart action, the development of collaterals, too, will be
similarly modified. Weeks and months may be required before the ultimate
collateral circulation has been formed.
Bolognesi! performed experiments to determine the effect of ligating the external iliac
artery in dogs. The ligation was done with a double catgut ligature under perfect asepsis
and by the extraperitoneal route. For the first two days following the ligation the femoral
pulsations disappeared but soon thereafter returned to normal. The animals were killed
after varying periods of time and the vascular systems of both limbs studied with the X-ray
after the vessels had been injected. The results of this study are summarized as follows:
(1) The arteries below the ligation were found to be enlarged and to possess more
numerous secondary branches than those of the corresponding area on the normal side.
(2) There was no return of circulation in the tract of the external iliac artery at the end
of one month but after two or three months a true collateral circulation had been established
which was represented either by communicating arterial branches or by complete restora-
tion of the segment of the main artery which had been excluded between the two ligatures.
(3) The gluteal branches of the iliac artery, and especially these of the inferior or
ischiatic gluteal artery, took part in the formation of the collateral circulation becoming
larger and richer in branches. These branches anastomosed fully with the femoral
branches.
The results verify the theory as to the establishment of collateral circulation which was
brought forward by Porta as far back as 1845. They demonstrate also that the increase
in size of the preexisting collateral arteries is of greater importance than a very great
increase of newly-formed vessels. This vascular dilation persists until the collateral
circulation established is sufficient.
It has often been pointed out that a congenital hypoplasia of the vascular
system (sometimes cardiovascular) may be one of the predisposing factors
that render certain individuals, possibly also certain races, susceptible to
vascular affections. Indeed, for some of the vasomotor groups this theory
has found adherents. So also, the hypothesis has been extended to the cases
of organic vascular disease.
Whether or not a congenital maldevelopment, implicating, therefore,
possible collaterals as well, is influential in preventing the proper and ade-
quate compensatory enlargement and dilatation of surrogate circulatory
paths, is a question worthy of consideration. If vessels are inherently too
small, it is not unwarranted to assume that when obliteration of important
avenues of circulation interrupts the blood flow, the collaterals will become
insufficiently developed and that gangrene may eventually ensue.
From the anastomotic by-paths already existing, certain laws can be
deduced as to the means of ascertaining the efficiency of the collateral circu-
lation. If we study the course of these anastomoses and that of the palpable
portions of the femoral and popliteal, we will learn that isolated compression of
either vessel might give reliable information as to the circuit through which
1 Bolognesi, G., Chir. a organi di movimenta, r1grq, III, 403.
84 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
the collateral circulation travels. If, for example, we arrest the femoral
artery at Poupart’s ligament, after having induced ischemia in the limb,
either through an elastic bandage or prolonged elevation, and the circulation
returns to the blanched parts in the pendent or horizontal position, we are
warranted in concluding that a new source of blood supply has been estab-
lished from a higher level. Such extensive central displacement of the point
of influx is of rare occurrence.
If the femoral and popliteal are patent and the latter is similarly tested,
a positive flush or reestablished circulation would denote, too, that the col-
laterals are adequate, arising above the level compressed. The anastomotic
paths could emanate then from any level between that tested and the femoral
test point above.
On the other hand, should color fail to return, the totality of arterial
supply must be derived at and below the point at which the circulation was
artificially arrested.
Unfortunately, the femoral artery is not easily accessible to extraneous
obliteration by compression except in its upper part, so that more accurate
findings of the collateral niveau cannot be easily ascertained. Enough data,
however, can be put at our disposal to warrant interesting deductions.
If the test fails (circulation does not return after compression) at the
popliteal level, certain prognostic inferences may be made, to wit, that a
sudden thrombosis of this region would leave the distal parts without efficient
by-paths. Conversely, those patients in whom the result is positive (circu-
latory return) would offer a better immediate prognosis.
With a positive test at the popliteal and a negative one at the common
femoral, the intervening artery, in its totality, offers possibilities for ascend-
ing blockage that must be compensated for by the remaining patent and cen-
tral portion of its course. 3
Demonstration of Collaterals in Obstructive Vascular Disease.—Some
indications, as to the existence of effective new vascular by-paths can
be obtained by compression of the femoral artery in the case of the lower
extremities. Whenever chronic rubor is present, compression of the femoral
artery for from 2 to 5 minutes may not suffice to efface the color of the foot
in the diseased extremity, whilst similar compression on the healthy side pro-
duces marked blanching (paradoxical ischemia on the healthy, paradoxical
rubor on the diseased side). This would indicate that new interanastomoses,
connecting points above and below the femoral artery, are more efficient in
the diseased than in the healthy limb.’
The Course of New Channels.—The usual concept of these vascular
by-paths is vague. All will concede their teleological significance—that they
act as surrogates, devious, but nevertheless, purposeful avenues; and that
through interanastomoses they succeed in delivering a sufficiency of blood
even when large arteries are occluded. Little is known, however, as to
the exact course along which the blood flows in any given case; whether the
circulatory stream is shunted back again into an important vessel and thence
to the periphery, whether altogether new routes are followed, or whether a
combination of both exists.
Perhaps it is not generally appreciated that, when ligation of an impor-
tant artery is undertaken, the blood tends to seek and enter the main chan-
nels again at some point beyond the occlusion. According to recent
observations the task of the collateral is mainly to reestablish communi-
1 See also tests for abnormal vasomotor reactions in thrombo-angiitis, Chap. LIV.
COLLATERAL CIRCULATION 85
cation with the continuation of the main artery, and not to form a new
arterial system of more extended course.
When we speak of the collateral circulation in pathological conditions,
we must visualize for ourselves the three factors upon which the new course
of the circulation depends. These are: firstly, the situation of the most
proximal point of obturation in the main vessel; secondly, the condition of
the vessels beyond the central point of blockage—as to whether they are
patent, narrowed (atherosclerosis, arteritis) or occluded (thrombo-angiitis
obliterans); thirdly, whether the sudden advent of a centrally situated
obstacle (obturation, ligation, thrombus, compression) is immediately or
remotely followed by secondary stagnation, or accretion thrombosis in the
arterial or venous channels.
The problem of even vaguely appraising the direction of the collateral
paths through existing anastomotic channels becomes difficult part passu
with the amount of impairment of the integrity of the arterial tree beyond the
point of occlusion. Whilst it is easy to judge approximately as to the new
current when a large artery is ligated, or when a small embolus is lodged and '
unaccompanied by secondary thrombosis in arteries that are healthy and
patent, a very perplexing and intricate condition obtains when we are
ignorant of the exact extent of a preexisting occlusion in the peripheral
arteries. Therefore, in arteriosclerotic obturation and occlusion and in
thrombo-angiitis obliterans, the sudden advent of thrombosis or embolism
in larger more centrally located trunks offers a more dubious outcome, neces-
sitates a more devious and circuitous route for the substituting arterial paths,
and may make reestablishment with the former currents impossible.
The Collaterals When the Peripheral Arteries are Patent.—The fre-
quently accepted assumption that the ends of the extremities are in more
imminent danger of gangrene, the nearer to the trunk the ligature is placed,
is not in consonance with experience. And so it has been observed that one
can tie off the axillary artery and the common femoral without much risk.
Often the ligation of the femoral below the profunda is dangerous, while
ligation of the popliteal artery is almost always followed by gangrene.
In some investigations (Hotz) it was found that adequate collateral paths
are in evidence, wherever large muscle masses require supply, and that at the
insertions of muscles in the regions where transition into tendons occurs,
there is but a sparse distribution of the arterial by-paths.
In an attempt to explain two striking clinical observations on the frequency
of gangrene after ligation at certain levels in the course of the main arteries
of the lower extremities, some authors have concluded that the multitudinous
smaller muscular branches are perhaps even more important than the larger
and discrete anastomotic channels nourishing tendons, fascia and bone. ‘The
lack of development of muscular branches is given in explanation of the
occurrence of gangrene, when the popliteal artery is ligated. Theanastomotic
channels about the knee (see Fig. 31), although apparently sufficiently large,
do not seem to suffice when sudden occlusion of the popliteal artery occurs.
On the other hand, when a process of slow development (such as tumor or
aneurysm) has gradually diminished circulation in this region, the collateral
paths may have become adequately enlarged. In these circumstances
they are able to cope with the sudden emergency that arises when complete
occlusion by thrombosis or ligation eventually occurs.
The arteria profunda femoris has been considered important, for through
its anastomoses with the pelvic gluteal and sciatic arteries, it may act to
reestablish the current below its site of origin, when occlusion of the common
86 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
femoral takes place. This explains the paradox that sudden obturation
below the profunda may be even more dangerous than arrest of the circu-
lation above its point of origin.
A reference to Fig. 31 will recall the anastomoses about the knee joint known as the
circumpatellar anastomosis or rete patellae. In this rich network are engaged vessels in
the superficial fascia surrounding the patella, with branches to the patella, the knee-joint,
capsule and neighboring muscles. The vessels partaking in its formation comprise: from
above (1) the anastomotica magna from the femoral and the descending branch of the
external circumflex; laterally, the internal (3) and external (2) superior, and the internal
and external (5) inferior articular branches of the popliteal, and the muscular branches of
Fic. 31.—Schematic rough drawing of Fic. 32.—Schematic rough drawing of
collateral paths about the region of the collateral paths about the region of the
knee. (Hotz) elbow. (Hotz)
the same artery; and from below, the anterior tibial recurrent. Although these vessels
would apparently suffice as anastomotic channels, according to Hotz none of these give
adequate supply to muscles. Merely the fascial planes, the tendinous insertions of the
thigh muscles below, and the points of origin of the calf muscles above, are supplied with
the tendons and capsules of the joints. These circumstances have been regarded as provid-
ing an explanation for the danger of necrosis after ligation of the popliteal artery.
In the case of the elbow (Fig. 32) similar conditions obtain. The superior profunda
(1) by a medial collateral branch (5) anastomosing with the posterior ulnar recurrent and
with the interosseous recurrent (7); and in front of the elbow establishing communication
(4) with the radial recurrent (6); furthermore, the inferior profunda (2) or A. collateralis
ulnaris superior, also anastomosing with the posterior ulnar recurrent (7) behind the internal
condyle, while the anastomotica magna (3) makes connections in front of the internal
condyle with the anterior ulnar recurrent; and posteriorly with the posterior ulnar and
posterior interosseous recurrent. In view of the fact that these vessels not only supply the
capsule of the joint and the tendons (as in the case of the knee) but take care of the circula-
tion of large volumes of muscle, the contention of Hotz seems to be supported in the observa-
tion that ligation of the brachial at the elbow may usually be carried out, without danger
of gangrene.
CIRCULATION IN THE EXTREMITIES 87
In the case of the shoulder region and upper arm, the paradox has been again pointed
out that ligation above the circumflex arteries (anterior and posterior or their common
trunk) is less dangerous than below that point. A reference to Fig. 33 clearly shows how,
by anastomoses of the anterior circumflex with the acromial thoracic with the posterior
circumflex and through the anastomoses of the posterior circumflex with the same arteries
and the superior profunda (see 6 and 8 in Fig. 33), blood can be directly delivered from the
Fic. 33.—Schematie rough drawing of collateral paths about the region of the shoulder.
(Hotz)
axillary and subclavian through these channels, through which it may find its way again
into the main artery below the point of ligation. When ligation takes place below the
circumflex, a more devious route has to be taken by the current. Indeed, ligation below
the origin of the profunda should be still more dangerous. Ligation high in the axillary
may be borne by reason of the presence of the large vessels, the mammary, subscapularis,
and long thoracic. :
Therapeutic Development of Collaterals.—Methods for enhancing the
circulation must necessarily include those that further the development of
collateral channels. Intermittent compression of the femoral or brachial
artery has been suggested, and is a procedure that may be of some value in
the treatment of obstructive arterial diseases of the extremities.
CHAPTER ReexItt
CIRCULATION IN THE EXTREMITIES UNDER PATHOLOGICAL
CONDITIONS
CLINICAL MANIFESTATIONS
There is no better teacher of the varied circulatory phenomena resulting
from pathological conditions of the vessels of the extremities, than the clinical
manifestations that shall hereafter be described. Careful observation and
comparative appraisal of the normal and abnormal clinical manifestations
88 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
are most illuminating. Through these we will more clearly appreciate the
circulatory phenomena in diseases of various types and causation, than
through theoretical and physiological considerations alone. Nevertheless,
it may not be amiss here to dwell briefly on the more abstract questions,
leaving their amplification, explanation and illustration for subsequent
chapters.
The interpretation of the phenomena of disturbed circulation meets with
an abundance of pitfalls, if we do not carefully weigh the various factors that
may enter into the resultant subjective and objective states. Although the
blood supply of the extremities, and especially of their more remote portions,
depends primarily on the size and patency of the arteries and veins, many
other elements, both general and local may act to modify the abundance and
rapidity of the flow of blood. We need hardly dwell upon the importance of
the cardiac factor and general systemic condition, but shall confine ourselves
to the agencies of more local source and effect.
For example, a maldevelopment or hypoplasia of the peripheral vascular
tree is a condition common enough to warrant serious consideration, both
because peripheral nutrition suffers then more readily when vascular dis-
ease is at hand, and also because of its vitiating action on the development
of adequate collateral channels. ‘The presence of such an inherent anat-
omical mediocrity or inferiority must be deemed possible in any given case,
and its participations carefully weighed in every instance of failing local
circulatory compensation. Just as aplasia and anomaly must be con-
stantly kept in mind when the clinician makes a critical appraisal of any
given case of surgical renal lesion, so here too, one must not lose sight of the
factor of congenital hypoplasia.
The multitudinous distribution of the vessels, their variation in capacity,
their subserviency to alterations both of organic, functional and neurotic
nature, allow of kaleidoscopic combinations of manifestations.
The effects of obstructive lesions will be distributed, in a measure, over
the area supplied by the vessel or vessels involved. But only with this reser-
vation, to wit: that these effects are limited in intensity and in extent by
time and the possibility of substitutions through other circulatory avenues.
So, whilst the quantity of blood and rapidity of flow may be objectively
and subjectively manifested in certain areas of the normal distribution at a
time immediately following the advent of a sudden arterial obstruction, the
intervention of preexisting and later of compensatory collaterals, is responsi-
ble for partial or complete disappearance of all phenomena.
Serious alterations (in the vessel integrity) may have as their consequence,
no appreciable manifestation other than those of diminished blood supply,
decreased warmth and slight sensory disturbances. But where a large
territory is affected, by virtue of the exclusion of more central, more impor-
tant and larger arteries, or through a larger number of arteries, associated
effects may be then evoked. These are:
(1) Immediate effects; or the residual changes persisting after rehabilita-
tion of the circulation.
(2) The induced or reactionary processes in the peripheral capillaries
and arterioles, viz. rubor, hyperemia, or erythromelia.
(3) The tendency to trophic derangements.
(4) The production of either transitory or permanent lability of the local
vasomotor mechanism.
Whereas both subjective and objective signs of a suddenly interrupted or
seriously disordered circulation in a given territory are usually definite and
CIRCULATION IN THE EXTREMITIES 89
vivid enough to be both experienced by the affected person and easily recog- |
nized by the physician, the slower and more gradual obstructive lesions of
the vessels may be easily overlooked. And so, it has been clinically proven
that insidious, progressive occlusion of main arteries of the lower extremity,
including the femoral, popliteal, posterior and anterior tibial arteries, may
take place without symptoms; and, indeed, the clinician may fail to recognize
the basic vascular lesions until gangrene or trophic disorders follow a slight
trauma or local infection. As shall be pointed out later, however, certain
objective signs can be usually elicited, and careful examination will lead
to the discovery of the condition long before grave consequences ensue.
The subjective appreciation of local deviation from the normal must
needs vary with the individual’s apperception and introspective psyche, as
well as with his threshold of sensitiveness. Our interrogations, therefore,
should be so put as to make up for the deficiencies of those who might lead
us astray. Pain in the affected territory, coldness, paresthesia, liability to
fatigue, may antedate by months or years, the appearance of the more
easily recognizable features. Coldness of the toes of spontaneous onset, or
after but slight degrees of exposure, is also a sign worthy of note. It must be
remembered, however, that pari passu with the gradual extension of the
vascular obturation, collateral paths may enlarge so that subjective symp-
toms may disappear. On the other hand, the liability to pain and cramps on
walking may increase as time goes on, and masquerade under the guise of
rheumatic pains, flatfoot ache, ‘‘cramps from varicose veins” and the like.
The signs that may be objectively elicited will be discussed in full elsewhere.
They include (1) the immediate result of circulatory inadequacy; (2) the
evidences of dilatation of peripheral capillaries and arterioles (rubor or
erythromelia); (3) vasomotor lability or instability; and (4) trophic dis-
orders and gangrene.
In the interpretation of the prognostic significance of these manifestations,
we must bear in mind their intensity and extent, the duration of their exis-
tence, their constancy and especially the progressive nature of the phenomena
of malnutrition. The immediate results of circulatory impairment may,
as already mentioned, be so slight as to escape notice. With sudden and
extensive interruptions of the current, however, pallor of the foot (or even
leg) on walking, on elevation, or in the horizontal position, is a significant
sign. Coldness of peripheral parts to the touch, with a distinct increase in
warmth of portions more centrally located, is an important objective phe-
nomenon. Other expressions of nutritive disorder include those more
delicate changes in the skin texture, the nails and the subcutaneous tissues
that are to be described in detail.
The condition of rubor (erythromelia) is such a characteristic manifesta-
tion as to warrant careful and detailed study. It may develop very gradually
or within a very short time; it may be a permanent sign or gradually dis-
appear; and is under the influence not only of the immediate state of the
circulation of the part, but also dependent on posture.
Vasomotor instability is not a constant attendant disturbance, although
well marked in some cases. Its expression may lead to confusion, and there-
fore, its rdle and its separation from evidences of purely hydrostatic or
mechanical origin may be occasionally difficult.
Trophic lesions and gangrene, too, are characteristic results of poor local
nutritive states. However, even the causation of these may not be altogether
clear, whenever signs of apparent vasomotor lability seem to dominate the
picture. Of the less striking, but nevertheless important effects of these
90 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
maladies, are the alterations in deeper tissues, particularly of the bones. The
changes in conformation of visible parts give usa clew as to abnormalities in
the subcutaneous tissues. But the condition of the bones requires elucidation
with the Roentgen ray wherever there is a doubt as to diagnosis. It is
noteworthy that the osseous tissues may suffer even greater absorption in
some of the true vasomotor neurogenic circulatory disorders than from the
more constant effects of organic vascular occlusion.
Evidences of disturbed nutrition may be hyperplastic rather than degen-
erative. And so hypertrophy of the subcutaneous tissues is occasionally
seen with chronic cyanosis of the hands.!
In the neurogenic or vasomotor derangements, sensory and objective
circulatory phenomena may be so closely linked in onset and duration, that a
causal interrelationship is often assumed to exist. The effects of the purely
hydrostatic depletion, stasis or deficiency of flow (through vasoconstriction)
are here also hard to separate from trophic disorders attributable to pure
neurotrophic abnormalities. In short, whereas in organic occlusive disease
of the arteries, a direct association between trophic disorders and circulatory
insufficiency can usually be invoked in explanation, the nutritive complica-
tions of the vasomotor affections, may be under the influence of one or several
different forces.
CHAPTER XIV
THE TROPHIC FUNCTIONS OF THE NERVOUS SYSTEM
The réle of the nervous system in the production of trophic disturbances,
wounds that refuse to heal, ulcers, necroses and gangrene should be
thoroughly understood as far as present day knowledge permits, in order that
the clinician may differentiate the neurogenic cases from those of organic
vascular origin. When we speak of trophic disturbances, we can, in a broad
way include not only those that are directly dependent upon poor circulation,
or the action of external insults (cold, chemicals, heat, etc.), but also some of
the clinical effects of nerve derangement. Classification is made difficult by
reason of the fact that we are at pains to conclusively differentiate between the
trophic lesions produced by external and endogenic causes. Some believe
that severe cold may produce its effects only by direct action, and others
attribute the tissue disturbances for the most part to the neuroparalytic
effects of cold upon the blood vessels. For our purposes, it would be well to
keep in mind two large categories; trophic disturbances of a nutritive or mal-
nutritive nature from whatever cause, and those of purely neurotrophic
origin.
Several theories have been put forth to explain neurotrophic disorders
in the peripheral tissues; firstly, that the inflammation extends along the
nerve until the innervated area is reached; secondly; that the inactivity
induced by the neurogenic condition is responsible; and thirdly, that the
anaesthesia produced by the nerve lesion results in an inability to avert
injury. Numerous clinical observations, however, have shown that none of
these causes must obtain. We are, therefore, constrained to accept the view
1See Chap. XCV, page 528.
THE TROPHIC FUNCTIONS OF THE NERVOUS SYSTEM 91
that there is a direct trophic influence exerted on the tissues through the nervous
system.
The Exercise of Neurotrophic Influences.—Several theories have been
offered in explanation of the paths along which trophic influences are exer-
cised.
One vasomotor theory presupposes that the tissue changes depend upon
vasomotor influences. Accordingly trophic lesions may result from neuro-
paralytic hyperemia, or from anemia due to neuro-irritation.
The theory of neuroparalytic hyperemia is based upon the supposition that in these
circumstances, inflammation and nutritive disturbances occur more easily than witha
normal vascular tone. Certainly experiments do not corroborate this theory; in that ten-
dency to inflammation through experimental lesions of the sympathetic in animals has not
conclusively shown increased tendency to inflammation.
The theory (Brown-Séquard) that a neuro-irritative ischemia is responsible
for certain trophic disturbances also has not found substantiation. Of recent
years some of the European authors have attributed late trophic disturbances
in gangrene (after exposure to cold) to neuroparalytic lesions of the blood
vessels.
It does not appear proven nor plausible that either vasomotor theory should account
exclusively for trophic disturbances. Alterations in the blood content of the affected part
have not been observed clinically to precede the trophic disturbances, except in those cases
(thrombo-angiitis) where the nutritive lesions can be explained otherwise. Certainly
in the neurotic muscular atrophies or in the neurotic glandular atrophies, or in the tabetic
arthropathies, no such prodromal vascular disturbances have been noted. In short, vaso-
motor derangements can only be regarded as contributory causes.
The Theory of Special Trophic Nerves.—According to another hypothesis
special trophic nerves are assumed to exist (Samuel!). Perhaps the only
affection which presents symptoms that would seem to substantiate such a view
is that called progressive facial hemi-atrophy.
This is a disease in which the skin, as well as the bones of one side of the face slowly
atrophy. According to Samuel this condition is to be attributed to an isolated lesion or
paralysis of trophic nerve fibers. However, in almost all such cases other nervous derange-
ments of sensory and secretory type, are present. The implication of other nerves, particu-
larly the trigeminal, and in some cases also the sympathetic, are facts that warrant a
modification of the above hypothesis and do not permit of the wilful assumption that
specialized trophic paths are present.
In short, the existence of isolated special trophic nerve paths and centers
has not been proven clinically or experimentally. Most observations and
investigations, therefore, agree in supporting the conclusion that the trophic
influences pass through the very same nerve paths and centers that possess
other special function.
As to how the trophic influences act, a number of different theories have
been advanced, and perhaps it is best to discuss these in connection with
the different tissues, since their actions may not be uniform, and then to
point out in what form and to what extent these tissues are subject to such
trophic influences. Of these theories, there are those that presuppose a diminu-
tion in nervous influences; others that interpret the trophic influences as
conditions of irritation or excitations; and finally those according to which
trophic lesions depend upon abnormal reflex stimuli from the periphery.
Closed Circuit and Nerve Impulses.—It is still a mooted question as to
whether direct contact of nerve elements is necessary for the exercise of
nervous forces.
1 Samuel, Trophoneurosen, Eulenburgs Realencykl., XX, IT, Aufl.
92 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
The Interdependence of Nerve Paths with Particular Reference to Trophic Function.—lf we
accept the neuron theory, we believe that the nervous system is made up of innumerable
nerve units or of anatomically or physiologically specially destined and characterized indi-
vidual cells. The constituents of such units are the cell bodies with their dendrites, their
nuclei and nucleoli, and the axis cylinders, the latter leading into medullated or non-medul-
lated fibers. According to the new tinctorial methods that show fibrils in the axis cylinder,
the histologic unity of these nerve cells and their processes has been subject to strong criti-
cism. These fibrils appear in the axis cylinder as long, parallel lines or threads, whilst they
split up in manifold fashion in the ganglion cells, intersect and intertwine. Besides these the
neurofibrils pass from one dendrite of one cell into its neighbor’s.
We are still uncertain regarding the manner in which communication
takes place between the intracellular neurofibrils, and those peculiar and
varied endings of nerve fibers that approach the cells from the nerve fibers.
We should not hold too tenaciously to the concept of an anatomical independ-
ence of the nerve units.
Be this as it may, the transmission of the nerve impulses from the phy-
siological standpoint from one cell to another can be carried out by nerve
streams that pass directly or through a gap; and it appears irrelevant as
to whether direct communication is present or not.
As for the réle of the nerve cells in the production of trophic influences, some authors
have regarded those ganglia cells that are included in the heaps of fibrillar substance as
having no other specific function than that of nutritive reservoirs. There have been but
very few adherents to this special doctrine.
The Interdependence of Certain Portions of the Nervous System as Studied in Nerve
Degeneration.—Three types of degeneration occurring in the nervous system throw con-
siderable light upon their function and anatomy. These may be divided into the Wallerian
degeneration, or Lenhossek cellifugal degeneration, the retrograde degeneration, and
secondary atrophy or indirect degeneration.
1. The Wallerian Degeneration.—Section of a motor nerve is followed by degeneration
distal to the point of the break in continuity and up to its endings in the muscle. Section of
a sensory nerve is followed by degeneration up to the endings in the periphery. Section
of a posterior root causes degeneration of the intramedullary course. Therefore, the
degenerative process is always away from the cell (cellifugal) in the sense of the physiological
direction of the impulses (towards the periphery, or caudad). It appears that the neuron
theory gave a satisfactory explanation of the destruction of the axis cylinder, when severed
from the cell, the accepted belief being that the neuron constitutes a nutritive entity. It is
hard to conceive, however, how parts situated at great distances from the cell can obtain
their nourishment throughit. Indeed, the nodes of Ranvier have been regarded as points
of entrance for nutritional fluids. Therefore, the trophic action of the nerve cell must be
interpreted in another light, possibly as exerting such influences on the axis cylinder that
enable it to attract nourishment from the neighborhood, and utilize it. The assumption
that a ferment substance emanates from the cell, gives no more satisfactory explanation
than the view that centrifugal impulses from the cells assure the axis cylinder of the power
of nutritive assimilation. Furthermore, we cannot adhere too strongly to the notion that
trophic influences are confined merely to an anatomic unity of the cell and its axis cylinder.
The observations upon which the whole theory is built up do not concern themselves with
single cells and their processes, but in fact we are always dealing with a multiplicity of cells
and fibers. When we speak of degeneration clinically and anatomically, also pathologically,
cell groups and fiber groups only are actually considered.
Concerning the dependence upon central nerve matter and peripheral fibers, observa-
tions are at hand that show that lesions in the spinal cord follow in the wake of amputation.
For instance, distinct alterations in the spinal cord not limited to the white matter,
but implicating the ganglion cells with diminution in size of the anterior gray horn have been
observed. Involvement of the anterior or posterior tract and varying amount of implica-
tions of the white and gray substance have been observed.
Theory of Cellular Excitation According to Monakow it would appear
that alterations in the ganglion cells, after section of the peripheral nerve,
depend upon two factors: firstly, as to whether the cell is in possession of
rich collaterals; and secondly, on the point of section. When the point of
section is very far removed from the cell, its action is minimal as compared
THE TROPHIC FUNCTIONS OF THE NERVOUS SYSTEM 93
to proximal interruptions. The degeneration of the cell, in his opinion,
would depend rather upon the amount of functional disturbance. The
degree of disturbance of the latter is directly related to the number of func-
tional impulses that are excluded, these including not only influences from
the axis cylinder itself, but of all the neighboring nerves that are in close rela-
tion to it. Perhaps all cells require similar stimuli for the conservation of
their trophic integrity.
Section of axis cylinders causes rapid changes in the related anterior hornand ganglionic
cells in most cases.
The intensity of these changes vary, and the cell may undergo a reparative process, a
return to the normal occurring to a considerable extent. Whenever the cut nerves become
reunited, the cells return to normal. Per contra, these undergo simple atrophy when the
function is in abatement by reason of a permanent break in continuity.
2. Retrograde Degeneration.—In this category belong the degenerative processes that
manifest themselves in a reduction of the size of anterior root fibers after amputation.
Similar narrowing of the posterior root leading into the posterior tract has often been
observed. Then, too, diseases of the peripheral nerves, either peripheral neuritis or the
action of compressing tumors, is followed by some degeneration in the corresponding pos-
terior roots and the corresponding posterior tract. Although in some cases these changes
have been interpreted as an extension of the toxins that led to the polyneuritis, in other cases
the changes have been believed to be of reactive nature in consequence of the peripheral
lesions. Such apparent retrograde degeneration is not confined to the territory of the
motor and sensory nerves. They have been found in the brain itself and in the centers of
the optic thalami after cortical lesions.
The Reflex Theory—Explanations of so-called retrograde degeneration
throw important light on the problem of trophic influence of the nervous
system. According to one view, the trophic functions of the nervous sys-
tem are not automatic, but reflex in nature. Marinesco expressed the
following hypothesis, in explanation of the central proximal atrophy occur-
ring after amputation. ‘The cause of the degeneration (in the cells and in
the central stump) is to be sought in the interruption of the continuity
between periphery and center. One may suppose that by irritation of the
sensory nerve endings biologic changes (probably of chemical nature) are
produced in the spinal ganglia, and that a trophic influence in the efferent
fibers from the ganglionic cells is thereby exerted. When section of an
extremity or of a nerve takes place, quantitative and qualitative changes
in the impulses through the nerve ends must needs result that are no longer
able to evoke the adequate trophic function; therefore, a slow progressive
degeneration of the nerve fibers ensues. Just as the fibers of the central
nerve stump show changes, so also the fibers which travel from the spinal
ganglia to the spinal cord become altered. This explains the atrophy in
the sensory sphere. According to this view, impulses travelling to the cells
simultaneously serve to conserve their trophic function.
According to a supplementary view, such activating nerve stimuli do
not necessarily have to emanate from the periphery, but may be of central
origin. ‘That is, other reflex impulses that are subconscious may be effec-
tive. Among these may be mentioned metabolic processes, emotion, and a
variety of constantly changing and repeated, almost continuous stream of
impulses of sensory and motor nature. These serve to excite the trophic func-
tion of the cells, and when absent, there result those atrophic alterations of
the ganglion cells and their processes that have been observed.
According to still another interpretation, it is the inability to give off impulses that is
the essential factor in the production of the degenerative cell changes (Lenhossek). For the
conservation of the normal integrity a continuous function of the cell is necessary.
94 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
That section of the posterior root is followed by degeneration of the spinal ganglionic
cells is difficult of explanation. Under such circumstances, impulses are still received, and
in spite of this fact, marked derangement in the anatomical conditions of the spinal gan-
glion cells is noted. From this we would have to conclude that an uninterrupted flow
of impulses from the cells or the cell responses, is essential for the conservation of the cell
equilibrium. Every derangement of function, be it an obstacle to the reception of impulses
or changes in the giving off of impulses leads to alterations in the anatomical structure of
the nerve cells. Unfortunately this theory is nothing more than another way of stating
the facts.
The Theory of Heterologous Stimulation.—Interferences with trophic
function are said to be also due to suppression of impulses in neurons that
are not in anatomical but in functional relationship. Observations on
secondary atrophy would substantiate such a view.
3. Secondary Atrophy or Indirect Degeneration.—Under this name, Monacow describes
secondary changes in the nerve fibers and ganglion cell groups characterized by qualitative
conservation of the histologic elements, but distinct diminution in volume of all parts.
The medullary sheath becomes very narrow, very thin, the nucleus poor in chromatin and
the Nissl bodies of the protoplasm become indistinct.
This degeneration has been explained on the assumption that through the suppression
of one neuron, changes take place in a second neuron that is functionally in relation with the
first. As an example may be mentioned the amyotrophic condition in tabes following
disease of the sensory protoneurons. So also Schaeffer would explain the changes in the
anterior horn cells as due to disease of the sensory neurons.
According to this view, trophic derangements extend not only through
homologous (motor-motor) but also through heterologous (motor-sensory)
neurons. The condition of certain nerve fibers is doubtlessly influenced
from the trophic standpoint, through systems that are in close functional
and anatomical relationship.
In short, the striking peculiarity of the nervous system is the interde-
pendence and relationship between function and structure of the cell. The
function consists of the reflection of the impulses or irritations, the elabora-
tion and the conversion of the irritant or impulse, and finally the giving off
of impulses. It is even possible that disturbances in any one of these three
functions may lead to localized trophic disorders. On theother hand, it is
doubtful that the integrity of any unit is absolutely essential for conservation
of its nutritive condition. Indeed, the neuron theory does not explain either
the so-called retrograde degeneration, nor the secondary atrophy. Cassirer
believes that if we consider the ganglion cells as a sort of center, that is in
spatial and functional relationship with a certain number of degeneration and
trophic disturbance, as upon the basis of the unity of the ganglion cell and
its processes.
Nerve Influences on Osseous Tissues.—A few words concerning the
dependence of the conservation of bony tissue on nerve influences may
not be amiss, since trophic alterations, particularly in the end phalanges
can give us valuable diagnostic information. The differentiation of pri-
mary atrophy of the distal phalanges associated with Raynaud’s disease
and sclerodactyly from nutritive disorders due to inactivity, syphilis,
syringomyelia and secondary infection may be thereby facilitated.
The nerve control of osseous nutrition is well exemplified by the retarded bone growth
of infantile spinal paralysis. There are also some clinical observations on disturbed growth
of bones after peripheral nerve lesions. Gayet and Bonnet described a case in which resec-
tion of a neuroma formation in the median nerve seven years previously was followed by
diminution in size of bones and rarifaction. A number of instances of intensive osseous
changes after traumatic lesions of peripheral nerves can also be found in the literature.
THE TROPHIC FUNCTIONS OF THE NERVOUS SYSTEM 95
Bone disease associated with diseases of the central nervous system is
more common. In syringomyelia, osseous alterations are not infrequent.
These are necroses particularly of the tips of the phalanges of the fingers,
or diminution of their size; or, even disappearance of small bones without
inflammation or suppuration. Roentgenograms may show bone atrophy
and lightening of the bone shadows, both of the diaphysis and epiphysis.
Even enlargement of bones has been reported without the presence of
acromegaly in cases of glia changes in the spinal cord.
Fragility of bones, too, occurs in paralytics, although this has been
interpreted by some as due to atrophy of inactivity. A rarifying process
may make the bones brittle when tabes is present, and liable to spontaneous
fracture.
There are cases in which after trauma of an extremity without wound or
suppuration, marked trophic disturbances appear. These may beaccom-
panied by slight vasomotor symptoms and sensory irritative phenomena,
but deficiency manifestations in the sensory nerve domain are absent.
Here it is believed that the trophic disturbances have a reflex cause through
excitation of the sensory apparatus. Cassirer mentions a case of Sudeck!
in which after injury of a hand, swelling, redness, pain and restricted motility
resulted. The X-ray picture presented the characteristics of bone atrophy
with clarified bone substance and typical atrophic changes in the carpal
bones. Even osteophytes are said to occur as an expression of continued
reflex irritation.
Characteristic in lepra are the resorptive and degenerative processes in
the peripheral phalanges with mutilation of the parts. The lime disappears
hand in hand with atrophy of the rest of the bony parts, and corresponding
changes inthe soft parts: The bony resorption in these cases is so character-
istic and so extensive, that it can hardly be mistaken either for the very
minimal changes of Raynaud’s disease or sclerodactyly; nor can it be readily
confused with the bone and joint destruction associated with perforating
ulcer, arteriosclerotic ulcers and gangrene.
The cause of the bony changes is said to be a trophoneurotic one due to
lesions in and about the peripheral nerves.
Trophic Influences on the Vessels.—If such a relationship exists, it is ali
the more important by reason of the secondary effects that could be thereby
transferred to the tissues supplied by the vessels in question. Lapinsky
claims to have demonstrated structural changes in the walls of arteries after
section of the vasomotor nerves. Cassirer accepts the experimental work of
this author as reliable even though others (Jores) could not offer confirmatory
facts.
As for the manner in which vessel alterations are dependent on the vasomotor nerves,
satisfactory explanations are difficult to find. In how far do these changes result from the
absence of functional impulses? Or, to what extent are direct nutritive stimuli responsible
for conservation of anatomical integrity? A complicated mechanism is put into action
when vasomotor nerves are experimentally cut off. For, the induced dilatation of the
vessel permits of new mechanical hydrostatic or circulatory forces to come into play and
possibly exert an effect on the arterial walls. Perhaps the therapeutic results of future
operations on the periarterial sympathetic fibers (Leriche) will throw additional light on
this obscure subject.
1 Sudeck, Monatschr. f. Unfallheilk., VII, 50, 1910.
96 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
CHAPTER XV
TROPHIC DISORDERS OF THE SKIN
Neurotrophic disorders of the skin include all those regressive, hyper-
trophic, and so-called inflammatory changes dependent upon the nervous
system. ‘The skin and the nervous system are brought into communication
through those sensory nerves in which fibers of the cerebrospinal and vege-
tative systems are contained. Probably the sensory nerves per se have no
direct influence upon the vital functions of the skin. When the sensory
paths are interrupted, the parts are placed in jeopardy, insofar as injurious
moments do not come to consciousness. Such is the case in syringomyelia
and in interruptions in the continuity of the peripheral nerves. As a rule,
trophic changes associated with sensory disturbances depend exclusively
upon lesions or irritations of the vegetative nervous system, whose paths and
centers are in intimate relationship and contact with the sensory fibers.
The distribution of blood, and therefore the nutrition of the skin, is under
influence of the nervous system through the vasomotor paths. And so, a
continued spasm of vasoconstriction and so-called neurogenic stasis may cause
functional derangement of the skin.
The immediate effects of injury of the peripheral nerves demonstrate
that the cutaneous vessels may functionate independently of the nervous
system. Later on, however, distinct disturbances in the blood supply
appear, such as anemia or cyanosis: and with this, other changes in the surface
of the skin, namely, purplish discoloration, thickening, changes in the nails
and glossy skin. The latter are evidences of dystrophic or maltrophic altera-
tions in the integument. And so also, the vascular responses to external
stimuli or conditions suffer a change. Under such circumstances there is
a tendency towards severe regressive or degenerative changes. Inflamma-
tory processes are intensified and the ability to heal is diminished.
In addition to the vasoconstrictor and dilator paths, vasosensory fibers
course in the peripheral cutaneous nerves. ‘They are important in the nutri-
tion of the skin. For we can only then expect an orderly nervous regulation
of the blood distribution when a harmonious and reciprocal association of
the vasomotor and vasosensory impulses obtains.
According to some it is hardly necessary, nor in accord with any observa-
tions to postulate the existence of a separate trophic nervous system. In
cases of nerve lesions trophic disorders may be absent for years. ‘The origin
of the so-called glossy skin has been explained upon the theory that the vaso-
motor relations have been disturbed. A thickened, brittle skin with hyper-
keratosis is also noted in cases of peripheral nerve lesions and in localized
spinal diseases, such as syringomyelia.
Of the so-called inflammatory types of trophic disorders herpes zoster is
an example. ‘This is the only one of the trophic disorders in which certain
distinct anatomical changes in the nervous system have been demonstrated.
There are hemorrhagic inflammatory processes in the spinal ganglia.
Certain cases of circumscribed edema and urticaria may be of neurogenic
origin, whilst in other cases a toxic cause is responsible. That neurogenic
cases can exist is proven by the examples of urticaria of psychogenic or reflex
creation demonstrable after the passage of bougies in the urethra; and also in
dermatographism. ‘The exact nature of the responses depends to a consider-
able extent upon the predisposition of the skin, and upon the individual.
TROPHIC DISORDERS OF THE SKIN 97
Trophic disorders of the nails manifest themselves in irregular growth.
The nails may become plump, easily torn, show furrows, may, degenerate,
and later may break up. External injuries or insults often give rise, in
predisposed individuals, to inordinate responses on the part of the skin.
Such a predisposition to trophic disorders is exhibited by certain weak cuta-
neous structures in cases of myelitis or nerve injuries or lesions.
A number of skin lesions have been regarded as due to trophoneurotic
causes. Amongst these may be mentioned: malum perforans, acute decubi-
tus, skin changes of peripheral nerve disease, and those associated with syringo-
myelia. All of these should be carefully studied before we can. possess
correct diagnostic appreciation of the varied clinical pictures of gangrene.
Mal perforant is fully discussed in Chap. LXXXIII. To what extent
this process owes its character to nerve lesions has not as yet been con-
clusively proven. In some cases at least we may accept the existence of
derangement of sensory nerves as well as of vessel reflexes.
As for acute decubitus, views differ as to the réle of mechanical infectious
or neurogenic influences in its causation. A careful perusal of the literature
permits us to cull a few authentic examples of undoubted neurogenic nature.
In such the skin necrosis is said to have developed a few hours after the onset
of the nerve disturbance (hemiplegia and hemianesthesia). That immediate
skin changes can follow cerebral lesions is recorded in the reports of pemphigus-
like eruption in the paralyzed, areas, extensive bleb formation in territories
with sensory and vasomotor disturbances, etc. In some cases ‘‘decubitus”’
is the product of a combination of factors, pressure, vasomotor weakness of
the skin, and infection.
Another manifestation of the relation of the nerve and cutaneous systems,
is the glossy skin described by Weir-Mitchell. Not greatly dissimilar are
some of the remarkable changes in the integument occasionally seen in the
feet, when slowly progressing but vast arterial obstructive lesions of arterio-
sclerosis impair the nourishment of the parts. Also, in rare cases of throm-
bo-angiitis obliterans, a condition of the skin of the hands, with trophic
lesions of the nail beds, without ulceration, may give deceptive pictures.
In glossy skin the skin is red, thin, shiny and stretched. With it there
may be burning sensations or neuralgic pain. The hair and rugae of the
skin may be absent, whilst sensation may be conserved. It is important
to note that this lesion appears when only partial section or interruption of
nerve continuity in the territory has taken place.
If the cutaneous disturbances correspond to the territory innervated by
certain nerves, their neurogenic nature is usually easy to recognize.
A word may not be amiss regarding neurotrophic skin changes attending
syringomyelia, which must also be occasionally considered in differentiating
trophic disorders and gangrene. Here the lesions’ are usually associated
with motor, vasomotor and sensory derangements. Nor can we always
establish a causal relationship between the cutaneous changes and other
evidences of nerve lesion, since the former may antedate the latter.
As for other lesions, such as herpes zoster and multiple neurotic gangrene
of the skin, these would seem to indicate the existence of a close neurotrophic
relationship. In the case of herpes, Head says that the eruptions are not
produced by disturbance of special trophic nerves, but by intense irritation of
cells in the ganglia, which normally subserve the function of pain. Probably
irritation of sensory end-neurons are responsible for the trophic changes in the
skin. Cassirer suggests a reflex disturbance of the vasomotor nerves through
sensory impulse.
7
98 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
In multiple neurotic gangrene of the skin such vasomotor derangement
has also been considered possible, the reflexes being either of toxic, electric
or psychic nature.
The so-called trophedema is a hard, white, painless edema of rather
chronic course. It is usually observed in youth and is progressive. It is
demarcated by a sharp circular line in a segmental fashion, being limited to
certain parts of the limb, and is not infrequently a familial disease.
Pathogenesis of Neurogenic Gangrene.—The question as to whether
gangrene may result solely from changes in, or functional derangement of the
nervous system without reference to effect of vasomotor spasm, has been a
much mooted one. As for the peripheral nerves, evidences are lacking that
these are the seat of degenerative changes either in Raynaud’s disease or in
other cases of spontaneous neurotic gangrene. When they are reported as
having been present, they are usually not the cause of the gangrene, but sec-
ondary, and result from the same forces that are productive of the gangrene.
As regards the central nervous system, it is known that marked nutritive
disturbances of the skin and its adnexa can be associated with the central
nerve changes, as in syringomyelia. Indeed, gangrene has been observed
complicating even gliosis.
Cassirer is unwilling to accept the purely ischemic theory or that of
angiospasm as sufficient to explain the gangrene in Raynaud’s disease. This
view receives additional confirmation in the manifestations of gangrenous
herpes and in the disease of multiple neurotic skin gangrene, where irritation of
the vasomotor nerves is believed to occur. Indeed, Kreibich! was able to
produce angioneurotic inflammation experimentally, and also, patches of
gangrene in the latter affection with the use of faradic current and other
irritants. He suggests that the nerve impulses excite paralysis of the vessels
through irritation of the vasodilators with consequent edema, exudation, and
necrosis; and that the necrosis is due to increasing pressure of the exudate.
These observations, however, cannot be invoked in explanation of the
Raynaud complex, since, in the latter, vasoconstrictor, and not vasodilator
irritation exists. Whilst Kreibich and others would interpret the necrosis
as the result of mechanical effect of an exudate of vasomotor origin, Cas-
sirer rejects this assumption, believing it more plausible that there is a direct
trophic action through the nervous system on the tissues; and with such a
theory he would interpret gangrene associated with both vasodilator (multi-
ple neurotic gangrene) and vasoconstrictor (Raynaud) impulses. Enough
data are at hand, however, irrespective of which view may be correct, to
warrant the belief that neither angiospasm nor ischemia satisfactorily accounts
for all types of neurogenic necrosis or gangrene; for this occurs where vaso-
dilatation has been shown to exist. It may be accepted therefore, that a
primary gangrene of the skin may take place by reason of alterations in, or
functional derangement of the nervous system.
A new French school has arisen that would regard even trophic ulcers of traumatic
peripheral nerve origin as explicable by the theory of deranged vasomotor function. Thus
the trophic ulcers complicating transverse injury of the sciatic nerve? have been recently
attributed to vasomotor reflexes produced by a neuroma of the nerve’s proximal end. Ac-
cording to this theory the active proliferation in the neuroma is the point of departure of
vasodilator reflexes that augments the existent circulatory disturbances. By virtue of
this effect minimal local peripheral traumata may give rise to sero-sanguinolent exudation
in the connective tissue meshes, in which the dilated capillaries have lost their function
and that consecutive cutaneous necrosis and ulceration ensue.?
1 Kreibich, Die Angioneurot. Entziindugen, Wien, 1905.
2 See Chap. on Trophic Disorders in Diseases of the Peripheral Nerves.
3Leriche, Lyon Chirurg., 18, 1921, p. 43-44.
EROPEIC DISORDERS. OF ‘THE SKIN. 99
Summary.—The passive tissues too, such as skin, bones and joints, are
under the control of trophic nerve influences. It would seem that a specially
attuned reflex mechanism is here essential for the harmonizing of their nutri-
tional condition and their specific functions. Cassirer offers the following
views: Pathologic changes of innervation exert a more injurious effect on
the nutrition of tissues, than when nerve impulses are completely in abeyance.
Excitation of sensory nerves calls forth marked reactions in vascular inner-
vation. Although the tissues, in general, are trophically innervated, they
may continue spontaneously to make up for nutritive defects. The special
trophic impulses would only then be significant when the nourishment of the
tissues is under special strain, as in the presence of unfavorable conditions
such as continued pressure, and unusual desiccating influences. But when
the normal innervation becomes pathologically altered through special
irritants, the nourishment of those tissues that are within the anatomic and
physiologic boundaries of the exciting impulses, may be reflexly modified
thereby; and as long as the special irritants continue. So that accordingly
it is not an absence of innervation, but rather a pathologically deranged form
of nerve impulse that comes into consideration in the development of trophic
lesions. Indeed Leriche has recently expressed the hypothesis that trophic
ulcers after nerve section (Chap. XCI) may be caused by reflexes set in
motion in the neuromata of the nerve’s proximal end. In an analogous
way, intense symptoms may be produced by the constant irritation of
posterior roots by a new growth, and manifestations may be wholly lacking
with complete destruction of such posterior roots.
Other authors have expressed the opinion that when nerve impulses are
interrupted, the nutrition of tissues goes on, but with diminished activity.
Under such conditions only special demands upon the functional activity of
the nerves may bring deleterious changes. The tissues are believed to be-
come more sensitive, so that increased pressure may lead to necrosis as in cases
of myelitis; or, the insensitive cornea may be injured through the very slight-
est external traumata with resulting ulcer formation. In many examples of
trophic disorder, the occurrence of a trauma might be regarded as sufficient
to explain the condition, since under normal circumstances the tissues of the
body demonstrate their ability to resist external influences and conserve
their nutritional integrity. Slight external irritants, when followed by trophic
derangement, indicate a disorder in trophic innervation (trophic function).
Whenever the skin cannot meet the exigencies of the normal external
accidents and stresses and reacts with evident nutritive disorder, we are
warranted in assuming that impairment of the neurotrophic function exists.
Conditions of deranged trophoneurotic function may escape our cognizance,
unless each set of the motivating factors resulting in manifest impairment of
tissues be carefully analyzed and weighed.
Most authors agree that the existence of isolated trophic nerves is not
supported by present evidence. ‘That the nervous system exercises a trophic
function cannot be denied, and the trophic influences doubtlessly pass through
paths serving other purposes. ‘The skin receives the trophic impulses by way
of the sensory and vasomotor paths, and may travel in a direction opposed to
the usual impulses travelling through them. The action of reflexes by way
of the sensory to the vasomotor paths is also of great importance in deter-
mining nutritional effects.
100 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
mCHAPLER ex
GENERAL CONSIDERATIONS OF THROMBOSIS
Forms of Thrombi.—To elucidate both the pathological and clinical
phenomena observable in cases of gangrene, a clear concept of the process
of thrombosis is essential. The practitioner should not be satisfied with a
loose notion regarding the pathology and causation of the thrombotic lesions
that partly or completely occlude the arteries and veins.
The coagulation and the loss of the fluid state of the blood, when it occurs
during life, becomes one of the morbid processes. For the recognition of
thrombosis as a disease, we must differentiate zntra vitam and postmortem
clots. Although the word thrombosis has been employed in a wider sense
to include also the intravascular accumulation of living cells of varying
types of tissue complexes and of bacteria, the presentation of this subject
will be restricted to descriptions of agglutination, conglutination and coagula-
tion of the blood elements, with the formation of clumps or solid masses of
various types and forms.
The intravascular solidification of the total blood in a vessel, or of any of
the component parts in the living organism, is the result of changes in those
factors which under physiological conditions preserve its fluid nature.
These factors are the physical power of the blood circulation and the chemical
constitution of the blood. The blood flow (circulation) can undergo changes
by reason of either general or local disturbances in the blood pressure, as
well as through alterations in the structure and capacity of the vessel wall.
The chemical composition of the blood depends upon the intrinsic vital
function of the blood cell as well as upon the action of the vessel wall. But
both the mechanics and the chemistry of the blood may suffer change through
the action of solid or fluid bodies of alien nature that penetrate into the blood.
These considerations would lead to a differentiation into mechanical and chem-
ical causes of thrombosis. It is difficult, however, to strictly separate causal
moments.
Authors differ as to whether all thrombi represent some form of decay (necrosis).
According to some, thrombosis should be regarded as a form of intravascular blood necrosis,
and that in the process following mechanical or chemical causes, there form certain materials
made up of single or a combination of confluent blood components.
The word thrombosis signifies plug formation within the blood vessel,
leading to partial or complete closure of the vessel lumen.
Various conditions lead to thrombosis. The following types have been
described: (1) coagulation with separation of a solid fibrous (fibrinous) sub-
stance (clotting); (2) an aggregation of various morphologic constituents
or agglutination; (3) the separation and cohesion of certain elements, called
conglutination. The healing and degeneration of these elements in the latter
process has also been called congelation.
The determining factor in thrombus formation seems to be the aggregation
of elements. This may be brought about through the influence of the vessels
themselves (injury of the vessel wall), through the action of the blood ele-
ments, or through agencies altering the blood elements, through hemolysis,
precipitation, agglutination or destruction. Coagulation or clotting then
follows as a secondary phase, and is rarely primary.
GENERAL CONSIDERATIONS OF THROMBOSIS 101
The distinction has also been made between pure conglutination throm-
bosis, in which the separation and aggregation of elements is essential and
determining, and a combined thrombosis, of the clotting type, called coagu-
lation thrombosis.
Thrombi form because of impairment of the blood stream, injury of the
vessel wall, or changes in the blood composition.
Types of Thrombi.—W hite thrombi may develop in flowing blood from the
heaping up of platelets or leukocytes, or both, with or without fibrin forma-
tion. When, with the blood at astandstill, the red blood cells participate
particularly, a red thrombus usually combined with a white one (mixed throm-
bus) is formed. Such segregation of blood platelets from leukocytes can
result from mechanical factors or chemotactic influences. Of the mechan-
ical factors, centrifugal dispersion or confluence in wave nodes may be
mentioned; chemotactic forces cause the attraction of leukocytes into platelet
centers, as the result of chemical changes in the vessel wall. When the ele-
ments that participate undergo death, they form a coherent, colorless mass that
offers resistance to the blood flow, and simultaneously delivers a ferment
necessary for the coagulation of the fibrinogen of the plasma.
White thrombi can be made up of pure platelets, but only so when they are recently
produced; or, where by reason of the strength of the stream, deposition of leukocytes and
fibrin is prevented. ‘This occurs in the aorta over atherosclerotic patches. Usually white
thrombi are made up of platelets and leukocytes, the leukocytes being attached to a ground-
work of fused platelets. Fibrin and red blood cells are admixed. When white blood
corpuscles preponderate, then we speak of a leukocyte thrombus, but platelets are always
present. The white thrombus is the typical segregation (Abscheidungs Thrombus).
It is formed when the vessel wall is injured, without added circulatory disturbances; or it
can constitute the essential structure of mixed thrombi.
Red thrombi occur either when there is rapid coagulation, or when the
stream is markedly arrested or retarded, usually over a deposit of white throm-
bus in a retraded stream. In the red thrombus there is a rich network of
fibrin with enmeshed red and white blood cells, which are not equally dis-
tributed. The red thrombus is particularly a coagulation thrombus and its
loose structure permits of the tearing off and the transportation of fragments.
Mixed thrombi form the greatest percentage of all. They are made up of
red and white portions (with head and tail, Aschoff).
Hyaline thrombi are found in small veins and capillaries as complete
homogenic bodies, or diffusely filling the lumina. They are made up either
of fibrin plugs or of a homogeneous mass of platelets and leukocytes. ‘Toxic
substances such as serpent venom, ferments, the products of the influence of
cold and heat, mushroom poisoning, and the toxins of eclampsia, infectious
diseases, (diphtheria, pneumonia, scarlet fever) have been known to pro-
duce these plugs. They are not so apt to occur in the extremities; more
usually are they observed in the kidneys, intestines, lungs and brains.
Blockage of the small vessels may be produced by the spodogentc thrombi,
where precipitates and destroyed fragments of blood corpuscles fill the lum-
ina. Poisons such as lead, anilin and the absorption from burns, are the
causes. A similar condition is produced through sudden hemolysis and after
blood transfusion, when so-called shadows of blood cells (thrombi) or plate-
lets and leukocytes fill the vessels.
102 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
CHAPTER XVII
THE FORCES ENGAGED IN THROMBUS FORMATION
Coagulation and Agglutination—These must be differentiated. They
will be described as they occur outside of the vessels, and then as they appear
in the cadaver.
Extravascular Coagulation.—Microscopic observations of the first changes in a fresh
clot, of blood (hanging drop) kept in a moist chamber, may be summarized as follows: The
platelets agglutinate and accumulate in small heaps, in which the contour of the individual
platelets shows dissolution of their peripheral margins. The platelets stick together and
to the glass chamber. The agglutination of the red blood cells into the coinstack form
takes place simultaneously, and the rolls sink gradually to the lowest part of the drop.
Later they fuse to such an extent that they form solid bodies simulating hyalin thrombi.
Shortly after the process of agglutination, the deposition of the fibrin elements takes place.
This probably depends upon the breaking-down of the platelets. At the inception of the
process, the ultra microscope shows fine linear crystal-like threads which grow under the
eye of the observer, and increase innumber. The fibrin masses in the hanging drop usually
show at the very beginning a relationship to the platelets radiating from these. ‘Then the
crystalline form becomes lost and the fibrin attains the appearance of threads, thicker in
the center than in the rest of their course.
In sterile tubes, if coagulation is rapid, the red blood cells may be thrown out at different
levels, giving the clot a variegated appearance. If agglutination and gravitation are
absent, the blood may solidify into a homogenous red column. ‘The process of coagulation
begins at the periphery and advances towards the center. Later the coagulum contracts
with the expression of clear serum. This filtration takes place through a dense fibrin
reticulum that allows neither red nor white blood cells to penetrate.
In the cadaver, coagulation of stagnant blood is modified through the continuance of
a certain degree of inhibiting action of the inner vascular walls. Its process is slower and
incomplete as compared with extravascular coagulation. Even if an abnormal amount of
ferment is present in the capillaries and small vessels (as in pneumonia) coagulation’ does
not take place. Inhibitory influences exerted through the vessel wall are held accountable.
Whilst coagulation incited by a foreign body takes place away from the periphery (as
in the glass tube), early clotting in the cadaver is seen in the central portion of the blood
column, the clot being separated by a layer of fluid from the vessel wall. The inhibitory
process is believed to be due to injury, and deterioration of fibrinogen and fibrin ferments.
Between the one extreme of fluid blood, and that of delayed coagulation (cadaver) with
its homogenous red clot, there are manifold mixtures of a bacon-like clot (speckgerinnsel)+
with the red masses or cruor. ‘The mixtures vary in that bizarre layers, combination clots;
islands, inclusions or white clots are enclosed in the red portion. Evidently in the cadaver
the coagulation takes place more slowly, at varying rates and at different points.
The red post-mortem clots (cruor masses) have the general appearance of the clot in
vitro. Microscopically there is very slight platelet agglutination. The more dense the
coagulation, the denser the fibrin net work, and the more complete is the absence of the
fibrin centers. In the post-mortem clot the fibrin is exhibited throughout and shows dis-
tinct platelet centers. In rapid coagulation, there is probably a sudden invasion or satura-
tion of the blood with fibrin ferments. This is artificially producible through the injection
of tissue juices. The fibrinous network may then become so dense, that its interstices are
smaller than the red blood cells. As a result, mechanical breaking-up of the cells may
ensue when the fibrin mass contracts. Where there is slow coagulation as in the bacon-like
clot (post-mortem), the absence of erythrocytes with the coarse platelet centers
is noteworthy.
The Process of Agglutination.—The agglutination of the platelet is the
signal for the rapid excretion of fibrin. So also blood whose red cells have a
special tendency to agglutinate, is apt to clot rapidly, although no morpholog-
ical relationship between fibrin formation and the agglutinating red blood
cells is demonstrable. Substances that inhibit agglutination also diminish
1 A term given to post-mortem clots in which the red blood cells have fully gravitated.
THE FORCES ENGAGED IN THROMBUS FORMATION 103
fibrin coagulation. However, the two processes of agglutination and fibrin
clotting cannot be regarded as identical, since either can occur independently.
Agglutination of platelets, and less frequently of erythrocytes occurs; it is absent
altogether in the case of leukocytes.
Agglutination represents a disturbance in the normal repulsion between corpuscular
elements on the one hand, and the surrounding plasma on the other. Spatial conditions
even with chemical integrity of the elements, may play a réle in the production of agglutina-
tion. ‘Thus, when, by virtue of mechanical conditions the cellular elements are approxi-
mated, the quantity of the inhibiting fluid between them may not suffice to prevent a’
tendency to cohesion. It is this mechanical relationship that may be a factor in the
production of thrombi of mechanical etiology; and it throws light upon the importance of
movement in the fluid, for the conservation of the blood.
If we believe that agglutination occurs by reason of dissolution of very delicate surface
coverings about the erythrocytes or platelets, we must also accept the view that the
microscopic cell limitation is only the boundary of the solids, but not of the fluid constit-
uents. According to Beneke, when no cohesion of cells occurs, any normal process of
attraction that may exist is inhibited by the opposing forces in the surrounding plasma.
Two forces are apparently necessary for agglutination, firstly the specific function of the
corporal elements, and a contrary force emanating from the blood plasma. From the
corpuscles, streams of fluid matter are supposed to emanate. The production of a cohesive
surface substance can be increased. Foreign bodies are known to have such influence on the
platelets, and overproduction of adherent or cohesive substances resulting, implicating more
and more new platelets, and attracting these to the incipient conglomerates. Chemical
injury of the platelets leads to overproduction of this surface substance, or to destruction
of platelets even without contact of a foreign body.
Fibrin Coagulation.—This is a complicated process in which a fibrous
substance, called fibrin, separates out from the plasma in the form of a reticu-
lar mass, and unites the corporal elements of the blood into a solid mass.
In the blood plasma there are fibrinogen, thrombogen and calcium salts. Thrombogen
is the incomplete antecedent of the ferments, and is converted by the activating substance
thrombokinase into the effective coagulating ferment thrombin. This can occur, however,
only in the presence of the calcium salts. This thrombokinase originates mostly out of the
blood platelets which agglomerate at the incipiency of the clotting process, break down and
form the center of radiating fibrin formation. Possibly leukocytes also participate in this
action. Ordinarily for the creation of thrombokinase out of platelets or leukocytes, the
latter must leave the vascular channel, and in this case some of this kinase is also delivered
from the salt of the wound surface. Through the action of thrombin (derived from throm-
bokinase, plus thrombogen) upon fibrinogen, the latter is broken down into fibrinoglobulin
and fibrin.
In the vessels themselves the intact endothelium of the intima is supposed to inhibit
clotting, partly in that the smooth surface exerts no irritation upon the elements that
deliver kinase, and partly in that it forms an anti-clotting, inhibiting substance
antithrombin.
More recently the following views have been expressed regarding coagula-
tion (Bordet!). The two so-called mother substances active in coagulation
are cytozym—a lipoid derived from the tissue cells and blood cells; and sero-
zym present inthe serum ‘These are the precursors or mother substances of
thrombin and prothrombin.
Serozym is easily destroyed by heat; whereas cytozym, the active princi-
ple of platelets resists eventoo° C. without losing its properties. The latter
also exhibits in extract the characteristics of lipoids, especially lecithin.
Bordet believes that cytozym and serozym unite in a manner similar to
the union of toxins and antitoxins, not from true chemical affinities, but from
contact or molecular adhesion. Serozym found in the serum is not there in
the same condition as in plasma. It is incapable of reacting at once with
cytozym in plasma. In other words, plasma contains a proserozym instead
of the active serozym, so that one of the first phenomena of the whole process
1 Bordet, Harvey Lectures, Oct., 1920, p. 36 (Lippincott).
104 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
of coagulation would be the conversion of proserozym into a body capable of
uniting with cytozym.
In short, the process of coagulation may be thus summarized: Plasma
contains fibrinogen and proserozym, the latter being converted into serozym.
by means of calcium and contact along the wall. The platelets deliver
cytozym, which is liberated by means of contact adhesion along the vessel
wall. Through a union of proserozym and cytozym (the former converted
previously into serozym) thrombin is formed; and this, with the fibrin derived
from fibrinogen, brings about coagulation.
SCHEME OF COAGULATION (Bordet)
= Plasma Cells (platelets) '
Fibrinogen | Proserozym converted Cytozym liberated by
into serozym by means means of contact (ad-
of calcium and contact hesion of the cells
along the wall. : along the wall). |
Union of serozym and cytozym
——_—_——> «<—_—————Thrombin (along the wall)
Fibrin
contact and calcium no more necessary).
The degenerative susceptibilities of the blood platelets towards certain
insults and their consequent tendency to clotting, are matters that become
easily comprehensible.
The importance of the platelets in clotting can be studied by noting the character of
radiating fibrin formation (fibrin stars). Such irradiation centers formed by the fibrin
and emanating from the blood platelets are now well recognized. They are no longer
suspected as being merely the consequence of fortuitous inclusion of platelets in the fibrin-
ous network.
However, close relationship between clotting and platelet fibrin formation cannot be
altogether limited to these bodies. For example, leukocytes and other cells (endothelial,
Zenker!) can embody fibrin forming forces. The grouping of fibrin about such cells in
inflammatory foci speaks for this assumption. But a special condition of the tissue
fluids and cells is necessary to evoke the development of their coagulins, or to activate these.
Both the quantity of ferment and the circulatory conditions play a clear role in the
clotting process. Kiister? was able to show that the clot could be modified artificially
according to the amount of fibrin ferment added, the delicate ones corresponding to smaller
quantities, the coarser clots to the use of larger quantities of ferment. The dilution of
ferment through the circulation is, therefore, of importance in intravascular clotting.
In ordinary life and under normal conditions (in which the ferment is probably present
only in small quantities) the circulation is active in producing a dilution up to a point where
the ferment is impotent.
Fibrin formation occurs in two varieties, in a reticular type of clotting, and in the form
of true crystallization. Since authors differ as to the exact nature of the processes and
division into such categories, it must be admitted that the exact limitations of crystalline
and amorphous forms are not always possible.
Fibrinolysis is believed to be a normal attribute of certain cells, since a fibrin network
may disappear. ‘The breaking down of fibrin occurs more rapidly in the cadaver than in
vivo. Just what particular kind of ferment is at work, whether it is a proteolytic ferment
of the leukocytes, or endothelial cells is not known.
Antithrombin which inhibits clotting, is a constant product of the vascular wall, and
may be regarded as a sort of vital reaction opposed to the chemical influence of the blood.
Blood collected from organs containing numerous capillaries and relatively slow circulation,
when taken from the living or the cadaver, has a tendency to remain fluid. Some authors
claim to have found antithrombin in the liver after washing the latter and after transfusing
this organ with arterial blood, anticoagulating properties then appeared in the transfusate
1 Zenker, Ziegler’s Beitr., XVII, 1895.
2 Kiister, Miinchen. med. Wchnsch., rg11, No. 46.
PHYSICAL EXPLANATIONS OF THROMBOSIS 105
Lipoid substances, or according to others, phosphatid substances containing C. N. and P.
are said to be responsible for the diminished coagulating powers. An observation of no
mean importance is the relative lack of clotting in the capillaries.
Source and Quantity of Fibrinogen.—This does not seem to be produced by the blood
corpuscles, since in defibrinated blood no new fibrinogen is elaborated upon standing. In
an animal that has been thoroughly bled and transfused with defibrinated blood, the fibrin-
ogen formation may attain or exceed the normal (Dostre & Mathews). Simultaneously
the blood platelets also.make their appearance, so that the fibrinogen has been considered
as arising either from the vessel wall, or from the platelets. The latter is unlikely, since the
lymph may contain fibrinogen without platelets. Therefore, the excretion and quantitative
control of fibrinogen in the blood and lymph seems to be a specific function of the tissuejcells.
The kinase or coagulin production is a function of the living tissues, particularly of the
platelets and leukocytes. Other cells, such as connective tissue cells, may participate.
Congelation.—In addition to cell agglutination and fibrin coagulation
there is another type of phenomenon whichis often associated with thrombosis,
namely, the hyaline conversion of albuminous bodies of various forms. This
phenomenon has been called congelation as a substitute for other terms—
hyaline degeneration, and coagulation necrosis... This process, however,
occurs only in dead material, even though this material forms but a part of
the respective cell or intracellular substance (intracellular hyaline degenera-
tion). Nor does it occur in every form of necrosis. The conditions for its
development are more favorable in the living organism than in the cadaver.
The exact nature of the process is not well known, some believing that a
proteolytic ferment is at work.
CHAPTER XVIII
PHYSICAL EXPLANATIONS OF THROMBOSIS
For a comprehension of the causation of gangrene of the extremities, it is
well to be acquainted with the present status of the question of thrombosis.
Much discussion has arisen since the time of Virchow as to the importance
of the infectious or mechanical factors in the production of thrombosis. In
his day the mechanical effects of slowing of the blood stream was regarded as
the all important factor. The tendency of late has been to stress infection
as the deciding factor.
According to Aschoff! the concept of thrombosis can be clarified by a
study of other physical processes with certain similarities.
The Appearance of Thrombi.—From the pathological point of view a
thrombus is any obstructing intravascular mass that arises intra vitam.
Thus we can differentiate blood thrombi, tumor, thrombi and parenchymatous
thrombi. We are merely interested here in the blood thrombi.
These latter are characterized by their distinct stratification, by their
friability and undulatory nature of their surface; and, are differentiated from
post-mortem thrombi by organized adhesions to the vessel wall.
In a well developed thrombus parts differing in color are recognized. The
proximal portion or head portion is usually pale or a white thrombus. Adyja-
cent to this, the neck portion is mixed in color, and the peripheral part is
dark red. The head may be very small, whilst the tail often measures many
centimeters. Such are their usual appearances in the venous system. ‘The
red thrombi are only found where the white portion obturates the vessel.
1 Aschoff- Beitr. z. Thombosefrage, Leipzig, 1912.
106 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
The red portion may be absent in parietal thrombi, the white portion
occasionally growing to considerable length in a continuing circulation.
The white portion is the essential part of an autochthonus thrombus, and is
the real causal factor in the whole process, whilst the red portion is only acci-
dental. A pure red thrombus without a head portion is a rare exception.
Such is the description given by Aschoff for the ordinary thrombus. That
these rules do not obtain in inflammatory thrombi, such as are seen
in thrombo-angiitis obliterans, will be learned in the section on that affection.
Macroscopic and Microscopic Appearances of the Caput.—Certain characteristic appear-
ances of the surface of an autochthonus thrombus correspond to the internal structure, and
have lead Aschoff to propose certain explanations of the method of its origin. The fluted
or reef-like markings, and the reticular and streak-like shadings seen in the caput and neck
portion of the thrombus are considered characteristic. An explanation of these markings
is offered by this author that should lead to a correct concept of the origin of this type.
A longitudinal section through the head and neck portion of the thrombus, shows that
the above described superficial reef-like elevations are but the summits of beams or skeleton
structures. These are coralliform or frame-like joistings, that form the supporting struc-
tures of the whole thrombus mass. This framework is constituted by the heaping up of
blood platelets in a fine granular mass. Above these beams or girders a fine layer of
leukocytes is disposed, whilst in the interstices between the main support, the red blood
cells fill out the structure.
The beams themselves are disposed to each other in a regular fashion, separated by
-interspaces of varied size, and with fine branches passing upwards and downwards. As we
approach the caput, the blood-filled interspaces become narrower, until the supports fuse
together into the white summits of the thrombus.
The fibrin is almost absent in this whole structure. When it is present, it is found at the
margin where the platelet structure is in contact with the red blood.
When it was shown (Deetjen!) that the blood platelets are independent elements
assisting in the circulating blood, it became comprehensible, that only in flowing blood
could such masses of blood platelets be deposited, as are to be found in the above described
framework of thrombi. The platelets do not originate from white or red blood cells,
but are independent elements arising from the giant cells of the bone marrow and in the
spleen. The platelets show a finely granular center, and a clear peripheral zone. They
are detached from the giant cells, megakaryocytes and attain spontaneous mobility.
These megakaryocytes of the bone marrow have been seen to interpose pseudopods into the
capillary blood channels, and in this way the transference of the blood platelets into the
circulation comes to pass.
It has been shown that when a section of vessel is tied off by ligation no platelet forma-
tion could be observed even after the employment of caustic irritation, whilst a typical
platelet thrombus develops under such conditions in a vessel in which the blood circulates.
A platelet thrombus, therefore, is regarded as arising in flowing or circulating blood.
Formation of the Thrombus.—The framework of this type of thrombus
is composed of a lamellar system (Fig. 41) with the elements more or less
parallel, either transversely or obliquely disposed to the long axis of the
vessel. In this sense, the structure resembles the effect of the ebbing tide
on the fine sand of the ocean beach. A similar step-like line formation is
produced by the flowing blood, the platelet masses forming the delicate
lamellar system. Just as in slowly running water, finely divided elements
may be deposited in a regular way so as to form reef-like formations, so in the
blood vessel, platelets are deposited in the above-described framework. Asthe
blood continues to flow, more and more platelets are attached, and further
elaborate the structure. In the oldest portion of the platelet system, the
renewed deposits are greatest, and finally the time arrives when the inter-
stices of the lamellar system (in the oldest portion of the thrombus) become so
minute that the blood stream becomes slower and slower, and finally ceases.
At this moment the primary thrombus formation has attained its finality,
1 Deetjen, Ztschr. f. physiol. Chem., Bd. 65, 1900.
PHYSICAL EXPLANATIONS OF THROMBOSIS 107
since no more platelet masses are added and its primary growth can continue
no further.
The leukocytes in this system follow the usual laws according to which the
specifically lighter white blood cells take the peripheral zone of the stream.
Here, since the stream is divided into numerous sub-streams by the regular
structure, the leukocytes follow the same law and are deposited along the
walls of the structure.
This 1s the manner of formation of the head portion of the typical thrombus
(Aschoff!),
The tail portion of the thrombus in which a platelet lamellar system is
absent, forms in the non-flowing blood. In microscopic structure this throm-
bus resembles a post-mortem clot, being made of an irregular admixture of
red and white blood cells, blood platelets and fibrin.
The Cause of the Development of a Platelet Thrombus.—If we compare
the blood stream to a river in which foreign particles are distributed, the con-
clusion would be warranted that any local heaping up of particles can only
take place under an optimum special rate of flow. And so, in the blood
stream we must presuppose that a certain diminution in the rapidity of the
flow must take place to furnish the optimum condition. Thus in the stream
in which barriers or dams are erected and changes in rate of flow are produced,
deposits have been observed. So therefore, we would expect that in the
formation of autochthonus thrombi we should find certain alterations in the
blood stream that bring about sudden flowing or refluxes, or vortices.
The causal factors in this type of thrombosis have been given as,
A. Changes in the rapidity of the blood stream;
B. Changes in the qualitative and quantitative state of the blood platelets;
C. Changes in the inner walls of the vessels.
A. Changes in the Rapidity of the Blood Stream.—The predilection of the venous system
to thrombosis is in keeping with the possibilities of impediments to the normal rapidity
of flow in them. In the venous system there are indeed sites of predilection, namely, the
veins of the leg, the proximal portion of the femoral vein, the pelvic veins, the veins of the
meninges, etc. Four factors contribute to the localization of venous thrombosis; (1)
the continuous pressure on the venous wall—as is exemplified by the constant pressure of the
column of blood in the veins of the lower extremities in the upright posture (or the action
of intra-abdominal pressure in causing dilatation of the veins); (2) the ampullary dilatation
of veins in the valvular pockets; (3) the possibility of reflux in the stream, first occurring in
the proximal valves of the femoral veins; and (4) the resistance to flow that Poupart’s
ligament offers to the current of the femoral veins in the recumbent posture. The position
of the patient is not unimportant in determining thrombosis in veins, for an extremity that
is constantly held under another one is more apt to show complicating thrombosis. The
compression of the left iliac vein through the iliac artery is not to be disregarded in its effect
in impeding flow in the veins and leading to left-sided crural thrombosis.
B. Changes in the Platelets —Whilst retardation of the flow is an important factor in the
production of thrombi, the accumulation of platelets may be influenced otherwise. ‘These
thrombi have been variously called separation or accumulation thrombi (Abscheidung und
Anhaufung). These terms have been applied because of the fact that the platelets are
more or less intimately agglutinated. And so, in the literature, we find besides the
appellation “‘accumulation,”’ also the words “‘conglutination”’ and “‘agglutination”’ descrip-
tively used in this connection. Here we presuppose an alteration in the viscosity of the
platelets. We do not know, however, whether increased coagulability of the plasma also
determines a more rapid agglutination of the platelets. Variations in the fibrinogen
content may have some influence. Increase in the fibrinogen content alone per se does not
lead to thrombosis, so that a direct causal relationship cannot be accepted in the present
state of our knowledge.
Certain it is, that in artificial anemia, the platelets become markedly increased in
number, and from this we may draw asa corollary the noteworthy observation that persons
1 Aschoff, Loc. cit.
108 CIRCULATORY ‘AFFECTIONS OF THE EXTREMITIES
rendered anaemic by operation or gynecologic or obstetrical conditions show an increased
tendency to thrombus formation.
C. Changes in the Vessel Wall.—The réle of alterations of the intima in the production
of thrombosis has been much overestimated. It is a well-known fact that the atherosclerotic
aorta, and other large arteries in spite of very intensive intimal changes, may be free of all
thrombus formation. It has been asked as to whether thrombosis can only occur when the
intima has been damaged; chronic changes in the intima of the vein alone do not play
a determining réle in causing thrombosis. Where, however, there is advanced phleboscler-
osis with rigidity of the vein walls and valves, with consequent circulatory impairment,
we may conclude that a causal relationship exists. When, however, the intima is suddenly
robbed of its endothelium covering, a pathological reaction of the tissues is necessarily
unavoidable. In such a case it is the alteration in the territory of the wound that causes
the thrombosis.
Coagulation in the Process of Thrombosis.—The observation (Baum-
garten) to the effect that fluid blood does not clot in a section of a vessel
that has been ligated in two places, would at first sight offer insurmountable
difficulties to any explanations of the clotting process.
Aschoff says that the breaking down of platelets sets free fibrin ferments
that admix with the surrounding plasma, and by a process of diffusion pass in
a peripheral direction where the effects can be manifested. In the origin,
therefore, of red thrombi, we presuppose not the separation of corporal ele-
ments of the blood (as in the platelet thrombi), but notably the throwing out
of fibrin (as in the ordinary clotting process). And so the red clot (coagula-
tion thrombus) is to be differentiated from the platelet (segregation or conglu-
tination) thrombus. Some authors distinguish between conglutination or
agglutination, and accumulation thrombosis and coagulation thrombosis.
Whilst in the segregation (conglutination) type of thrombosis, the slowing of
the blood stream and the quantitative and qualitative conditions of the plate-
lets and their viscosity are the essential factors, so, in the case of the coagula-
tion (red) thrombosis, the cessation of the stream and the ferment elaboration
are essential.
It is evident, then, that one type of thrombus (the platelet thrombus)
leads directly to the other type, the coagulation thrombus. Similarly we see
in thrombo-angiitis obliterans a specific type of clot doubtlessly of inflam-
matory nature, directly associated with a coagulation clot that caps the
terminal portion of the former (Chap. LXI).
Primary Coagulation Thrombosis.—It is a difficult matter to produce a
primary coagulation thrombosis experimentally. Cessation of the blood
flow alone does not suffice when the ferment development is not adequate.
Indeed, optimum conditions, with a proper relationship between rapidity of
flow and quantity of ferment are necessary to bring about the result. For, if
ferment is present in large enough quantities, even the flowing blood may clot.
In some of the experimentally produced clots we may be dealing either with fibrin
coagulation or what is known as “‘precipitation thrombosis.”’ ‘Two other factors, however,
are known to bring about coagulation thrombosis. These are ligation and infection.
When the fibrin ferment that originates in an injured vessel wall through
ligation can adequately exert its influence on the continuous non-flowing
blood column, coagulation thrombosis may occur. The platelet thrombosis
may also develop where the dead portion of the vessel is in contact with the
blood stream. Both forms of thrombosis are possible, whilst with very slight
injury to the wall neither one of these may follow.
In the so-called infectious type of thrombosis, the thrombus formation may
precede the infection or be caused by the infection. In the puerperal throm-
bosis, and in post-operative infectious thrombus formation, by virtue of the
PHYSICAL EXPLANATIONS OF THROMBOSIS 109
liberation of fibrin ferment, coagulation thrombosis may occur in numerous
veins, and where the blood flow is interfered with, the platelet thrombosis
may develop. If infection (particularly streptococci) be superadded, an
inflammatory reaction within the vessel wall with the migration of leukocytic
elements from the periphery into the vein wall, is to be expected. Puerperal
cases often evidence a puriform condition within the veins, with marked
periphlebitis, the picture simulating abscess rather than infectious throm-
bosis. In such cases the infection travels through the vascular walls rather
than by way of their lumina.
The thrombosis that occurs in direct association with an inflammatory area is a compli-
cated process. At first the venous tributaries become the seat of thrombosis, probably of
the coagulation type, by virtue of the liberation of the fibrin ferment in the inflammatory
toxic process. Then secondary invasion of bacteria takes place, and finally the larger veins,
by reason of interference of the circulation, become the seat of platelet thrombosis. It is
difficult to differentiate accurately in all cases between thrombosis as the result of an infec-
tion, or a thrombus secondarily infected.
Metastatic (?) or Distant Thrombosis.—It is possible to explain distant thromboses in
three ways: (1) the microorganisms in the blood cause a local change in the wall of the
vessel with secondary thrombosis; or (2) that in some unknown way, coagulation phenom-
ena are brought about in the blood by the organism; and (3) that the primary thrombosis is
independent of the infection, the manifestations of thrombophlebitis being produced by
secondary invasion of the clots with the organisms.
(1) Metastatic inflammatory changes in the wall are clinically rare, but may possibly
explain the occurrence of tubercular and syphilitic thrombophlebitides.
(2) Direct coagulation through the action of the circulating organism is only a hypo-
thetical explanation, since experimentally such action of bacteria could only be produced
when stasis in the blood stream is an added factor.
(3) Primary thrombosis with secondary infection is the most common type. In the
femoral vein where thromboses so frequently occur in post-operative cases, the thrombosis
according to Aschoff, was found to be of the platelet type. Distant thrombosis in the iliac
veins occurs with no direct connection between the site of operation and the site of the
thrombosis. Here, too, platelet thrombosis is the rule and when infectious thrombi are
found, these show the bacteria in the platelet masses. The thrombosis, therefore, just as
in the non-infected cases is the result of local alterations in the stream, and not the imme-
diate result of infection, the bacteria invading secondarily. Then, as the bacteria multiply,
degeneration of the thrombus elements takes place, and infiltration of the vessel wall with
leukocytes follows. Superadded to such a thrombus there may be a secondary thrombosis
extending centrally.
Thrombosis in Thrombo-angiitis Obliterans.—How are we to explain
this variety of thrombosis, one that is exquisitely of the red variety, but in
which three different forms are in evidence? The pathology of this form will
be described in detail elsewhere. Here, for clarity it may be well to
anticipate by stating that a red (or mixed) form is the immediate sequence
of lesions in arteries and veins, whose walls have become the seat of an
acute inflammatory process. Stasis probably plays a role, for only ‘n this
way can we explain the predilection of the vessels of the lower extremities
for this disease. Secondary changes occur in the clot by the transmigra-
tion of corpuscular elements through the walls of the vessels. A “‘specific”’
architectural picture is thus evolved that seems in the light of our present
knowledge to be pathognomonic. ‘The latter changes are reactive, resorptive,
and (teleologically speaking) paradoxically curative and baneful in nature.
The characteristic form of clotting could, in the interpretive system of
Aschoff, be regarded as of the type due to “‘ metastatic inflammatory changes
in the vessel walls,’ although a specific organism has eluded the search of
investigators. So also, could the process be included in the above-mentioned
third category. For, the inflammatory and abscess-like foci in the clot
might be regarded as indicative of secondary infection.
110 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
A bland, red form of thrombus within normal vessel walls, and evidencing
no inflammatory andnone of the specific reactive and resorptive phenomena
is often found as a sort of cap surmounting the typical variety (accretion or
stagnation thrombus). This, it would seem, is due to local cessation of the
stream, possibly aided by the liberation of fibrin ferments.
The third form includes only the intermediate and final products of the
first type.
Precipitation Thrombosis.—This is another form of thrombosis that has a rather
theoretical than experimental interest. It may be described as that form in which thrombi
result from the action of chemicals precipitating albumin. Whenever mucous membrane is
cauterized chemically, such thrombi develop in the smallest veins; so also, when a heterolog-
ous serum or a specific precipitating serum is introduced into the veins. ‘This phenomenon
belongs to the type known as agglutination, the agglutinating red blood cells playing an
important réle. In the thrombi resulting from the action of poisons (ricin, adrin, snake
venom), the clotting is partly due to agglutination phenomena, and partly to the obstruc-
tion of the smallest vessel with broken-down red blood cells. The effect of burns is a similar
one. Aschoff has designated the type with breaking down of red blood cells as spodogenic
thrombosis.
CLASSIFICATION OF THE THROMBOTIC PROCESS!
According to form According to causal genesis
Immediate causes Remote causes
1. Seggregation (separation or} Local retardation of the (a) Physiological narrowing or dilata-
conglutination thrombo-| stream. tion. . phys. dilatation thrombosis.
sis). Quantitative and qualita- (b) Dilatation with pathological changes
tive alterations in the in the walls.pathological dilatation
platelet. (c) Static factors..... static thrombosis
(d) Compression. .compression thrombo-
sis.
(e) Vesselinjury..traumatic thrombosis.
(f) General weakness of the vascular
SVStetnerene marantic thrombosis.
(g) Alterations in the blood............
blood deterioration thrombosis.
(h) Inflammatory wall changes.........
inflammatory thrombosis.
. Coagulation thrombosis; Local cessation of the Ligation
(clotting). the stream. Placentar | stagnation thrombosis.
Fibrin ferment. detachment
Inflammation. Inflammatory thrombosis.
iS)
3. Clumping thrombosis (ery- | Agglutination of the red
throcytic agglutination).| blood cells through blood
poisons.
4. Precipitation thrombosis. jAlbumin precipitation
: A ON cote Ge Ce TOxice met is.
through caustic chemi- fo) hrombosis
cals:
5. Spodogenic thrombosis. Breaking down of red cor-
puscles through blood
poisons.
1 Aschoff, L, Beitr. z» Thrombosefrage, Leipzig, 1912.
Ribbert? differs in his conception of thrombosis from the views above expressed in that
he believes that the platelet structure is a secondary formation after platelets have become
adherent to an injured intima. When there is a small circumscribed lesion of the intima
1 Ribbert, Virchow’s Arch., 220, 1915, p. 133-147.
MECHANICAL TYPES OF THROMBOSIS 111
(experimentally produced) a small rounded mound of platelets covering the area is noted.
An intimate relationship is always seen between the injured area and the platelet deposit.
According to his view a retardation of the blood current, although it favors the adhesion of
platelets, is not the determining factor, but the very beginnings of platelet deposit permit of
continued deposition including also leukocytes and fibrin. In this way lamellae perpen-
dicular to the blood stream originate. Where there is a ‘“‘system”’ of platelet framework,
Ribbert presupposes the existence of numerous platelet mounds, each giving rise to its
platelet beam.
CHAPTE REXCLX:
MECHANICAL TYPES OF THROMBOSIS
For a better understanding of the origin of thrombi within the body, a
brief resumé of results of experimental work and of observation on effects
of intravascular physical phenomena may elucidate the subject. In the
following exposition the work of Beneke,! Lubarsch, Zahn and others has
been extensively drawn up.
The deleterious influences can set in acutely or slowly, or may take the
form of a variation in the character of the stream of flow. The former of these
constitutes stagnation thrombosis, the latter the pulsion? thrombosis. The
former of these corresponds to a certain extent to the coagulation type of
of thrombosis, the latter with the accumulation or seggregation type.
Stagnation Type of Thrombosis.—Experimentally, it has been shown that blood con-
tained between two ligatures in a living vessel with uninjured vessel walls, will remain fluid.
But such a section of vessel when cut out of the body and exposed to ferments, or when
tissue extracts are injected (coagulins), undergoes early coagulation. In such stagnant
blood, coagulation does not take place until by virtue of marked injury of the vessel wall at
the site of ligation, or through chemical lesion of the wall and thermic influence, localized
special causal moments have become established.
In territories undergoing stasis, increasing degeneration of the vessel wall is believed to
take place by reason of inadequate gaseous interchange, with resulting breaking-down of the
blood corpuscles. ‘Their hemoglobin-free detritus may then fill the lumina, or lead to
hyalin thrombosis. Then fibrin ferment develops, resulting in coagulation in spite of the
inhibiting influences of the vessel walls.
In short, experiments seem to warrant the conclusion that true thrombosis results only
then in stagnant blood when added mechanical thermic or toxic influences play a rdle.
Pulsion Thrombosis.—In this group we presuppose that through special modalities of
flow, the normal mixture or distribution of the corporal blood elements is disturbed with
a tendency to local aggregation of special groups or types, particularly of blood platelets.
In this way agglutination, coagulation and congelation leading to plugs or thrombus
formation are favored. Essential for such modifications are principally an abnormally
strong development of the plasmatic marginal stream. These currents can be observed
in flowing blood at the vessel wall, and they form the peripheral zone in which erythrocytes
areabsent. The physiologic significance of this territory is the constant reciprocal exchange
of chemical relations between the blood and the vessel endothelium. Through this
exchange the plasmatic marginal current is doubtlessly influenced. ‘The rolling motion of
the leukocytes independent of the axial current is believed to be partly due to the osmotic
processes that are an expression of the secretory activities of the mural vascular elements.
For an understanding of the mechanical forces the excellent description of Beneke
will be extensively used.
According to general hydro-dynamic laws the forte of the axial current (in a non-living
tube) is the strongest and diminishes in intensity towards the wall of the tube. Theoret-
ically there is a thin resting layer directly against the wall. The rapidity and breadth of
the marginal current depend upon the energy and form of the total stream. A rapidly
1 Beneke, Krehl-Marchand Handb. d. allg. Path.
2 Terms used by some of the Continental writers.
te CIRCULATORY AFFECTIONS OF THE EXTREMITIES
+ ce al AL
Fic. 34.—Schematic representation of increasing size of marginal zone with diminution of
pressure. (Beneke)
A
te
Fic. 35.—Schematic representation—changes in marginal zone at points of local dilatation.
(Beneke)
Fic. 36.—Schematic representation—formation of whirls or eddies in vessels by reason of
abrupt changes in the character of the lumen. (Beneke)
MECHANICAL TYPES OF THROMBOSIS 113
flowing axial current develops considerable natural pressure, and the marginal current can
become insignificant; the less the lateral pressure, the broader the slow marginal zones may
become.
In Fig. 34 the dark central area to the left represents a strong rapidly flowing stream
that develops an increasingly broader marginal zone at a, where its diminishing intensity is
also expressed by lighter shadings.
»>—> a
} { |
i \ H
i
Fic. 37.—Schematic representation—the effect of dam-like obstructions (a) here depicted
(Beneke)
cd
i
j
Fic. 38.—Schematic representation—formation of whirlpool where two marginal cur-
rents (x-y) meet ata. (Beneke)
Local dilatation (Fig. 35 at a) and general dilatation at (b) are accompanied by similar
changes in the marginal zones.
Abrupt changes in a tube or vessel wall with generalized or local changes in diameter of
the lumina (Fig. 36) may cause the formation of whirls or eddies or vortices. The propel-
ling force of the stream current perpetuates these eddies, whilst any contained particles at
the periphery of the eddies are cast off tangentially.
5
114 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Narrowings in the stream through projections from the walls cause quite different
phenomena. In Fig. 37 it will be seen that the upper portion of the stream conserves its
strength, whilst the lower is altered through the presence of the dam-like obstruction at a.
Behind the dam, condensation and attenuation of the axial current are produced together
with waves. The altitude of these waves diminishes as they recede from the obstacle,
varying according to the strength of the axial stream, their length being related to the
height of the obstruction. Beyond the obstacle an eddy is formed that tends to flow ina
everse direction.
It will be noted that just beyond the dam (to the right at a) there is a space, and
then follows the eddy. The course of this eddy or whirlpool has been shown to be so
great that solid particles in an experimental stream are thrown backward against the
stream into the dead space. A correct understanding of these phenomena will enable the
reader to properly interpret the theories of Aschoff. ;
Fic. 39.—Schematic representation—the effect of ligation seen in the formation of whirl-
pools at the closed vessel ends. (Beneke)
Fig. 38 shows the development of a whirlpool where the two marginal currents of « and
y meet at a. Whichever of the two streams is the stronger (let us suppose y) will displace
the eddy into the lumen of the other, into a point of rest (a). The stronger the pressure
differences between the two streams, the greater the transference into the lumen of the
weaker current.
The effect of ligation is depicted in Fig. 39 at a, with the current running in the direction
of the arrow. ‘The current flows with accustomed full rapidity through the branch (w’),
and forms a whirlpool in the blind end. A collateral (y’) which leads from the distal vessel
becomes the seat of a reverse current. In the blind end of this part of the eddy a larger
eddy is formed.
According to Eberth-Schimmelbusch (Fig. 40) the marginal current of the blood
contains normally only white blood cells, whilst the platelets are admixed with red blood
cells in the axial stream. Simple diminution of the rapidity of the current is followed by a
distinct increase in the parietal leukocytes. With further diminution in flow the blood
platelets are cast into the marginal zone in increasing numbers until the latter occupy most
of this region. Even with this phenomenon a true thrombus does not form, and with a
change in the rapidity of the current, these corporal elements can be again withdrawn into
the central portion of the stream.
According to mechanical laws, the heavier red blood cells must follow the axial current,
and according to the law of centrifugal motion must move in the periphery of the eddies.
The marginal zone, as also the center of the eddies, must therefore under favorable cir-
cumstances contain mostly leukocytes and platelets. The breadth of the marginal zone,
as also the extent of the whirlpool centers decrease with the intensity of the lateral pressure
in the channel. Increased pressure tends to force the corpuscular particles into the eddy,
against the latter’s centrifugal tension. Per contra, when there is little pressure the eddy
tends to broaden and the steadier elements can be more easily precipitated externally, and
MECHANICAL TYPES OF THROMBOSIS 115
the separation of specifically lighter articles from the heavier is favored. «Since the eddy
becomes broader with diminution in rapidity of the stream, the number of platelets and
leukocytes increases with weak current.
Solid plugs develop experimentally with mechanical vascular lesions. When acupunc-
ture is used in experimentation, all the blood corpuscles are pressed against the injured
area, and then become converted under pressure into a hyalin stagnation thrombus.
Where circulation is still present with waves and eddies, leukocytes and platelets coalesce.
The latter agglutinate and form the beginnings of true thrombi. Where the current is very
rapid, the thrombi may be absent, because the platelets are torn away soon after attach-
ment. Changes in direction and weakness in the current are important factors in
the formation of thrombi in experimentation.
Fic. 40.—(1) Normal circulation showing central axial current and plasmatic marginal
zone with discrete leucocytes.
(2) Circulation of diminished rapidity, the red blood cells visible in the axial current,
accumulation of leucocytes at the parietes and beginning mural attraction of the platelets.
(3) Markedly slow circulation, marginal accumulation of platelets and leucocytes with
sluggish, narrowed axial current. (Eberth-Schimmelbusch)
It has been shown, however, that although trauma is an important predisposing factor
in thrombus formation, pure mechanical agglutination up to complete thrombus formation
can occur, as the result of changes in the current alone.
In addition to the mechanical factors, chemical influences have been thought to explain
thrombosis. Indeed, the experiments with hirudin seem to show that venous tears after
hirudin or pepton injection are followed by typical platelet thrombosis, usually without
fibrin, in inverse proportion to the amount of anti-coagulin injected.
When foreign bodies are introduced into the circulation, agglutinated platelets accumu-
late in thrombus-like formation over the foreign body in very few minutes. About such
bodies, eddies and waves develop that lead to agglutination of the platelet elements.
That chemical influences must be taken into consideration, however, is demonstrated
by the fact that foreign bodies covered with paraffin do not show such platelet agglutination.
Perhaps in the case of foreign bodies, just as in the traumatic thrombi, the death of isolated
leukocytes and platelets adherent to the foreign body evokes the incipiencey of further
agglutination and attachment of the mechanically concentrated platelet masses. Plate-
lets occur in places in which the current is relatively retarded.
116 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
In the ligated vessel, whirlpools of varying size and density are occasioned by the
current. Usually with adequate collateral and intensive circulation thrombosis does not
occur, since small agglutinates are easily detached by the current. In the presence of weak
currents, however, thrombus formation occurs with growth of the latter into the free lumen
of the vessel without contact with the walls.
But the retardation of the stream alone after ligation of a vessel does not seem to be the
only factor in thrombosis. It must be conceded that at the present state of our knowledge
it has not been possible to simulate the marantic thrombi in an experimental way. Some
other chemical constituent of the blood must be sought for, which in the presence of
mechanical contributing factors suffices to bring about thrombosis. Lipoid substances are
believed to be not unimportant in this connection.
Stagnation Thrombosis.—Some observations would seem to indicate that thrombosis
does not normally occur in a stagnant flow. The fact that it is absent in the umbilical
artery after ligation of the cord is cited as an argument against the mechanical theory;
and also the fact that vessels in the case of atherosclerotic closure of the crural arteries do
not necessarily become closed by thrombi.
The instances where plugs do occur, however, in these circumstances cannot be ignored.
Here possibly an additional factor besides the stagnation, either a change in the vessel wall
or of the contents, is responsible.
In the case of the capillaries and small vessels, stasis contributes a certain essential
condition, be it through simple mechanical interference to the outflow with a continuous
inflow, or be it through the chemical changes in the tissues and vessels that are thus engen-
dered. The phenomenon of stagnation does not seem to be the only effect of retarded
circulation. In addition to the diapedesis and capillary dilatation, the erythrocytes are
massed together and compressed, so that a homogenous fusing can take place. Then
hemolysis, through the influence of mechanical or chemical injury to the endothelium may
take place, the hemoglobin of the red blood cells may disappear, and their stromata left as a
colorless, dense reticulum. In such agglutinates, platelets and leukocytes then degenerate
and form foci for the production of fibrin clots. Such stagnant blood columns in small
vessels and capillaries then have as a characteristic the rapid degeneration of all the cells
implicated, and are thus differentiated from the stagnant blood in the cadaver.
The compression of the erythrocytes and the necrosing influence of slowly flowing but
stagnant blood with the concomitant degeneration of other cells, particularly endothelial
cells, seem to be the essential factors in the genesis of stasis thrombosis. In this sense
mechanical and chemical moments combine to produce the end-results.
Red or mixed hyaline thrombi correspond to stagnation of the total blood. But color-
less hyaline thrombi can develop in capillaries and small vessels without admixture of
erythrocytes when tissue is injured, either through cold or long continued ischemia. In
such case the residual leukocytes, the fibrin masses, and the transuded substances then form
a hyaline substratum which is not unlike a hyaline urinary cast in form and genesis. Simple
ischemia, even when of considerable duration does not cause thrombosis. In the local
asphyxia of the fingers occurring after exposure in susceptible individuals, the vitality of the
blood and tissues remains intact, only the flowis retarded. After excessive cold, there may
be simultaneous death of the surrounding tissues as well as of the blood in the vessels, so
that no vital exchange is possible; then, too, thrombosis is absent. Thrombosis takes place
only when the remaining living tissues can exert their effects.
As compared with the stagnation thrombi in the smaller vessels, those in the larger ones
are not essentially different, except that the separation of the colorless elements is not so
complete as to produce obturation with these alone. In larger vessels one occasionally sees
gross clotting of blood, not unlike cruor, following sudden interruption of the circulation
(as in ligation of the plexus pampini formis). A sudden cessation of the blood flow results.
However, even in the larger vessels such red thrombosis is usually under the influence of
undulating currents, as manifested by the grouping of platelets and leukocytes, within the
coagula. These form smaller and larger conglomerates that are evidences of the effects of
the current’s waves. .
It is believed that there is always a necessity for a certain quantity of ferment for the
development of red stagnation thrombi in the large vessels. Simple compression or even
invasion of a vessel with an obturating tumor mass may not produce thrombosis.
Further observations speak for the immediate importance and relationship of local
increase in ferments in the formation of stagnation thrombi. A primary thrombus as
soon as it becomes obturating, may bring about a secondary red thrombus. This is also
noticeable in the specific type of thrombi in thrombi-angiiti sobliterans where secondary
thrombi of red type are apt to cap the terminations of the specific clot. By reason of the
action of the ferments, these secondary clots may extend for varying distances into the
vessels and even into their branches. The extent of the secondary red thrombi exceeds
the primary pulsion thrombus. Appearances of the secondary clot, too, speak for the
MECHANICAL TYPES OF THROMBOSIS 1a ie
diminution in the amount of ferment as the clot recedes from its point of origin. Where
the secondary coagulum is attached to the primary thrombus, it is firmly connected, whilst
farther away it tapers out and gradually shows an imperceptible transition into the fluid
blood.
In short, the origin of red stagnation thrombi is traceable to two principal factors—
firstly, a weakening or deficiency in circulation and secondly, the presence of substances 1n
loco that further fibrin clotting.
Pulsion Thrombosis.—This is the most frequent form of human thrombosis, and was
first given complete study by Zahn,! who called attention to the relationship between
the wave motion transmitted in the pulse and the conformation of thrombi.
Virchow, von Recklinghausen and Zahn, therefore, were the founders of the mechanical
theory. They conceived that retarded flow, whirlpool or eddy formation and undulatory
movements were possible factors in thrombus formation. The participation of blood
platelets as important components of white thrombi was first called attention to by Osler?
Fic. 41.—Schematic representation ot stratified formation of thrombi reproducing the wave
currents. (Beneke)
and Hayem.’ Pure platelet thrombi are. not common inthe human organism. They occur
only there where the platelets can stick together and form firm masses, whilst the depo-
sition of leukocytes and fibrin is prevented by the current. ‘These conditions obtain
where there is a strong current, particularly in arterial territories, as for instance, over
areas of aortic sclerosis, aneurism, etc. In the venous channels leukocytes can become
attached by reason of the diminished flow and agglutinate. Platelet thrombi are very
often seen in the furrows in the arterial walls over atheromatous ulcers. There-
upon the blood stream may model such thrombi. They cover the arterial wall with
protecting hyaline covering and later may become calcified.
White thrombi made up of platelets and leukocytes, with or without fibrin, are more
common than the pure platelet thrombi. They begin with the deposition of the platelets;
then occurs the attachment of leukocytes and fibrin.
The most important forms are the wave and whirlpool or eddy thrombi. The aggluti-
nated cells lie in the nodal points of the waves and in the centers of the eddies. According
to the intensity of the blood stream they may be dense and narrow, or they may be loose
and broad.
The deposition of fibrin then follows by reason of the participation of the degenerate
leukocytes. The agglutinates forming in the retarded stream lie in the nodal points of the
1 Zahn, Virchow’s Arch., LXII, 1875; also XCVI, 1884, and CII, 1885.
2 Osler, Ztschr., f. med. Wissensch., 1882.
3’ Hayem, Recherches sur l’anat. norm. et path. du sang, 1878.
118 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
waves and in the centers of the whirls. Even the very smallest agglutinates show deposits
of leukocytes. All the various degeneration forms can be seen, namely, detached granules
of platelets, karyorrhexis, breaking down of the nuclear substance—are noted. Because of
the large number of leukocytes one gains the impression that chemotactic influences attract
them. The participation of leukocytes is of importance for the growth of the white
thrombi in typical formations, in which a central agglutinate free from nuclei forms,
and about which there is a zone of leukocytes. The breaking down of leukocytes goes hand
in hand with the deposition of tissue material.
Fibrin formation follows the chemical participation of degenerating leukocytes, beginning
from the degenerating center. Fibrin threads surround the centers, and attain their great-
est size between two coagulating centers. Histologic pictures are often observed which
correspond accurately to the wave conditions present. Thus one finds at intervals more or
less oblique masses of thrombus made up of platelets and leukocytes corresponding to the
nodal points. Between these one finds the fibrin threads like water plants taking the direc-
tion of the stream, and whose obliquity and curve depend upon the strength of the lateral
pressure of the current. Lamella formation is another product of the mechanical hydro-
static conditions. The parallel formations are due to repeatedly new depositions in the
nodal points in a direction perpendicular to the current. This forms the reef-like surface
of thrombi being a replica of the wave current (Fig. 41).
The erythrocytes only play a subsidiary réle in the process. When they are included
between the layers of fibrin, they may persist for a long time without degenerating. They
may be absent between the layers, as in the case of the white thrombi, which arise in the
plasmatic part of the stream. Only then when the strength of the stream becomes so
diminished that the peripheral portions of it are stagnant, and the erythrocytes also taken
up in the wave thrombus, just as in the stagnation thrombus, then are produced those
peculiar mixtures of red and white layers or mixed stratified thrombus (Fig. 41).
In the mechanically produced thrombi the process sets in through agglutination of the
platelets and the secondary fibrin formation and leukocytic accumulation that results from
the autolytic poison. Therefore, to a certain extent even the mechanical thrombi are of
chemical origin. The active substances causing the thrombosis emanate from the midst of
the stream and from the constituent elements of the blood aided by the absence of inhibiting
influences. The inhibiting influences under normal conditions are the constant dilution
of the toxic substances in a normal blood current, and the checking action of the vessel wall,
both of which are disturbed when mechanical influences are at work.
CHAPTERS:
THROMBOSIS OF CHEMICAL ORIGIN
By true chemical thrombosis we designate those forms in which the plug
formation arises by reason of chemical influences that penetrate from without
through the vessel wall, or that are carried by the blood. Several varieties
of thrombi are thus formed, the so-called spodogenic thrombi due to preci-
pitation, and fibrin forming or agglutinating types. Fluid substances
diffuse rapidly in the blood and have a general effect; more solid substances,
by reason of their concentration, act locally and mechanically on the blood
and vessel wall.
Amongst chemical influences are included fluid and solid chemical agents, effects of
general blood intoxication (from endogenic and exogenic poison), with injury of the vessel
wall, and also thermic and actinic factors.
Substances injected into the veins experimentally for the production of thrombosis,
naturally exert their effect upon all the blood elements, although they may specifically
alter certain elements more than others, particularly the erythrocytes. Injection of ox
blood serum into the veins of rabbits produces fatal agglutination in the lung vessels.
Hirudin injection does not prevent such agglutination which indicates that this process is
not a fibrin coagulation. Fibrin formation has been produced experimentally in dogs by
a injection of foreign serum. Hirudin injection prevents death by inhibiting fibrin
clotting.
THROMBOSIS OF CHEMICAL ORIGIN 119
Other forms of blood clotting have been experimentally produced through the injection
of substances, that either destroy the blood corpuscles at once, or break them up (spodo-
genic thrombi), or that cause precipitation thrombi by granular deposition of the soluble
albuminoid substances in the plasma (Dietrich!). Von Bardeleben? found that even rich
cultures of streptococci when introduced into the blood, did not cause thrombosis, but
only when stasis was caused in a vein in which cocoi were developed.
Dietrich, when he injected hemolytic agglutinating or precipitating substances into the
blood stream, encountered typical seggregations or platelet thrombi whenever the blood
stream was diminished in intensity.
The simultaneous injection of chemicals and injury to the vessel wall is especially effec-
tive through the latter agency. With complete necrosis of the vessel wall the hyaline and
static type of thrombi develop (stagnation thrombi). More mild degrees of vessel injury
cause thrombus formation corresponding to the pulsion type, insofar as they are derived
from agglutinates of platelets and develop into white thrombi. The removal of the vital
function of the endothelial cells alone leads to agglutination thrombosis, whilst simul-
taneously cooperation of fused toxic substances may lead to precipitation or to
agglutination.
In the larger arteries the same insult (e.g. caustics) are not so apt to cause thrombosis as
in the veins, in which agglutinates are more likely to adhere. The degree and the nature of
the mural changes are important for the origin of thrombi. Whenever reaction is present
in the walls, particularly with fibrin formation, the conditions for thrombus deposition are
present. On the other hand, when the toxin diffuses, precipitates or agglutinates are more
apt to form.
Inflammatory Processes.—Hyaline thrombi often accompany inflammatory processes,
So long, however, as the inflammatory irritation of the vessel wall does not interfere with its
vital functional capacity, thrombosis may be absent. Even accumulating leukocytes may
not give rise to thrombosis, and it is not until these necrose and degenerate that thrombosis
ensues. When, by virtue of specific action, fibrin deposition occurs in the lumen, then
thrombosis immediately occurs.
In the larger vessel fibrin formation may occur within the vessel wall and layers. This
may extend into the vessel lumen. Then thrombosis occurs. It is easily understood that
inflammatory exudation. of fibrin on the inner surface of the vessel wall would be relatively
stronger when the current is slow, asin the veins. This is in accord with the more frequent
combination of thrombosis with phlebitis than with arteritis. Talke* was able to produce
obturating thrombosis in the sheaths of vessels in which staphylococci were inoculated.
The thrombi were probably evoked through the diffusing toxins, and the bacteria secon-
darily entered these clots. At first platelet deposits were noted by this author, and later,
red or mixed clots.
In the case of staphylococci it has been found more difficult to produce such thrombosis,
other factors being necessary such as marked retardation of the stream. Other authors
were able to produce thrombi, with the injection of bacterium coli in the walls of the vessels.
In all of these experiments it is not the specific toxins of bacteria that predispose to
thrombus deposition, but the total inflammatory exudate with its plasmatic, fibrinous and
leukocytic accumulation, that evokes fibrin coagulation and platelet agglutination.
Chemical Varieties. Endogenous Poisons.—In extensive burns poisons
are doubtlessly formed in large quantities, in contiguous tissues. Their
absorption can be regarded as the cause of death. It has not been decided
as to what réle these poisons play in the production of thromboses in the
organs. Thrombi, indeed are found in the form of hyaline masses in the
small vessels and capillaries of the organs, particularly in the stomach and
duodenum, sometimes associated with small peptic erosions. Aschoff
reports small white thrombi in the lung arteries inacase. A thrombophilic
tendency after burns, as an expression of the general intoxication, has not been
proven.
In eclampsia there is a characteristic predisposition in certain organs to
the formation of autochthenous capillary thrombi. Perhaps certain chemical
local changes including degeneration of red and white blood cells in the liver,
or the protagon and cholesterin contents in the brain, lungs and kidneys, are
1 Dietrich, Path. Zentralbl., 1912, X XIII, ro.
‘ Von Bardeleben, Arch. f. Gynec., 1907, LX XXIII.
a-Vaike, Beitr. z;klin. Chir., 1902, X XVI:
120 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
the factors that increase tendency to thrombosis. ‘The increasing leukocy-
tosis of pregnant women has been regarded as a morphological expression of
a particular status of intoxication, perhaps of ferment production. On the
other hand, it is well known that the coagulation time is not notably changed
in pregnant women, nor is the cadaveric blood of eclamptics more prone to
clot. It is believed, therefore, that whatever thrombosis occurs in such cases
is rather due to an intensive local chemical action in which lipoid substances
play a special rdle.
The occasional occurrence of sinus thromboses or similar implication of the lung arteries
in children suffering from severe dysentery, has been explained on the supposition that there
is absorption of poisons from the intestines. Circulatory weakness, however, is more
important in these cases. Here, just as well as in the thrombi associated with carcinoma
cachexia, it is found that the thrombi correspond in structure to the mechanical pulsion
thrombi, and not to the experimental intoxication thrombi.
The so-called ferment intoxication can be brought into play through injection of
defibrinated blood of the same species, through foreign blood, or special ferment solutions.
It has been known for a long time that foreign blood as well as tissue extracts produced
clots, a condition most apt to occur in the large blood vessels.
When tissue extracts are introduced into the circulation, sudden death from intravascu-
lar coagulation may result. An albuminoid substance, foreign to the blood, and not the
precursor of thrombin, is believed to be found especially in the tissues.
Fibrin ferment in solution such as serum has been shown by Dienst to cause sudden
death in rabbits through embolism of the lung with coagulation in the right heart. Small
quantities produced very toxic injuries to the parenchyma of the kidney, up to necrosis
with the formation of hyaline and platelet thrombi in the capillaries.
Exogenous poisons, such as ether, benzol, chloraform, pyrodin, ammonia,
potassium chlorate, amyl] nitrite, ricin, etc. have been known to bring about
similar results. As for the influence of bacterial poisons—Loeb reports
formation of red thrombi following injection of staphylococcus toxins.
The Action of Exogenous Poisons and Infectious Agents.—Changes in the
total blood in the sense of increased coagulability are rare. Extensive cruor
formation in most of the vessels is seen post-mortem after carbon monoxid
poisoning. After transfusion of foreign blood lethal clotting has been
observed. In eclampsia, anemic infarcts have been observed in the kidneys,
due to hyaline thromboses with a picture of anuria. In the transfusion of
foreign blood hemolytic processes leading to ferment over production and
to local accumulation of erythrocytic fragments may occur. -Thrombi of
various types appear in the capillaries in various types of poisoning forte
ide and anilin).
All poisons that act in a destructive way upon the blood, do not neces
lead to thrombosis. Thrombosis is absent in the cases of methhaemoglo-
binemia after potassium chloride and nitrite poisoning.
As a rule the larger parasites do not cause thrombosis when they are
found in the blood. The trypanosomes, even in large numbers, do not lead
to clotting. This is also the case with bacteria. Even when there are
atheromatous ulcers, bacteria do not seem to further the deposition of clots.
The presence of bacteria does not essentially modify already existing
mechanical thrombi, such as occur at points of ligation in the placenta.
One would expect a favoring influence upon the growth of bacteria by reason
of the presence of a clot, but indeed it is noted that bacteria are sometimes
inhibited in their proliferation by just such a thrombotic process.
One may conclude, therefore, that infection with a variety of different
bacteria does not suffice, as a rule, for the creation of thrombosis. Even in
diseases such as fibrinous pneumonia in which conditions are present that lead
to a saturation of the blood with fibrin ferment, thrombi are not so frequently
THROMBOSIS OF CHEMICAL ORIGIN 121
found as one would expect. When, however, bacteria such as streptococci
invade the lumen of vessels in considerable number, fluid pus develops in
veins very frequently without thrombosis. Sometimes such pus is separated
from the current through a clot. Thus, we may conclude that the bacterial
contents of the blood and bacterial poisons are not essential for the origin of
thrombi in infection. Septic thrombosis is produced rather by disease of the
vessel wall.
In atheroma Lubarsch does not consider the intima changes as playing an
important part in thrombus formation. When the current is strong, thrombi
rarely become attached to such patches. When there is mere fatty degen-
eration of the endothelium, thrombosis is usually absent. Even extensive
change in the vessel wall, such as amyloid alterations of a large vessel or
capillaries, does not necessarily lead to thrombosis. Chemical factors are
however, important when smaller or larger vessels suffer necrosis through the
action of poisons. Essential for thrombosis, therefore, would be the presence
of diffusible poisons that enter the blood and modify it; or an active partici-
pation of an altered vessel wall through unusual special responses. In
some cases the injury to the blood elements through the vessel wall is a chief
factor; as following the injection of poisonous substances, or following the
action of strong poisons through surface defects.
The form of thrombosis then varies according to the peculiar character-
istics or qualities of the toxic substances. ‘Thus, in the case of acid poisons
entering through the stomach, such as sulphuric acid, a sort of stasis thrombo-
sis occurs, with distension of the capillaries and smaller vessels with red
thrombi. Or, in the case of putrid cystitis or pyelitis, hyaline thrombi occur
in the neighborhood of ulcers and degenerate tissues.
In clinical pathology most interesting are the local vessel wall infections,
particularly of the veins. A vein that is inflamed with staphylococci and
streptococci shows the same leukocytic infiltration as any other tissue. With
this a fibrinous excretion within the walls takes place. ‘The process may be
limited to the wall itself, particularly when only the adventitia is involved,
the blood flowing within the vessel without being affected. When the fibrin-
ous deposition is more diffuse, and enters the inner layers of the wall of the
vessel, then platelet masses become attached to the intima. It is believed
that the fibrin masses combine with the platelets, and can be traced to com-
municate directly with the intramural fibrin deposit. Most of the fibrin,
however, has its origin in the flowing blood and does not emanate from the
vessel wall. As the thrombus grows, it presents a mechanical obstacle to
flowing blood, and there results the usual wave and eddy formation with cor-
responding mechanical accumulation of new thrombus masses.
Infectious processes vary in their influences on thrombus formation.
Whilst thrombosis is seen in the superficial veins in syphilis during the preco-
cious form of syphilitic migrating phlebitis, it may be absent in the umbilical
veins, even though circulatory conditions are favorable for clotting. In the
secondary stage, with endo- and periphlebitis syphilis does produce thrombo-
sis (Hoffmann, Chap. LXXX). In tuberculosis extensive phlebitis migrans
has been seen to occur without thrombus formation (Schwarz!). Glassy
masses are known to fill the veins in the neighborhood of severe diphtheritic
lesions, an expression of the reaction of the circulating toxins.
The tubercle bacillus may develop nodules in the vascular wall (vessel wall), which may
later give rise to mechanical thrombus deposition (Benda?). But, even here the thrombus
1 Schwarz, Virchow’s Arch., 1905, CLX XXII.
2 Benda, Berl. klin. Wchnschr., 1908, XLV, 7.
122 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
formation is usually rather insignificantly organized. Parietal thrombi were seen in the
case of Beneke where there were about a dozen such deposits in a number of veins of the
lungs. They had the appearance of droplets that had become congealed as they flowed
along the wall in a central direction.
In- meningeal tuberculosis, however, the thrombi caused by fresh tuber-
cles in the pia usually are obturating.
In the inflammatory diseases of the arteries, with the exception of thrombo-
angitis obliterans, thrombosis is not as common as would be expected.
Inflammation of the vessel wall, as a rule, only produces thrombosis then in the
large vessels, when mechanical deposition is facilitated through changes in
contour, such as aneurismatic dilatation. A very striking type of thrombus
formation is that of periarteritis nodosa (Chap. LX XIX) or polyarteritis.
Here foci of intensive inflammation develop in the smaller vessels, leading to
destruction of the vascular wall. As soon as the intima is reached, aneuris-
matic dilatations occur with thrombosis. Fibrin, leukocytes and hyaline
masses occupy the clot. Destruction of the arterial walls furthers the throm-
bus formation. In the veins the circulatory sluggishness; in the arteries
transitory vasoconstriction with consequent fibrinous deposits, are factors
that predispose to thrombosis.
In the case of capillaries in an inflammatory area, leukocytes may clog
their lumina and lead to the formation of hyaline masses. This occurs in
pneumonia, in which glassy thrombi are characteristic.
Thrombosis Due to Solid Bodies.—Here we deal with the blockage of vessel lumina
through migrated body constituents, with or without bacteria, as well as intravascular
parasites.
In fat embolus there is but little tendency to thrombosis. In the neighborhood of
fractures, the veins may contain fluid fat that is held fast by thrombi. Air (air embolus)
does not incite clot formation.
Normal tissues have not identical chemical actions. We deal usually only with solitary
cells (placentar). These circulate and do not act in a deleterious fashion on the blood
elements. When they die off, the injury produced is so minimal as to exert no thrombotic
effect. Where larger fragments of tissue, such as pieces of liver, are mechanically displaced
after liver traumata, the action is mechanical.
The displacement and the distant transportation of material containing ferment, such as
detached thrombus particles, produce much more extensive additional thrombosis. Trans-
ported thrombi by reason of their ferment properties, predispose to further coagulation, and
after death are even known to be the points of origin of fresh cruor masses. Very long
secondary thrombi are often attached to such emboli, an evidence of their chemical action.
Thrombosis Due to Thermic Influences.—Thermic forces are exerted
through injurious action on the blood itself, or through lesions of the vessel
walls. Both heat and cold can produce thrombosis.
The general effect of extensive burns has been regarded as an expression
of blood destruction due to ferment intoxication and attended with extensive
blood coagulation. Other authors deny that extensive coagulation takes
place. It is believed that large quantities of ferment are developed at the
site of the burn, enter the blood and cause thrombosis.
The observations in the human conform to the experimental investiga-
tions. In the case of extensive burns the picture of intoxication preponder-
ates over the thrombotic lesions.
Mild degrees of heat lead to hyaline thrombi in the affected locality. The clots fill the
vessels, inflammatory reaction of the vessel wall being absent. Probably congelation of the
dead leukocytes produces the plugs here. In the capillaries and small veins, at the margin
between dead and healthy tissues, thrombi are not infrequently found. In some cases the
clots have been regarded as precipitation phenomena.
GENERAL CAUSES OF THROMBOSIS 123
Effects of Local Refrigeration.—The experiments of Zahn! showed that
cold produces stasis and then thrombosis in the arteries, veins and capillaries.
Experimental freezing in rabbits and guinea pigs demonstrated the develop-
ment of typical inflammatory pictures. True thrombi do not necessarily
form, but when the leukocytes attracted in this process, are caused to die off.
Then these are converted into hyaline masses; and, together with the fibrin
they fuse into masses that are regarded as thrombi. Even the vessel wall,
when the action of cold is intensive, may participate in the degenerative proc-
ess, become hyaline, and fuse, as it were, with the thrombus. In this way,
extensive congelation thrombi may form in the region of the frozen area.
In the necrotic areas themselves, the thrombi may be absent, being confined
to the marginal zone between healthy and dead tissues.
The longer the cold effects are allowed to act upon the tissues, without direct necrosis,
the more the circulation is impaired, and the more extensive the formation of hyaline
thrombi. The circulatory conditions are determining factors in many cases. It has been
shown that experimental section of the sympathetic nerve in the necks of rabbits was
followed by more marked thrombosis than in those in which the vascular nerve mechanism
was Intact.
Thrombosis Due to Actinic Causes.—Electricity, X-ray and other actinic
influences seem to exert about the same effect upon the blood and tissues as
thermic insults. Local thrombi are caused by these whenever their action is
sufficiently intensive to produce necrosis in blood or tissues. Jansen? describes
local thromboses after light treatment; and Askanazy* observed thrombosis
after the use of ultra-violet rays.
CHAPTER XXI
GENERAL CAUSES OF THROMBOSIS
Thrombosis may depend (1) on factors inherent in general diseases; (2)
on local mechanical or chemical alterations; and (3), on special conditions.
1. Thrombosis and General Diseases.—Beneke in his excellent work in
this field proposed a grouping into general mechanical and chemical
causes.
Cardiac weakness, whatever may be its origin, is an important factor.
This may be brought about by toxic and infectious degeneration, excessive
stress through stenosis, valvular insufficiency, or local disease of the cardiac
muscle, as well as through senile change. In many of the post-operative
thromboses and the marantic group, such conditions play a réle. For, the
clotting is most apt to take place where circulation is sluggish, as in the venous
system, or where waves and vortices are likely to occur.
Local stasis, too, may be regarded as a contributing cause and with general circulatory
weakness eventuates in thrombus formation. Indeed, Beneke states that ligation or tumor
invasion of large veins need not give rise to this process until marked stasis occurs as the
result of cardiac weakness.
Changes in the character and form of the stream, associated with currents interrupted by
vortices and waves are important forces making for thrombosis. Examples are varices,
aneurysms with variations in the size of the arterial lumen, sclerosis of the coronary,
A Z7ahny Loc. cts
2 Jansen, Ziegler’s Beitr., 1907, XLI.
3 Askanazy, Pathol. Anat., (L. Aschoff), Fischer, Bd. 1, 1919.
124 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
cerebral, and popliteal arteries. Ifa sudden alteration in the lumen is met by the flowing
blood, eddies and vortices ensue, which with other agents such as cardiac weakness or
special local muscular demands, may lead to thrombosis.
All these aforementioned factors are potent in proportion to the weakness
of the general circulation. And so the preponderance of venous thrombi
over the arterial is explained. Conversely, a strong current will inhibit
thrombus formation.
Although the mechanical forces may suffice to generate thrombi, the latter may fail to
develop where all the conditions for their production seem at hand. Hence qualitative and
quantitative alterations in the blood corpuscle elements and their chemical relationship to
the plasma, have been invoked in explanation. These possible motivating agents may be
summarized as (1) anomalies of the blood cells including increase or diminution in the
number of erythrocytes or platelets, leukocytosis and leukopenia; (2) anomalies of the plasma
such as altered carbon dioxid, calcium ions, fibrinogen, fibrin ferment content; and (3)
diverse conditions, such as increased agglutinability of the platelets, effects of age,
cachexias and infection. All these may be of chemical nature.
Although it is often impossible to gauge the importance of chemical fac-
tors in a given case, the following brief summary may help clarify our inter-
pretation of etiology.
The Alterations in Corpuscular Elements.—An increase in the number of erythrocytes
seems to have no essential influence on thrombus formation. Polyglobuly or plethora may
cause disassociation or separation of plates and thereby diminish the tendency to clot.
A superadded factor, however, such as cardiac weakness, may nullify this and thrombosis
nevertheless supervene.
A diminution in the number of red blood cells (erythropenia) may further the clotting
process by an association of factors. Perhaps the diminution in the size of the vascular
marginal zone in erythropenia may be a mechanically conducive element. To the coinci-
dent numerical increase of platelets must be also ascribed a certain réle. So also, has been
explained the mechanical thrombosis occuring in anemic persons. However, there is not a
great tendency to thrombosis in anemic conditions, unless cardiac weakness is added as a
factor.
In chlorosis, however, we have an exception, in that the inferior vena cava, the crural
and renal veins are reported as being more than ordinarily predisposed to thrombosis.
Leukocytosis is a condition which theoretically would favor thrombus formation.
Beneke believes that this could occur through deposition of leukocytes at any platelet
center, and through the elaboration of ferments.! And so in leukemia the frequency of
thrombosis has been especially noted (thrombosis of corpora cavernosa in priapism).
Whether there is an overproduction of fibrin ferment, as has also been suggested by Dienst?
in eclampsia, has not as yet been definitely proven. Leukopenia does not seem to influence
thrombus formation.
Increase in the number of platelets has very frequently been recognized as conducive to a
state of thrombophilia. Some of the post-operative thrombi occurring 4 to 5 days after a
severe loss of blood, at a time when platelet production is most intensive, has been regarded
as due to this phenomenon. It has not been satisfactorily proven, however, that a platelet
increase per se is a cause of thrombosis. Diminution in the platelets, similarly, in severe
anemias and acute febrile conditions does not explain tendency to thrombosis.
2. Chemical; Alterations of the Total Blood.—The carbon dioxid content of the blood
may inhibit coagulation by reason of the altered sensibility of the platelets, for these are
said to degenerate through such chemical changes in the blood. In spite of this chemical
restraining element, conditions in which there is increased carbon dioxide in the blood, such
as stasis, show an increased tendency to thrombosis, due to the fact that the mechanical
conducive moments more than counterbalance the chemical inhibitory.
The Ca- Ion content of the blood has been regarded by some authors as important in
thrombus formation.
1See the case of Dr. G. in whom extensive obliteration of the vessels of the lower
extremities, probably due to thrombosis had occurred, and in whom leukocytosis was
present for many months and possibly years without known cause (Chap. LX XXII).
2 Dienst, Archiv. f. Gyn., 1912, XCVI, 1.
GENERAL CAUSES OF THROMBOSIS 125
The fibrinogen content, according to Welch and Aschoff is not responsible for altered
susceptibility to thrombosis. Of more importance is the fibrin ferment content of the
blood. Sudden increase of this element in experiments causes extensive clotting in the
large vessels and immediate death. This lends confirmation to the view that excessive
local ferment production may enhance thrombus formation. In the circulating blood
neutralization or the destruction of ferments goes on constantly. The experiments of
Dienst would indicate that in some cases sudden, in others a more or less continuous,
overproduction of ferments may occur.
Cases are reported of extensive sudden thrombosis following small, mini-
mal, primary, mechanical thrombi, and requiring but a very few minutes for
their development. ‘Two cases are cited in menstruating women. In one of
these after a clean appendectomy, sudden coagulation of the blood in the
inferior vena cava took place, resulting in pulmonary embolism and death
within a few minutes, in the other case a red thrombus in the uterine veins
seemed to be the starting point. In both of these, the authors concluded
that there was sudden invasion of the blood with fibrin ferment, that enabled
a very small mechanically produced thrombus to give rise to extensive coagu-
lation. Mixed thrombus formation over a large territory has been reported
in chronic nephritis where a more or less continuous state of increased ferment
production was assumed to exist.
In the extremities we have not infrequently observed the association of
extensive red thrombosis with emboli after infectious diseases and pneumonia.
The sudden extension of thrombus formation throughout all the larger arteries
and veins does not always occur in various embolic processes. Indeed, the
absence of such secondary thromboses in most of the cases of arteriosclero-
tic blockage is noteworthy. The frequency thereof is striking in the above
mentioned cases. Perhaps here, too, an overproduction of fibrin ferment, is a
factor.
3. Special Conditions.—Little is known regarding the influence of
increased viscosity as a factor in thrombosis. Increased viscosity of the
blood is said to take place with increasing age,' and in certain infectious
diseases (tuberculosis and pneumonia).
Welsh found no direct relation between coagulation time and viscosity.’
‘Holmgren,’ however, takes the view that the polymorphs influence viscosity
and the latter coagulation. His experiments tend rather to show a relation-
ship between the polymorph content or polymorphlymphocyte quotient, than
upon viscosity of the blood per se.
Except in the case of cholera, in which concentration of the blood follows
the withdrawal of water, no particular tendency to mechanical thrombosis
has been observed in conditions with increased viscosity.
The relation of thrombosis to age, has given rise to much specula-
tion. The chemical differences in the blood and the quantitative relation of
the platelets and the changes in the vessel wall have all been regarded as
factors in the tendency of adults to thrombosis. That cardiac weakness may
be a factor in the senile cases must be admitted. Nevertheless chemical
alterations must not be lost sight of, and are probably of considerable impor-
tance.
In the thrombosis of cachectic conditions and in the marantic conditions,
the quantity of blood and its composition, or the chemical relationship
between the corporal and fluid elements have undergone change. Pathological
1 Hess, Deutsch. Arch f. klin. Med., 1908, XCIV, 404.
2 Welsh, Heart, Vol. III, 1, 1rorr.
3’ Holmgren, Deutsch. med. Wchnschr., Jan. 30, 1913.
126 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
products of metabolism circulate in the blood, or the blood is depleted of
certain substances. Malignant cells may have a special affinity and attrac-
tion for blood components.
In the present state of our knowledge we must admit the possibility of a chemical
component in the production of the marantic thrombi. Only in this form is their depen-
dency upon mechanical forces brought to our notice.
The Role of Infection in Thrombosis.—Infection can indeed play an impor-
tant part in thrombosis. According to some authors this is due to an exten-
sive vasculitis. Inflammatory foci with or without ‘bacilli in the vessel wall,
and the action of toxins have been regarded as the causes of parietal or other
thrombi in typhoid fever. Systematic investigation of the occurrence of
endophlebitic foci in the various infectious diseases has given rather negative
results. The evidence seems to show that although focal infection of the
walls of the vessel cannot be denied in infectious processes, no important
role can be ascribed to these lesions in usual thrombus formation. The occlu-
sive thrombosis in certain special types of phlebitis of unknown origin and in
thrombo-angiitis is an exception (Chap. LXXXI). It would appear that
the direct effect of bacteria and their toxins upon the total blood (or the
forces engaged in circulation) are more important. The cardiac degeneration
brought about by infection affords one of the mechanical conditions. So also,
the existence of other coincident conducive agents cannot be denied.
Aschoff points out that embolic infarcts even in sepsis are not necessarily bacterial, but
frequently agglutination thrombi with secondary invasion of organisms. Up to the present
time we are unable to properly estimate the effects of the various chemical components of
infection upon the alterations of the fibrinogen, the fibrin ferment; on the increase in
number of leukocytes and platelets, the erythrocytes and their degeneration. Nor do we
know whether specific agglutinins (platelets) are produced. Indeed, experimental methods
have shown that certain toxins and bacteria have a specific action upon certain parts of the
total blood. If we accept the theory that the essential moment in thrombosis is the coagu-
lation, the absence of thrombi in many cases of hemolytic streptococcus infection and the
frequent development of thrombi in pneumonia or staphylococcus infection could be
explained on a specific toxin effect. Such assumption, however, cannot be admitted as yet,
since thrombosis is not merely a process of coagulation.
Even the possibility of a diffuse chemical influence of infectious poisons upon the vessel
walls has been considered, and paralysis of the inhibitory activities of the endothelial cells
in so far as these have a defensive mechanism against thrombosis. These, however, are
speculative theories.
Although infection can thus play a rdle, it is not necessarily followed by
thrombosis, unless some other special factor is brought into operation.
Mendel! suggested the appellation “thrombophilia” to designate a general
predisposition on the part of a patient with infectious disease to thrombosis.
This was extended to include that state of heightened susceptibility to throm-
bosis that may occur after an infection has been overcome. Such an acquired
state would be opposed to hemophilia in which an absence of thrombokinase
has been believed to occur. There is still some doubt as to the correctness
of this assumption.
Various causes? have been given for the tendency to thrombosis in infection. Very few
cases of thrombosis occur in the cadaver in which we are not able to demonstrate an infec-
tious malady of some sort as a possible cause. (1) Thrombi are particularly frequent in
the neighborhood of infectious processes; (2) in varices, the blood is apt to remain fluid as
long as infection in the neighborhood is absent; and whenever a wound in the skin permits
1 Mendel, Miinchen. med. Wchnschr., 1909, LVI, 42.
2 Lubarsch, Berl. klin. Wchnschr., March 11, 1918.
GANGRENE—GENERAL CONSIDERATIONS 127
of the entrance of bacteria, thrombosis occurs; (3) in post-operative thrombosis, there is
usually associated elevation of temperature; (4) microscopic search and bacteriological
cultures of thrombi have demonstrated the presence of bacteria; and (5) it has been found
possible to produce thrombi in animals by the injection of bacteria.
Kretz states that of 6511 cases he was unable to find a single instance in which thrombus
formation was not associated with previous infection. Lubarsch, on the other hand, in his
material notes 13 per cent of thrombi in which no infectious process could be discovered.
If the remaining number (87 per cent) is critically reviewed for a possible regional relation-
ship between the infectious process and the thrombosis, it appears that only 55 per cent
showed any association, and these would have to be still further reduced to 52 per cent if
thrombi are excluded that might have antedated the infectious process.
Autopsy material then would suggest that the infectious process plays a considerable
réle in about half of the cases.
How can the action of bacteria be brought into harmony with the usually accepted
theories as to the genesis of thrombosis? Firstly, the influence of the infectious agent upon
the heart and the circulatory centers; secondly, on the blood and the blood forming organs,
particularly the bone marrow; and thirdly, the action on the blood vessel wall:—these are
the theories that have been advanced.
If we emphasize the rdle of alterations in the blood constituents as a determinant in
thrombosis, the action of organisms in a chemical and morphological sense can be easily
brought into consonance with existing theories of thrombus formation. Thus, bacteria
not only destroy the red blood cells, but also through their action on the bone marrow,
particularly on the giant cells (megakaryocytes) may play an important part. Both red
blood cells and giant cells are influential in the formation of blood platelets, be they con-
sidered as products or degeneration products. For, it is known that giant cells are thrown
out into the blood stream by reason of irritation by bacteria, so that the influence of strepto-
cocci, for example, can easily be understood both on the basis of their destroying influence
on the red blood cells, as well as on the basis of their irritative effects on the bone marrow.
CHAPTER XXII
GANGRENE—GENERAL CONSIDERATIONS
Gangrene (Fr., gangréne, Latin gangraena, from Greek ydyypatva an
eating sore Ypaw, ypaev to gnaw) signifies the death of macroscopically
visible portions of the body, the invisible liquefaction of tissue being known
as molecular death or ulceration.
Mortification is synonymous with gangrene, being more frequently used in
the parlance of the laity.
Mummification refers to that type of gangrene in which drying or desic-
cation of the tissues takes place.
Sphacelation means total death of all of an affected part, the dead tissue
being known as a sphacelus.
Sloughs are dead masses of tissues, the result of a process of sloughing.
The act of sloughing which results in the formation of sloughs may be brought
on by ulceration or inflammation. Thus, a core is aninflammatory slough;
when it is sufficiently large and possibly putrid, it is termed gangrenous
slough.
Properly speaking, necrosis is a general term that should include all types
of tissue death. Although used in this way by the Germans, in English
medical parlance, it is more frequently applied either to the disintegration or
death of internal organs, when the mortification is unattended by decom-
position, or to the death of bone tissue.
Gangrene is usually the result of imparied or absent blood supply. Other
causes, however, must be able to bring about mortification in the presence of a
128 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
patent and apparently intact or adequate circulatory system, as in the so-
called vasomotor varieties of gangrene, of which Raynaud’s disease is an
example. It is by virtue of the development of an adequate collateral
circulation, that gangrene can be prevented, so that we can distinguish
between the clinical picture of impaired or arrested circulation with gangrene
as a sequence, and where gangrene has been averted through the development
of sufficient secondary circulatory paths.
In addition to the factors, impairment of circulation and establishment of
collaterals, other influences may determine the development of gangrene.
These are the general condition of the patient and the local condition. An
enfeebled general condition, a weak heart, the debilitating effects of pro-
longed illness, of infection or diabetes, all these, not only lower the vitality,
but also militate against recovery. Local conditions such as extravasations
of blood, inflammatory exudates, localized vascular disease, stasis or con-
gestion resulting from tight bandages, and improper posture, are additional
impediments to the formation of collateral paths. The tissues, too, vary as
to their vulnerability, the vitality of bone, cartilage, tendons and fascia being
apparently greater than that of muscles and nerves, whilst the glandular
organs and the elements of the simple nervous system seem to succumb
within a very few hours after complete blockage of the main avenue of
blood supply. In certain tissues, such as muscles and nerves, impairment of
circulation produces temporary ischemia, which, if not of too long duration,
leads to degeneration, functional disturbances, so-called ischemic contracture
and palsy, but not to gangrene.
For a thorough comprehension of the clinical manifestations of gangrene
or impending gangrene, it is essential to be able to recognize not only the
signs that appear when the condition is definitely and well developed, but all
those objective evidences of impaired circulation that may precede by months
or even years the advent of true gangrene or even of trophic disorder. The
signs and symptoms of gangrene and those of impaired circulation will be
merely mentioned here, a detailed description being given under the dis-
cussion of the various types of gangrene.
Signs of death of a limited part are the following: first, loss of pulsation in
the usually palpable vessels; second, coldness of the part; third, absence of
sensation or paresthesiae followed later by anesthesia; fourth, loss of active
motion in the part, or loss of function; fifth, change in outward appearance,
chiefly in color. At first there may be intense blanching, the skin having a
waxy, cadaveric or ivory tint. Or, if the part be engorged with blood by
virtue of intense venous stasis, a cyanotic livid hue will predominate. Later,
the color and appearance of the part will change, as the condition of dry or
moist or mixed gangrene is developed.
Premonitory Symptoms of Gangrene.—These are best illustrated when the
extremities are the seat of impaired or arrested circulation. Jt is quite as
important to be cognizant of the objective and subjective phenomena antedating
the advent of gangrene or trophic disorder, as tt is to recognize the death of tissue
itself, for, in most cases in the clinic, the diagnosis of the arterial lesion leading
to gangrene Should precede by a longer or shorter period the onset of the gangrene
itself.
Symptoms of Impaired Circulation.—Certain definite clinical manifestations
of diminished blood supply are frequently the precursors of gangrene. Or,
gangrene may occur in one limb and never develop in the other, although both
limbs offer the signs of diminished blood supply. The most important of
such clinical signs are the following :—
GANGRENE—GENERAL CONSIDERATIONS 129
1. Intermittent Claudication.—By this term is meant cramp-like pains in
the calf of the leg brought on by walking or running, and causing the patient
to rest the limbs. ‘The pain regularly disappears when the muscles are in a
state of repose. Less typical pain referred to the ball of the foot or the ankle,
or the instep, must be regarded as of the same nature. Erb’s syndrome
called “‘intermittent claudication”’ should not be regarded as a clinical
entity, for the symptoms described as intermittent limping do not belong
to any one group of cases, but occur in almost all of the cases in which
obstructive or obliterative disease of the arteries of the lower extremities is
present. Thus, intermittent claudication is a symptom of thrombo-angiitis
obliterans, athero- or arteriosclerotic disease, arteriosclerosis with diabetes
or with thrombosis, or endarteritis, and aneurysm of the popliteal artery.
The feeling of weakness in the affected part also influenced by motion, prop-
erly belongs here, since it is so frequently associated with the pain and
cramp-like phenomena. Clinically similar manifestations may have been
described (Dejerine) with apparently patent peripheral arteries where a
lesion in the spinal cord is held responsible.
2. Coldness of the extremity, when chronic, is a significant sign. It may
be influenced by climatic conditions and intensified by exertion. It is
manifested subjectively and objectively.
3. Bluish discoloration (cyanosis) of the tips of one or more toes, particu-
larly the great toe, sometimes of the ball of the foot, intensified by walking
and associated with coldness—is another important manifestation.
4. Ischemia or blanched condition of the extremity may occur when the
limb is in the horizontal position, more rarely in the dependent, but can
usually be elicited by elevating the affected limb 60 to go° above the
horizontal.
‘5. Redness or rubor involving the toes, sometimes the dorsal and plantar
aspects of the foot for varying distances (to the ankle or even higher), is a
feature of diagnostic importance. It frequently involves the lower extremi-
ties when these are allowed to hang down, occasionally occurring even in the
horizontal position of the limb, and independent of infection, gangrene, or
trophic disorder. ‘The author has termed this phenomenon “erythromelia.”’
6. Absence of pulsation usually occurs in the palpable vessels of the
extremities, the dorsalis pedis, the posterior tibial, popliteal, or femoral of the
lower extremity, the radial, ulnar or brachial arteries of the upper extremity.
7. Trophic disorders include indolent fissures, ulcers, hemorrhagic areas,
superficial ulcers, perforating ulcers, a withered or atrophic condition of por-
tions of the extremities, foot or hand, and impaired growth of nails.
8. Thrombosis may occur in attacks with the following symptoms refer-
able to the sudden closure of vessels; pain in the calf of the leg or foot, in-
ability to walk, pallor of the forepart of the foot, coldness, blanching of the
foot on elevation, loss of pulsation in the dorsalis pedis, posterior tibial or
popliteal arteries, or all of these, sometimes followed by the development of
trophic disturbances, and even gangrene, or at other times eventuating in
more or less complete recovery.
130 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
CHAPTER XXIII
METHODS OF INVESTIGATION OF GANGRENE
The identification of specific minute architectural peculiarities in
thrombo-angiitis obliterans, the understandable and acceptable explana-
tions therefor given elsewhere;! the gross and microscopic recognition of the
atherosclerotic lesions, the demonstration of constant and immutable differ-
ences between the thrombotic obturating changes in the blood vessels,
and the hyperplastic endarteritic processes; all these have permitted us to
correlate accurately a clinical, pathological and structural classification.
On the other hand, the vasomotor and trophic neuroses, by reason of our
imperfect knowledge of anatomic as well as functional derangements of the
vegetative and sympathetic nervous systems, must be grouped principally
upon a basis of clinical characteristics and similarities.
Since a correct concept of the distinctive clinical features of certain vascu-
lar lesions must needs depend upon repeated mental comparative association
of the gross and minute visual findings obtainable from the vessels of ampu-
tated limbs, with the anamnestic, subjective and the objective physical
signs, it is advisable that the student have the opportunity of viewing as
many pathological specimens as possible. Through these he should be
able to supplement his routine observation with the anatomical comple-
ment essential for thorough comprehension. Then, too, will the disassocia-
tion of hydrostatic and mechanical factors from the attendant evanescent
or transient neurotic symptoms be more readily understood; and then will
the striking differences and peculiarities of symptomatology and clinical
course in the vasomotor neuroses be better appreciated.
In lieu of actual pathologic material intensive application to the study of
the lesions described in other chapters may act as a good substitute.
In consonance with the trend of modern medicine, which is not satisfied
with barren labelling and dividing of morbid conditions into classes according
to the presence or absence of certain qualities, we must endeavor to supple-
ment clinical phenomena with a well-grounded and searching method
of investigation such as will be herein described. It was through the results
obtained by it and the hypotheses evoked by its application, that a satis-
factory differentiaton of the neurotic and the physical symptomatology was
made possible.
For the sake of clearness and emphasis let us recapitulate by title what a
correct method of approach should include |
(1) The general appearance of the limb
(2) The presence or absence of rubor or cyanosis in the pendent position
of the limb
(3) The existence of ischemia on elevation of the limb and the interde-
pendence of change of position and blanching
(4) The absence of some or all of the usual arterial pulsations
(5) The angle of circulatory sufficiency
(6) The possibility of eliciting reactionary or induced rubor
(7) The presence of migrating phlebitis
(8) The existence of trophic disorders and gangrene, and
1 The author’s interpretation of the acute and chronic lesions in the vessels is given in
detail in Chap. LXI-LXII.
METHODS OF INVESTIGATION OF GANGRENE 131
g. The other refinements of physical diagnosis or special tests described
elsewhere.
Certain salient facts in connection with the distinguishment and classi-
fication of the varied clinical morbid complexes here under discussion, deserve
mention and careful consideration. Without the correct mental approach
in our methods of differentiation, the confusion in diagnosis now so wide-
spread will tend to become perpetuated. Let us then focus our attention
on certain essentials that should be borne in mind.
First, there are two distinct, clinically discrete and pathogenetically
separable types of morbid process in the extremities, both associated with
manifestations of circulatory derangement, exceedingly similar in many of their
objective and subjective phenomena. These are the organic and the neuro-
pathic affections of the blood vessels or vasomotor, or vasomotor and trophic
disorders.
Second, these two forms may be again subdivided into clinical entities
some of which represent essentially diverse pathological lesions, others how-
ever, corresponding in the present state of our knowledge, to different kinds of
derangement in the vegetative and sympathetic nervous systems, the exact
nature of which is unknown.
Third, whereas the anatomic alterations in the vessels in the organic type
of vascular disease have been satisfactorily classified by virtue of the recogni-
tion of gross architectural and histological differences in the blood vessels, and
whilst the causal relations between structural changes and symptomatic
effects have been explained beyond question, such harmonious relatively
has not been established between the characteristic phenomena of the vaso-
motor affections and the nervous system where the motivating agency is
supposed to reside. In the latter, theoretical assumptions alone are offered in
the interpretation of the varied and bizarre manifestations, since microscopic
and microchemical deviations from the normal have not been obtainable.
Fourth, the organic types may be attended with vasomotor phenomena,
but the latter do not justify the assumption of the coexistence of the two
forms of disease. Some of the appearances imitate true vasomotor symp-
toms, but are clinically dissimilar under the application of proper tests, and
of wholly different origin. Others are veritable vasomotor manifestations,
the expression of irritative and exhaustive influences in the sympathetic
system, usually of transitory or even fugitive nature, surely of insufficient
duration to be recognized as, or segregated into clinical or pathological
entities.
Fifth, the clinical phenomena attending organic vascular lesions of the
extremities when manifested as rubor, ischemia, nutritional and circulatory
disturbances—including atrophy, swelling, edema, trophic disorders and
gangrene—may not be sufficiently characteristic to permit of precise differ-
entiation from the true vasomotor affections. Even with additional sub-
jective data, decision may not be possible. It is through an investigation of
the circulatory functions in the affected limb in the manner previously de-
scribed that pathognomonic signs may be obtained. The dictum to refrain
from diagnostic conclusions based on anamnestic and visual information
alone, is applicable here, and worthy of the strongest emphasis. Any
scheme which has the identification of the various interrelated or even com-
pletely diverse morbid entities in view, is inadequate and unsatisfactory
unless the data obtainable through physical examination are accorded due
weight and consideration.
132 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Before proceeding to the discussion of the various forms of gangrene and
to the symptomatology, pathology, diagnosis, and treatment of both organic
and neurogenic morbid processes that result in, or threaten to bring about
tissue death, it may be well to dwell more in detail on some of those salient
phenomena upon which their advent is often foretold. These are pain,
arterial pulsation, and ‘intermittent claudication.’’ The other phenomena
already alluded to, namely the coldness of the extremity, cyanosis, lividity,
ischemia, rubor or erythromelia, trophic disorders, and thrombosis shall
receive more comprehensive attention under each and every separate malady
in which they may present themselves.
CHA PRE Rees L Vy
DIAGNOSTIC SYMPTOMS—ARTERIAL PULSATION
The detection of the presence of pulsation in the palpable arteries of the
extremities, namely the ulnar, radial, brachial, dorsalis pedis, posterior tibial,
popliteal and femoral—is one of the most valuable physical signs for the
recognition and differentiation of a symptom-complex due to vascular disease
or of vasomotor incitement. Whilst the pulse in the above mentioned arteries
of the upper extremity can usually be elicited in the normal individual except
aberrant radial and deep seated ulnar vessels, a number of extraneous con-
ditions, seem to influence the demonstrability of the pulses in the lower limbs.
Both an anomalous course as well as concealment through adiposity can
invalidate the palpatory physical findings.
The incidence of pulsation in the normal has been investigated by Erb’s
assistants, who found that single pulses eluded detection, in somewhat less
than 1 per cent of the 700 ward cases that he examined. In the author’s
experience, tests of some 200 cases—that were regarded as normal, and in
which the possibility of any excessive compromise of arterial integrity
could be excluded—failed to evidence more than one instance of absence
of the dorsalis pedis pulsation (14 per cent).
Therefore, the demonstration of palpable evidence of obliteration through
the disappearance of pulse, is to be accorded great weight as a sign of organic
vascular occlusion, particularly if elicited at a period free from possible
vasomotor spastic phenomena and demonstrated repeatedly under varying
circumstances.
Fortuitous interference with the demonstrability of the arterial beat
through changes in the skin, as edema, eczema, elephantiasis, adiposity,
and other exceptional causes, must be given proper consideration.
The popliteal pulse can be best felt in the following manner: With the
patient prone and the leg flexed to the vertical and with muscles relaxed, the
examining fingers enter the upper half of the popliteal space where the vessel
can be readily discovered by pressure downward against the femur (Fig. 42).
It is only in very stout individuals that pulsation fails to manifest itself in
non-occluded arteries.
Elsewhere will be discussed those occasional examples of vast functional
exclusion of the arterial tree, where the femoral, popliteal, posterior tibial
and dorsalis pedis pulsations are imperceptible, and in which arterial oblitera-
tion of indeterminable nature is believed to exist. Enough clinical observa-
DIAGNOSTIC SYMPTOMS—ARTERIAL PULSATION 133
tions are at hand to bear testimony to the view that embolic closure of some
of the larger arteries of the extremities may take place with apparently no symp-
toms, or such minimal ones as to completely escape the notice of the patient.
This conclusion has been arrived at through the study of incipient clinical
stages of embolic obturation of larger arteries in patients already under obser-
vation for definitely proven embolic or thrombotic gangrene of another
extremity. With the sudden advent of the signs of impaired circulation in a
foot, or with a vague history of pain and coldness of abrupt onset, the
(WS
| is ;
yes
yee?
Fic. 42.—Author’s method of palpating the popliteal artery.
absence of pulses and other phenomena makes the diagnosis clear. And
still, by virtue of the developing collateral channels, all evidences of circu-
latory disturbance may disappear except the absent pulses; and a clinically
unrecognizable phase may then present itself to a future observer. For such,
the clinician will have but the altered pulses and the accompanying mani-
festations, if any, to guide him. The history of trouble in another territory
may be an aid; but only a vague record, if any, in the limb now examined will
be at his disposal.
Two types have come under our observation.
(1) Embolic closure of a large artery of the lower extremity, symptoms of
imminent gangrene, rapid and adequate substitution of the collateral circu-
lation, a latent or functionally cured stage, without trophic lesion being the
issue.
(2) Embolic closure of the posterior tibial artery above its bifurcation in
cases of multiple emboli of the extremities, with an identical sequence.
A more complete discussion of this subject will be found in Chap. LII.
Whilst the absence of pulsation at the usual palpable sites may be regarded
as indicative of arterial closure in most instances, the existence of pulsating
vessels does not preclude vascular obturation in certain other territories.
Both clinical observation and pathological examination of amputated limbs
have conclusively shown that extensive closure of the plantar arteries. and
even the digital and dorsalis hallucis can exist, whilst the posterior tibial,
134 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
dorsalis pedis and anterior tibal arteries pulsate strongly. Clinically too, the
usual symptoms of thrombo-angiitis obliterans and even gangrene may be
coincident with pulsating vessels, when the plantars alone are affected. As
the disease progresses, both the posterior tibial and dorsalis pedis may become
occluded.
Many observations, clinical, operative and anatomic through dissections
made by the author attest to the fact that arteries in which pulsation is usu-
ally perceptible may fail to beat, although at the site of palpation their patency
is conserved. Blood may trickle or flow through such channels without pulsa-
tive effect on the vessel wall. So ina case of embolism of the brachial artery,
in which arteriotomy and embolectomy were performed (Chap. LXXXV) the
flow through the section beyond the obstacle could be readily demonstrated.
Exceedingly interesting and conclusive evidence was also obtained in another
case of embolectomy of the brachial artery, where, although an additional
more remote territory was opened, by removal of the clot, the radial pulse
remained abolished, not to return until 7 months after the occlusion.
Absence of Pulsation Distal to Occlusive Thrombi.—That the absence of
pulsation does not always indicate organic occlusion, but may signify empty
vessels distal to the occlusive embolus or thrombus, has been frequently
observed in thrombo-angiitis obliterans and may also occur in cases
of embolic gangrene of cardiac origin or in thrombosis complicating athero-
sclerosis. It will be pointed out elsewhere how the return of circulation
through collaterals demonstrates the patency of such seemingly closed vessels,
and how this reappearance of pulse has often been misinterpreted as evidence
of the beneficial results of treatment.
Here it may be well to emphasize the occurrence of imperceptible pulses
beyond the point of thrombotic occlusion in cases of atherosclerosis. As an
example may be offered the following interesting case.
J. R., male, aged 47, diabetic with advanced atherosclerosis; sudden advent of gangrene
of the right foot and leg with absence of pulsation in the popliteal, femoral and external iliac
arteries for a distance of about 1 inch above Poupart’s ligament.
Amputation below the level of the origin of the profunda artery through the upper
fourth of the thigh. At this level the femoral artery was partly closed by atherosclerosis,
partly by recent thrombosis; almost no bleeding at this level, amputation being performed
without a tourniquet or Esmarch. Five days after the operation a strong pulse could be
felt in the femoral artery down to within about 4 inch from the point of section, the wound
having been left wide open.
In explanation of the return of sucha pulse, two theories can be advanced;
one, that the occlusive thrombus in the external iliac was dislodged into the
femoral just above the point of ablation, or that the common and upper super-
ficial femoral had been patent; and that through establishment of the
collateral paths the pulse became reestablished. ‘The latter is in the author’s
opinion the correct explanation, since the character of the thrombi and their
age would preclude their having been detached after the amputation.
Similar reestablishment of circulation is described elsewhere as occurring in
the vessels of the upper extremity after embolic closure of the brachial
artery.
DIAGNOSTIC SYMPTOMS—PAIN 135
CHAPTER XXV
DIAGNOSTIC SYMPTOMS—PAIN
Pain is such a varied phenomenon both as regards its appearance, con-
stancy, methods of excitation in the organic and neurogenic forms of arterial
affection of the extremities, that it may be well to analyze its method of
origin and some of the characteristics in the maladies in which gangrene may
occur.
In erythromelalgia, it is interesting to note that in the majority of the
cases the pain does not follow the path of any of the peripheral nerves, nor is it
encompassed within the territory or distribution of any nerveroot. Further-
more, in the quality of the pain there seems to be a difference here as
contrasted with the common neuritic and neuralgic forms of pain. ‘There is
a deep-seated burning, poorly limited, constant, susceptible to exacerbations
that is quite different from the pain described in the neuralgic cases. A
similar condition is noted in cases of frozen extremities, when they suddenly
enter into a warm room, the blood rapidly returning. This would arouse
the suspicion that the pain is related to alterations in the vessels.
Centripetal conducting elements of the sympathetic (Chap. IV) are
numerous according to anatomical investigations. It would not be too auda-
cious, therefore to believe that irritation of the centripetal fibers may evoke
pain. If we accept the notion of the possibility of pain of sympathetic
origin, we must seek a special form of irritant for the excitation of such pain.
This is true, since in affections of the sympathetic nerve of the neck,
excitation leads to mydriasis, and narrowing of the vessels without pain.
We may assume that in certain arterial diseases, such as arteriosclerosis,
irritation of the sympathetic plexus in the adventitia could cause stimuli
that are transmitted or transferred in the spinal segments to sensory tracts,
causing the so-called referred pain. But we cannot exclude the possibility
that pain may be occasioned by alteration of the centripetal nerve fibers
emanating from the blood vessels themselves, even though these under ordi-
nary circumstances do not carry such impulses.
In erythromelalgia it is possible that pain is occasioned by direct irritation
of the sensory sympathetic elements in the vessel wall; for, the vasomotor
and sensory symptoms often occur almost simultaneously in this condition.
In thrombo-angittis obliterans, the acute pain that is associated with the
attacks described as the attacks of acute thrombo-angiitis obliterans, may also
be, and probably is of the same origin. The vessels themselves become pain-
ful. This pain is of a different nature from that which is associated with
exercise (intermittent claudication) and that which precedes and attends the
development of trophic lesions of the distal parts. Impulses along the
usual sensory paths would account for the pain accompanying ulcers, fissures,
and gangrene; but even here the abnormal intensity of the sensory impressions
would lead one to believe that a distinct alteration in the threshold for pain
often exists.
In Raynaud’s disease sensory phenomena, be they anesthesia, hyperaes-
thesia or pain, do not correspond to the territory of a single nerve, but extend
rather diffusely over the extremity, being rather confined to the area in which
there are vasomotor and trophic disturbances. The difference noted is that
the pain is apt to extend farther proximally, and radiates to a greater degree
136 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
towards the root of the extremity. The absence of relation between its
situation and the course of distinct nerves, the diffuse distribution, the
simultaneous occurrence of pain in both extremities, and its extension into
the deeper tissue, these are facts that speak for a more central lesion. Be-
cause of the return to normal in certain cases, and the transitory nature of
the symptoms, Cassirer concludes that in the Raynaud complex there may
be lesions that are easily repaired, possibly superinduced by vasomotor
influences and their consequent trophic effects. This assumption, however,
could only be extended over a limited number of cases.
In most of the cases of true Raynaud’s disease an exact localization of
the lesions cannot be made. The nature of the pain and its distinct rela-
tionship to vasomotor phenomena point to a very evident association with
the vasosensory fibers.
In organic obstructive arterial diseases various explanations may be given
for the relationship between the advent of pain and its intensity to the position
of the limb. It is usual (though not without exception) to find that pain will
be evoked whenever the limb is elevated sufficiently long to produce a very
marked ischemia, or at least, if this position be maintained over a sufficient
period of time. It is impossible to assert just how important is the ischemia
itself, with its power to cause irritation of the sensory nerves, and to what
extent the secondary reflex or direct spasm of the vessels is an exciting moment.
Doubtless both agencies may play a rdle.
Paroxysmal pain of a diffuse variety is occasionally severe; it may come on
in insufferable nocturnal attacks, especially in those arteriosclerotic cases in
which recent thrombosis has been superadded. No satisfactory explanation
for this manifestation has as yet been presented. Possibly it results from a
summation of the excitant action of cumulative chemical effects, or of pro-
longed circulatory stasis. The latter would be favored by inactivity during
resting (sleeping) periods, and might attain a climax sufficient to incite spasm
in still non-sclerotic smaller arteries (discussed more fully in Chap. XXVI).
This phenomenon would be analogous to that of intermittent claudica-
tion, but of different causation—a paradoxical intermittent claudication
of inactivity.
The pain induced by prolonged pendency of the limb, particularly if this
position be preceded by a period of elevation, is perhaps more difficult to
account for. It is not uncommon to find patients who are unable to allow the
legs to hang down for a protracted period, particularly if well marked rubor
and trophic ulcers or fissures be associated phenomena. Here, we may pre-
suppose inadequate oxygenation of the blood as evidenced by the ensuing
lividity when the posture is continued. The manifestations do not seem to
be unlike those that are expressed by tingling, formication and pain in the
fingers of a person who had exposed them to excessive cold; or in whom a con-
stricting (Esmarch) bandage had been applied and released. In such a case
the effects of ischemia and subsequent hyperemia or even stasis, cause
responses in the sensory nerves. Or, perhaps, even the vascular channels,
themselves are the source of sympathetic sensory impulses. In the present
state of our knowledge we must be content to attribute to both the inherent
vascular nervous paths and also to the sensory nerves a réle in the incitement
of the above types of pain sensation.!
The alteration of tonus (change in threshold) in the spinal cord that may
be produced by persistent pain and its influence on vasomotor stability are
+ A more detailed statistical and clinical description may be found under the Chapters on
Thrombo-angiitis obliterans.
DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 137
discussed elsewhere.’ It is not infrequently stated that the distress is
especially intense at night. This may be in part due to variation to threshold
for pain perception; but it is in part referable to the lack of motion and
resulting stasis.
The pain associated with trophic disorders, such as ulcers over the distal
parts of the phalanges, may be exceedingly intense and quite out of propor-
tion to that which we would expect from lesions of similar nature and extent
complicating other affections. It is apt to be noteworthy in its degree in
thrombo-angiitis obliterans, and may be so excruciating as to render the
patient neurotic and to beg for amputation of a toe or even of the leg. The
threshold for the pain sense is indubitably altered in these cases, and a con-
dition of hyperexcitability of the sensory domain probably exists. Indeed,
persistence of pain of similar nature may continue for days or weeks after
amputation of the limb.? On the other hand, it is reported that injection
of absolute alcohol into the posterior tibial nerve may completely abolish
pain attending trophic ulcers of the foot. Whilst no doubt is cast on the
correctness of such observations, it is difficult to reconcile this therapeutic
effect with the above statement of the persistence of pain after amputation.
| CHAPTER XXVI
DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION
_ Thoroughly intrenched in medical parlance, this term, though giving rise
to much confusion, may still be retained, if its import, limitations, and exact
significance be comprehended. Suggested by Erb as applicable to a dis-
tinctive clinical picture, it has by virtue of incorrect interpretation, been
transferred to a multitude of affections, the true nature of which has oft been
unrecognized, and has been confounded with Raynaud’s disease. Although
believed by some to denote morbid entity, it should more properly be confined
and restricted, as a designation for a complex of symptoms, such as may be asso-
ciated with a number of different pathological processes, or even vasomotor
affections. In this sense, not indicative of any particular disease, but as a
composite of manifestations, it will be used by the author. That there may
be an association of other manifestations of vasomotor neuroses or that it may
itself be of neurogenic origin cannot be denied. Nevertheless, much progress
will be made in the differentiation of vascular affections of organic from those
of neurogenic derivation, if the limitations above suggested be adhered to.
SYMPTOMS
The characteristics of the Erb type of intermittent claudication are
complete or almost complete absence of pain or discomfort in a limb when at
rest, commencement of disturbances, pain, tension, paresthesize, weakness
shortly after walking is begun, gradual intensification of these until walking
is embarrassed and finally impossible, and the disappearance of the disorders
1 See page 42.
2 See page 250.
138 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
after a period of rest. Objectively there may be coldness, cyanosis, transi-
tory patches of rubor interspersed with the cyanosis, with a marmorated
appearance of the skin. At times cadaveric ischemia is noted: one or more
arteries of the foot usually fail to pulsate. Trophic disorders such as dry
skin, ungual dystrophies and gangrene may complicate the picture.
This is the symptom-complex as it is associated with organic vascular
disease in contradistinction to the angiospastic or functional variety that is
to be grouped with the vasomotor neuroses. ‘This description of a symptom-
complex is incorrectly extended to include a number of diverse infections.
Intermittent claudication may be described as a manifestation accompany-
ing two totally diverse processes:
(1) Vasomotor neuroses (angiospastic neurosis) ; and
(2) Obstructive arterial disease (arteriosclerosis, thrombo-angiitis oblit-
erans, etc.)
Oppenheim! distinguishes a (1) benign and (2) malignant form, the former
a functional or purely angiospastic phenomenon, the latter associated with
diseased arteries. . .
I. The Vasomotor Type-—A concomitant neurosis of the neuropathic
diathesis, is said to coexist with znéact arteries and to depend on spasm of the
arterial wall. Oppenheim mentions the following characteristic instance in
which transitory pain on walking with disappearance of pulse, coldness and
blueness of the toes were significant.
A male thirty years of age had been suffering for two years from painful sensations in the
feet on walking, these becoming gradually more severe so that at time cramps and numbness
in the feet and legs were pronounced even after fifty paces. After walking two hundred
steps in the office, painful fatigue with coldness of the skin and bluish discoloration set in,
together with a disappearance of both dorsalis pedes pulses (?). After a rest of a minute,
the right dorsalis pedis pulse was again perceptible. Several years later, all the symptoms
had disappeared, and the arteries of the foot were distinctly discernible.
Another case quoted by the same author is equally valuable.
Miss S., 22 years of age had frequent attacks of local syncope in her finger since her
sixteenth birthday. In the winter of 1898 there was much emotional strain, and in the
early summer of the same year she took a long and arduous tramp. Immediately after this,
the following condition developed. After walking 100 to 200 steps she experienced severe
pain and coldness in the left leg, and to a lesser degree in the right; the calf of the leg seemed
to become stiff and there were pricking and stinging sensations. After standing still for a
few minutes, she could go on again for a short time. The patient was a slender, anemic
individual. The pedal pulses were present though weak. When the patient was allowed
to walk around the room some 15 to 20 times, the foot became pale and bluish, and the dorsalis
pedis pulse was no longer perceptible. Five to 10 minutes later the beat returned.
These forms may have to be differentiated at times from Raynaud’s
syndrome and erythromelalgia. When the angiospastic phenomena affect
not only the territory of the muscles but implicate the cutaneous arteries,
vasomotor manifestations in the integument appear that may mimic the
above conditions.
The points valuable in differentiation are: In zutermittent claudication,
the dependence on motion is characteristic even though the picture is ob-
scured by evidences of vasomotor irritation (blanching, cyanosis and reactive
rubor), and the temporary or permanent absence (?) of pulses; in Raynaud’s,
the spontaneous, symmetrical and paroxsymal appearance with patent arteries
is the rule.
Whilst the careful observations of eminent authorities on the occurrence
of the angiospastic, functional or vasomotor type of intermittent claudication
deserved respectful consideration, a study of a large number of cases of
1 Oppenheim, Deutsch. Ztschr. f. Nerven., XLI, p. 376.
DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 139
organic disease of the vessels of the lower extremity, has convinced the author
that the incipient stages of true vascular obliteration when accompanied by similar
symptoms 1s frequently overlooked, and interpreted as a vasomotor affection.
Il. The type accompanying organic vascular disease is seen in athero-,
arteriosclerotic and syphilitic affections as well as in thrombo-angiitis
obliterans. Here the attendant vasomotor phenomena must not be regarded
—as Erb would have it—as integral elements of the syndrome, intermittent
claudication, but as irritative manifestations, frequently due to external
thermal influences, emotions or other excitants. The associated vasomotor
symptoms should not be regarded as part of the Erb complex, since they are
present even when the symptoms of intermittent claudication are wholly absent.
The grouping of vasomotor signs with the spasmodic and sensory phe-
nomena of Erb, is insufficiently warranted, therefore, and it is for this
reason that the author shall merely include the sensory symptoms in the
designation ‘intermittent claudication.” Cases of organic vascular dis-
ease, such as thrombo-angiitis obliterans, therefore, may present vasomotor
phenomena, side by side with these regarded as “intermittent claudication.”
HISTORICAL
Keeping in mind that many authors have described intermittent claudication as a
morbid syndrome of varied pathogenesis,! it may be well and of historical interest to recount
some of their observations.
In 1858 Charcot described a clinical picture typical of intermittent claudication. A
male 54 years of age complained of weakness, numbness, cramps and stiffness in his right
leg after walking for about one quarter of an hour. After a pause of some 5 to 10 minutes,
walking wouid again call forth the symptoms.
The relationship between these manifestations and similar occurrences in animals
peel described by veterinarians, was noted and commented upon by Charcot at
that time.
Erb gave a classical and extremely illuminating description of the symptoms in the year
1892. A number of different designations and appellations had been employed by various
authors, amongst which may be mentioned the following:
Charcot? described a Claudication intermiitente par oblitération arterielle; and also,
Paralysie douloureuse ischémique. Erb* suggested Dysbasia intermittens arteriosclerotica;
Higier,* Angiosklerotische paroxysmale Myasthenie; Oppenheim,*® Dysbasia angiosclerotica;
Walton and Paul, Angina cruris. Grossman,’? Angioscklerotische intermittierende Muskel
Parese; and Determann,’ Akinesia or Dyskinesia intermittens angiosclerotica.
Charcot had previously called attention to an affection in horses that had its analogy in
the human, and to which he assigned the term “Intermittent Claudication.’’ Boullay®
had noted—as had also other authors, subsequently (Rademacher,!*® Bother,!! Voétsch,!
Sommer!’ and Goubaux"4) that an ischemic condition of the hind legs regularly appeared as
a causal or concomitant phenomenon, so that it was a priori clinically acceptable to surmise
that impaired circulation could also account for similar symptoms involving the muscles of
locomotion in the human.
1 Erb, Deutsch. Ztschr. f. Nervenh., 13, 1898, 76.
2 Charcot, Compt. rend. Soc. de Biol., 2, Série 12, 1858, p. 225.
$Loc. cit.
4 Higier, Deutsch. Ztschr. f. Nervenh., 19, 1901, S. 438; Neurol. Zentralbl., 1910, g11.
’Oppenheim, Deutsch. Ztschr. f. Nervenh., 17, 1900, S. 317; Deutsch. Ztschr. f.
Nervenh. 41, S. 376.
6 Walton, Boston Med. and Surg. Jour., 146, 1902, p. 351.
7 Grossman, Deutsch. Arch. f. klin. Med., 66, S. 500.
8 Determann, Deutsch. Ztschr. f. Nervenh., 24, 1905, p. 152.
®Boullay, Ac. roy. de Méd. Séance du 11 Oct., 1831. Arch. gen. de Méd., 1831,
MAVIL, p. 425.
10 Rademacher, Gwilt u. Hertwig’s Magazin f. d. ges. Tierheilk., 1838, IV, S. 455.
11 Bother, Ztschr. f. d. ges. Tierheilk., 1839, VI, S. 425.
12 Votsch, Herings Repertorium d. Tierheilk., 1839, VI, S. 425.
13 Sommer, Gwilt u. Hertwig’s Magaz. f. d. ges. Tierheilk., 1843, IX, S. 461.
14 Goubaux, Recueil de Méd. Vét. prat., 1846, XXIII, p. 578.
140 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
In the so-called “‘Boiterie intermittent des chevaux’’, (intermittent limping of horses)
one may observe that an affected horse presenting no symptoms at rest or when going at a
slow pace, will, after five to fifteen minutes of hastened gait or trot, drag one or the other
hind leg. Even a short run may cause it to perspire, and to turn its head in the direction
of the hind quarters. Its expression becomes anxious and breathing is accelerated. In
short, all the signs of pain, and weakness in the limping extremity become evident. The
affected limb becomes simultaneously cold and pulseless. If the horse be now driven still
further, the functional enfeeblement may increase to such an extent, that the horse breaks
down completely, lying helpless and paralyzed. After a pause or rest of five to thirty
minutes it becomes wholly restored and capable of assuming normal pace. Since such
attacks recur whenever the animal moves at a moderately rapid gait, the horse becomes
practically useless.
Autopsies have revealed an obliteration of the distal portion of the aorta in the bilateral
cases, and closure of the iliac or femoral artery in unilateral, when one limb alone is involved.
Gangrene does not occur because of the relatively favorable conditions that obtain for the
establishment of a collateral circulation.
In Charcot’s first and analogous case an aneurysm of the right iliac artery with oblitera-
tion of the distal portion of the artery was present. This aneurysm and consecutive
thrombosis had followed a bullet injury sustained some twenty-one years previously.
Curiously enough this first reported and clinically observed case of intermittent claudi-
cation in a human being had for its anatomical basis a most uncommon lesion, since, as
subsequent investigation revealed, symptoms of intermittent claudication usually accom-
pany and are due to disease of the peripheral vessels of an extremity (Erb).
CLINICAL TYPES
Although the organic vascular form of intermittent claudication seems
to be the most common, the literature abounds in clinical examples warrant-
ing the recognition of additional types. We may summarize.
I. Charcot—Erb’s variety (Dysbasia angiosclerotica intermittens).
II. The functional vasomotor type (Oppenheim).
III. Intermittent claudication in other territories.
IV. Acute forms (so-called) probably thrombo-angiitis obliterans, or
V. Apokamnosis or artificially induced intermittent claudication.
I. DYSBASIA ANGIOSCLEROTICA INTERMITTENS
This type (according to the literature), includes the typical symptoms
associated with diseased arteries and has been variously called, claudication
intermittente par obliteration artérielle (Charcot). Paralysis douleureuse
ischémique (Charcot), angiosklerotische paroxysmale Myasthenia (Higier),
angiosklerotische intermittierende Muskelparese (Grossmann), and Angina
cruris (Walton).
Whilst the symptom-complexes here described are alluded to by most
authorities as indicative of a morbid condition of which they are the most
important manifestations, the author wishes to emphasize in advance that
he cannot subscribe to such a view. For he will show that intermittent
claudication is more correctly merely a designation for a group of associated
phenomena that may be evoked by a number of varied and diverse patholog-
ical conditions. Nevertheless, for a thorough comprehension of the subject it
may be well to give a brief review of the symptomatology, etiological factors,
clinical course and pathology, as they have been set forth by other authors.
Oppenheim and Cassirer! describe the following picture. The manifes-
tations begin slowly as a rule, affecting both lower extremities simultaneously,
or successively one and then the other after varying intervals in different
1 Cassirer, Loc. cit.
DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 141
cases. First, there appear sensory symptoms such as disagreeable sensations
in the foot, toes, soles, and calf of the leg with paresthesia, or with a feeling
of coldness, alternating possibly with burning sensations, sensory symptoms
in the foot or calf of the leg—all of these, or a combination of several develop-
ing after walking, and disappearing after repose. Vasomotor symptoms are
frequently associated at the very onset of the symptoms, the patient noticing
that the feet become blue and cold, sometimes strikingly cyanotic after walk-
ing, or when allowed to remain in the pendent position for some time. Such
discoloration may alternate or be associated with areas of redness, or the toes
may become ischemic. These vasomotor phenomena also are apt to be
intensified or appear only after locomotion.
Cassirer remarks that as the pain and cramp-like sensations increase,
the muscular disturbances become intensified, so that the patient can walk
only with difficulty. In this stage frequent rests become necessary, and
finally walking may have to be given up altogether until the symptoms have
wholly abated. Such recovery after rest comes on after several minutes,
when a continuance of locomotion is resumed with the greatest difficulty.
There may be considerable variations in the degree of suffering and func-
tional interference.
Subjective manifestations of vasomotor nature were noted in 25 out of 36
cases. As arule there was a feeling of coldness whilst more rarely the oppo-
site condition obtained. Local ischemia particularly over the plantar aspect
of the feet could be evoked by permitting the patient to walk rapidly around
the room, when sensory and motor derangements could also be elicited.
Goldflam! states that some of the latent cases of intermittent claudica-
tion can be recognized by noting the onset of vasomotor symptoms after
exercising the feet and legs. Thus he describes changes in the color of the
feet, blanching, disappearance of the small veins with collapse of the veins.
In the advanced cases the feet and lower legs may present a spotted cyanotic
appearance with possibly hyperemic areas between the patches of cyanosis,
the skin temperature usually subnormal, rarely elevated.
Erb, Cassirer and others speak of the absence of the dorsalis pedis and pos-
terior tibial pulses as the most important objective signs. In most of the bilat-
eral cases all four pulses of the feet are wont to be missing.
In the clinical picture above described, it is remarked by a number of
authors, that symptoms other than those mentioned are generally absent.
The reflexes are usually normal, objective sensory disturbances do not occur
and there are no neurologic findings. However, certain trophic disturbances
of the skin of the feet may be noticeable, such as dystrophy of the nails and
ulcers. Very frequently a decided degree of arteriosclerosis can be detected.
Two facts stand out prominently as having a causal relationship with the
symptom-complex: first, certain circulatory and vasomotor Phenomena, and
second, the absence of the pedal and crural pulses.
The circulatory and vasomotor phenomena that usually precede the
manifestations of intermittent claudication and may be given the importance
of prodromal signs, are described as attacks of peculiar paresthesiz (feel-
ings of heat and cold, formication and sensation of “falling asleep’’) with
cyanotic, livid, marmorated or cadaveric discoloration of the foot and
leg. The same interdependence of symptoms and locomotion, as noted with
intermittent claudication obtains in the production of these visible signs.
When the well marked motor disturbances of intermittent claudication are
1 Goldflam, Neurol. Centralbl., 1910, S. 1.
142 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
fully developed, such objective and subjective paroxysms as here given may
appear simultaneously.
Coldness, cyanosis and pallor of the affected parts are noticeable when the
patient complains of numbness or strange feelings in the toes.
Erb called attention to the fact that in the well developed cases the feet
are apt to show abnormalities in appearance, even with the absence of par-
oxysms, that is, during the free intervals. When the extremities are allowed
to hang down, they are apt to be cold, cyanotic, swollen. The skin is said to
be abnormally dry, and the growth of the nails impaired. Bright red spots
may be interspersed with the cyanotic areas, lending a marble-like appear-
ance to the skin. Or, anemic areas may appear usually involving one or
more toes, the feet becoming cadaveric and cold for varying periods of time,
these phenomena being associated with prickling or sticking sensation when
the normal redness or cyanosis returns. All these manifestations may be
absent when the patient is at rest in bed, or in a warm temperature. A/]
of these appearances, we believe, may belong to any of the types of organic arterial
disease, and cannot, therefore be regarded as a separate entity.
Examination of the Pedal and Crural Arteries.— This may be regarded as
of pathognomonic value in the diagnosis of dysbasia, angiosclerotic inter-
mittens. The absence of pulses in one or more of the four pedal arteries is
almost a regular finding, and may be accompanied by demonstrable thicken-
ing and tortuosity of the vessel. Thus Erb reports that of 30 bilateral cases
there was an absence of the beat in all four arteries in 16 cases; three in 2 cases
and in 1 case absence of one pulse. All four pulses were palpable in but 4
cases, and in these they were weak, three of the patients having evidenced
thickening and sinuous vessels. Of 16 unilateral cases absent pedal arteries
were noted in 13.
Almost as important according to the above author is the examination of the popliteal
and femoral arteries which often give positive findings, such as absent beat, or the above-
mentioned organic changes. In the case of Bourgeois! there was an aneurysm of the
popliteal artery. Simon? recorded similar symptoms in a case of embolus of the anterior
tibial artery. Although a number of observations definitely offer conclusive proof that
localized arterial disease such as aneurysm, embolism, etc. can also cause the symptoms of
intermittent claudication, as a rule a more diffuse impairment of the circulation as produced
by obstructive diseases of the peripheral arteries of the lower extremities is present.
Clinical Course.—A perusal of the literature convinces one of the fact that
a progressive and obliterating arterial infection is usually present. Striking
also is the circumstance that spontaneous gangrene of the affected extremity
is so frequently the issue. In the cases that are not treated, or in those which
were refractory to all measures, there was described a progressive aggravation
of the condition, or periodic recurrences with increasing intensity of symp-
toms, finally eventuating in almost complete abolition of locomotion. With
increasing intensity of the degree of circulatory disturbance and the con-
comitant symptoms, gangrene of the toes of the foot, with proximal
extension, is said to occur.
II. FUNCTIONAL VASOMOTOR TYPE (OPPENHEIM)
Nothnagel* recorded the following symptom-complex in a patient in
whom the arterial circulation of one arm was impaired by reason of thrombo-
sis of one of the axillary arteries.
1 Bourgeois, F., Thése de Paris, 1897.
2 Simon, Deutsch. med. Wchnschr., 1905, 19, p. 754.
3 Nothnagel, Berl. klin. Wchnschr., 1867, No. 51, p. 536.
DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 143
A girl of twenty-five years was afflicted with striking fatigue, weakness, with pain and
paresthesie in the fingers and hand on doing but the lightest of work, all symptoms
disappearing after a rest.
Such observations confirm the assumption that any occlusive process in
the arteries may serve as the basis for the manifestations of intermittent
claudication. Therefore, not only the extremities, but other territories
should offer clinical evidences of corresponding symptoms.
Doubtless many of the cases of so-called vasomotor or angiospastic forms
of intermittent claudication belong more properly to the vasomotor neuroses,
intermittent claudication being only one of the manifestations, just as are
cyanosis, ischemia and other phenomena. That Oppenheim! had been
compelled to take this view and to renounce, in part, the classification of
intermittent claudication previously suggested, was due to the publication
of cases that were quite different from the classical forms of intermittent
claudication, except for some of the motor and sensory symptoms.
Thus, Westphal? called attention to spastic phenomena in the vessels of
the lower extremity with disappearance of the anterior tibial and posterior
tibial pulses during the attacks, (coincident with disturbances in locomotion)
—in a case of hysterical pseudotetanus—a complex which surely cannot be
classed with intermittent claudication, but which, because of the wide and
indiscriminate application of this term, had been considered as another
variety.
In a woman with symptoms of pseudotetanus, there were associated attacks of vaso-
motor manifestations involving the upper as well as lower extremities. At the beginning
of a paroxysm, there was a pricking sensation in the fingers or the toes, gradually increasing
in intensity to actual pain. At times the whole of the hands and feet would be involved, or
but parts of these, either on one side or symmetrically. The affected regions would become
cyanotic, or violaceous in color, or sometimes ischemic, pale and cold. Pallor would
occasionally give way to cyanosis, and a deep prick with a needle could not entice a drop of
blood to the surface. Variations in color would be manifold in distribution of time of
appearance and duration.
Most striking was the disappearance of the pedal beats during such attacks, whilst
during the free intervals the feet were found normal, both as to color and as to the intensity
of the arterial pulsations. The radial pulses, however, were always present.
With the advent of these vasomotor phenomena, disturbances in locomotion were also
noted. The patient would complain some time before the beginning of an attack of fatigue
on walking and paresthesiae in the feet. With the actual onset of the attack, walking would
become impossible.
What an exquisite example of a pure vasomotor neurosis and how futile
to force a clinical relationship between this disease and “‘intermittent claudi-
cation!” That some of the cases described as intermittent claudication were
said to have had evidences of an angiospasm in the pedal arteries, cannot be
denied; but that the case of Westphal has any clinical or pathological affilia-
tion with either the so-called organic or the functional types of intermittent
claudication, is to be doubted.
Record of an instance that was said to be due to toxic factors is that of a
young man, in whom the symptoms of intermittent claudication seemed to
depend upon psychic or emotional states (Schlesinger?). The symptoms
disappeared after one and a half years, only to return eight years later.
Perhaps the most convincing example of the neurotic type of intermittent
claudication is a case in which symptoms of this disease were associated with
1 Oppenheim, Deutsch. Ztschr. f. Nervenh., tg00, Bd. XVII.
2 Westphal, Berl. klin. Wchnschr., Dec. 9, 1907, XLIV, p. 1567.
3 Schlesinger, Deutsch. Ztschr. f. Nervenh., Bd. 41, p. 235.
144 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
the Raynaud phenomenon. The following description and case report will
elucidate.
Angioneurotic Intermittent Claudication with Raynaud’s Disease of the Fingers.—
An example of so-called neurotic intermittent claudication is described (Riilf!), in which
there were combined Raynaud’s disease of the fingers, intermittent claudication of the
lower extremities, rubor of the tip of the nose and symptoms of migraine.
A woman 30 years of age, always of nervous temperament, began 6 years previously
with severe attacks of migraine.
For the past 2 years the tips of the fingers would become numb and white as if dead.
Rubbing or motion would restore the circulation. At first the fourth and fifth fingers were
involved, later the others. For about 3 months the attacks of syncope were followed by
asphyxia. The severity of the symptoms has been increasing; recently have been appearing
several times weekly.
The symptoms referable to the lower extremities antedated those of the upper slightly.
There have been associated cardiac symptoms, in that attacks of weakness, feeling of
faintness and prostration come on after walking. Recently pain has developed in the left
leg after walking, necessitating frequent periods of rest. After a short walk, a feeling of
tiredness appears in the left sacral region, the weakness and tiredness advancing so as to
implicate the left thigh, knee and upper part of the leg. If the body were supported by
the right limb, the left leg seemed warm again, and the symptoms would disappear.
The dorsalis pedis and posterior tibial arteries could be found pulsating, but were “‘diffi-
cult to find” (?). The radials arteries were abnormally small.
The temperature was found reduced over the left leg and foot, but not always, usually
only after walking. The blood pressure was 115 systolic.
This case is described as one of intermittent spasm of the vascular capil-
/aries, since the pedal pulses were neither diminished nor abolished during
the attacks. The diminution of temperature over the left lower extremity is
attributed to vasoconstrictor action.
Curschmann,? also, accepts the possibility of an intermittent claudication
with apparently intact (?) arteries, where the symptoms are referable to a
genuine constriction of the pedal arteries. In two females (between the
ages of 19 and 22) he found the typical manifestations associated with absence
of the pulses of the feet and without any evidence of arteriosclerosis. He
claims that such instances are analogous to the intermittent asphyxia of
the hands, differing in that the pulses are permanently absent in the former.
It is, however, just this constant lack of beat in the pedal vessels that
throws considerable doubt on the accuracy of his observations. A permanent
arterial spasm is so foreign to analogous conditions elsewhere, that our mental
approach to such a possibility can hardly divest itself of the suspicion that a
true organic obliteration did exist.
Relation of Angiospasm to the Organic Type of Intermittent Claudication.
—We have purposely retained here the designations, angiospastic (neurogenic
or vasomotor) and organic intermittent claudication (dysbasia angiosclerotica
—Erb), in order to express more clearly the views of the authorities who have
employed these terms. For it must be borne in mind that amongst a large
number of the continental observers, the conception of the malady ‘‘inter-
mittent claudication” had taken root so strongly, that, with the discovery of
diverse, contradictory and inconsistent physical findings, in arteriosclerotic
arteries (Erb), in acute arteritis (Higier), in obstructed arteries (Higier), and
with patent arteries (Oppenheim’s angiospastic form), a confusing collection of
clinical descriptions had found their way into the literature. To clarify some
of these notions, reference must be made to theories according to which vaso-
motor neuroses are regarded not only as the antecedents, but also as actual
harbingers of organic vascular changes in a causal sense.
M-RUulti Arch: f)'Psychiat,..50;:f121, pscoo:
2 Miinchen. med. Wchnschr., 1907, No. 51, p. 2522.
DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 145
Oppenheim entertains the belief that the angiospastic neurosis with symp-
toms of intermittent claudication may be a prodromal stage of what he terms
organic intermittent claudication or ‘‘dysbasia angiosclerotica.’’ In defense
of this proposition he cites a case of a young man in whom vasomotor mani-
festations preceded by years, the final appearance of intermittent claudication
with evidences of arterial obliteration.
H. H., male, 28 years, gave a history of neuropathic tendency, insomnia, frequent
attacks of ‘‘dead fingers,” and even local syncope in these, with sensation of “‘pulsations’’
in various parts of the body, with excessive sexual irritability. The feet showed nothing
abnormal (February, 1895).
Two years previously after emotion, he had pain with coldness in the calf of the legs on
walking 1 to 3 minutes, necessitating a pause before further progression was possible.
After lasting about a year, these symptoms disappeared.
In 1899, a recurrence of difficulty in walking, with the right leg especially affected, was
noted. The plantar aspect of the toes of this limb would become pale with slight cyanosis
after fatigue. The corresponding dorsalis pedis artery could not be felt pulsating.
In tort the pulses of the right foot were altogether absent, present on the left. Cold-
ness and cyanosis were also striking signs. Pain and cyanosis appeared after walking
30 to 4osteps. X-ray examination showed distinct calcification.
In short, evidence has been brought forth, at least in this case, that the
phenomena of intermittent claudication may coexist with pulsating vessels in
a neurotic individual with other stigmata of a labile vasomotor system; that,
later, such a patient may, after free intervals, pass over into a stage in which
the peripheral arteries are arteriosclerotic and obturated. While such a
chronological sequence of events doubtlessly may occur, the causal relation-
ship between the stage of angiospasm and the subsequent development of
organic disease, be this arteriosclerosis, thrombo-angitis obliterans, or throm-
bosis, is not so clear. To conceive of peripheral thromboses as a compli-
cation during the history of repeated attacks of vasomotor constriction, is
logically permissible, and, certain observations of the author would support
such an assumption. An analogous condition obtains in cases of gangrene
in anatomically normal arteries and in the cases of thromboses in peripheral
arteries without arteriosclerosis or other disease.!' In some of these acro-
cyanosis had been noted although intermittent claudication was usually absent.
But to assume, as does Oppenheim, that there is an intimate motivating
dependency between a prior neurotic status and a succeeding arterial disease,
would appear an audacious hypothesis, in light of the fact that in that most
intense and exquisite form of angiospastic condition, Raynaud’s disease, such an
organic vascular eventuality is altogether lacking.
A perplexing situation, diagnostically speaking, will not infrequently
confront us, one that may be interpreted as reliable testimony in favor of
Oppenheim’s belief. This is the circumstance that marked vasomotor
symptoms, occasionally with, but usually without intermittent claudication
may occupy the clinical picture, weeks, months, or almost years before the
typical objective manifestations of thrombo-angiitis obliterans are recog-
nizable. References to this type will be made in Chap. LIX.? To deduce
a causal association between the excessive lability of the vasomotor func-
tions and the consequent inflammatory and obstructive vascular lesions,
would, in our opinion be unwarranted.
Whenever pronounced neurotic vascular symptoms participate in the early
stages of an insidiously developing organic obstructive arterial lesion, we
must consider the following possibilities.
1 See Chap. XCVIII. ae
2See Vasomotor Symptoms in Thrombo-angiitis Obliterans of the Upper Extremities,
and also Chap. ‘‘ Borderline Cases’? CIV.
10
146 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
First, two independent diseases may overlap, coexist or follow each other.
Second, minimal unrecognizable peripheral vascular obturating processes
(as in thrombo-angiitis obliterans of the plantar arteries or peripheral pedal
vessels) are present for a long time, and are a factor, not only in evoking the
cyanosis or pallor of the digits on exertion, but also secondarily elicit a super-
abundant quota of vasomotor response; and this, either by virtue of the super-
fluity of waste products (toxins, COs, etc.) developed in poorly nourished
territories, or by a relative ischemia when the circulation is impaired.
Third, thromboses of the popliteal artery of clinically unobserved,
stealthy advent, with adequately dilated collateral paths filling the dorsalis
pedis and posterior tibial arteries may be accountable for a complex that is
wont to be diagnosticated as a vasomotor form of intermittent claudication.
A more complete exposition and an analysis of this subject are given in the
section on the critique of so-called angiospastic forms of intermittent claudi-
cation also in Chap. CIV.
While Oppenheim lays great stress on two factors, namely, a neuropathic
and an angiospastic diathesis, as being important in intermittent claudica-
tion, he seems to have overlooked the possibilities above mentioned. Higier,
himself, to whom he oft refers, was not clear as to the pathology of most of his
cases. Amongst the latter’s cases can be recognized exquisite examples of
thrombo-angiitis obliterans in the chronic or in the acute relapsing stage.
Just how important are the other predisposing moments to which Oppenheim
alludes, to wit, the congenital Anlage or congenital mediocrity or inferiority
of the vascular and nervous systems, it is impossible to say.
In short, this author recognizes a “‘genuine”’ or true organic form of inter-
mittent claudication and an angioneurotic. But even for the former variety
he would postulate the existence of a congenital mediocrity or inferiority of
the vascular system, a degenerative stigma that runs parallel with the neuro-
pathic diathesis of these individuals. The finding of abnormally small
femoral arteries 7m vivo during their exposure for the performance of the
Wieting operation of arteriovenous anastomosis, convinced him of the cor-
rectness of his hypothesis.
III. INTERMITTENT CLAUDICATION IN OTHER TERRITORIES
In fact a number of authors have observed phenomena attributable to
occlusive conditions in the arteries of the affected parts, and Ortner+ described
what he calls:
(a) Dyspragia Intermittens Angiosclerotica Intestinalis.
In a male 55 years of age, an inveterate smoker, there were attacks of pain in the umbilical
region 2 to 3 hours after a large meal, the symptoms lasting 2 to 3 hours. For several
months there would be periods of intermission with recurrences. Exitus occurred after
an operation.
Autopsy showed marked atheroma of the aorta, the superior and inferior mesenteric
arteries being markedly sclerotic. ‘There was nothing else to account for the symptoms.
Determann described a case of intermittent claudication, involving an arm, one lower
extremity and the tongue. This latter case, however is open to the criticism that there
were not multiple arterial obturations, but that some of the cerebral arteries were involved.
(b) Intermittent Claudication of the Spinal Column.—Even an affection
of the vessels of the spinal cord has been described by Déjerine,? who men-
1 Ortner, Wien. klin. Wchnschr., 1902, p. 44.
Ibid., Volkmann’s Vortrage, N. F., 347, Leipzig, 1903.
2 Déjerine, Rev. neurol., 1906, 14, p. 341.
DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 147
tions in the clinical picture an onset with cramp-like contracting sensations
of heat and cold in one or both legs brought on by walking and disappearing
after repose. With this, gradual aggravation of the symptoms, weakness
after the slightest exertion become so accentuated that the legs are practi-
cally functionally useless. Paralysis and evidences of contracture are absent.
Increased reflexes and ankle clonus appear during the attack, as well as the
Babinski reflex. Urinary and sexual disturbances may be associated,
although sensory phenomena are absent.
The histories reported by Déjerine? describe cases in the third or fourth
decades with lower extremities that show no disturbances when in repose.
After a short walk the limbs become heavy, motion more and more impaired
until locomotion becomes impossible. Motor power returns after a few
minutes of rest. Parasthesia, cramp-like sensation, formication, coldness
and heat may be associated and also disappear during the period of rest.
At the onset of this disease the patient must pause but rarely, being able
to walk considerable distances, possibly even a mile, but later on the patient
may require a rest after twenty or thirty steps.
An ankle clonus, occasionally also a Babinski sign, that are absent,
during rest can be elicited after motion. Occasionally urinary frequency and
urgency and sexual hyperexcitability are associated symptoms.
At the same time one can demonstrate all evidences of pathological altera-
tions in the vessels; the pulses are present and also the vasomotor manifes-
tations that usually accompany intermittent claudication.
The prognosis is bad in these cases since a spastic paraplegia eventually
develops. ‘This outcome speaks for the assumption that an organic altera-
tion is responsible for this affection.
Déjerine believes that there is a deficient circulation in the dorsal portion
of the lumbar cord by reason of a chronic arteritis. In all probability the
permanent changes in the cord do not develop until a long period has elapsed
since the history of the cases is long with marked remission in the
symptomatology.
Other authors, such as Grasset? and Sollier have confirmed the above
observations. In contradistinction to the two forms of dysbasia and angio-
sclerotica intermittens, syphilis probably plays the most important part in
determining endarterial lesions in the cord.
Other authors, amongst whom Hardy,‘ Long,’ and Rekord,* may be
mentioned, have made similar observations.
(c) Intermittent Claudication of the Upper Extremities.—The upper
extremities may be the seat of similar phenomena.? The author has
described their occurrence in thrombo-angiitis obliterans as well as in arterio-
sclerotic lesions of the vessels.
A number of cases have been reported in which the complex, intermittent
claudication, involves both upper and lower extremities, with absent pulses in
both. Whilst in some of these the findings would point to atherosclerotic
vessels, in others the data given are not conclusive.
1 Déjerine, Thése Paris, 1894, p. 170.
2 Grasset, S., Rev. neurol., 1906, XIV, No. 10, p. 433.
8 Sollier, Presse med., Oct., 1906, No. 85, p. 677.
4 Hardy, Thése de Paris, 1909.
5Long, Rev. med. de la Suisse romande, 1910, p. 7.
6 Rekord, Amer. Jour. Med. Sc., 1912, 114, p. 721.
7 Buerger, Loc. cit.
148 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
In the case of a man 58 years of age (Tobias!) symptoms were present in both lower
extremities and in the /eft arm. In the legs, there was a feeling of coldness and pain in the
calf muscles upon walking, and for 1 year similar manifestations in the left arm. Striking
was the early fatigue occasioned in the latter after using it. The intense feeling of coldness
of the left hand necessitated the wearing of heavy gloves.
Physical examination showed an absence of the dorsalis pedis and posterior tibial pulses
of both lower extremities; in the left upper, the axillary and subclavian pulsated, whilst
all other large pulses were absent.
Determann employs the term dyskinesia intermittens angiosclerotica to
which the adjectives cruris and brachii are added for the leg and arms
respectively.
In a case of Nothnagel (1867) there was a thrombotic occlusion of the right
axillary artery.
In an arteriosclerotic woman of 25 the right axillary artery had been converted into a
hard cord, easily palpable in the axilla and below this. The pulsation in the radial artery
was absent, and in the ulnar and brachial there was but a slight beat. When the girl used
the right arm even for the lightest kind of work, weakness soon resulted, with pain and
paresthesiz in the hands and fingers. Work became impossible; after rest it could be begun
again. It was not clear as to how the thrombus had developed in the artery. A somewhat
insufficient collateral circulation had resulted.
Whilst in the above-mentioned case extensive vascular disease was not
present, but a localized thrombotic process was held responsible for the
impaired circulation, other instances are reported where one or both upper
extremities were involved in a manner similar to that of the lower extremities.
In a case of Wedensky? the right arm was involved as follows:
A male 38 years of age was suffering from intermittent claudication of the right leg, with
symptoms also in the right arm. He could not write for any length of time without
experiencing pain in the fingers and also in the wrist. At the same time there was hyper-
hidrosis and later coldness of the whole right arm. In moderately cold weather the wrist
and fingers would get blue. There were periods of improvement and intensification of the
symptoms, until finally ulcers appeared on the second and third fingers, which, however,
healed under treatment. At about this time gangrene of the third toe of the right foot
occurred, necessitating exarticulation of the toe.
Examination revealed the fact that the right arm was somewhat atrophic and colder
than the left, and that the pulses in the right radial and ulnar arteries were absent.
As a rule the symptoms in the upper extremities are associated with
similar symptoms in the lower. Up to the year 1907, Bing was able to find
about one dozen cases described in the literature.
An interesting case is reported by Determann? where the tongue also gave
symptoms.
A Russian (Hebrew) who smoked 6 cigarettes a day complained, in addition to the
usual symptoms in a leg and arm, of the following, very annoying manifestations: after
speaking from 5 to 8 minutes, the mechanical act of articulation was impaired, although no
interference with the mental functional mechanism was present. Gradually the tongue
would become heavy and thick, motility returning after a short period of rest. “The examina-
tion of the lingual pulse revealed bilateral weakness.
IV ‘“‘ACUTE’’t FORMS OF INTERMITTENT CLAUDICATION
An inchoate, unreliable and unsatisfactory classification has resulted
from the trend of a number of excellent observers to accentuate the impor-
tance of the symptomatic association called intermittent claudication, and
1 Tobias, Ztschr. f. d. ges. Neurol. u. Psychiat., 1921, 71, 300.
2 Wedensky, Langenhecks Arch. f. klin. Chir., 1898, LVII, p. 98.
3 Determann, Deutsch. Ztschr. f. Nervenh., 1905, X XIX, p. 152.
*“ Acute” in quotation marks since this is an appellation of other authors.
DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 149
also from a neglect of the pathologic basis or true morbid process. Some
time prior’ to such reports as to those of Higier? the author had already
studied vascular material from identical cases, and had been able to recognize
a clinical and pathological entity, to which the designation thrombo-angiitis
obliterans had been given. Intermittent claudication was regarded as one of
the manifestations of occluded arteries accompanying this as well as other
maladies.
The acute form of intermittent claudication of other authors corresponds
to two essential vascular lesions; first, to the acute stage of thrombo-angiitis
obliterans with sudden extension of the inflammatory and thrombotic
obturation over varying territories; and second, to the deposition of keystone,
parietal or even completely obliterating thrombosis in arteriosclerotic vessels.
(a) Acute Stage of Thrombo-angiitis Obliterans.—The contributions to
the literature of “acute intermittent claudication” have added considerably to
the clinical confusion already sufficiently ingrained and impressed by multitu-
dinous and variant descriptions of types of intermittent claudication. Whilst
Higier® reports a clinical picture of subacute or chronic course as intermittent .
claudication or angiosclerotic paroxysmal myasthenia in one publication,
he speaks of “‘arteritis acuta with intermittent claudication’”’ elsewhere,‘
when the onset of the malady is sudden. In the former® he was, we believe,
dealing for the most part with cases of thrombo-angiitis obliterans of the
chronic progressive type; in the latter, with the same malady during a period
of acute manifestations. In neither instance, was this author justified in
speaking of a disease ‘“‘intermittent claudication.”
The case of Higier* reported in 1910 corresponds with the author’s ‘‘acute
stage”’ or acute thrombotic exacerbation in thrombo-angiitis, and can in no
sense be regarded as a rarity. He cites the following history.
A Polish Hebrew, 25 years of age was suddenly seized with pain in the right foot.
Fever, chills and general depression were absent at the onset, and there was no local swelling,
abnormal redness or heat, abnormal pallor, cyanosis or coldness. Examination of the
internal organs was negative. There was no increased blood pressure and no anemia.
The urine was free of albumin and sugar. Intense pain in the right foot and leg made
walking impossible, but abated with the patient in bed and at rest. Walking, even after
some 30 or 40 paces, produced a feeling of numbness and fatigue in the calf of the leg,
necessitating immediate cessation of locomotion. A certain degree of pallor of the foot
seemed to follow repeated or prolonged movements of the extremity, whereas the pendent
foot turned to a livid or rose color (erythromelia). The temperature of the extremity was
lowered. The right dorsalis pedis and posterior tibial arteries did not pulsate. Later,
exceedingly painful ulcers of the second and third toes developed. Radiography showed
no arterial calcification. The pulses of the leg were present: In the past history nothing
of moment could be elicited, no lues, no exposure to cold nor to trauma.
The insomnia which did not respond to sedatives and hypnotics made the patient des per-
ate and he was anxious to accept the physician’s proposal of amputation. However, after
three months the ulcers healed, and the pain as well as the intermittent claudication
diminished greatly. Six weeks later he was able to get up.
The physical examination made about ten months after the first symptoms, showed
persisting coldness, moderate lividity of the foot, and absence of the pulses.
In the light of the author’s’ studies, and in a comparison with almost
identical observations in which pathological material through amputation
1 Buerger, Amer. Jour. Med. Sc., Oct., 1908; Proc. New York Path. Soc., March, 1908.
* Neurol. Centralbl., 1910, p. 911.
3 Higier, Deutsch. Ztschr. f. Nervenh., tg01, XIX, p. 439.
4 Higier, Neurol. Zentralbl., rg10, X XIX, p. 911.
'See “Intermittent Claudication,’’ p. 255.
6 Higier, Neurol. Centralbl., r910, X XIX, p. 912.
7 Buerger, see literature on Thrombo-angiitis obliterans.
150 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
was available for study, there can hardly be any doubt but that the case
reported by Higier was one of thrombo-angiitis olbiterans. That extensive
acute inflammatory thromboses occur throughout the territory of the dorsalis
pedis, posterior tibial, peroneal and popliteal arteries in thrombo-angiitis oblit-
erans, the author has demonstrated beyond the shadow of a doubt. And, the
manifestations called forth correspond in almost every detail to those in the
story above related.
How misleading an attempted grouping of unrelated diseases under the
caption “‘Intermittent claudication”? can be, is well illustrated both by
Erb’s quest for a special category in which to put the so-called ‘‘acute form of
intermittent claudication, ’’ and Higier’s renewed necessity for separation of
his ‘‘angiosklerotische paroxysmale Myasthenie” from the “acute type”
subsequently called “‘arteritis acuta with intermittent claudication.”
(b) Arteriosclerosis with Thromboses Diagnosticated as Acute Intermit-
tent Claudication.—Elsewhere will be described a characteristic picture of
“acute attacks of thrombosis” in cases with arteriosclerotic vessels (Chap.
LXIX). In some of these intermittent claudication has preceded by many
months or years; in others, vo clinical evidence of vascular affection has made
itself manifest. When, therefore, a patient with no past history referable
to the lower extremities, suddenly develops intermittent claudication or other
phenomena resulting from vascular occlusion, a thrombotic lesion is the
most probable cause, although palpatory evidences of such occurrence may be
absent. Cases such as that reported by Pelnar! may be classified from the
pathologic standpoint as latent arteriosclerotic vascular lesions with second-
ary parietal and occlusive thromboses. The history report may be
summarized thus :—
An engineer, 61 years of age, developed the following symptoms rather rapidly. After
walking but a few (2 to 3) steps he experienced a peculiar uncomfortable sensation in the
whole left lower extremity, as if the limb were foreign to him, this feeling gradually giving
way to heaviness and lack of control of the affected part. This necessitated pausing to
rest, immediate recurrence of these manifestations following renewed attempts to move
about. So severely was he affected that only the most necessary steps were taken, the
sitting posture offering considerable relief.
His wife noted that his toes would be cold, pale and ‘‘like dead,”’ the left leg colder than
the right. Because of tenderness in the left groin, the respective region was protected from
all pressure and contact. There had been a previous history of mild apoplectiform attack
with recovery.
Physical examination November 5, 1909, revealed increased blood pressure (180 mm.
systolic) generalized arteriosclerosis, and cardiac enlargement. The femoral artery
below Poupart’s ligament was tender and its pulsation weaker than that of the other side.
The left dorsalis pedis beat was also diminished.
Iodides were administered and in 1 month the subjective symptoms abated consider-
ably, and walking became easier. So also the tenderness in the groin became limited to a
ane a Objective signs remained stationary and the blood pressure rose to 210 mm.
systolic).
In August, 1910, he was again seen and found to be suffering from the results of an
apoplexy whose onset was recorded as January, 1910. ‘The right side was the seat of slight
paresis. The symptoms in the /eft lower extremity were noticeable only after prolonged
exertion and locomotion, and were of only moderate degree. The left femoral and popliteal
beats were weak, whilst the dorsalis pedis artery could “‘hardly be felt.”’
In short, a case of marked arteriosclerosis, high blood pressure, apoplecti-
form attacks, with rather sudden advent of enfeebled pulsations, the arterial
distribution of the left lower extremity being accompanied by the usual symp-
toms of intermittent claudication with gradual improvement and practical
disappearance of the dorsalis pedis pulse. Such examples have frequently
1Pelnar, Neurol. Zentralbl., 1911, XXX, p. 9.
DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 151
been observed by the author, and when gangrene eventuates—as occurs in a
certain percentage of the cases—the existence of thrombosis superimposed
upon the arteriosclerotic lesion has been demonstrable at autopsy or dissec-
tion of the amputated limb.
Doubtless parietal, keystone, and completely occlusive thrombi are re-
sponsible for similar clinical pictures. Syphilis also, and still unknown forms
of arteritis—(thrombo-angiitis obliterans being a distinctive, well differenti-
ated type), by virtue of complicating thrombosis and obstructive impairment
of the circulation can give rise to like symptom-complexes.
V. APOKAMNOSIS (GOLDFLAM!) OR ARTIFICIAL INTERMITTENT CLAUDICATION
Goldflam employed this term to denote abnormal liability to fatigue in
myasthenia, and transferred its application so as to designate also a feeling
of tiredness, numbness, heaviness and tension evoked by actively lifting the
affected limb. Whilst these manifestations can be artificially induced in an
extremity in which intermittent claudication occurs, in the normal only
slight pain or a feeling of fatigue will be tardily produced. Latent cases of
intermittent claudication may be brought to light by this test—instances in
which the typical signs have not as yet developed—and in which pallor,
rubor and cyanosis may dominate the clinical picture. As a comparative
method of investigating two corresponding limbs, it may reveal sufficient
differences to be of diagnostic worth.
Artificial pallor is also producible in cases with symptoms of intermittent
claudication, if the foot—whilst in the horizontal position—be flexed and
extended some thirty to forty times. The color contrast is even more strik-
ingly forthcoming, if the leg be permitted to hang down when the exercises
are carried out. Blanching of the fingers and hand can also be made to
occur by repeated flexion and extension of the fingers with arms hanging.
But most noteworthy is the ischemia of the foot following walking, particu-
larly if a test of locomotion be tried after the patient has been standing for
some time.
_ Goldflam attempts to explain the cutaneous ischemia in the following
manner. With the active motion of the extremity and the implied muscular
contractions, a hyperemia of this territory with dilatation of the arteries
occurs. With this ‘functional hyperemia” of the muscular vessels, a
collateral cutaneous anemia is to be expected. Invoking also the participa-
tion of the vasomotor nervous system, he calls attention to the autonomous
self-regulating mechanism that is an inherent rdéle of its activities, so that
with the necessary dilatation of the deep arteries a corresponding constric-
tion of the capillaries and arterioles of the integument, is an essential compen-
satory sequence.
PATHOLOGY
A study of the literature is exceedingly unsatisfactory, because of the
fact that authors have not differentiated between the obliterating lesions of
arteriosclerosis those of so called ‘‘endarteritis obliterans,’ and the
obturating process of thrombo-angiitis obliterans. The failure to properly
interpret the histological picture resulting from the canalization and vasculari-
zation of obturating thrombi has produced confusion in the literature; no
cognizance having been taken of that special, inflammatory and thrombotic
1 Goldflam, Neurol. Zentralbl., r9g10, X XIX, p. 2.
152 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
lesion described by the author. In fact, the lack of distinguishing criteria
between arteriosclerosis, endarteritis obliterans and thrombo-angiitis
obliterans, has permitted an incorrect conception of the pathology of these
conditions to persist.
Thus, the cases of Charcot, Dutil and Lamy,! Laveran,? Panas,* Goldflam,
Erb, and others are described by authors who have made a critical study of
their publications, as examples of a productive or obliterating endarteritis.
Endarteritis obliterans in this sense is considered to be a progressive thicken-
ing of the intima, through proliferation of a cellular, new-formed connective
tissue, leading to complete closure of the arterial lumen.
This interpretation is incorrect, for, some of the cases mentioned are
examples of arteriosclerosis, others of syphilitic endarteritis, and still others
of thrombo-angiitis obliterans.
Bing? in his resumé of intermittent claudication is unable to differentiate
between endarteritis obliterans of Friedlénder—which in all probability is
identical with thrombo-angiitis obliterans—and that of arteriosclerosis.
Be that as it may, it can be gleaned from the literature, that in spite of
uncertainty as to the exact pathological nature of the obstructive arterial
conditions observed, most authors are in accord in the opinion that organic
impoverishment of the circulation by an obturating vascular affection is
usually the pathological substratum.
In the consideration and treatment of the subject of etiology and
pathogenesis, the lack of proper recognition and segregation of types of
pathological process have also entered into the production of inexplicable.and
conflicting statements and circumstances on the parts of various authors. It
can therefore be readily understood how the views of one observer who de-
scribed only the arteriosclerotic form of intermittent claudication can be
diametrically opposed to those of another author dealing with cases of thrombo-
angiitis obliterans, as to the question of the particular age at which the
process is most apt to occur. In the former, older individuals, in the latter
the young, and predominatingly the Hebrew race will be affected. It is
just this inability to differentiate between the types of cases that has called
forth much academic discussion and many controversial argumentative
publications. |
Causal agents of varied nature such as chemical toxins, static, and even
neurotic influences have received the attention and _ recognition of
commentators on this subject.
According to one set of statistics regarding age (Erb), there were but 3
cases under 30 years; from 30 to 4o, there were g; from 40 to 50 years, 20;
from 50 to 60 years, 27; and from 60 to 70 years, 14 patients. So the largest
number occurred between 40 to 60, the age at which arteriosclerosis is most
pronounced.
Some authors report cases in even young individuals. Higier’ and
Idelsohné cite such cases in young people, the latter also referring to a patient
34 years of age. Some of these were doubtlessly cases of thrombo-angiitis
obliterans. Indeed, Higier concludes that of his 23 cases at least one-half
were under the age of 4o.
1'Dutil and Lamy, Arch. de méd. exper. d’anat. path., 1893, p. 102.
*Laveran, Acad. de Méd. Séance du 27 fév., 1894.
3 Panas, Acad. de Méd. Séance du 5 juin, 1894. Sem. méd., 1894, p. 265.
4 Bing, Beiheft z. med. Klin., 1907, p. 117.
5 Higier, Loc. cit.
6Idelsohn, Deutsch. Ztschr. f. Nervenh., 23, S. 285.
DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 153
The affection occurs more frequently in men than in women, and accord-
ing to Erb there were but 9 cases in females amongst his 168 cases. The
Hebrew race is said to be particularly predisposed, as well as the inhabitants
of East Russia, Poland, the Baltic Provinces and Finland.
Excessive use of tobacco is cited by Erb as one of the most important
causal factors, and he gives the following statistics:
Of 500 males taken from the better classes, who did not present the symp-
toms of intermittent claudication, 4 classes could be distinguished according
to indulgence in tobacco (smoking), as follows:
Non-smokers or almost non-smokers; a second class of moderate smokers (3 to 6 cigars or
10 to 15 cigarettes); a third class (7 to 12 cigars or 15 to 40 cigarettes); and the fourth class
of excessive smokers (40 to 100 cigarettes). Of the 500 males, 44.8 belong to the first class,
31.6 to the second, 17.8 to the third, and 5.8 to the fourth. Of the cases of intermittent
claudication, however, 7 per cent belong to the first class, 14 per cent to the second, 50 per
cent to the third, and 28.6 per cent to the fourth. From these statistics one may conclude
that there is a preponderance of smokers amongst patients suffering from intermittent
claudication.
Idelsohn attached some importance to the existence of flat feet in certain cases. Deter-
mann observed a hereditary tendency to arteriosclerosis in one family, and a neuropathic or
neuro-angiospastic disposition is held by others to play a significant rdle.
A neuropathic habitus is regarded by Oppenheim, Erb and Goldflam, as
of some importance as a contributing etiologic factor. Its frequent incidence
in Hebrews and the coexistence of hereditary psychoses, congenital anomalies
and functional neuroses have given weight to this view. Oppenheim has
suggested that an angiospastic disposition is not uncommonly associated with
intermittent claudication, and further inclined to the hypothesis that a con-
genital narrowness of the arterial system may be in some way related to such
vasomotor inclination.
In another publication Erb concludes that intermittent claudication corresponds in the
age at which it afflicts individuals with the period during which arteriosclerosis is most
apt to occur. A preponderating number of his cases was over 4o years of age. Of 57
cases only 1 was under 30 years; between 30 and 4o there were 8; between 40 and 50 there
were 19; between 50 and 60 there were 20; and over 60 years there were 9g cases.
Higier (whose views have been considered elsewhere) and who undoubtedly had for the
most part cases of thrombo-angiitis obliterans under observation, reported that of 23 cases,
50 per cent were under 40 years of age.
The mere fact that the intermittent claudication described by all of these
authors is extended to include the totality of symptoms ina number of different
pathological processes, and in the case of Erb said to be connected with
arteriosclerosis of the vessels of the lower extremities, and in the case of
Higier to correspond to the disease, thrombo-angiitis obliterans—is sufficient
argument in favor of the view oft expressed by the author, that associated
symptoms common to a number of different lesions and morbid processes
must not be exalted into the equivalent of the morbid processes themselves.
Had some of these observers the opportunity of being convinced of the
absolute pathologic differences that underlie the vascular obturation in the
various cases, their classification would in all probability have been carried
out on a pathologic rather than on a clinical foundation.
The circumstance that the symptoms of intermittent claudication may be
absent in cases of outspoken arterial disease, suggests the importance of a
functional factor—an angiospastic condition—as responsible for the symp-
toms. So Erb concludes that the necessary vasodilatation that normally is a
concomitant of increased function is absent in these cases, and even accepts
the possibility of vasoconstriction in the pathologically changed vessels. So
154 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
also is Bing willing to agree in this assumption basing his view upon the
significance of the ischemia and cyanosis of the skin—phenomena dependent
upon vasomotor action.
We shall discuss these matters critically in another section, and it may
suffice here to say that whilst these views may be correct in part, they lack
foundation insofar as vasoconstriction of the obliterated vessels is incon-
ceivable. However, that an additional moment, namely, a vasomotor
process is active in other vessels, that is, in the normally patent vessels, be
they of the skin or of the subcutaneous tissues, or uninvolved muscular
vessels, is not only possible, but undoubtedly takes place. It occurs in two
types of cases. :
Firstly, in cases in which the symptoms of intermittent claudication are
dependent upon and associated with marked obliteration of some or many of
the large vessels and
Secondly, cases in which the patency of the larger vessels is unimpaired.
CRITICAL SUMMARY
When described as a clinical entity by certain authors (Higier, Idelsohn,
Kahn, Kohler), the symptomatology will be found to correspond to patho-
logic processes of different nature and to be inclusive not only of thrombo-
angiitis obliterans, arteriosclerosis of the vessels of the extremities, but also of
certain vasomotor affections of doubtful nature. Let us summarize the
symptomatic history as described by these and other authors, so as to illus-
trate most vividly the misconceptions that such a grouping will create.
Then only will the fallaciousness and incoherency of a mere clinical associa-
tion of wholly unrelated morbid processes, be well appreciated.
Thus Cassirer’ summarizes the course of intermittent claudication as follows:—
“The malady (intermittent claudication) usually takes a chronic course,
although the severe symptoms may arise rather suddenly. Prodromal
signs are usually to be observed. The symptoms, the paresthesie, pain,
tension, gradually increase to the severity of well marked intermittent
claudication that materially intereferes with occupation.”
In this very first descriptive paragraph, the simultaneous usage of the
appellation, intermittent claudication, both as a noun and as an attribute or
adjective, is illuminating. Then follows:—‘‘If now, an arrest cannot be
brought about through correct therapy and diet, progressive gangrene of the
toes, of the foot or of the leg with the usual severe consequences, is the issue.
Sometimes a stationary period intervenes after gradual improvement; an
adequate collateral circulation may be developed or the arteriosclerosis may
abate,
Such a clinical picture is no more applicable to intermittent claudication
than it is to any of the other striking phenomena of obstructive vascular
disease of the extremities. It corresponds to arteriosclerosis, as well as to
thrombo-angiitis obliterans and other types of thrombotic lesion. By the
same token, and by similar reasoning, rubor or erythromelia, or ischemia,
mere manifestations, may be elevated and exalted into the rank of separate
maladies. For both of these examples, mentioned to illustrate by analogy,
are just as frequent concomitants of obstructive arterial processes as is
“intermittent claudication.”’
1 Cassirer, Loc. ett.
DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 155
The pathognomonic evidence of intermittent claudication is termed
“paroxysmal myasthenia” by Higier.1_ He describes the typical phenomena
just as Erb and Cassirer have, and adds that for diagnostic purposes, the
coincidence of weakness or absence of pulses in the affected territories is an
essential accompaniment of the paroxysmal recurrent dysbasia. He, too,
therefore, accepts an anatomical pathological substratum in the arteries
as the basic lesion.
Indeed, a study of Higier’s article? on “‘ Angiosclerotic Paroxysmal Myas-
thenia (claudication intermittente of Charcot) and Spontaneous Gangrene”
will engender the conviction in any observer conversant with the disease
thrombo-angiitis obliterans, that the latter malady and not intermittent
claudication had come under that author’s observation. Although he recog-
nized the existence of a vascular affection in his cases, a lack of pathological
material is responsible for his view that a neuropathic diathesis plays the most
important réle in the symptomatology. Conceding to functional neurotic
factors a preponderating influence in the clinical manifestations, he neverthe-
less recognizes the existence of arterial disease and secondary nerve degenera-
tion. That his own conception of the interrelationship between arterial
affection and intermittent claudication is discordant and at variance with the
author’s is to be gleaned from his belief that the vascular processes are
secondary in some cases to a primary nerve lesion.
EXPLANATION OF PHENOMENA
Many explanations have been given to account for the symptoms induced
by exercise, most authors invoking a vascular spasm as the most plausible.
Such vasoconstriction would be pathological, since our physiological
concepts presuppose dilatation as a response to excessive demands. Some
assume that an abnormal vasoconstriction or reflex is the reaction of patho-
logical arteries. This view is, however, not altogether satisfactory, firstly
because the diseased vessels in blocked territories (such as thrombo-angiitis
obliterans) must surely have lost their contractile powers, and secondly,
since the more peripheral disturbances in the supplied muscles and other
tissues are then not taken into account as a possible source of origin for special
or abnormal reflexes.
Intermittent Claudication with Healthy Arteries.—Zak has shown? that
identical symptoms are producible after exercise in a normal upper extremity
when the brachial artery is artifically compressed.
If the brachial artery be compressed with the finger with the arm in a horizontal
position, and then repeated opening and closing of the hand be carried out some 30 or more
times, increasing weakness and fatigue set in; on further motion a cramp-like sensation
appears in the hand up to the wrist, and later such pain as to make flexion and extension
impossible. Simultaneously a cadaveric hue of all five fingers develops, which is limited
about at the metacarpal phalangeal level, or extends somewhat up the dorsum of the hand.
Sometimes the pain extends up to the elbow, together with a sensation of fatigue.
When the blood is allowed to enter again, a typical red hyperemia (reactionary) takes
place over the arm and hand, but the pallor of the fingers may persist for 10 or more
seconds, yielding gradually to pale pinkish or rose colored patches.
This experimentally or artificially induced symptom-complex is compar-
able to that of intermittent claudication, and can be demonstrated to occur
1 Higier, H., Zur klinik d. angiosklerotische paroxysmalen Myasthenia, etc., Deutsche
Zeitschr. f. Nervenheilk, 1901, 19, pp. 438-466.
2 Loc. Idem.
3 Zak, Wien. Arch. f. inn. Med., 1921, 2, p. 408.
156 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
with vessels altogether healthy. Explanations for the genesis of the phenom-
ena, other than reflexes emanating from the diseased vessels themselves,
therefore must be resorted to.
Not only can the sensory manifestations of intermittent claudication
be stimulated in the above way, but data seem to indicate that in an ischemic
limb, conditions are at hand which predispose to angiospasm or heightened
vasoconstriction of the small vessels as the result of exertion.
And so it has been observed that whereas the resting limb will react (reactionary hyper-
emia) in a sudden fashion upon the release of an Esmarch bandage or compression of a main
nutrient artery, a considerable delay of this vasodilating response, and a persistence of
vasoconstriction occur, if such an artificially ischemic limb be allowed to exercise. From
this it has been concluded that a state of vasoconstriction or spasm in a multitude of vessels
in the ischemic vascular territory, responding in this heightened way to exercise, may be
responsible for the symptom-complex, intermittent claudication.
Theories as to the Cause of the Angiospasm.— More recent views tend to
the acceptance of a chemical or chemiconeuro reflex explanation. When the
main artery of a limb is compressed or an Esmarch bandage or a tourniquet
is applied, a consequent ischemia or anemia depends not only upon a lack of
blood in the arterioles and capillaries, but also upon arterial constriction.
This is demonstrated by the author as obtaining in thrombo-angiitis obliterans
upon elevation of the affected extremity. The small vessels do not collapse
in their true sense, but contract—possibly a functional response or defense
against reflux or venous blood. Indeed, Hering concludes that venous blood
exercises a vasoconstricting influence on the arterial wall.
The Role of Chemicals in an Anemic Territory—Many other data! discovered by
physiologists have disclosed the influence of chemicals on the contractility of the smaller
blood vessels. Fleisch? showed that weak concentration of carbon dioxid causes vascular
dilatation, whilst strong concentration causes contraction. Dearth of oxygen causes
vasoconstriction. Thus, it has been assumed that the diminution of oxygen may be
responsible for vascular constriction. Not only a direct chemical effect upon the arteries
has been thus revealed, but even an indirect vessel reflex through nervous influences was
demonstrated by the author; for similar contraction was produced in territories only. in
nerve connection with that in which carbon dioxid accumulation has been experimentally
produced.
Therefore, two antagonistic reflexes may be at play in a member, whose
circulation has been put in abeyance but allowed to exercise; firstly, the
normal vascular dilating reflex of a functionating part with normal circulation;
and secondly, a vasoconstricting one, which is especially active in the badly
nourished territory. In the latter accumulation of carbon dioxid or defi-
ciency in oxygen may account for the abnormal reflex. When the constricting
influence overbalances the dilating, the subjective and objective phenomena
of intermittent claudication may be produced. In the presence of increased
carbon dioxid concentration and deficiency in oxygen, a normal vaso-
dilating response is diminished or put in abeyance. This is the theory
advanced by some of the more recent observers.
More recent work (Hopkins*) emphasizes the importance of the develop-
ment of lactic acid in muscle physiology. The prime, if not the sole, cause
of fatigue in muscle is believed to be the accumulation of this acid. Although
the author has been unable to find any investigations of illuminating nature
regarding the direct effects of lactic acid in evoking a vasoconstrictor reflex
action, the general trend of interpretations seems to regard the deficiency of
1 See Capillary Circulation.
2 Fleisch, Pfliigers Arch., 1918, Bd. 171.
3 Hopkins, Harvey Lectures, April 2, 1921 (Lippincott).
FORMS OF GANGRENE 157
oxygen and the accumulation of acid waste products as responsible; lactic acid
would be one of these.
Whether failure to eliminate lactic acid and the consequent change in the
elastic properties of the muscles may be translated into a direct response in
sensory nerves, without implication of vasomotor mechanism, is another
hypothesis worthy of consideration. It would presuppose a direct analogy
between the cramp-like pain of excessive fatigue in healthy, well nourished
tissues, and the symptoms of intermittent claudication, both explicable in the
light of the above theory.
DIFFERENTIAL DIAGNOSIS
1. Myasthenia Gravis Pseudoparalytica.—In this affection, too, we also
note an intermittent disturbance of motor function that returns with each and
every exertion, but is distributed over wide muscle territory, is characterized
by a typical electrical reaction, and is unaccompanied by sensory or vasomotor
phenomena.
2. Dysbasia Neurasthenica.—This type is somewhat more difficult to
diagnosticate particularly from intermittent claudication of the spinal cord.
Charcot cites an example of a lieutenant who could walk fairly well in the normal
march, but at a faster pace would become unsteady after 20 to 30 minutes, his right limb
particularly becoming heavy. With this there was marked numbness of the sole of the foot;
all of the symptoms disappeared after rest. The patient, who was markedly neuropathic,
was neither arteriosclerotic, leutic, nor diabetic. Objectively the pulses were negative and
vasomotor phenomena absent. ‘The knee reflexes were increased, and there was a right
sided ankle clonus. Because of the marked neurasthenia, an affection of the spinal cord
was believed to be absent. ‘This diagnosis was confirmed 7 years later by Bourgeois, who
observed that the same patient was still unable to carry on his activities.
3. Sciatica.—Here we must consider those relatively mild cases of sciatica
in which paroxysmal attacks of pain are evoked only by motion, and call forth
restriction of function. ‘The pain in these patients does not abate as quickly
as in intermittent claudication, and furthermore during the free intervals,
pressure on Walleix’s point should provoke the latent pain.
4. Akinesia Algera.—In this psychasthenic affection pain is aroused
immediately upon the beginning of motion, and can occur not only in the
extremities, but also in the back, in the head and elsewhere.
5. Tarsalgia and Metatarsalgia.—Here too pain follows short periods of
locomotion and is localized to the tarsus and metatarsus. ‘The arteries are
intact and vasomotor phenomena are absent. There is usually a circum-
scribed area of tenderness.
6. Certain Rare Cases of Neuritis —Cases have been described by Hallion
and Charcot! as examples of neuritis, but the histories are not convincing,
since the evidences of arterial involvement are sufficient to make it impossible
to exclude these as a factor in the symptomatology.
CHAPTER XXVII
FORMS OF GANGRENE
One of the oldest classifications and one which has but little value since
it throws no light upon the etiology, is the subdivision into dry and moist
‘gangrene. Some authors add another variety, microbic gangrene.
1 Hallion and J. B. Charcot, Arch. de Neurol., Feb. 28, 1895, X XIX, p. 81.
158 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Dry gangrene ensues when the arterial circulation is suddenly impeded
while the venous flow continues, the tissues being drained of their fluid
through the veins. Mummification follows and the part becomes desiccated.
or dry by reason of loss of water. - In man it is usually the peripheral parts
that are affected. Perhaps mummification is a more descriptive word.
This variety is not infrequently met with in the aged, when, by virtue of the
slow process of athero- or arteriosclerosis, the lumina of the arteries become
occluded, the blood supply diminishes progressively, and finally gangrene of a
distal part occurs. Although the words senile and dry gangrene have at times
been used synonymously, this restricted application of the term is incorrect,
since dry gangrene takes place in many other conditions.
After preliminary blanching, paresthesia, coldness and loss of sensation,
cyanosis usually follows. The skin gradually becomes dry, then brownish or
black, the whole part being converted into a shriveled, hard, blackish mass.
The changes in color are ascribed to the disintegration of hemoglobin with
the elaboration of black by-products.
Moist Gangrene-—Moist gangrene results when there is an impediment
both to the influx of arterial blood and to the venous return, so that the
affected part retains sufficient fluid to leave the dead tissues moist. Com-
plete obstruction of the chief veins of a part, without occlusion of the
arteries, may also lead to gangrene, although this is of rare occurrence.
The condition of the circulation in the limb before the arrest of arterial cir-
culation takes place, may be the determining factor in the production of
either the moist or dry type of gangrene. Intense edema associated with
nephritis or impaired heart action usually favors the development of moist
gangrene, as in the embolic or thrombotic gangrene, complicating pneumonia
or other infections.
Because of the putrefactive condition characteristic of this process,
putrid gangrene would be an apt designation. The sequence of events is first
degeneration of the blood with the appearance of dirty red patches and
zones. Then the connective tissue and muscles undergo change, whilst
epithelium, tendons, elastic fibers, cartilage, and bone are most resistant.
The parts become doughy, edematous, the epidermis is separated off in
blebs; there may be gas formation (NH3, SHe, or S (NH4)s), crepitation and
foul odor. Leucin, tyrosin, triple phosphates, blackish pigment and fat
crystals are to be found in the fluids. In addition to putrefactive organisms,
streptococci often develop and may enter the blood stream. Bacillus coli
may also be associated, and the bacillus proteus vulgaris may grow in
symbiosis with either of the above and enhance their virulence.
The general clinical picture is an expression of the absorption of toxins
(especially of proteus) with or without the effects of streptococcus or bacillus
coli bacteriemia.
Characteristic for moist gangrene are the following clinical stages:—
first, a stage of pallor which may pass so rapidly as to be overlooked; second,
a stage of extensive ecchymosis; third, a stage of subepidermal exudation with
reddish discoloration of the part; and fourth, a stage of disintegration.
Although these stages are not always clearly defined, they may be recog-
nized in a fairly large percentage of the cases. The initial pallor may be
evanescent; it may be accompanied with paresthesia but more regularly
with frigidity and anesthesia. Soon a bluish and purplish mottling that
rapidly spreads over the affected part becomes the striking objective mani-
festation, being succeeded by the exudation of bloody serum under the epi-
dermis. When the latter is lifted off, larger or smaller bullae are formed
PEATE
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Early Stage of Moist Gangrene, Showing Bulla. (Buerger in Ochsner’s
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FORMS OF GANGRENE 159
(Plate I) many of which attain considerable size. When the epidermis has
been separated and no considerable fluid is present, the angry red cutis vera
shines through (Plate II). Higher up, the limb is usually cold for a variable
distance, often intensely edematous and brawny, mottled here and there by
areas of purplish discoloration (ecchymosis). Later the intense red dis-
appears, as the disintegrating cutis vera and the gray green epidermis com-
bine to form a peculiar ashen purplish hue (Plate III). The serum from the
bullae now makes its escape in many places, the separated epidermis lying in
folds over it, here and there torn off, exposing the weeping derma. With the
advent of putrefaction, an intensely foul odor develops. Secondary pyogenic
infection complicated by lymphangitis and cellulitis above the site of gang-
rene may supervene and be associated with toxic general symptoms.
Microbic gangrene has been termed acute microbic gangrene, fulminating
gangrene, emphysematous gangrene and traumatic spreading gangrene.
Here a virulent infection usually with a gas producing micro-organism is
responsible for the mortifying process, injury usually preceding the infection.
If descriptions of this type be taken from older authors, a rather confused
clinical picture will be obtained. Latterly, our notions have been consider-
ably clarified since advances have been made in bacteriologic recognition
of varying types. Special attention has been focussed on the gas-bacillus
forms of infection, which will be discussed at length in anotherchapter. A
number of different micro-organisms have been isolated and identified as
the causative agents in this severe form of infectious and gangrenous process.
There is still another “‘infectious” or microbic type of gangrene in which
gas formation is absent and in which the streptococcus can often be isolated
in pure culture. A more comprehensive description of this variety will also
be given elsewhere.
Course and Termination.—Gangrene is very frequently self-limiting, a
definite line, separating the dead and the living tissue known as the line of
demarcation, being ultimately formed. At this line granulation tissue is
developed, as the result of a reactive inflammatory process. By virtue of the
- action of the emigrated leukocytes, certain ferments are elaborated which
bring about the separation of the dead from the healthy tissue. Soft parts
yield relatively soon to the sequestrating effects of the inflammatory process,
whilst bone is very much resistant. When a considerable part of a
member is thus separated off, so-called spontaneous amputation results.
When the area of necrosis or mortification is infected, the process of sepa-
ration is accomplished in a different manner. ‘The usual phenomena of sup-
purative inflammation of greater or lesser virulence are manifest, the products
of inflammation being instrumental in causing disintegration of the part at its
junction with the living, but may also spread in the healthy tissues requiring
surgical intervention. If sufficiently severe, a rapidly ascending lymphangi-
tis may occur, general infection, bacteriemia and toxemia. In these cases the
end-result will depend upon the virulence of infection, and of the possibility
of its control.
160 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
CHAPTER XXVIII
CLASSIFICATION OF GANGRENE
From the clinical standpoint, a pathological and etiological grouping is most
satisfactory. It must be remembered, however, that an absolute classifica-
tion is impossible, both because case may simultaneously belong to several
groups, and because the causative factor in certain instances is not well
understood.
Three large groups may be recognized: first, gangrene due to external or
direct causes, such as bring about immediate death of tissue; second, gangrene
due to internal or indirect causes, which act by impeding or arresting the
circulation of blood in the larger vascular channels; and third, neuropathic
gangrene in which the cause is an abnormal, pathological, functioning vaso-
motor nervous mechanism, or resides in the vegetative nerves.
A. External or Direct Causes.—(1) Mechanical Causes in which death or
necrosis is the direct result of the physical injury. Tissues may become
completely separated in continuity and thus die; or, necrose because of the
disorganizing effect of a crushing force. Continuous pressure upon bony
prominences, particularly in the emaciated, produces gangrene or necrosis
to which the name decubitus has been given. Compression by a tight bandage,
torsion acting upon a portion of the intestine, or strangulation at the neck of a
hernial sac—all are mechanical causes of gangrene.
2. Thermic Causes, intense heat or cold, may cause death of tissue in a very
short time, either by the direct coagulating or carbonizing effect, or indirectly
by the formation of thrombi in the vessels, or by paralytic action on the
vessels of supply.
3. Chemical Causes include the action of a fairly large number of sub-
stances. Some authors include some of the bacterial toxins, although many
of these would not properly belong here, if their action were understood. The
action of tissue juices in the normal secretions and excretions may, however
be included here, since they produce digestion necrosis.
The most common chemical substances leading to gangrene are strong
acids, hydrochloric, nitric, sulphuric, acetic, trichloracetic; also carbolic
acid and lysol when applied as wet dressings. ‘The secretions and excretions
that bring about necrosis through their specific ferments are gastric juice
escaping through a gastric fistula, extravasated urine, and the feces.
4. Microbic Agents, certain virulent bacteria, particularly in the presence
of intense traumatism, may bring about a combination of infection and
gangrene often called microbic gangrene.
The toxins produced in bacterial inflammation are also regarded as being
responsible for destruction of tissue, or even for gangrene.
B. Internal or Indirect Causes.—Injury of the main nutrient vessels may
be brought about by mechanical force in several ways, as when a limb is
crushed or receives an intensive traunia, when a large vessel is pierced by a
gun-shot, when pressure effects are produced by an aneurysm or a malignant
tumor, then the circulation may be impaired indirectly, through interference
with the continuity or patency of the chief nutrient vessels. Ligation of a
vessel, such as the spermatic artery during an operation upon the testicle, or
for hernia, or ligation of a renal or middle colic artery, may lead to necrosis and
gangrene. Ligation of the internal carotid artery is followed by necroses of the
CLASSIFICATION OF GANGRENE 161
brain, in almost 50 per cent of the cases. In the case of the extremities, liga-
tion of one of the main arteries may be followed by gangrene if adequate
collateral circulation does not become established. ‘The general condition of
the patient, the heart action, the presence of complicating diseases (such as
anemia, diabetes, infections and atherosclerosis), of inflammatory conditions,
exudates or hematomata in the affected limb, and tight bandages—are all
contributary causes that hinder the establishment of collateral circulation.
Diseases of the blood vessels including first athero- or arteriosclerosis (senile,
presenile, diabetic, with or without thrombosis and embolism); second
thrombo-angiitis obliterans; and, third, endarteritis (including syphilitic endar-
teritis); and fourth, acute arteritis and miscellaneous affections.
Thrombosis or Embolism.—Complete obliteration of the lumina of either
normal or diseased vessels through thrombi or emboli may lead to gangrene.
When these occur in diseased vessels, they may be regarded as compli-
cations of the primary vascular lesion. Therefore only such obturation in
vessels relatively patent will be discussed under this caption.
_Emboli and thrombi may be composed of red clot, mixed clot, bacteria,
purulent or even tumor material. For practical purposes we need consider
merely clots; other embolic material more frequently evokes small areas
of necrosis, suppuration or aneurysm, than true gangrene.
Embolism most frequently affects the femoral or popliteal artery and may
then result in gangrene of the foot and leg. More rarely the brachial and
axillary arteries are involved. It occurs most commonly in the course of
severe infectious diseases, or as a complication after the disease has subsided,
also with valvular heart lesions, and after abdominal or pelvic (particularly
gynecological) operations. In typhoid fever, pneumonia and influenza,
sudden blockage of the popliteal or femoral artery may occur, or there may be
extensive thrombosis of the femoral vein. Although it is not generally
understood why an embolus in the popliteal artery should cause extensive
gangrene, when there are adequate avenues of blood supply through collaterals,
the explanation is often to be found in the fact that extensive red thrombosis
is soon superadded above and below the site of the orignal clot, red and mixed
thrombi extending in both directions with great rapidity into many of the
smaller vascular branches and tributaries, preventing in this way the estab-
lishment of a subsidiary collateral circulation.
C. Neuropathic Gangrene.—In this group may, be placed all those cases
in which the arteries and veins are organically intact, or have suffered
no alteration of their patency, and in which, in the present state of our
knowledge, we assume that a neurogenic causal agency is responsible.
The following symptom-complexes, Raynaud’s disease, erythromelalgia,
acroparesthesia, multiple neurotic gangrene, and chronic acro-asphyxia be-
long here. It has been generally accepted that in some of these, the vascular
disturbances and arrest of circulation may be accounted for on the theory of a
spastic condition of the nutrient vessels, but in others, the true mechanism
still remains unrecognized.
The various clinical forms of gangrene will be grouped and described
according to the following classification:
I. Gangrene due to external or direct causes, viz.:
A. Trauma.
B. Thermal influences.
C. Chemical causes.
D.. Microbic action.
11
162 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
II. Gangrene due to indirect or internal causes, including
A. Injury to main nutrient vessel of a part.
B. Diseases of blood vessels.
1. Arteriosclerosis.
2. Thrombo-angiitis obliterans.
3. Endarteritis (luetic).
4. Miscellaneous arterial affections.
C. Thrombosis and embolism.
III. Neuropathic gangrene.
CHAPTER XXIX
CLINICAL EXAMINATION IN GANGRENE
Examination in Prodromal Stages.—In order to understand and give the
proper dignity to all of those clinical manifestations that constitute the
prodromal signs of symptom-complexes that eventuate in gangrene, it is
wise to follow a certain scheme of procedure in the examination of all cases
in which we suspect impaired circulation. When we are confronted
with cases of vasomotor disturbance, of trophic disorder, such as ulcers
and atrophy, when the patient complains of pain which arouses the sus-
picion of intermittent claudication, as well as in the presence of true gangrene
of the lower extremities, the following method of the author will be found
of value in diagnosis. It includes the investigation of the following points:
First, the general appearance of the limb in the horizontal position; second,
in the dependent position; third, the presence or absence of ischemia in
the elevated position; fourth, the estimation of the angle of circulatory
sufficiency; fifth, pulsation in the palpable vessels, iliac, femoral, popliteal,
posterior tibial, anterior tibial and dorsalis pedis in the case of the lower
extremities, radial, ulnar, brachial and axillary in the upper extremities; and,
sixth, the occurrence of induced, reactionary rubor or erythromelia. ‘The
value of nerve status need hardly be emphasized.
1. General A ppearance of the Limb.—Any departure from the normal should
be noticed, such as the presence of fissures, ulcers, perforating ulcers, bullae,
ecchymoses, impaired nail growth, gangrenous areas, distinct gangrene,
signs of infection or lymphangitis or venous thrombosis. Evidences of
malnutrition, such as atrophy, exceptional prominence of the bony landmarks
and extensor tendons, conservation or effacement of the normal irregularities
of contour through edema or through thickening of the skin and subcutaneous
tissues, are features of importance. Variations from the normal color—partic-
ularly marked pallor in the horizontal position, a play of color over the foot,
even in the horizontal position; cyanosis, increased redness—all these, are
manifestations of either impaired circulation or vasomotor disturbance.
2. Rubor or Erythromelia.—With the foot in the pendent position and in
the absence of inflammation, a red flush involving the toes and dorsum, as
well as sole of the foot, extending upward for a variable distance, rarely
farther than the ankle, is a phenomenon that is characteristic of many cases
and many types of reduced circulation due to vascular obturation. Thisisa
CLINICAL EXAMINATION IN GANGRENE 163
condition of rubor or erythromelia: (Gr. erythros-red, melia- limb). It is
brought about by a compensatory dilatation of the superficial capillaries, and
is most characteristic of the disease, thrombo-angiitis obliterans, although
also found in other arterial affections attended with closure of larger vessels.
It is frequently present in arteriosclerotic and diabetic cases as well. It
seems to be an effort on the part of nature to make up for the impairment of
circulation by virtue of dilatation and engorgement of the superficial capil-
laries. Although more striking in the pendent position, the rubor may also
be present in the horizontal position, and when continuously in evidence,
may be termed chronic rubor, chronic erythromelia, in contra-distinction to the
reactionary rubor that may be induced by depressing the limb after previous
elevation. These terms, erythromelia, chronic rubor, reactionary rubor,
induced rubor, angle of circulatory sufficiency, as well as others employed
here, have been adopted by the author in an attempt to facilitate expression
of various conditions of circulation, and if adopted, must be carefully applied
in the sense here suggested.
3. Ischemia or Blanching.—This usually sets in rapidly when the affected
limb is elevated, whenever mechanical interference with the circulation is
present. The extent of the blanching and the rapidity with which it
appears, are both valuable aids in the estimation of the amount of obstruc-
tive arterial disease. When the affected limb is cold, the tips of the toes
may remain slightly blue or cyanotic. Should the blanching be slow in
appearing, or very hard to determine, pressure upon the tips of the toes
after the limb has been elevated for some time will demonstrate whether the
part has become depleted of blood or not. Before elevation, pressure over
the toes will cause an anemic area in which the color returns tardily
(Expression test). Compression of the toes of the elevated foot in normal
cases will reveal the presence of sufficient bright arterial blood (rarely
slightly cyanotic), whilst a varying degree of ischemia, with or without
marked cyanosis will accompany obliterated or obstructed arteries.
4. The Angle of Circulatory Sufficiency (Fig. 43).—The estimation of this
angle is based on the supposition that the normal limb, when elevated so as
to be perpendicular to the horizontal plane, that is 180°, still retains most of
its color. When the circulatory mechanism is defective, and the limb is
elevated to the vertical, a variable degree of blanching of the foot occurs. If
the leg is then gradually depressed, the angle at which a reddish hue returns
(angle of circulatory sufficiency) will be found to vary considerably. In some
cases it will be necessary to depress the limb to the horizontal before evidences
of return circulation are manifest. The angle of circulatory sufficiency would
then be go°. If the reestablishment of visible circulation in the skin neces-
sitates depression below the horizontal, the angle will be correspondingly
less than 90°. In many cases of arterial disease, the estimation of this angle
is a valuable adjuvant, not only in the recognition of the extent of the circu-
latory disturbance, but also in prognosis.
When the deficiency in color of the foot appears but slight or doubtful, it
is well to examine the sole of the foot flexed at right angles with the patient in
the prone position. The difference in the color of the two feet may thus
become more apparent. When infection is present, tenderness over the
plantar region will often be elicited, and indicate deep necrosis or suppuration
complicating a gangrenous digit, even though no superficial sign thereof—
such as redness—be in evidence.
1 Not to be confused with ‘‘ Erythromelia”’ a term used by Pick to designate an atrophic
cutaneous malady.
164 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Vasomotor symptoms may interfere with the estimation of the angle of
circulatory sufficiency. Sometimes the blanching of the foot together with
the cyanosis induced after elevation may remain so long, that the angle can-
not be determined. In these cases it is not the obstruction of the vessels,
but the special vasomotor irritability that is responsible for the lack of usual!
reactive hyperemic response; for, neither is it constant, nor does it regularly
interfere with the test. Such vasoconstriction is also not always present to
the same degree. It is, therefore, incumbent upon us to apply the test on
several occasions, to preclude the fallacies that vasomotor lability may
occasion.
ee
90°
Fic. 43.—Method of determining the angle of circulatory sufficiency.
By a comparison of the circulation of both lower limbs, valuable informa-
tion can be gleaned as to the degree of involvement of the arteries in each,
also in the corroboration of a presumptive diagnosis of obliterated arteries in
the limb that gives no subjective symptoms.
So it may be necessary to depress one limb from 180 to go°® (horizontal)
in order to effect a return of color into the toes, whilst in the other, a complete
blush occurs at 135° (45° more elevated). The circulation may show visible
advance up to a certain point (such as the base of the toes) at one angle, and
still greater pendency may be required to promote a flux into the toes. These
or even more of the foot may remain cadaveric in hue until the horizontal or
possibly a lower position is reached.
5. Absence of Pulsation as an Indication of Arterial Occlusion.—We should
be able to feel the femoral, posterior tibial, popliteal, and dorsalis pedis
arteries, pulsating in almost all individuals who possess patent arteries.
In rare cases the dorsalis pedis may be aberrant in its course, and there-
CLINICAL EXAMINATION IN GANGRENE 165
fore not palpable in its usual situation, or, neither the dorsalis pedis nor
popliteal may be accessible to the touch because of the stoutness of the
patient.
To palpate the popliteal satisfactorily, the patient is placed on his abdomen,
lying prone. ‘The leg is held at right angle, that is, vertical, the patient being
asked to relax the hamstring muscles. The artery is then sought in the upper
half of the popliteal space, just outside of the semimembranosus and
semitendinosus tendons (Fig. 42), the fingers being pressed downward against
the femur. In the upper extremities, the radial, ulnar and brachial and
axillary arteries should be examined for pulsation. !
The absence of pulsation is as arule, an indication of occlusion at the point
palpated, although in some instances dissections have shown that the site of
obliteration 1s somewhat higher up.
6. Reactionary Hyperemia, Rubor or Reactionary Erythromelia.—By this
term we mean an induced rubor that manifests itself in the dependent position
of the foot, after it has been previously elevated to the vertical. It is a physio-
logical phenomenon, that ischemia or blanching of a limb artificially produced
by an Esmarch or Martin bandage, will be followed by sudden dilatation of the
capillaries of the peripheral parts, when the circulation is allowed to return.
So, also blanching will occur in a leg whose larger arteries are occluded, on mere
elevation from 60 to go° above the horizontal, without the use of any artificial
means. When such a blanched limb is then depressed to the pendent posi-
tion, a similar induced or reactionary rubor will become manifest. This well-
known manifestation may be invoked in the examination of cases in which
impaired circulation due to arterial occlusion is suspected. It will be found
particularly useful in cases of thrombo-angiitis obliterans, although also
demonstrable in other cases of organic vascular disease. In early cases, it is
a particularly valuable sign, for it may be present long before the chronic
condition of rubor or erythromelia develops.
It is a manifestation analogous to the hyperemia (Bier) induced by the
application of an Esmarch or similar bandage or tourniquet to a limb, imme-
diately after the arterial compression is removed.
In a sense all chronic rubor of the pendent position is a reactionary rubor,
when it accompanies obstructive arterial disease. For, is there not always
a relative ischemia of the peripheral parts; and is not this brought about in
varying degrees by every elevation of the limb, even if only to the horizontal?
Indeed, it will be elsewhere shown (page 238) that in cases of marked
impairment of the peripheral circulation, the foot is already blanched
in the horizontal position, or even when flexed slightly below this level.
Tests for Circulation.—It is indeed desirable to possess a sign, criterion or
symptom that would afford a measure of the circulatory intensity of the leg,
above the usually gangrenous parts of the foot. Search has been made for
single phenomena that might fulfill this desideratum and a number of tests
have been evolved. Among these may be mentioned those of Moskowicz,
Matas and the author.
We shall refer later to the limitations of such evaluations and to the impor-
tance of that incommensurable and inestimable factor—the excessive demands
for healing. For, when investigations of the degree of force and extent of
collateral circulations are practically applied, they have been regarded by many
authors as especially valuable in determining the lower safe limit for amputa-
tion. In our own experience, all such tests are more reliable in fore-telling
1 Some of the anomalies of the radial and ulnar arteries are mentioned in Chap. II.
166 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
the probabilities of the healing of the trophic disorders, or in fore-casting
the advent of gangrene, than in setting indications for the site of operation.
The Moskowicz Test.\—This depends on the phenomenon that soon after
removing an elastic bandage that has set the circulation of a limb in abeyance,
an active hyperemia replaces the cadaveric hue. ‘This striking rubor begins at
and is sharply demarcated above, at the level of the constrictor. Thence it
extends rapidly, down the extremity (peripherally) till it reaches the tips of the
toes or fingers.
After holding the extremity high for a short time (and this concerns
especially the lower) an elastic bandage is firmly applied as far up as pos-
sible,and allowed to remain for 5 minutes. After removal of the constrictor, a
prompt hyperemic blush is to be expected, when the circulation is adequate.
When vascular obturation exists, the reaction is weaker and the extension of
the blush towards the distal parts is slow. Often ischemic islands in the
skin seem to tarry for some time, and in some instances a marmorated appear-
ance will be prolonged. The hyperemia may progress rapidly to acertain
level where its further spread is arrested or allowed to descend very slowly.
In comparison with the less affected normal limb, the persistence of periph-
eral pallor in the more diseased extremity will be found most striking.
Moskowicz is of the opinion that the lower boundary of the hyperemic zone
or point just above this, marks also the level of the obturation of the arteries.
Reasoning thus, he sets the indications for the proper niveau for operation
by selecting a level within the area of reactionary rubor—namely a short
distance above its peripheral limitations.
In our own experience this test is unreliable. Indeed, certain dogmatic
and arbitrary rules that we have adopted as the result of a multitude of
clinical observations are to be followed, in the selection of the level for ampu-
tation, rather than teachings such as the above.
The Matas Test.z—This is a modification of the Moskowicz test for
estimating circulatory sufficiency in cases of aneurysm. Although the pur-
pose and technic of the Matas method are somewhat different from that of
the latter, they are similar in utilizing the hyperemic blush following arti-
ficial ischemia to determine the limits of adequate circulation. The principle
according to which this test is employed is based on the fact that whilst the
main arterial trunk is compressed in close proximity to the lesion (wound,
aneurysm, tumor) sufficiently to arrest pedal pulses or fill an aneurysm, the
collateral distribution is allowed to give evidence of its extent and magnitude.
This segregation of the visible signs of collateral from those of the normal
circulation is obtainable by excluding the main artery as a factor through com-
pression, simultaneously with the abolishment of all impediments to arterial
flow through other channels.
An elastic bandage, after preliminary elevation, is applied from the digits
to the level of the lesion, usually the aneurysm, after which a compressor is
applied to the artery above the aneurysm. ‘The elastic bandage remains in
situ for 10 minutes in the young, 5 to 6 minutes in the aged, and is then
removed, whilst the main artery is completely occluded. Immediately upon
removal of the bandage, a hyperemic blush descends downward rapidly,
progresses onward to variable extent, in proportion to the development of the
collateral circulation. More often, the hyperemia may stop at a distance of 5
or 6 inches from the compressor, or about 14 distance down the limb, then
1 Moskowicz, L., Mitt. d. Grenzgeb. d. Med. u. Chir., Vol. XVII, p. 216.
2 Matas, Jour. Am. Med. Assn., 1914, p. 1441.
CLINICAL EXAMINATION IN GANGRENE 167
continuing in a subdued color, traveling towards the periphery, but the
extreme end of the limb, foot, or hand retains a cadaveric waxy pallor for
several seconds or even 40 minutes, according to the development of
collaterals. ‘Then this waxy color gives way to a pale living color. Where
collaterals are well developed, the hyperemic wave spreads in a few seconds,
as if the artery had never been compressed.
Matas in 1914 had used this test in 26 cases of aneurysm and other lesions, and the
conclusions furnished by this test have been invariably confirmed by operative demonstra-
tions and results. He used this test therapeutically in several cases, where the reaction
was long delayed, for the purpose of increasing the collateral circulation, as follows. He
postponed operations for days or weeks, in order to develop collateral circulation by system-
atic compression of the main arteries, conjointly with dry hot air, baths and massage.
Whilst the Matas and Moskowicz tests may have a sphere of applicability
when a limited arterial territory suffers obturation, they are not very reliable
in peripheral vascular disease. In thrombo-angiitis obliterans or marked
arteriosclerotic disease of the vessels, certain elements of these tests would
need modification. ‘The application of an Esmarch bandage is not to be
recommended in view of the deleterious effects of such intensive ischemia,
and the direct mechanical lesions that mightensue. Furthermore, the periph-
eral pulses are not usually palpable, and therefore no guidance. It has
been the author’s custom to employ a method based on hydrostatic prin-
ciples which has been previously described. In view of the extensive vascular
obliteration that accompanies thrombo-angiitis obliterans, it is noteworthy
that no great differences can be elicited at times, between the color reaction
that follows the depression of the limb after prolonged elevation (gravity
depletion), and that resulting after separate compression of a main artery.
This is comprehensible when we consider that the very main vessel compressed
may have become a negligible factor in the delivery of blood even through
collaterals; and when we take into consideration the multitude of occluded
branches emanating from this trunk. In other words, such main arteries
are not essential to complete the collateral circuit and the latter depends on
even more remote and deeper channels and anastomoses.
Allan and Matas have also experimented with the occlusion of the main artery by flat
and pliable aluminum bands. Such a band is applied about the vessel supplying the part
to be tested. If the collateral circulation is adequate, the band is left in place, and becomes
encysted in the tissues. If gangrene threatens, the band is made more lax, so as to facilitate
a better collateral circulation. The bands are made long and narrow so as to pass through
aneurysm needles. After such a band encircles the vessel, it is tightened with the fingers
until the pulse is obliterated distal to it.
Value of Tests for Circulation in Thrombo-angittis Obliterans.—The
Moskowicz test according to some authors is of value in determining the safe
point to amputate in presenile and in senile gangrene. Matas cites examples
in which he was successful in recognizing that amputation could be performed
below the knee, because the hyperemic blush extended well below this level,
thus indicating that a flap would be viable.
The author’s experience in cases of thrombo-angiitis obliterans has con-
vinced him that, although the test may demonstrate to what extent a
collateral circulation has become established or even how far a compensatory
hyperemic state has been developed, it does not, with any degree of precision
or reliability, denote where amputation should be carried out. This is true
because it cannot correctly gauge the likelihood of healing after an incision
is made, even though it demonstrates the centrifugal limit of collateral skin
circulation. For, it must be remembered, that not only is it necessary to
168 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
have blood enter the most peripheral parts after amputation, but nature
makes excessive demands for purposes of healing. The exigencies evoked
by the new conditions may be incommensurate with, and far exceed those
hydrostatic factors that are sufficient to give a red color to the part. Not
infrequently has gangrene of the flaps and other tissues at the point of
ablation been observed when the Moskowicz test indicated ample collateral
paths. Even when healing of the greater part of the wound does occur, an
ulcer may remain at the point of drainage. ‘This is then wont to enlarge and
gives rise to gangrene or phlegmon formation.
In short, experience in thrombo-angiitis teaches that an indication for
amputation below the knee or below the level of the Gritti-Stokes method, set
according to tests, is of theoretical rather than of practical value. In arterio-
sclerosis amputation below the knee is also unreliable, although in rare cases
it may be attended with good results.
Henle-Coenen Method.—Almost simultaneously Henle, Lexer, v. Frisch
and Coenen recorded an observation which they regard of value in estimating
the degree of collateral circulation. It was applied by these authors to the
treatment of aneurysms by ligation. In their judgment, indication for ligation
would depend upon the positive result of the test. If a larger artery be
sectioned transversely, not only the central but the peripheral stump should
bleed copiously in a strong stream (Positive test).
It is based on the fact that in many arterial territories (external carotid,
arteries of the hand and foot), the normal collateral circulation suffices to
give a copious reflux when the centrifugal current is interrupted at any point.
Tests for the Patency of the Veins.—Whereas it is a relatively easy matter
to determine with a fair degree of certainty whether the patient possesses
patent superficial veins, the question as to the involvement of the deep veins is
a most puzzling one. Thrombotic lesions in the palpable veins are des-
cribed in detail in Chap. LVIII. In these latter cases one can watch the
recurrences of thrombophlebitis throughout the thigh and leg and find it
extending even to the sole of the foot. And, when personal observations
are not at hand, anamnestic data may be forthcoming.
What signs and symptoms are of value in indicating the patency or
occlusion of the deep veins? It is here that we have to concede the inade-
quacy of our clinical methods. In looking over the histories of the cases
in which amputation revealed marked obliteration of the deep veins, only
in very few was there mention of marked cyanosis in the pendent position
of the limb. Whilst an unusual intensity and rapid advent of cyanosis after
rubor may be a serviceable sign in this connection, it is not absolutely depend-
able since vasomotor agencies play an important réle in the determination
of color phenomena. Inadequate vis 4 tergo and constricted arterioles in a
pendent limb may suffice to give cyanosis without obstructive lesions of
the veins.
CHAP TEREX XS
TRAUMATIC GANGRENE
Traumatic gangrene results from the direct action of a mechanical force.
A rapid and direct disorganization of tissue may follow mechanical insults
such as contusion, crushing, machine injury, injury through blunt force, and
TRAUMATIC GANGRENE 169
pressure. The latter force acts in the main by interference with circulation.
Tissue which has become totally separated must needs become necrotic or
gangrenous, if the conditions for healing and restitution of the circulation in
the wound are not favorable. Such adverse conditons arise when severe
traumata bring about crushing and mangling of tissue, extravasations of blood
and bacterialinfection. Only inthecase of transplantation by operation under
strictest aseptic conditions, are the conditions favorable for restitution and
growth of the transplant.
A blunt crushing force may also lead to gangrene of tissue, partly by reason
of the disintegrating and destructive action of the force itself, and partly
through thrombosis in larger vessels. The severe traumata inflicted in
various accidents by machinery, which produce extensive laceration of tissues,
may be followed by gangrene of a part or the whole of an extremity.
We may distinguish a number of varieties. ‘Through separation of con-
tinuity a mass of tissue may be detached and become necrotic, its attachment
and healing being prevented by hemorrhage and infection, or through dis-
placement of tissue elements (Décollement) and distortion, a blunt force
leading to the formation of a subcutaneous pocket. Blood then fills this
space; thrombosis of the torn and squeezed vessels takes place, and gangrene
and necrosis are expedited. Or, ligations of vessels may lead to a similar
issue, whenever the chances for the establishment of collateral circulation are
slight.
Observations on the results of traumata during the Great War have
awakened interest in the indirect effects of trauma. Through the stimulation
of the vessel nerves, contraction and later dilatation of the smaller blood
vessels occurs. Intense trauma may evoke dilatation and finally complete
vascular paresis with stasis and diapedesis. An ischemic necrosis of muscle
is described as due rather to the implication of nerves, spastic contraction of
vessels, dilatation and stasis, than asthe result of direct forces.
Finally, injuries leading to rupture and consequent ligation of larger
vessels are not infrequently complicated by gangrene. Such an eventuality
may be expected, when extensive hemorrhagic extravasations are present.
Symptoms. Manifestations of threatened gangrene of an extremity begin
with the picture of ischemia or venous stasis, coldness, and absence of pul-
sations in the usually palpable arteries. After initial paresthesiz, or dull
pain, complete absence of sensation and motor paralysis set in. Intense pain
and tenderness, however, may persist above the area of gangrene. Within
forty-eight hours, the evidences of beginning dry or moist gangrene make their
appearance.
It would be possible, although not fruitful, to make groupings according
to the nature of the injury, its extent, whether the main arteries of a limb
are implicated, as to whether the issue be gangrene of part or whole of a
member, or merely limited necroses.
The following classification although not all-embracing has some clinical
value.
1. Gangrene of limited extent involving larger or smaller areas of the
integument, possibly attended with injuries (fractures or dislocations) of
deeper parts.
2. Gangrene of part of an extremity, usually the lower, due to direct
compressing forces with or without complicating thrombosis of the, main
artery; and
3. Gangrene of almost the whole of an extremity (usually the lower).
The most striking and characteristic examples of this variety are those
170 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
severe injuries resulting from accidental entombment, so frequently observed
during the Great War.
1. Gangrene of limited extent requires no detailed description. When- ~
ever a limb is subjected to such compressive or percussive force that the
vitality of the tissues is compromised, local necrosis ensues, When such
devitalization with subsequent sequestration of slough is of limited extent,
we usually speak of a “decubitus.” This may occur after the application
of too tight bandages, or after even slighter insults in those in whom neuro-
trophic and functional derangements already exist. More severe injuries,
such as compressing, sliding and crushing forces against the extremities may
result in more extensive death of tissue. These are seen in automobile,
railroad and “‘shoot-the-chutes”’ accidents, where the living force and
momentum cause an extraordinary degree of local stress when resistance
is encountered. Even gangrene of a part or the whole of a limb may eventu-
ate, especially if the main artery be traumatized and thrombosed.
2. Gangrene of an Extremity.—Traumatic gangrene of the lower extrem-
ity is best exemplified by that resulting from accidental entombment. The
cases may be grouped into:
A. Gangrene with, and
B. Gangrene without blockage of the main arteries.
3. Accidental entombment, formerly of rare occurrence and rarely seen
except in mining and building operations or earthquake, was not infrequently
the cause of extensive gangrene of the extremities during the Great War.
The injury to the extremities following such trauma is attributable to
external pressure and is characterized by the absence of external wounds,
the absence of severe external contusion, and of infection.
Similar injuries have been described as occurring during earthquakes
and Colmers! reports acute decubitus as the result of such injury. The
contusing force acts for many minutes or hours by reason of the fact that
the injured person is imprisoned and incarcerated under earth, stone, debris,
etc. Gangrene of a portion or the whole of the extremity, resulting from
such a trauma is characterized by the absence of external wounds and of
infection.
Acute traumatic decubitus is a condition resulting from incarceration of
the body or entombment for many hours, the compressing forces bringing
about localized gangrene. ‘The skin, the soft parts, as well as the bones may
become involved. Strange to say the integument may remain intact, whilst
the fascia and muscles become necrotic. Subsequently infection leads to
extensive phlegmon formation. The gluteal and trochanteric regions are
the sites of predilection. After sequestration of the dead tissue, large
punched out holes or cavities are left behind (Colmers).
A. Gangrene with Arterial Thrombosis.—The trauma is usually exerted
over the thigh. The symptoms include rapid development of necrosis of
the lower extremity without the presence of any wound or an infectious
process. The lower extremity becomes enormously swollen, tense and
indurated; the skin of the whole leg is discolored, has a livid hue, is mar-
morated with areas of pallor, sometimes with superficial excoriations. The
whole limb is immobile and cold up to the knee or even higher. The pulses
in the dorsalis pedis and popliteal are usually absent.
If the patient is not already in shock, the usual symptoms of the latter
develop, and exitus occurs in most of the cases within a few days after the
injury.
1 Colmers, Arch. f. klin. Chir., 1909, 90, p. 703.
TRAUMATIC GANGRENE ea
The femoral artery at the site of the greatest compression may be throm-
bosed, the intima injured and detached, or the seat of suggillations. Second-
-ary thrombosis in the femoral vein develops later, and may contribute to
the development of gangrene.
B. Gangrene Without Involvement of the Main Arteries.—Here we may
distinguish gangrene of the leg with mortification of (1) the superficial
ae or (2) the deep tissues.
Traumatic Superficial Gangrene with the Main Vessels Intact—This
Pecty is characterized by the fact that but a short time after release from
entombment the picture of impending gangrene rapidly develops. The leg
may be markedly swollen, cold and tense, the peripheral pulses absent.
Changes in the appearance of the skin are striking in that the color is first
bluish red and marmorated in places. Soon there develop large vesicles
or bull partly filled with hight colored fluid or blood. Signs of infection
are usually absent. Shock is associated only in the cases sustaining severe
trauma, but local pain may be severe. With the progress of the gangrenous
process, temperature is common and amputation becomes indicated.
The cause of the tissue death seems to be the force of external pressure.
Whilst complete mortification may involve all of the tissue lying upon the
deep fascia, the underlying parts are the seat of hemorrhagic infarction and
thrombosis of the smaller vessels. In spite of the fact that the vitality of
the deeper tissues is not altogether compromised, their integrity and future
outlook gives little promise of functional restoration. In spite, therefore, of
only superficial necrosis, amputation usually becomes necessary.
Pathology.—The skin of the leg is usually extensively infiltrated with
blood and the veins thrombosed. The subcutaneous tissues, too, show
brownish black discoloration with numerous thrombosed vessels. As for
the tissue under the fascia, the muscles may show but slight changes save for
some hemorrhages. Except for some bloody extravasation, possibly bony
fractures, all of the deeper tissues may escape the destructive mortifying
process.
2. Traumatic Gangrene of the Deep Tissues (with main arteries intact).—
Although the limb will here also give early evidences of interference with its
nutrition, gangrene develops more slowly. Indeed, months may elapse
before amputation seems warranted. The circulation of the skin may
appear unimpaired for some time (Orth!); or coldness and pallor may be
present (Kuttner?) from the beginning.
The characteristic feature of this variety of traumatic necrosis is the dis-
turbed nutrition of the musculature and the intensive swelling of the deeper
tissues, the skin and subcutaneous tissue suffering relatively little. The
latter may, however, become secondarily involved. Gangrene of the
extremity does not necessarily follow especially if no secondary infection
supervenes. Or the muscle alterations may subside if not too severe. In
these circumstances function may become restored, or more or less perma-
nently impaired.
In short, primary necrosis of muscles is believed to occur in these cases.
Prolonged action of an equally distributed contusing, compressing force
may explain the involvement of muscle and escape of the integument, in
contradistinction to the more intensive stresses that bring about mortifica-
tion of the skin.
1 Orth, Miinchen. med. Wchnschr., 1916, No. 39, Feldirz. Beilage, No. 39, p. 1407.
? Kuttner, Bruns’ Beitr., 112, 1918, p. Sgr.
172 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Treatment.—The treatment of traumatic gangrene includes first, the
surgical treatment of the wound produced by the injury, according to the
principles of aseptic surgery; second, the methods for enhancing the circu-
lation, so as to limit the gangrenous process, as much as possible; and third,
the amputation of the affected part. These methods will be given due
consideration in Chap. LXV.
CHAPTER XXXI
THERMIC GANGRENE
Intense heat or cold may bring about necrosis of tissues within a very
short time, while a moderate degree of heat and cold may have the same effect
when in action for longer periods. Gangrene from cold apparently differs
in no essentials from other forms of mortification. The death of tissue may
occur first, from the direct action of cold upon the protoplasm; second, from the
ischemia due to vascular spasm; and third, thrombosis. Although gangrene
may be due to the fact that the part has become completely frozen, restitution
would occur in most instances were it not for the fact that extensive thrombosis
of the arterial and venous channels has already occurred.
For a thorough understanding of the gangrenous processes depending
upon the action of cold, it is well to have some knowledge of the observations
that have been made on the effects of such influences during exposure in time
of war. It was during the recent Great War that a multitude of lesions depen-
dent upon exposure to cold and moisture developed, many of which were
accompanied by gangrene.
General Consideration.—In studying the effect of cold on human tissues
we must take into consideration both the local and the general action. The
human organism can adopt itself to very marked diminution in the surround-
ing temperature, without any considerable loss of body temperature. ‘The
body compensates for loss of warmth by increased heat production. So
important is the matter of tissue nutrition that in the absence of an ade-
quate delivery of blood the body warmth may be reduced to a degree incom-
patible with a continuance of the vital functions. The consequences of
the local action of cold on the tissues vary according to the degree of tem-
perature, the duration of the action, and the character of the environmental
circumstances.
Cold, dry air has an effect different from cold water or snow, whilst the
effect of air in motion is notably at variance from that of an absolutely tran-
quil atmosphere. These variations are due in part to the fact that loss of
body warmth to the air is effected through radiation, whilst the physical
process is one of conduction in a watery, humid, or moist medium. ‘The
red blood cells are said to be destroyed through freezing. Lesser degrees of
cold produce primarily a constriction of the vessels, first of the smaller then
of the larger arteries. The pain due to cold results from the direct action of
loss of warmth upon the sensitive nerve endings. Consequent upon vaso-
constriction comes vasodilatation, when the temperature rises; and redness
and cyanosis of the exposed part ensue.
THERMIC GANGRENE 173
A wet cold is especially apt to bring about marked redness and swelling
of the part, in anemic individuals. Such individuals easily develop chil-
blains (pernio). The protracted action of moderate degrees of cold (not
approaching the freezing point) may so disturb the arterial circulation, as to
produce ischemia of the peripheral parts—toes and fingers—and gangrene.
This ischemic type of gangrene must be distinguished from the immediate
and actual result of freezing of a part.
Experimental work on the local lesions due to cold has produced a number
of interesting lesions, among which may be noted the following; thromboses
of the vessels (Hodara and Riehl); dehydration and ice formation in the
tissues (Rischtler).
Symptomatology of Local Freezing.—Freezing of the tissues may be
divided into three types. First, simple freezing with erythema as the chief
symptom (first degree chilblain); second, with formation of vesicles; third,
with gangrene. A fourth type has been suggested by Flércken,! without
skin lesions.
It was found during the Great War, that robust and strong individuals,
who had been exposed for a considerable period of time in wet trenches, or
had worked in cold water, presented the following clinical picture. There
was severe pain, stiffness in the legs and back, with inability to use the muscles,
Muscles, tendons, periosteum and the shin bone, as well as nerves seemed to
be tender to the touch without any palpatory lesions, without objective changes
of sensibility or altered reflexes. The most frequent localization of these symp-
toms was the region of the shin bone. Certain German authors have given
the name “‘Schienbein Schmerz” to this syndrome.
The result of exposure during the war sometimes gave clinical pictures
simulating influenza, typhus, perityphus and other diseases. Thus, Sipp-
mann described headache, chills, fever, malaise as preceding the attacks of
pain. The relationship between the characteristic tibial pain, and the general
symptoms has been a mooted question. ‘There can be no doubt, however,
but that the intense pain in the extremity can be brought in direct causal
relationship with the exposure to cold.
_ Local Changes Due to Cold. First Degree.—Portions of the body exposed
to cold become reddened, whilst severe burning and prickling sensations are
experienced (nerve irritation). As a result of vasoconstriction the parts
become blanched and anesthetic. Rubbing of the parts may restore circu-
lation. Following the vasoconstriction, intense reddening of the peripheral
parts with itching and pricking sensation follows, the extremities becoming
swollen. All of these symptoms my subside completely or lead to the develop-
ment of chilblain. These are represented by bluish red, flat swellings, or
nodular elevations surrounded by a red zone. The sites of predilection are
the extensor aspects of the fingers and toes, the margin of the foot, the heel,
the ball of the foot and the back of the hand. However, ears, nose, cheeks,
and more rarely the penis, the gluteal region, and the chin may be affected.
Second Degree.—Freezing of the second degree is characterized by the
presence of bullae or vesicles on a reddened or violaceous skin. ‘The con-
tents of the vesicles differ from those of gangrenous vesicles in that there is
clear fluid just as in the blebs of burns. After the bursting of the vesicles
the superficial epithelial defects heal rapidly. In rare cases, however, ulcers
may form that are of indolent character. Certain authors have brought these
lesions into relationship with subsequent arterial changes eventuating in gan-
1Flércken, Ergebn. d. Chir. u. Orth., 1920, p. 185.
174 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
grene (Von Winiwater). The particular disease, however, described by this
and other investigators has been shown by the author to be none other than
thrombo-angilttis obliterans.
Third Degree-—When the fingers or toes suddenly turn blackish and
cannot be moved, lose their sensation and become cold as ice, we have the
typical picture of this form. When the superficial portions have been dam-
aged, then needle pricks and incisions are not experienced as pain, but only
merely as pressure sensations. Later, the affected parts become swollen,
cyanotic, bluish-red and congested. If this circulatory stasis does not
abate, then gangrene occurs. ‘The fingers and toes may become totally gan-
grenous whilst proximally merely the superficial tissue layers are involved.
A rather characteristic type of gangrene is that involving the heel, and when
this type is more extensive, the larger part of the sole of the foot becomes
gangrenous.
In certain instances, smaller or larger areas of skin and subcutaneous .
tissue of varying size over the shin bone, or in fact, over any portion of the
leg may become frozen as the result of exposure in wet stockings or large
indolent ulcers may result.
Clinical Course.—The following clinical picture is described by Volk and
Stiefler.1 The affected extremity is swollen, exceedingly painful, and
temperature may accompany the local phenomena. ‘The skin is livid and
bluish and is lifted up here and there into large blebs or is easily cast off.
Subsequently, extensive gangrene of the distal parts occurs, particularly
when anesthesia has lasted for a few days. In the severe cases of freezing
necrosis of the superficial tissues, involving muscles and tendons, and even
mummification or moist gangrene of the fingers, toes or a portion of the foot
may occur. Spontaneous amputation has been noted, and erosion into the
large vessels may take place. Some authors? describe the occurrence of a
moccasin-like gangrene involving the sole and big toe of the foot.
Rather characteristic features are the implications of the heel, and the
freezing of the finger tips without involvement of the thumb. Meyer and
Kohlschiitter’ describe typical pictures where the tips of all the fingers are
frozen, ulcerate or become gangrenous, the thumb often remaining free.
Regarding the symptoms of pain when parts are frozen, authors vary
considerably. Zuckerkandl reports cases in which mortification of the
affected part can occur without pain. Patients may have no knowledge of
the state of the parts until, after removal of the shoes, the condition becomes
manifest. In such cases spontaneous pain begins only then when the
superficial blebs are opened, and the corium becomes exposed to the air.
Other authors, such as Dreyer‘ report that in the moist gangrene observed
during the Balkan war, pain appeared as a late symptom and was followed
after seventy-two hours by swelling and gangrene.
Still others have observed that practically all patients have subjective
manifestations in the affected territory complaining of paresthesiz such as
feeling of numbness, a wooden feeling, stiffness, prickling, formication,
burning and sensations of heat and cold.
About one-third of the cases under the observation of these authors
developed, what they termed “ Erkaltungsneuralgie”’ or neuralgia due to cold.
This term was employed to designate a complex of pain in the feet, soles, and
1 Volk and Stiefler, Wien. klin. Wchnschr., 1915, No.
2 Coenen, Thorn, Cilimbaris, Beitr. Kriegsheilkunde, Berlin, J. Springer, 1914.
3 Meyer and Kohlschiitter, Deutsch. Ztschr. f. Chir., Bd. 127, March 2, 1914.
4 Dreyer, Zentralbl. f. Chir., TOTS. INT:
THERMIC GANGRENE bogs
toes, with tenderness over the anterior tibial and perineal groups of muscles,
manifestations that would subside after rest and the use of salicylates. When
pain appears shortly or some time after the action of the cold, paresthesize
were often noted as prodromal signs; these were in no way related in inten-
sity to the degree of the exciting process. Freezing of even moderate degree
can evoke intensive paresthesiz.
Quite in contrast to the sensory phenomena, in cases of ordinary gangrene,
these authors observed derangement in sensation over much larger areas and
extending much higher than was expected from the extent of tissue injury.
Anesthesia may extend well above the line of demarcation (if gangrene occurs)
and may be delimited above by a zone of hyperaesthesia.
Etiology.—It is known that a reduction of temperature down to the
freezing point of blood or below is not necessary to bring about what is
known as freezing of the tissues; but that temperatures even above zero
centigrade suffice provided that predisposing factors are at hand. Indeed
gangrene may take place at a temperature considerably above the freezing
point of blood (even 6° to 8° C.).
Such predisposing factors are firstly, moisture (wetness); secondly, local;
and thirdly, general predisposition, these including all the noxious factors
that may lead to ischemia of the vessels. Whilst reduction of temperature
of any part of the body through the action of cold air takes place by radiation,
chilling of the body by reason of moist cold, such as wet clothing and snow,
takes place more rapidly through direct conduction. The most dangerous
degree of cold is at the thaw and melting point. It has been noted by Sticker
that most cases of freezing during the Great War occurred during the time when
the snow began to melt.
Local predisposition is still further conducive. Thus, the distal parts of
the body are most prone to become frozen, especially parts that are least
well provided with blood. A disproportion between the surface extent and
the volume of a part is another factor that makes fingers, toes and ears
susceptible.
Loss of heat is greater when the airisin motion. The presence of bodies of
good conductivity, such as metal, is dangerous. Water, too, is to be feared
when in direct contact with the skin. Those portions of the body which are
not only exposed to cold, but suffer impairment of circulation through
restricted motion, and constriction of the circulation are particularly sensitive
to gangrene. The deleterious effects of tight shoes, shrunken and wet
boots, and tight and wet stockings are well known.
Internal causes are bodily weakness and disease. These minimize the
body’s protecting forces. Lack of power of adaptation to surroundings
is a predisposing cause. Thus, individuals who are able to withstand unusual
climatic changes including exposure to moisture and cold are less susceptible
to gangrene. A certain amount of resistance can be acquired gradually
through artificial exercises. Statistics demonstrate that most cases of gangrene
of this type occur in the autumn, whilst later in the season, when a certain
degree of adaptation (acclimatization) has become possible, its incidence
diminishes.
Patients that have just recovered from a malady are also susceptible;
which is in keeping with the frequency of gangrene in post-typhoid and in
cholera cases.
Pathogenesis. Direct Tissue Injury.—Life is dependent upon the continu-
ance of definite temperature in the protoplasm. ‘There are upper as well as
lower limits under which it can no longer continue. The lower limits vary
176 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
considerably in different animals. In man and many of the warm blooded
animals 25° C. is considered incompatible with existence. The circulating
blood usually causes renewal of warmth. With impairment of circulatory
activity, however, the two factors may combine to exert a deleterious result.
The direct effect of cold, from the physical standpoint, is a change in
the colloid solution of the protoplasm. Within certain limits it is rather
the duration of the lowering of temperature than the degree that is impor-
tant, so standing in cold water for many hours leads to gangrene, whilst
freezing with the ethylchlorid spray for several seconds does not. It has
been shown by Schade that the elasticity of the tissues may return to normal
when the loss of warmth lasts but a short time. In addition to the changes
in the colloids, chemical changes occur—changes in the crystalloid solution.
The Effect of Freezing in This Type of Gangrene-—The temperature of
o° C. does not indicate a critical point. J vitro the blood and human fluid
freeze at a temperature of —o.66° C. but in the body a much lower tem-
perature is necessary. With the formation of ice, however, an additionally
injurious factor is added. Freezing is only of significance in that a rapid
and intensive loss of water is occasioned thereby. It is well known that
plants that have been frozen show macroscopically and microscopically the
same appearance as dried ones. Indeed, those forms of life that are not
dependent upon water cannot die by reason of cold.
Experiments have shown that with a marked lowering of temperature, an alteration
of the protoplasma from the sol condition into the gel condition takes place; that is, the
substances in solution approach the precipitate or solid state. The body cells do not
possess the same characteristics or qualities at a temperature of 20° that they do at 30° C.
The microscopic examination, however, does not always show corresponding changes.
The elasto-metric method of Schade is a new procedure for the investigation and demon-
stration of this subject. In a specially constructed apparatus, this author showed that
elasticity of the subcutaneous tissues diminished in a state of fatigue, general disease,
and local cold, even though the fluid contents did not change. Elasticity is the quality
or capacity for alteration of form and return to a previous state. A measureable loss of
elasticity can take place in fat-free tissues only through a change in the physical condition
of tissues, namely, in their protein substances.
After return to normal temperature, the disturbance in the colloid mixtures does not
cease when the degree of what is known as ‘‘reversible’”’ has been exceeded.
The formation of ice in the tissues is another deleterious factor. As a matter of fact,
the whole watery solution of colloids and crystalloids which we recognize as the fluid proto-
plasm, the lymph and the blood plasma, does not become converted into ice. The ice forma-
tion takes place in the precipitation or congealing of pure water in a solid form out of the
tissues, with simultaneous concentration of the remaining solution. By virtue of the higher
concentration of the colloids themselves, and particularly the crystalloid substances, the
tranference of the colloids into their gel condition is intensified. ‘At the same time carbon
dioxid and oxygen previously held in by the water become free. ‘The microscopic pictures
noted in frozen ameba bear out this view.
For the living cell therefore, freezing exerts its influence by virtue of a rapid and inten-
sive withdrawal of water. And, furthermore, forms of life which we regard as latent, do
not appear to suffer from cold. The time factor is important because the changes are slow.
After a certain lapse of minutes, a portion of the cell protoplasm becomes converted into the
gel condition so that the remainder does not suffice.
The alterations in the protein substances are not reversible after long periods of freezing.
This corresponds to the condition of frozen solutions of devitalized colloid substances, such
as egg albumin which, even after being thawed, show their spongy structure, and do not
return to their sol condition. These changes are ‘the same for all degrees of temperature and
the time required for annihilation of life varies. When the human skin is frozen with ethyl
chlorid for from one to two minutes, it is assumed that during this period, an adequate
portion ofthe protoplasm retains its sol condition, and can subsequently resume its vital
function. ‘Thus, some animals can withstand freezing for longer periods of time. It has
been shown that medusae can remain frozen for hours.
The manner of thawing does not seem to be as important as is believed. Clinically,
acute gangrene does not ensue immediately after exposure to cold. The rdle of the blood
vessels seems to be an important one.
THERMIC GANGRENE er be
The Role of the Blood Vessels —Authors are at variance, as to whether in
gangrene due to cold (freezing) the reduction of temperature per se, or the
cessation of circulation plays the greater réle. Wieting! and Marchand?
have applied the word “‘ischemic”’ (Kalte-Gangrin) to this variety. Accord-
ing to this view the thermic influence produces a spastic contraction of the
arteries, even to the extent of complete obliteration of their lumina. And
because this effect may last for a considerable period of time, and other pre-
disposing factors are at work, gangrene is the issue. Wieting believes that a
vessel palsy together with true impairment of the vascular innervation, is an
important activating factor, for with it go stasis and thrombosis.
From what has been said it is clear that immediate action of withdrawal
of heat from the protoplasm plays an important part in the production of
gangrene due to cold, but it is not the only cause. The blood carries
renewed calories to the refrigerated tissues, and it is only when the loss of
heat preponderates over that which is received that injury to the tissues
sets in.
When the action of cold is very intensive, a deleterious result is obtained,
even if the vascular system functionates with normal or accelerated activity.
It is generally believed that contraction of the blood vessels follows stimulation by cold.
If contraction of the vessels were the only and regular reaction on exposure to cold, the
condition of gangrene due to cold would be adequately explained. Loss of warmth without
ae a absence of oxygen and nutrition would act similarly in bringing about cell
eath
Marchand? holds this view when he says that the anemia produced by contraction of the
small vessels can become complete and can thus lead to death of affected parts. However,
as a rule, the reaction of the blood vessels is somewhat more complicated.
The first sequence of the action of cold water is, indeed, a contraction of all of the
vessels in the affected parts, including arteries as well as capillaries and veins. The skin
becomes pale and the extremities lose in volume. This condition may persist for some time
in anemic individuals, the part remaining pale and cold, rigid, and permanent injury to the
parts may ensue. In anemic people as a result of mere contraction of the blood vessels,
death of tissue in the sense of an ischemic gangrene may eventuate.
The cases in which gangrene occurs immediately after exposure to cold are
telatively rare. Usually, days, weeks or months intervene before the injured
rissues die off. Doubtlessly the condition of the blood vessels is responsible.
To explain the delayed mortification, the question has been put as to
whether the tissues are not found ina condition of diminished vital energy after
the action of cold; also as to whether limited portions of tissues or cells can be
injured or comparatively devitalized in the multicellular organisms and remain
in such a state even after the causal agent has ceased to be active. Histo-
logic and biologic observations, however, do not seem to lend acceptance to the
view that single cells can remain in a state of permanent deterioration or
devitalization, in a multicellular organism. Indeed, it seems rather more
plausible that when such permanent or protracted local morbidity exists,
lesions in the blood vessels are at fault.
Animal experimentation has shown that the vessels may permanently contract as the
result of the action of cold. When the extremities and ears of rabbits were put into a cold
solution at 20° below o° C., they were found to remain bloodless until freezing took place.
When the same cold mixture was brought into contact with the femoral arteries, so inten-
sive a contraction was obtained, that no blood passed through it (Catiano‘). In healthy
individuals and under atmospheric conditions in which adaption has taken place, a dilata-
HWieting, Centralblof. Chir., 1913, p.
2 Marchand, Krehl- Marchand, Handb. a eee Bate oco, Tip. aids
3 Marchand, Handb. d. allg. Path. , 1908, Bd. 1, also 1912, Baar.
4 Catiano, Langenbecks Archiv., 1883, Bd. 28.
12
178 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
tion of the vessels follows sooner or later. Further investigation has shown that transitory
reduction of temperature of an artery is followed by immediate contraction, but after a few
minutes circulation is restored, and the vessel dilates beyond its original calibre. Even when
cold is applied for a longer period of time it is found that in the frog after preliminary
vasoconstriction, dilatation takes place beyond the normal, and whilst the cold is still in
action. After restoration of the external temperature, the vasodilatation may continue
for from ten to twenty minutes or more (Sartorius!). In the case of the rabbit, too, when
cold acts slowly, excessive dilatation may occur after preliminary contraction, and persist
for many hours, even though the snow be still in contact. It is believed that this reaction
of vasodilatation takes place whenever the organism has become accustomed to severe and
excessive fluctuations of temperature. That this is true, experimental observations
attests, whilst the unexposed portions of the body, such as the mesentery or internal organs,
manifest none of the above reactive phenomena.
We know that the face and hands become pale as the direct effect of
cold, but subsequently flush if the individual is accustomed to cold and is in
good health. In chronic disease, and in anaemic people, the reactionary
reddening may not take place. The nude body, when exposed to cold and
wind, may remain pale, with the surface vessels contracted whilst the skin
of the face that is used to exposure, may react with a marked flushing. These
well known phenomena of reactive hyperemia following cold are of importance.
They should be borne in mind in prophylaxis. For, when the reactive
dilatation is adequate, even severe degrees of cold fail to bring about gangrene.
The factors that constitute the closing links in the chain of deleterious
moments, and to which the gangrenous outcome is greatly due, may be
summed up as follows.
Firstly there may be an inadequate adaptation of the vascular system.
Since the reaction of the vessels is intensified and prolonged through exer-
cise, and climatic experiences, an absence of the latter would conduce to
inadequate or insufficiently long dilatation, and subsequent vasoconstriction.
In such circumstances the influence of cold, would bring about total plasmic
changes and necroses, both by virtue of the action of the cold itself, as well as
through the insufficient oxygenation and nutritive supply. This explains
the observation that soldiers are better able to withstand the cold and wet
during the winter or early spring, than in the fall.
Secondly, disease and weakness may cause the absence of insufficient
reaction. Such individuals are unable to deliver as much blood and as many
calories as are necessary for the conservation of any particular portion of the
body when threatened. Gangrene due to freezing also was noticed more often
when the extremities had been injured by bullet wounds, than when intact.
Thirdly, tight body coverings, shoes, stockinettes, stockings, etc., may
cause ischemia and constriction of the vessels by interfering with adequate
reactive vascular dilatation. ‘There must be enough room to accommodate
the increased volume incident upon the dilatation of the vessels.
The Effect of Stasis—When the action of cold is prolonged and does not
directly lead to freezing, the dilatation of the vessels loses its reactive nature.
Whilst, it is ordinarily superseded by vasoconstriction, it would under such
circumstances induce marked congestive dilatation of the capillaries.
The flow of blood would become slower until the circulation finally
ceases. ‘The skin then takes on a bluish red or crimson red discoloration and
edema of the tissues follows. ‘Then blebs form. There is loss of the active
muscular power, and loss of sensibility. In such a case, tissue death sets in
and, after a time, macroscopic evidences of gangrene in the dry or in putrid
wet stages, make their appearance. The important observations in this
1 Sartorius, Inaug. Diss., Bonn, 1864.
THERMIC GANGRENE 179
respect are those which have demonstrated that with a certain degree of tissue
injury, the blood flow ceases in the dilated capillaries, although the afferent
and efferent paths are open. Coagulation does not appear to occur at first,
which is in keeping with the fact that occasionally the circulation can be
again restored. This so-called stasis with interruption of circulation has not
been altogether explained mechanically. This much, however, may be said,
that when the tissue injury or insult has attained a certain degree, the blood
ceases to circulate through the affected territory. This applies not only for
the chemical or caustic injuries, but also for refrigeration. In the case of
congelation it is probable that the tissue degeneration is the most important
effect of freezing, whilst the circulatory disturbances and the stasis are accom-
panying and secondary. When stasis occurs, tissue death is predestined.
The Importance of Vessel Palsy—A number of authors have attributed
death of the tissues from cold to paralysis of the blood vessels. Wieting?
thinks that the essential factor in cases of protracted action of cold is the
paralysis of the vessels which is occasioned by injury to the vascular inner-
vation, and is followed by stasis and thrombosis. For this reason he speaks
of the necroses occurring during the Balkan War as paralytic vessel gangrene,
(neuroparalytic) gangrene of the vascular paralytic type (Marchand).?
Reference will be made on pp. 571 and 578 to the history of previous effects
of cold in some of the cases observed.
Both endarteritis and thrombosis have been considered as the causal
factors, when the action of cold precedes the mortifying process by weeks or
months. Indeed, it is assumed that the vessel endothelium is exceedingly
susceptible to the action of cold.
A number of authors in experimenting with the action of ether spray on vessels found
that degeneration of the media and consequent proliferation of the intima with narrowing of
the lumen took place.* It is interesting to note not only the immediate degenerative
phenomena but the late proliferative condition of the endothelium. This suggests that the
lesion is a replacement phenomenon, with substitution for the cells that had been destroyed
(cicatricial in nature). The consequent narrowing of the lumina of the arteries is held
responsible by some for the late gangrene. The eventual mortification is said to occur
either by reason of the gradual impairment of circulation, or may ensue in such poorly
nourished territories, whenever a secondary insult still further jeopardizes the circulation.
Thrombosis.—Thrombosis is regarded as a rare cause of gangrene after
freezing. Observation of experimenters along these lines, however, has
shown that arteries dissected free and exposed to the strongest and severest
degrees of cooling contained fluid blood so long as the vasoconstriction was
insufficient to well nigh obliterate the lumen. Uschinski‘ could demonstrate
thrombi only in some of the veins.
There are three cases found in the literature in which extensive throm-
bosis‘! occurred after freezing. One of these was reported by von
Recklinghausen’ in a woman whose feet were frozen, and in whom the veins
leading to the gangrenous toes were found thrombosed. Von Winiwarter®
described a case of widely distributed arterial thrombosis in a man who had
been exposed to cold. Niagelsbach? described a case in which all of the large
arteries of the foot and leg were thrombosed after freezing. It would appear
1 Wieting, Zentralbl. f. Chir., 1913, p. 593, p. 1985.
2 Marchand, Handb. d. allg. Path., 1908, Bd. 1.
3 Zoege v. Manteuffel, Zentralbl. f. Chir., 1902, 3.
4 Uschinski, Ziegler’s Beitr., 1893, p. 115.
5 Recklinghausen, Deutsch. Chir. Lief. 2 and 3.
6 Von Winiwarter, Langb. Arch., 1879, Bd. 23, p. 202.
7 Nagelsbach, Miinchen. med. Wchnschr., 1919, p. 353.
180 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
therefore that although thrombosis may occur after freezing, it is a rather
rare cause of gangrene.
Prognosis.—Opinions vary as to the criteria according to which a prog-
nosis of the viability of a part subjected to cold is to be based. A persis-
tence of pallor, coldness, lividity and anesthesia, has been regarded as of
valuable prognostic significance. Certain authors (Meyer and Kohlschiitter+)
believe that if spots of cyanosis, lividity and areas of anesthesia are present
after a week, the affected part cannot be expected to recover. Other authors
suggest the making of minute incisions in order to determine whether well
oxygenated blood trickles forth from the wound. It has been suggested to
apply the Moskowicz test. This in our opinion, would be contraindicated
because of the danger of inducing thrombosis and vessel injury.
Therapy of Local Freezing.—Calcium salts, (particularly calcium lactate)
because of their influence on the phagocytic power of the leukocytes and their
stimulation of connective tissue formation, have been suggested as a means
Fic. 44.—Multiple incisions for the prevention of gangrene. (H. Flércken.)
of combating the effects of freezing. In freezing of the third degree, it has
been traditionally accepted that the thawing or warming should take place
as slowly as possible. ‘This does not pertain merely to cases of actual freez-
ing, but also where the reduction of temperature has been less intensive.
Cases of extensive gangrene are reported, and the occurrence of this compli-
cation is attributed to sudden change of temperature. Some authors suggest
rubbing with snow, others, such as Bundschuh,? employ cold water for
almost an hour until the bath reaches the body temperature. If the frozen
part regains its sensation and becomes red, minor lesions of the tissues
may be prognosticated. When anesthesia and pallor persist, massage is
recommended. Other authors recommend massage over long periods of
time, continuing over twenty-four hours in half hour intervals. Kroh? is
said to have revived extremities that presented all signs of impending
gangrene.
Other authors use the hyperemia treatment with or without baking. Ele-
vation of the affected extremity is advised by Sonnenburg and Tschmarke.‘
1 Meyer and Kohlschiitter, Deutsch. Ztschr. f. Chir., March, 1914, 127.
2 Bundschuh, Miinchen. med. Wchnschr., 1915, No. 12.
8 Kroh, Cit. by Flércken, Ergeb. d. Chir. u. Orthop., 1920, Bd. 12, p. 202.
4Sonnenburg and Tschmarke, Die Verbrennung u. d. Erfrierung, Ferd. Enke, Stuttgart,
IQI5.
GANGRENE DUE TO CHEMICALS AND DRUGS 181
Multiple incisions are regarded as of great value where the return venous
circulation is impeded and are said to have been the determining factor in the
saving of many limbs threatened by gangrene (Noesske,! Wieting?).
When the greater portion of the peripheral phalanges, is frozen,
Bundschuh makes multiple incisions over the ventral and dorsal aspects of
the phalanges. The schematic drawing (see Fig. 44) shows the situation of
such incisions. The hyperemic treatment with elevation has been combined
with this method. Other authors recommend the use of quartz light sub-
sequent to the making of the incisions. Alternating hot and cold baths have
also been suggested.
It has been recommended by various writers that an effort should be made
to convert moist gangrene into dry gangrene, and to this end the removal
of the detached epidermis (Strohmeyer) has been advised. The application
of dry dressings and powders, such as dermatol, finely pulverized charcoal
and similar preparations, with or without the use of dry heat is frequently
followed by good results. Even X-ray treatment (Wachtel) is said to
have been of service.
Operative Treatment.—Conservatism is the watchword, and should be
followed wherever possible. One should not be too hasty in pronouncing
judgment regarding the eventual outcome, and operation should be deferred
when one is in doubt. Early amputation is only then indicated, when com-
plicating infection with phlegmon formation is imminent; or, when the septic
resorption from a typical gangrenous territory serves as indication.
Whilst the larger number of surgeons urge conservative therapy wherever
possible, waiting for a line of demarcation to form and for sequestration to
take place spontaneously, others lay great stress upon the advisability of
obtaining a valuable functional stump. ‘The latter proceed shortly after
demarcation has become established, to the surgical measures that will
assure such an issue.
a
CHAPTER XXXII
GANGRENE DUE TO CHEMICALS AND DRUGS
Certain chemicals or drugs taken internally and applied locally may
cause gangrene. Ergot, although not taken in the form of a drug, may be
considered here as one of those substances that may produce gangrene
when taken internally. Mercury, orthoform, phosphorus, carbolic acid,
trichloracetic acid, strong acids and alkalies, may produce gangrene under
certain conditions.
The action of chemicals on cells and tissues is of manifold variety. They
may combine with the proteids of the protoplasm and form more solid com-
binations; or effect coagulation, dissolution and precipitation; or alter
especially the colloids; or have an affinity for certain tissue constituents
causing solution of lipoids and thereby destroying the construction of the
cells. Poisons do not act like nutritive substances in proportion to their
1 Noesske, Chir. Kong., 1920, Stuttgart.
2 Wieting, Zentralbl. f. Chir., 1913 Nos. 16 and 52.
3 Wachtel, Wien. klin. Wchnschr., 1917, No. 18.
182 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
caloric value. They resemble rather the catalytic ferments in that they
become the exciting factor in the mutation of normal stresses or forces, or
exert a sort of restraining (paralytic) action on the normal processes. There
does not seem to be any relation between poisonous activity and atomic
weight, but rather some conformity with their valency. Varying effects may
follow the application of one and the same substance according to its concen-
tration; namely, stimulant, or paralyzing in weak solutions, inflammatory or
suppurative in stronger concentration, or even with capacity for causing
necrosis or gangrene.
The source of these poisons may be the mineral, plant or animal kingdom.
To these may be added those produced by pathogenic and saprophytic
organisms, and those synthetically made up. Examples are arsenic, lead,
mercury, and barium; of alkaloids, glycosides, proteins, toxalbuminates,
enzymes, bacteria, and alien (heterologous) blood, (such as causes hemo-
lysis, agglutination or precipitation).
Substances that irritate the tissues severely may produce inflammation,
suppuration or necrosis. Such are acids, alkalies, alkaline salts, metals,
nitrogenous bodies and the irritating combinations of organic compounds.
All acids have varying degrees of caustic action locally, according to the
quantity applied and the concentration. When the cells, are killed off,
direct necrosis, gangrene or mortificationensues. Even weak solutions (about
5 per cent of muriatic, nitric or sulphuric acid, and caustic potash), may
produce gangrene when applied as moist compresses for 20 to 24 hours.
These drugs lead to maceration of the epidermis, necrosis, the deeper tissues
becoming subsequently affected. ‘Trichloracetic acid is also dangerous, if
it be incorrectly used in the form of a wet dressing, when applied to remove
surface warts.
Sulphuric acid causes coagulation of albuminous substances of the tissues
through withdrawal of water and heat production. The black eschars
occasioned by it, however, are not expressions of carbonization, but due to
the presence of derivants of blood pigment, such as hematin, acid methe-
moglobin and hematoporphyrin.
Nitric acid (over 33 per cent solution) causes immediate brownish-yellow
discoloration. Proteids are precipitated by nitrification and changed into
xanthoproteinic acid. ‘There occurs coagulation of the blood 3 in the vessels
of the territory affected.
Chromic acid also precipitates in its local action, its salts causing oxi-
dation of cells. A greenish discoloration may result.
Oxalic acid is caustic and dissolves collagenous tissues.
Formalin or formaldehyde roughens the skin, hardens it, and brings about
coagulation of albumin, having caustic and necrosing action on mucous
membrane when sufficiently concentrated.
In short, the acid group are caustics that may effect rapid disorganization
of the protoplasm. This eventuality may be the result of withdrawal of
water (suphuric acid), albuminous precipitation (organic and inorganic salts,
fatty acids, trichloracetic acid), or through salt combinations with proteids
(acid albumins).
The halogens destroy the protoplasmic structure, in that they take up
water and thus make salts that precipitate proteids. Chlorine and fluorine
have the strongest action. Hydrochloric acid may lead to ischemic necrosis
of the skin. So also chromic acid combinations may produce necrosis.
The alkalies are not unlike the acids in their effects. However, these are
characterized by the development of soft, smeary shreds of swollen disin-
GANGRENE DUE TO CHEMICALS AND DRUGS 183
tegrated tissue—a true example of their dissolving effect (also called colli-
quation or colliquation necrosis).
Arsenic may have a caustic action in its oxidizing powers.
Phosphorous is especially dangerous for its peculiar necrotizing effect on the
jawbone, and there may even occur involvement of the vomer and sphenoid.
These are the sequences of the inhalation of phosphorous fumes in the manu-
facture of matches. Of the mercurial poisons calomel is a weak bichloride
(sublimate) of mercury, an intensive caustic. The oxide, chloride and
iodides combine locally at the site of application with the proteids, causing
death and destruction of the cells. Mercury is reported to produce local
sloughing at the site of injection, gangrenous patches in the gastro-intestinal
tract, and sloughing of the skin.
Silver nitrate combines with the proteids of the tissues to form a silver
albuminate, appearing as whitish eschars that become dark through the
action of light. In the blood this salt exerts a specific action on nerve cells,
causing spinal paralyses, temporary paresis, paralysis of the vasomotor cen-
ters and of the respiratory center.
Although caustic effects have been noted in the stomach from the contact
of lead, this poison is of no special significance as a clinical factor in the pro-
duction of necrosis. The same may be said of zinc and copper.
Local necrosis has resulted from the subcutaneous injection of the poison
of bees and wasps. Serpent venom, too, has produced gangrene (in case of the
crotalidae).
Finally, we may mention the distinctive effects of some of the microbic
poisons. Tuberculin (old) and mallein in concentrated form may bring about
necrosis. Substances of similar action have been derived from the bacillus
pyocyaneus, prodigiosus, proteus and penicillium glaucum. Cell necrosis,
too, may follow the action of ectotoxins.
The bodies of bacteria endotoxins have similar effects.
A gangrenous form of eruption is recorded in the literature as following
the use of orthoform. Gangrenous patches and ulcerations are said to com-
plicate the use of this drug about the fingers, anus and nipples.
_ Carbolic Acid Gangrene.—The fingers or toes are usually affected follow-
ing the local application of ointments or wet dressings. The gangrene may
result after the application of even a very weak solution (such as 0.5, I or 2
per cent). After the dressing has been applied for a few hours, the finger or
part becomes blanched, and a pricking sensation is felt. Within 24 hours
or less, the skin becomes dusky, discolored, dry gangrene may occur, the part
becoming gradually mummified.
Various theories have been offered to explain the cause of gangrene from
the use of weak solutions of carbolicacid. According to one view, thrombosis
is produced in the peripheral vessels; according to another, a particular
action upon the trophic functions and vascular nerves is exerted.
Amputation is advisable according to the view of Leclerc! who bases his
conclusion on the following observation.
A woman 50 years old, despite the fact that she was given accurate proportions for a
phenol dressing, to be applied to the finger, applied a compress saturated with the pure
solution for 24 hours without any sensation of pain. Upon removal of the dressing the
finger was found dead white, shriveled, and at the end of 6 days it became gangrenous.
Two days later pain of the hand was experienced and “‘erythema”’ on the back of the hand
developed. Symptoms of disturbed mentality now followed, with extension of the gan-
grene, and the following day elevation of temperature (38° in the morning and 38.3° in the
evening) and pulse 140. Then came a state of collapse and exitus on the following day.
1 Leclerc, Bull. de l’Acad. de méd., Paris, Feb. 25, 1919, 81, 205.
184 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Lysol, too, may be regarded as dangerous in solutions that are not
thoroughly mixed, as the case of Sowles! demonstrated.
In a patient who soaked his right index finger over a total period of about 15 minutes in
a basin of water, into which an “indefinite amount”’ of lysol had been admixed, the distal
half;of the finger became intensely swollen the following day. Examination, 24 hours later,
demonstrated marked redness and swelling with a sharp line of demarcation. The epider-
misfof the dorsal distal half of the finger was white and raised from the subcutaneous tissue,
appearing to be dislodged by serum or pus. However, on removal of the dead skin, the
subcutaneous tissues were evidently dry and gangrenous.
In the following case observed by von Stapelmohr? the agent was a 5 per
cent solution of lysol.
A woman of 53 had cut her left thumb 4 days before coming to the clinic. Two days
after the accident she had wrapped her thumb in a lysol drenched bandage for 12 hours,
and later had held the thumb for 2 hours in the same 5 per cent lysol solution.
Upon examination the skin was slightly red with occasional small blisters. In the next
few days the terminal phalanx became black, and 11 days after the injury the finger .
was amputated, at which time the soft parts were also attacked by dry gangrene.
Gangrene Due to Poisonous Gases.—Thrombosis in both deep and
superficial vessels (veins) may succeed the inhalation of a number of differ-
ent toxic fumes and gases. As examples of such we may quote some of
the records of gangrene due to carbon monoxid and illuminating gas. After
exposure to carbon monoxid from a charcoal stove, the following condition
is reported as having resulted in one case (Thandavaroyan!).
Areas of hyeremia were observed confined entirely to the left side of the face, left hand,
lower part of the chest and left thigh. Although the hyperemic areas on the face and chest
disappeared ‘after a few days, raised anesthetic areas appeared on the left hand and thigh.
Four days later gangrene of the little finger of the left hand set in, with absence of circula-
tion in the other fingers of that hand. The dry gangrene was well demarcated; the swelling
of the hand and thigh improved under treatment; amputation was refused.
Briggs‘ relates this instance.
After accidental disconnection of a pipe line on a motor boat unbeknown to the patient,
he retired to his cabin, where he was soon after found unconscious.
Upon examination it was found that the backs of both hands and feet were covered with
large tense blebs. In spite of conservative treatment, extensive gangrene of both upper and
lower extremities rapidly developed, and on January 24, 1919 his condition was as follows.
Right hand—gangrene of the entire three middle fingers, inner border of the thumb and
little finger.
Left hand—gangrene of the distal phalanges of the four fingers and flexor surface of the
thumb.
Right leg—gangrene over outer border of tibial region, external malleolus, outer border
of dorsum of foot and small patches on three toes.
Left foot—gangrene of two toes.
The necrosis attacked the skin, muscle tissue, tendon, periosteum and bone, as also
several joints.
January 28, 1919 (37 days after the accident) amputation of the following members was
performed. Right-hand—disarticulation of 3 fingers; left hand— 4 fingers.
Riedelé reports a case of gangrene of the leg after z//uminating gas poisoning.
Several days after an attempted suicide with illuminating gas a woman was attacked by
nausea, abdominal pains and stiffness of both legs attended with pain in the legs. After
7 days the posterior tibial and anterior tibial arteries became thrombosed (probably as the
result of the prolonged retention of carbon monoxid in the blood).
1 Sowles, Boston Med. & Surg. Jour., 1919, p. 5Io.
2von Stapelmohr, Hygeia, 1917, 79, 438.
§ Thandavaroyan, Lancet, April 30, 1921, I, 910.
4 Briggs, Jour. Am. Med. Assn., Aug. 30, 1910, 73, 678.
6 Riedel, Deutsch. med. Wchnschr., June 9, 1921, 47, 651.
GANGRENE DUE TO CHEMICALS AND DRUGS 185
Gangrene Following the Injection of Medicaments.—A few examples of
gangrene following hypodermatic or subcutaneous injection of adrenalin,
arsphenamin, quinine, and after simple hypodermoclysis, may suffice to
illustrate.
Following injection of glucose solution with adrenalin, Guilera! reports a
case.
A primipara of 23 years after receiving 2 injections of 350 grams of glucose solution with
adrenalin into the right thigh developed a gangrenous area. ‘The necrosed zones were
extirpated and the dead tissue removed ‘‘en bloc”’ down to the aponeurosis.
In this case the gangrene was not due to the volume of the liquid injected
nor to any defect in preparation of the solution, or in the technic of the injec-
tion. ‘The writer attributes it to the vasoconstrictive action of the adrenalin
contained in the glucose serum in an anemic, infected person.
Muller? reports gangrene after subcutaneous injection of sodium chlorid.
Because of post-partum hemorrhage in a female 29 years of age, 1000 cc. sodium chlorid
solution were injected subcutaneously into the thigh. Two days later about 20 cm. from
the site of injection the skin of both thighs became dark blue and blistered. Gangrene
spread rapidly. The patient left the clinic unrelieved.
In explanation of the gangrene the author believes a chemical effect could be ruled out
inasmuch as the solution was made up correctly; that a thermal injury was not responsible,
inasmuch as the temperature was controlled, and was in reality too cold (35°); that no
bacteria which might cause the infection were found at 37.4°; and further, that injection
into the fascia (which Jungmann believes to be an important cause of gangrene following
sodium chlorid injection) did not occur in this case. The only remaining etiological factor
could have been the pressure necrosis such as is described by Liepmann. ‘This is caused by
delayed resorption and consequent prolonged pressure effect upon the surrounding tissue
and capillaries.
Gangrene Following Injection of Quinin.—According to Prat, Flottes and
Violles quinine necrosis is exemplified by the following report. ‘The patient
received about 10 aseptic injections of chlorhydrate of quinine into the
gluteal region, and after about 2 weeks a small focus of induration was
observed. ‘Three to 4 days later the region began to swell, the skin became
stretched without reddening, and sensitive to pressure, soon resulting in a
deep mass.
If an incision be made in such a case at this period, necrotic tissue is
exposed. The quinine determines an amicrobic mortification, an aseptic
necrosis of the tissues. The cellular tissue is the most altered, the skin in-
tact. The muscles are changed later; groups of fascia become indurated and
mortified; veritable blocks of necrosed fibers are easily detached from the
healthy muscle fascia. Finally the cellular tissue is filled with pus and the skin
drops off in gangrenous shreds.
Left to itself, quinine necrosis would end in sphaceli, extensive detach-
ment and bacterial suppuration. In the “quinine abscess”’ globules of pus,
degenerated leukocytes, pyogenic microbes, blood corpuscles and fatty
granulations are observed. ‘The formidable decay of quinine necrosis gener-
ally necessitates surgical intervention under chloroform anesthesia. This
consists in wide and deep incisions, going beyond the limits of the affection
and excision of the mortified tissues. |
Sutter‘ records gangrene of the fingers due to the injection of arsphenamin. -
1 Guilera, Rev. espan. de med. y cirug., Barcelona, 1919, 2, 664.
2 Muller, Med. Klin., Aug. 1, 1920, 16, 804.
3 Prat, Flottes and Violle, Bull. de Acad. de Paris, April 10, 1917, 77, 506.
4Sutter, Jour. Am. Med. Assn., Nov. 22, 1919, 73, 1611.
186 CIRCULATORY AFFECTIONS: OF THE EXTREMITIES
In case O. P. M., aged 35, immediately after the injection of 0.4 arsphenamin diluted
in 250 cc. of normal salt solution, into a vein of the left arm, there was severe pain in the
hand and the peripheral circulation was poor. According to the history there was evidently
some infiltration about the site of the intravenous injection. Subsequently dry gangrene
of the distal portion of all the fingers took place, the index finger being involved up to the
middle phalanx, and the middle finger to a somewhat less degree, the ring finger up to the
middle of the second phalanx. Amputation of the thumb distal to the first phalanx,
of the index finger 1 cm. proximal to the middle phalangeal joint, disarticulation at the
middle phalangeal joint of the middle finger, and of the middle phalangeal joint of the ring
finger were carried out approximately 3 months after the injection of arsphenamin.
Gangrene Due to Ergot.—This results from eating bread made of spurred
rye, and has not been observed when ergot is taken for medicinal purposes.
This disease was not uncommon in the eighteenth and early part of the nine-
teenth centuries, particularly in Europe, where epidemics of so-called ergotism
are known to have occurred. At present it occurs but rarely, and then only
sporadically. ‘Two types are described, a convulsive and a gangrenous type,
although both types may be combined.
After prodromal gastro-intestinal disturbances, such as diarrhea, colic,
occasional vomiting, disturbances of the circulatory and nervous systems
appear. ‘The extremities may become cold, numb, blue; the pulses may
become weak and muscular spasms may occur. When thespasms become more
general, seizures of an epileptic nature develop. In the gangrenous type of
case, either the toes or fingers are usually affected. They become cold pain-
ful, show cyanotic or purplish patches which gradually mortify, gangrene
being usually of the dry type.
Cases described as occurring in southern Russia are said to begin with
formication, coldness, numbness of the fingers and toes, gradually resulting in
bluish black discoloration, drying and detachment of nails with necrosis of
parts or whole fingers or toes. Either dry or moist gangrene may affect the
peripheral parts, including even the nose and the ears, and may be accom-
panied by severe pain that disappears. with sequestration of the tissues. In
the mild cases small islets of epidermis only are separated, or blebs appear and
the hairs fall out. The gangrenous blebs are analogous to those of herpes
zoster gangrenosa.
At other times the malady may remain latent until an intercurrent disease
such as pneumonia, scarlet, typhoid, and so forth activates it. Then severe
lesions, such as gangrene of the lung, skin, intestines and of the female sexual
organs, may develop.
The three chief actions of ergot, namely, its spastic influence, uterine
stimulation and production of gangrene have been referred to three different
toxic elements; the first, to ergotin and ergotoxin; the second to p hydro-
xyphenylacthylamin; and the third to sphacelinic acid and to sphaceotoxin
(Kobert’s appellation, sphacelinic acid so derived from the Greek word
sphakelos meaning gangrene). Other authors, however, ascribe this action
to an amorphous alkaloid ‘“‘ergotoxin.’’ The preparation of Kobert? is effec-
tive on the peripheral parts, when diluted solutions are taken internally;
while in concentrated form it causes necrosis at the site of application—
pharynx, and gastro-intestinal canal. Even fowl (especially the cock)
when fed with ergot show symptoms, and the tips of the cock’s comb are
reported as showing necrosis as well as the tongue and wings. 2% Von
1 Kobert, Arch. f. exper. Path., XVIII, 1884; also Lehrbuch der Intoxikationen, Stutt-
gart,1906.
? Griinfeld, Arb. d. pharmak. Inst. z. Dorpat, XI, 1890; VIII, 1892; XII, 1895.
# Jacoby, Arch. f. exper. Path, XX XIX, 1807.
MICROBIC GANGRENE 187
Recklinghausen found hyaline thrombi in the arterioles, and hyaline degener-
ation of the vessel walls in the affected regions of these experimental animals.
In explanation of the physiologic action of the poison on the vessels von
Recklinghausen offers certain conclusions deducible from his pathologic
findings. Noting a ring-like zone of red blood cells between the hyaline vessel
wall and the hyaline thrombus, this author concludes that a primary vessel
contraction, attended with stasis and hyaline thrombosis of the contents, is
followed by relaxation, dilatation of the vessel allowing a renewed current to
be established between clot and vessel wall. According to this theory, the
necrosis would be due to the vascular disturbances, and gangrene of this type
should more correctly be grouped under the vascular forms. Such a theory
would find confirmation in the similarity of the poison’s action on the uterine
and vascular musculature, on both of which a contractile effect is produced.
CHAPTER XXXII
MICROBIC GANGRENE
The more important types of microbic gangrene are (1) hospital gangrene,
(2) noma, (3) emphysematous gangrene, and (4) gangrene due to virulent pyo-
genic organisms (streptococci, etc.).
1. Hospital gangrene (sloughing phagedena, pulp y gangrene, putrid degen-
eration, traumatic typhus, nosocomial gangrene) has practically disappeared
since modern antiseptic methods have been introduced into surgery, and need,
therefore, but slight mention here. It occurred either in epidemics, or was
endemic in hospitals, particularly in the military hospitals. Hospital gan-
grene may be regarded as an acute progressive gangrene with putrid decom-
position or degeneration of the wound, initiated by local symptoms, but
followed rapidly by severe constitutional manifestations. The cause is doubt-
less an infectious one, anaerobic bacilli being probably responsible. Mat-
zenauer claims to have isolated a bacillus' which however, he could not
demonstrate in pure culture. Nasse? found an ameba.
According to the clinical course, authors have described a superficial and
a deep form, and according to the external manifestation an ulcerative and a
pulpy variety.
Erichsen? describes the-disease as follows. ‘‘A disease characterized by a
rapidly destructive and spreading ulcer, covering itself as it extends by an
adherent slough, and attacking open sores and wounds. When sloughing
phagedena invades a wound that is previously perfectly healthy, the surface of
the sore becomes covered with gray, soft points of slough, which rapidly extend
until the whole of the ulcer is affected. At the same timeit increases rapidly in
superficial extent, and commonly in depth; the surrounding integument
becomes edematous, swollen, and of a vivid red color; the edges of the ulcer
are everted, sharp-cut, and assume a circular outline, and its surface is covered
with a thick, pulpy, grayish green, tenacious mass, which is so firmly adherent
to the sore, that it cannot be wiped off from it, being merely swayed to and
1 Arch. f. Dermat. u. Syph., Bd. 55.
2 Arb. aus von Bergmann’s Klinik, ster Teil, 1891.
’ Science and Arts of Surgery.
188 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
fro when an attempt is made to cleanit. There is usually some dirty, yellow-
ish green or brownish discharge, and occasionally some bleeding; the pain is
of a severe burning, stinging, and lancinating character, and the fetor from the
surface, is considerable. ‘The ravages of the disease when fully developed are
extensive. The soft parts, such as the muscles, cellular tissue, and vessels,
are transformed into a gray, pulpy mass and the bones are denuded and
necrosed.”’
The diphtheritic form is characterized by certain alterations in previously
healthy, granulating wounds. Associated with fever and pain, there appear
yellowish-brown areas of discoloration in the granulation, hemorrhages and
superficial sloughs. The diphtheritic form may become wlcerative when dis-
integration of the surface takes place. The discolored areas will soon give
rise to a foul odor, leave sharply demarcated ulcers which rapidly fuse together,
or the bottoms of the ulcers become hemorrhagic and gangrenous, their mar-
gins eroded, the neighborhood, tender and painful, and inflamed far beyond
the zone of the wound.
The Pulpy Form.—Marked swelling takes place here, gas may develop
in the tissues, a mass or pulp being developed, which may be likened to brain
substance. Associated with it, extensive hemorrhages may give rise to the
hemorrhagic type. In the superficial form the process would often be self-
limited, whereas in the deep form a putrid phlegmon would develop, leading
to bone necrosis, even ulceration of vessels, and death due to hemorrhage.
Or, the deep form may be associated with toxic general symptoms, that lead
to a lethal outcome within two or three days.
As complications, erysipelas, metastatic foci of pus, and lymphangitis
have been described.
Treatment.—This consists of the rapid and energetic cauterization of
putrid areas with Pacquelin cautery, opening of the abscesses and surgical
cleanliness. Sloughs are to be removed, and general stimulants freely
administered.
2. Noma.—This form of gangrene, also called cancrum oris, gangrenous
stomatitis, cancer aquaticus, is a special form of ulcerative stomatitis with
gangrene, that occurs almost exclusively in children between the ages of two
and twelve, and often follows some debilitating disease. The affection has
its origin in an infiltration of the mucous membrane in the neighborhood of
the angle of the mouth. The exudate or infiltration then becomes gangre-
nous, and converted into a bluish-black, dry mass, which is cast off, the morti-
fying process progressing, however, in the depth and laterally, so as to involve
the lips, chin and cheeks. Within a few days a considerable portion of the
cheeks becomes destroyed and even the bone becomes exposed and necrotic.
Rather characteristic is the perforation of a cheek which may ensue within a
few days. Externally, in the pale, swollen cheeks, a bluish-black hard spot
with a reddish zone of demarcation appears, or with this, there may be
associated a large bleb. After the gangrenous area is cast off, the perfora-
tion or hole is left leading into the cavity of the mouth (Fig. 45).
The disease seems to affect poorly nourished children, often in the course
of an infectious disease, such as measles, scarlet or typhoid. As a rule,
fever, cerebral symptoms of loss of consciousness accompany the malady
which is fatal within two or three weeks. 7
The etiology does not seem to be the same in all cases. Schimmelbusch!
and Babes? isolated a special type of bacillus. Perthes found a streptothrix.
1 Deut. med. Wchnschr., 1880.
2 La Romaine Med., 1894.
MICROBIC GANGRENE 189
Others, such as Buday' believe that a spirillum and a fusiform bacillus growing
in symbiosis are responsible for the affection.
Rods and spindel shaped elements were found by Perthes? and regarded as variant
developmental forms of a streptothrix (cladothrix of Seiffert). Baumgarten takes excep-
tion to the theory of bacterial causation, believing the organism found to be secondary
invaders. However, the finding of spirillae in the areas of advancing gangrene is believed
to be suggestive of a bacterial influence. Bernheim and Popsischill* found fusiform bacilli
Fic. 45.—Defect in cheek produced in noma. (Lexer.)
and spirochetae, but in the depth a mere plump rod. This latter is regarded as the true
exciting organism. Hoffmann and Kiister‘ also identified a bacillus as the causative agent.
The peculiar sharp delimitation and separation of the pulpy putrid tissue has been inter-
preted as indicating some nerve derangement. Latterly, however, the dominant view
seems to be that noma is a form of putrid infection with gangrene as a prominent feature.
Being frequently one of the complications of other diseases, measles, typhus, diphtheria,
dysentery, mercurial stomatitis, syphilis, etc., it is still a mooted question as to whether
it is a reactionary sequel of other infections, or of unique causation.
In view of the varied results of bacterial studies, it is quite compre-
hensible that noma cannot as yet be considered an entity as far as etiology
is concerned.
Treatment.—This consists in the destruction of the gangrenous areas with
the Pacquelin cautery, frequent irrigations of the mouth, prevention of aspira-
tion pneumonia, and, according to some authors, the extirpation of the
affected area with the knife. As prophylactic measures, the mouths of all
children suffering from severe debilitating illnesses should be kept scrupu-
ously clean, all ulcers should be cauterized, and carious teeth carefully
attended to.
1 Beitr. zu path. Anat,, 1905, *~X VIIT
2 Perthes, Miinchen. med. Wchnschr., 1902.
3 Bernheim and Popsischill, Jahrb. f. Kinderh., 1898, XLVI.
4 Hoffmann and Kiister, Miinchen. med. Wchnschr., 1904, 43.
190 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
CHA PTE Ren hy
MICROBIC GANGRENE (CONTINUED)
GAS GANGRENE
Emphysematous Gangrene (microbic or traumatic spreading gangrene,
gangrene foudroyante) produced by rapidly spreading infection of the sub-
cutaneous tissues is a clinical symptom-complex produced by a number of
different virulent gas-producing organisms. Much confusion has arisen
regarding the nomenclature and etiology, authors, however, being generally
agreed regarding the intensity of the infection, its virulence, the production
of gangrene and the presence of gas in the tissues. It has been variously
termed, traumatic emphysema, gas phlegmon, acute microbic gangrene,
fulminating gangrene, gangrenous cellulitis, malignant edema, anaérobic
gangrene.
Numerous appellatives have been employed, most of which have merely
historical interest. The French authors describe it as bronze erysipelas, a
gangréne foudroyanie. If the gas bacillus or the bacillus of malignant edema
alone were responsible, the terms, malignant edema or malignant emphysema
would be apt. However, numerous other organisms are known as causative
agents. Gas edema as been suggested by Aschoff. Other names are gas
inflammation and phlegmon, or gas gangrene. ‘The last of these has found
wide acceptance, even though the pathological process does not attain the
state of tissue mortification, and is more correctly a gas phlegmon. The
multiplicity of names is partly due to the diversity of the infecting organisms
and the consequent variations in the objective phenomena.
The Bacteriologic Etiology.—Although the gas bacillus (B. aerogenes
capsulatus) of Welch (and Nuttall) or of Frankel and the bacillus of malig-
nant edema were formerly regarded as the sole causative agents, more recent
researches have shown that a number of other obligate anaerobic bacilli can
be cultivated. The bacteria can be described in two groups; (A) the non-
putrefactive, and (B) the putrefactive form.
A. The Non-putrefactive Type.—1. The Welch or Frénkel gas bacillus (bacillus
phlegmones emphysematose).
Morphology—The Welch or Frankel gas bacillus (described by French authors as
Bac. perfringens) is found in the earth, dust, soiled uniforms of soldiers, trenches and in the
intestines. It is a short plump bacillus with square end, immobile, without flagellae. It is
absolutely Gram positive, and can be demonstrated to possess a capsule (Buerger method).
Spores.can be but rarely demonstrated.
It is easily cultivated according to the usual anaerobic methods. It can be most easily
recognized and cultivated by animal inoculation with the employment either of a rabbit in
whose ear vein a culture is injected intravenously, or by subcutaneous injection into a
guinea pig. In these animals, if they be killed shortly after inoculation, and placed into the
incubator, intensive gas production can be demonstrated.
Toxins and Antitoxin Formation.—The question as to the production of
toxins is still a mooted one. Certain authors have found that sterilized
cultures are not virulent for guinea pigs. Passini, however, claims to have
found toxic substances in the cultures of gas bacilli that are lethal for the
animal. Klose reports the isolation of a toxin in cultures, which produces
hemorrhages and local necrosis in guinea pigs; and, when injected intraperi-
toneally, causes dyspnoea, fever and death. Intravenous injecotin was
MICROBIC GANGRENE 191
followed by spasm and rapid exitus, the liver and spleen showing hemorrhages
and marked anemia.
By the appropriate treatment of dogs and rabbits, this author was able
to produce an antitoxin with which he could protect guinea pigs against a
lethal dose of the organism.
2. The Bacillus of Malignant Edema.
Morphology.—Several types of bacillus of malignant edema have been described; a
Gram negative type with flagellae, and highly pathogenic for rabbits and goats. These
animals succumb in a very short time with severe symptoms of malignant edema. In stab,
gelatin cultures, a cylindrical or bell-like fluid liquifaction takes place.
A Gram positive type has been recognized. ‘This is pathogenic for guinea pigs, the
animals dying within 24 hrs. with marked edema. Rabbits, however, are non-sensitive to
this type, except for slight local edema that rapidly disappears.
A third type is also Gram positive, is also pathogenic for rabbits and guinea pigs and is
said to be identical with Aschoff’s gas edema bacillus.
Pfeiffer and Bessau! distinguish between the bacillus of malignant edema which is unable
to produce putrefaction, and similar bacilli of the putrefactive type, and which can produce
edema, although considerably less malignant than the true bacillus of malignant edema.
The latter bacillus is longer and more slender than the Frainkel-Welch bacillus, its ends more
slender and may grow in long forms. It has motility by reason of numerous flagellae. It
is variable to the Gram stain and frequently the majority of the bacilli are negative to Gram.
The spores are oval, usually central, in no way causing bulging of the bacillus. .
In guinea pigs subcutaneous inoculation with the bacillus of malignant edema, a charac-
teristic bloody exudate is produced without or with very slight gas production. Exitus
takes place early, and the bacilli can be cultivated after death both locally and in the inter-
nal organs and blood. Intravenous injection in rabbits is so toxic that death occurs within
a period insufficient to warrant the expectation of multiplication of the bacilli. The toxic
effect of the cultures seems adequate to cause death.
Toxin Production.—Ficker? and Silberstein’ were able to isolate toxins and the latter
author by the elaboration of a goat serum could neutralize the effect of a lethal dose
in guinea pigs.
3. The Aschoff Gas Edema Bacillus.
This author was able to isolate (1915-1916) a plump motile anaerobic bacillus appearing
in diplobacillus or chain forms, usually Gram positive, but occasionally negative. Spores
were noted in a central or terminal situation. In milk, gas formation and coagulation
take place. It is distinguished from the Frainkel-Welch bacillus through its motility.
It differs from the Ghon-Sachs bacillus being more virulent for rabbits.
B. Putrefactive Organisms.—1. The Pfeiffer-Bessau bacillus. ‘This organism has been
called the watch-hand (Uhrzeigerbazillus), has constant characteristics, more probably
identical with the bacillus putrificus (Bienstock). These are short Gram positive rods with
rounded ends and marked motility. Their spore formation is active, so that most of the
bacilli contain large mobile spores. These are usually terminal and cause an intumescence
in the body of the bacillus. hey are but slightly pathogenic. Subcutaneous injection in
guinea pigs produces local inflammatory infiltration; intravenous injection into rabbits is
harmless.
2. The Pfeiffer-Bessau Paroedema Bacillus ——This organism has morphologic similarities
with the bacillus of malignant edema, but differs from it in its putrefactive powers. ‘This is
not a single group, but its members show considerable variation.
The paroedema bacillus varies in size resembling that of malignant edema, poorly
motile or non-motile; some Gram positive, others Gram negative. The spores do not
alter the width of the organism and are usually central. They are but slightly pathogenic.
This type includes a group of organisms not absolutely similar.
3. The von Hibler Bacillus.~—This is a motile rod and usually a diplobacillus. The
spores are frequent and dilate the bacillus. It is Gram positive, but not as strongly as the
Welch bacillus. It is pathogenic for guinea pigs, white mice, rats, rabbits, etc. Except
for the observations of von Hibler, there are only those of Chiari regarding the occurrence
of this in gas phlegmon of human beings.
1 Pfeiffer and Bessau, Deutsch. med. Wchnschr., 1917, p. 1217, 1255, 1281.
2 Ficker, Med. Klin., 1917, No. 45, 118.
3 Silberstein, Wien. klin. Wchnschr., 1917, No. 52, 1672.
4von Hibler, Zentralbl. f. Bakteriol. Parasitenk. u. Infectionskr., 25, 513, 1899 also
Untersuchungen u. d. path. Anaeroben, Fischer, Jena, 1908.
192 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
4. The Ghon-Sachs Bacillus.——This is a strong anaerobic pleo-polymorphous coccoid
bacillary organism sometimes, shred-like, or fusiform. In some of the preparations
bifurcations have been noticed. It is motile and has lateral flagelle. Spores may be
central or terminal. ‘The bacilli are Gram labile, the young forms Gram positive, the older
ones but weakly so. There is no capsule.
Guinea pigs are killed by 0.5 cc. of a 48 hr. sugar culture, death being preceded by gas
formation, edema and hemorrhage. Intravenous injection into rabbits produces death
with extensive edema.
Toxins have been produced by Ghon and Sachs. The Welch experiment of intravenous
injection into animals results positive for gas formation when the animal is kept in the
incubator after death.
Anaerobic Bacilli—Organisms have been found in gas gangrene, whose causal relation-
ship to the lesions has not been established. Of these, there are the Novy? bacillus and the
Conradi-Bieling® bacillus.
The former is an aerobic, motile Gram positive bacillus without spores, characterized by
the presence of long and fixed forms, but slight motility, absence of spores, poor growth on
agar and strong pathogenic action on experimental animals.
The Conradi-Bieling bacillus resembles those described by Aschoff. The vegetative
form is a non-motile, Gram positive thick rod, producing marked gas formation, in carbo-
hydrate media, and liquefaction of proteid media, very pathogenic for guinea pigs that die
of hemorrhagic edema and gas formation, whilst rabbits are non-sensitive.
Relationship of the Various Bacteria.—The most dangerous of the bacilli that produce
gas gangrene are the Frankel-Welch and the bacillus of malignant edema, neither being
putrefactive types.
The organism found in gas gangrene has been detected in the earth and in the intestinal
tract. ‘This explains their easy entry into wounds, particularly during war. The Frinkel-
Welch bacillus is the most common of the organisms found.
Next in frequency is the bacillus of malignant edema as a causative agent in an aerobic
wound infection.
Clinical gas gangrene, it is true, is most frequently due to the Welch or edema bacillus,
but anaerobic mixed infection is common. ‘Thus, the tetanus bacillus is not infrequently
admixed in such infections.
Furthermore, anaerobic bacilli may be associated with aerobic organisms, namely, with
streptococci, staphylococci, bacillus coli, bacillus pyocyaneus, proteus and others. The
streptococcus is particularly important, indeed, may be so preponderating so as to appear
to be the gas producing organism.
Some authors believe that certain of the gas producing organisms may be changed into
other types. Thus such mutation is said by Aschoff to occur, also by Conradi and Bieling,
when a vegetative form of gas bacillus is without spores and flagellae and is grown upon
proteid media. A conversion into a flagellated, spore-bearing form results. Other authors,
such as Frankel, desire to controvert this assumption, suggesting that such observations
were due to the presence of a mixed infection.
Pathological Anatomy.—The most important lesions in gas gangrene
are those occurring in the musculature, the alterations in the other tissues
being secondary. ‘The muscle becomes pale red, dry and filled with small,
glittering, silver-like gas bubbles. Later, it takes on a brownish or blackish
tone with greenish tint and the gas bubbles enlarge. ‘Then fluidification of
the muscle into a blackish, brown, pasty substance with large gas bubbles
occurs. Ata distance from the primary focus, the muscle undergoes areas of
waxy necrosis, becomes greyish-yellow and like fish meat. Associated are
small hemorrhages giving the muscles a variegated appearance. ‘The inter-
muscular connective and subcutaneous tissues are at first infiltrated with a
brownish yellow edematous fluid, that is striking because of its large amount.
Microscopic examination also reveals characteristic changes particularly
in the muscle tissues. The gas bacilli are present in large numbers, accumu-
1 Ghon-Sachs, Zentralbl. f. Bakteriol., 34, No. 4-7, 1903; also 35, No. 6, 1904; also
36, No. 2, 1904.
2 Novy, Ztschr. f. Hyg., 17, 18094.
3 Conradi-Bieling, Feldiarztl. Beil., Miinchen. med. Wchnschr., 1916, 133 (49), 1023
(455), 1561 (705); also Berl. klin. Wchnschr., 1917, No. 19, 440.
MICROBIC GANGRENE 193
lating in the connective tissue and fatty septa, extending to the subcutaneous
tissue and diminishing in number towards the skin itself. In the lumina of
the veins, occasional gas bacilli will be found, but not in the arteries.
Microscopically, therefore, the situation of the bacilli corresponds to the
assumption that the lesion is primarily one of the muscle. However, to be
exact the bacilli actually lie first, in the perimuscular or perifascicular con-
nective tissue and in the lymph spaces. By virtue of the activity of the bac-
teria the muscle fibers undergo fluidification with gas formation, there being an
absence of any inflammatory and cellular reaction. Rounded spaces about
the muscle fibers represent the gas bubbles. Pari passu with gas formation
there is a continuation of the degenerative condition of the muscle. The
fibers of the latter become fragmented, degenerate into hyaline bodies and into
minute particles. All of these detached and separated pieces of muscle
element become fluidified into a structureless mass, in which no recognizable
histological elements are then to be found. The absence of inflammatory
reaction is characteristic for pure gas bacillus action, for leukocytic infiltra-
tions usually indicate mixed infections with cocci. In addition, there is
marked edema of all of the tissues.
The three stages in the development of the destructive lesions are recog-
nized by certain authors.
First.—A primary focus develops characterized by the entrance ofa foreign
body (piece of clothing or shot) in a bullet tract; in it there is more or less gas
formation in the subcutaneous tissue and musculature. In this zone there
are numerous bacilli with spores and also free spores.
Second.—Adjacent to this and varying in width there is a zone of strong
hemolytic edema of the subcutaneous tissue with gas bubbles, containing
bacilli without spores.
Third.—A third zone without bacilli but with toxic yellow edematous fluid
infiltrating the tissues.
Gas Formation in the Internal Organs.—Welch and Nuttall! called atten-
tion to gas formation in organs due to the action of the bacillus aerogenes
capsulatus. Although the occurrence of gas formation in the organs was at
first demonstrated postmortem in experimental animals, Welch believes
that such gas formation can occur during life. Other authors take excep-
tion to this view.
‘The more recent observation during the war period would concede the
possibility of antemortem changes of this nature, with, however, the reser-
vation that such occurrence precede the lethal outcome by but a short time.
The Blood Vessels.—In cases of gangrene due to infectious processes, it
has always been a mooted question as to whether the vascular lesion or
direct bacterial action is responsible for the gangrene.
In gas phlegmon blood vessel lesions have been regularly encountered.
Some authors have described a fatty degeneration of the vessels and a prolifer-
ating endarteritis with gas gangrene. Legros describes also an obliterating
endophlebitis. Inasmuch as the entry of the bacteria into the blood vessels
has not been demonstrated, it is believed that the lymphatics are invaded and
possibly the capillaries, the latter portal of entry explaining the bacteriemia.
Bacteria, however, have been shown to enter the vein walls, in gas gangrene
when the bacilli of malignant edema are associated.
Period of Incubation.—Since the gas bacillus can vegetate in the wound
for some time, the period of incubation varies. As a rule, manifestations
appear within the first four days.
1 Welch and Nuttall, Bull. of the Johns Hopkins Hosp., 1892, 3, 81.
13
194 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
According to Hancken! the gas phlegmon appears on the first day in 21 per cent; on
the second day in 33 per cent; on the third day in r5 per cent; on the fourth to the sixth day
in 4 per cent; on the seventh to the eighth day in 3 per cent, and from the eleventh to
the twentieth day in 1 per cent of the cases. Of 119 cases studied by Franz? gas for-
mation was noted 29 times within the first two days; 18 times after three days, 14 times
after four days.
Occasionally there is a very short period of incubation no longer than a
few days after injury. It is said by certain authors that infection may be
carried through field hospitals, through kitchen utensils, dishes and instru-
ments. This is doubted by others. For it is known that war wounds
often harbor anaerobic organisms that remain dormant for weeks or months, ~
and then by reason of subsequent tissue injury light up and become activated.
Latent Infection with Anaerobes.—It is believed (Melchior) that organisms of this type
may be buried for a long time even in healed wounds and become active after weeks or
months. ‘This has been shown to be the case with the tetanus bacillus,? when buried
bullets or shot fragments are removed from old scars and the symptoms of tetanus develop.
The spores of the tetanus bacillus are said to remain for a long time in the scar and are
activated and made virulent through the trauma of operation. Similarly, gas bacilli can
be reactivated. Indeed Wieting‘ reports a gas phlegmon following grenade wound with
healing. Six months later, after an attempt to remove the imbedded metal, gas infection
occurred with a lethal outcome. Enough cases in which the primary wounds had already
healed with good cicatrization have been described to confirm the correctness of such
observations (Melchior,® Kiittner,® Hodesmann’).
Pathogenesis of Gas Gangrene.—It has been said that the majority of all
war wounds contains anaerobes. Bacteriologists working in the neighbor-
hood of the battle fields have found gas bacilli in a large percentage of wounds
during the Great War, though no clinical manifestations were present. Even
in ordinary infected wounds gas bubbles were not infrequently seen, so that
from the practical standpoint it must be accepted that almost all of the
wounds contain gas bacilli. This does not signify however, that all wounds
become gas phlegmons, inasmuch as special factors must be present to facilitate
the activity and develop the virulence of the anaerobes.
Two additional factors, namely, earth infection and special wound con-
ditions are necessary. Entrance of earth carries with it anaerobes that have
been derived from the excreta of animals. Such earth is carried there by
hand grenades, fragments or even when pieces of clothing are carried in by
bullet shots.
The bad wound conditions referred to include laceration, contusion,
extensive compression and detachment of tissue fragments with tearing of
vessels and circulatory insufficiency of the wound. Anaerobic organisms
develop rapidly in the necrotic tissue. The leucocytic poisons elaborated
and the negative chemotactic reaction induced by the organisms explain the
absence of the usual cellular exudate.
The Incidence of Gas Gangrene.—Amongst the wounded in the late
war, gas symptoms are said to have occurred in the following frequency.
Wieting 3—5 per cent, Marwedel$ 2.8 per cent, Rumpel® 3 per cent and Franz ”
1 Hancken, Feldiarztl. Beil. z. Miinchen. med. Wchnschr., 1916, 1030 (462).
2 Franz, Deutsch. med. Woch., 1917, 39, 1220; also Bruns Beitr. z. klin. Chir., 1917,
106, 443; also Deutsch. med. Wchnschr., 1917, 14, p. 446.
3 Buerger and Heimann, Am. Jour. Med. Sc., Aug. 19, 1905.
4 Wieting, Deutsch. Ztschr. f. Chir., 1917, 141, 1.
5 Melchior, Berl. klin. Wchnschr., 1915, 5; 97.
6 Kiittner, Bruns’ Beitr. 103, 300, 1916.
7 Hodesmann, Deutsch. med. Wchnschr. 1917, 22, 687.
8 Marwedel, Feldarztl. Beil. z. Miinchen. med. Wchnschr., 1915, 30, 1023, 479.
® Rumpel, Samml. klin. Vortr., 1917, '736, 39, 329.
10 Franz, Bruns’ Beitr. z. klin. Chir., 1917, 106, 443.
MICROBIC GANGRENE 195
2percent. Where hand to hand battles occur gas bacillus cases are frequent;
also where rescuscitation facilities are poor and wounds are neglected.
During the wet period with considerable rainfall, cases are more frequent
than in dry periods, probably due to the wetting of the clothes and accumu-
lation of anaerobic organisms in clothing already soiled with earth.
It was by far more prevalent while fighting took place on the well ferti-
lized fields of Belgium and France, than in the mountainous regions of the
Italian and neglected forests of the Russian fronts.
Localization of Gas Gangrene.—In view of what has been said, gas
gangrene must be expected in those portions of the body where muscle tissue
is present, particularly where large muscle masses occur, namely, in the
extremities. Thus, the lower extremity is more frequently affected than the
upper (2/4 times). It occurs in the trunk, where there are large muscle
planes; but rarely is it found in the region of the head and neck, infrequently
affecting the foot and hand. It may be multiple, implicating more than
one extremity.
The cases in which gas phlegmon of the brain occurred are not due to the
organisms described here, and doubtlessly are the result of extension from
head wounds containing anaerobes. Gas gangrene of bones does not occur, nor
of the abdominal organs. Reports of authoritative cases of gas infection of
the liver have not been forthcoming, and the spongy liver reported at some
autopsies (Schaumleber) must be regarded rather as a postmortem process.
Types of Gas Gangrene Infection.—Epifascial gas phlegmon of more
benign nature has been differentiated from the malignant subfascial form
(Payr!). The former usually heals after multiple incisions; the latter is
fulminating, converting the muscle into a pasty mass; the extremities die off
and require amputation or exarticulation to save life. The deep form of
infection corresponds to the gas gangrene and gas phlegmon of other authors
and is well accepted. The superficial form is regarded as a less virulent type
of infection, and is thus described.
The Superficial Form.—Its seat is between the skin and fascia, the muscle
being uninvolved. The skin is edematous and shows deep orange or almost
coffee colored patches. The subcutaneous tissue is infiltrated with amber
colored fluid; the skin may show blebs; and subcutaneous crepitation due to
gas can be elicited. The fascia is not necrotic, but the underlying muscle
seems to be healthy. The general systemic condition shows marked disturb-
ance, with fever and rapid pulse; but the prognosis is good. Some authors
(Bier?) refuse to accept this type as being one of true gas phlegmon, believing
that the epifascial form of Payr is also a muscle disease due to infection of a
bullet wound and represents an extension of a deep focus, one of such slight
virulence as to give the above described manifestations. It is noteworthy
that true gas phlegmon does not occur after bullet wounds that fail to
implicate the musculature.
In short, according to some the epifascial form may be regarded as a mild
distribution of this infectious process in superficial planes, and arising from a
primary deeper focus. It differs from the true gas bacillus infection, in that
it usually yields promptly to conservative treatment with multiple incisions.
Summarizing the types of gas infection we may speak of the following:
First, local gas phlegmon which is benign and has no tendency toward
unlimited extension, but localizes itself involving single muscles.
1Payr, Miinchen. med. Wchnschr., 1915, 57; also Med. Klin., 1916, 442.
2 Bier, Med. Klin., 1916, 14, 355.
196 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Second, progressive gas phlegmon which is malignant, in that muscle disin-
tegration may extend over the whole of a portion of the body (member) and
usually ends in gangrene; and
Third, anaerobic sepsis which extends rapidly without bounds, is attended
with severe general symptoms, and terminates fatally.
A. The Toxins of Gas Gangrene.—The general symptoms correspond well to the clinical
picture of a severe poisoning, the toxins being partly of bacterial, partly of tissue origin.
The question of the development of a true toxin from the gas producing organism is a
mooted one as regards the Frinkel-Welch bacillus. However, in the case of the bacilltis
of malignant edema, true toxins have been demonstrated (Ficker!), the intravenous injec-
tion of very small quantities of which, produces a lethal effect in rabbits. This finding
would lead to the expectation of appropriate serological treatment.
According to Wassermann? all gas bacilli produce a similar poison, just as staphylococci
produce a staphylolysin, so that this author believes that the poison is derived rather
from degeneration of the bacterial bodies, than from products of their action.
Clinically, however, there seems to be evidence in favor of the elaboration of a bacterio-
genic blood poison. Indeed, one that attacks the hemoglobin of the blood. The Frankel-
Welch bacillus, also the Aschoff, have a lytic effect on the red blood cells. Other authors
(Kamen*) speak of a toxin with a specific action against the leukocytes (leukocidin),
in addition to the active, negative chemotactic action of the poison. The most injurious
effect of the bacillary poison is the chemical action on the hemoglobin, which is liberated
from the red blood cells, and converted into methaemoglobin. Hemoglobin, therefore,
appears in the blood serum and inthe urine. Clinically, this action has been observed in
puerperal processes, and an attempt made to correlate the brownish, cyanotic skin color,
air-hunger, and a brown blackish appearance of the urine, with the production of the
hemoglobinaemia and the hemoglobinuria. Such severe disturbances in the blood, however,
have not been observed in gangrenous processes, but rather in the puerperal. Enough data
has been forthcoming to confirm the theory of the existence of a toxin. The yellowish and
brownish spots of the skin have been regarded as due to hemolysis, and the marked icterus
in the lethal cases, as due to the rapid degeneration of blood cells.
The histogenic poisons developed locally have not been thoroughly studied. It has
been shown that autolysis of tissues produces a poison, and here the muscle tissue in its
degeneration might be considered as the origin of a toxin. The symptom of marked collapse
has been due to anaphylactic shock. As the muscle protein breaks down through the pep-
tonizing action of the bacilli, toxalbuminates or foreign body proteins are absorbed, cause
hypersensitization and anaphylactic symptoms. Furthermore, acids—carbonic, lactic,
butyric, propionic, etc.—as they are formed in the process, are said to irritate the respira-
tory centers, and produce Kussmaul’s type of breathing.
General Symptoms.—In the severe cases of gas gangrene the general
symptoms are marked, collapse being an early sign of a rapidly progressing
gas gangrene. ‘The face has peculiar pale appearance, whilst the tongue
remains moist. The pulse becomes very rapid, so that a frequency of 140-
160 is not unusual. The blood pressure sinks rapidly, the lips become cyan-
otic. Striking changes in respiration are noted, often of the Kussmaul type,
similar to that of diabetic coma. Dyspnoea with the employment of all the
accessory respiratory muscles is characteristic, due to central irritation of the
respiratory center. This manifestation has been explained on the assump-
tion that acids elaborated in the gangrenous process are absorbed, or that
bacteria produce carbonic acid in the blood itself (Pribram) that acts directly
upon the respiratory center.
The temperature is not usually high, may be normal or subnormal, and
it is only when there is slow development of gangrene that there is elevation.
Icterus is a dangerous and grave manifestation, an indication of anaerobic
sepsis, and that the hemolytic process is making itself manifest in the circu-
lation. The assumption that liver changes are responsible does not seem
1 Ficker, Med. Klin., 1917, 45, 1181.
2 Wassermann, Med. Klin., 1916, 17.
* Kamen, Zentralbl. f. Bakteriol. Parasitenk. u. Infectionskr., 1904, 35, 554-686.
MICROBIC GANGRENE 197
tenable, in view of what has been previously said regarding liver lesions.
Vomiting and singultus are often associated with the icterus. Marked
hyperhidrosis is striking.
The blood picture very soon becomes altered, the hemoglobin being diminished, and the
erythrocytes showing the picture of anemia with marked anisocytosis (macro- and micro-
cytes). The white blood cells show changes, there being eosinophilia and leukopenia.
The absence of increase in the number of neutrophiles is said to be characteristic for gas
gangrene. The blood picture persists even after convalescence for a considerable period
of time, with a marked anemia, poikilocytes, polychromasia and megalocytes.
There is diminished coagulability of the blood. The urine contains
albumin, granular casts, often blood.
All of these symptoms may be present with complete conservation of
consciousness. Often euphoria is noted, and the picture is not unlike that of
poisoning by serpent venom, and sometimes of pancreas necrosis, all being
manifestations of severe intoxication.
Local Symptoms. Zhe Wound—Where the wound is wide open, the
musculature becomes dark, blackish and crepitates, and the uninvolved
muscles are glassy by reason of extensive infiltration with edematous fluid.
Gas bubbles glitter here and there like pearls in the tissue. The skin edges
become necrotic. The absence of inflammatory reddening and heat is charac-
teristic. Whenit is present, it is due to mixedinfection. The fluid of the pure
cases of gas bacillus infection is serous or resembles laked blood filled with
bubbles of gas. Swelling and pain are always present, the result of collateral
edema. ‘The regional glands are not enlarged.
The Skin.—Where the process is developed in the depth, the skin is at
first but little involved. Often, over the muscle focus, the integument has a
white, glistening, swollen appearance, in which the dilated veins are promi-
nent. When the gas formation approaches the skin, characteristic changes
appear, namely, a brownish or orange colored patch, or bluish or violet areas
of discoloration. With the former there may be blebs with watery or yellowish
fluid, that are distributed in geographic figures or discrete fashion. In the
region of the brownish spots, the skin may undergo a leather-like necrosis,
and an incision into it evokes no bleeding. Where the bluish discoloration is
present, the gangrene is more intensive, the skin dies off rapidly together with
large parts, or the whole of the extremity. Such blue patches are always
the precursors of total necrosis and gangrene involving all the layers. The
brownish patches indicate more limited necrosis often only of the skin.
When patches of skin are sequestrated, secondary infection with suppuration
may take place.
The Gas Formation.—This is the most characteristic symptom, being the
product of the breaking down of the muscle carbohydrates and the decompo-
sition of proteins. This accumulation of gas may be so. enormous, and its
migration so distant that when the lower extremity is involved, gas bubbles
are said to have travelled into the subcutaneous tissues of remote parts. The
distension may be so great that incision into the skin gives rise to a blowing or
puffing sound. Palpation or percussion suffices to detect the presence of
gas. X-ray examination shows free gas in the tissues. In the picture, spots
or streaks between the muscle and into the subcutaneous tissue can be visual-
ized, in territories far removed from the bullet wound.
The Edema.—Usually marked edema accompanies gas production, and is
responsible for the appellation “‘gas edema.”’ The places vary, according to
reports, some having marked gas production without gas edema, others marked
edema without gas. The edema of gas gangrene is rather characteristic. It
198 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
is of yellowish color or serous, causing marked bulging of the subcutaneous
tissue, and muscular interstices and vascular sheaths. This is very striking
about the sciatic nerve. The edema can become brownish due to blood
admixture. Two views as to the significance and purpose of the edema have
been suggested. According to one it is defensive and tends to combine and
nullify the action of the toxins and lytic products. According to other views
the edema has a contrary function, namely, in that it contains aggressins
which are toxic for the cells of the body. As such it would assist the bacterial
action as an advance guard.
The Gangrene.—This should be described under the classification of infec-
tious gangrene, being the direct clinical expression of the action of certain
bacteria. Gas gangrene, occurs directly in the infected wound, and not at the
termination of an extremity. In this way it differs from the gangrene that
results from injury of important vessels. The necrosis begins in the muscle.
The action of the bacilli and the development of gas produce a pale red
discoloration of the muscle which gives way to a darker color. Finally, as
fluidification takes place, a chocolate porridge-like mass is formed. All the
individual muscles are not equally affected, so that on cross-section, at ampu-
tation, or autopsy, the mottling with the contrasted involved and non-
involved groups is striking.
From here the gangrene extends into the external skin which becomes
bluish or violet in color, and then grayish black. The epidermis is lifted off
with the formation of bloody blebs, and the process extends more rapidly
peripherally than centrally.
When the gas necrosis surrounds the limb so as to involve all! the circu-
latory channels, the peripheral parts show evidences of impaired circulation,
in absence of pulse, anemia, and coldness. In this way a secondary anaemic
gangrene of the peripheral portions of the extremities may result because of
poor nourishment. These two processes, therefore, may meet and become
confluent, one descending, the other ascending.
The process of mortification may be so rapid as to implicate a whole limb
within a very few hours, and is due to the enormous rapidity of the multi-
plication of the organism. ‘Thrombosis of the large veins may add to the
rapidity of the mortifying process. Some authors attribute the fulminating
form of gangrene to the contractile effects of the toxins on the vessels; others,
to the accumulation of products that cause necrosis by pressure.
Vessel Injury and Gas Gangrene.—When large vessels of an extremity are injured by
bullet wound, or when it becomes necessary to ligate large vessels such as the popliteal
because of hemorrhage, the liability to gas gangrene infection is already present and the
progress of such infection is greatly enhanced. Thus, after ligation of the popliteal during
the Great War, it was observed that gas infection developed frequently, necessitating ampu-
tation. Of 39 cases studied by Bier and Specht! in which amputation for gas gangrene
was necessary, there were 33 in which injuries to the large arteries had occurred. Accord-
ing to some authors, however, the gas formation is a secondary process, consequent upon
the arterial thrombosis, when anaerobic, saprophytic organisms multiply in the dead tissue.
Clinically, however, it is difficult to differentiate the two types, and it must be accepted
that circulatory disturbances are an important factor in predisposing to anaerobic infection.
Diagnosis.—In severe cases the diagnosis is easy. The so-called anaer-
obic sepsis is characterized by the altered breathing, the deep collapse,
the weak pulse, with conservation of consciousness. The progressive gas
phlegmon with its edema, emphysema, foul odor, discoloration of the skin,
the gangrenous change of the muscle tissue, the peculiar pallor of the face
1 Bier and Specht, Bruns’ Beitr. z. klin. Chir., 1916, 101, 271.
MICROBIC GANGRENE 199
with the poor general condition—all these are characteristic manifestations.
Severe pain often initiates the onset of the process, and when it occurs, a few
hours or a day after the injury, is a premonitory sign of significance. When
in doubt, an incision is indicated which may bring to light the peculiar
change in the muscle, or possibly even gas. Severe streptococcus phlegmon
may also produce gangrene of the extremity, but gas is not present, nor is
there a characteristic sound on percussion.
Morbidity and Mortality.—Early in 1918, Gross! had 2,796 wounded men pass through
his hands, of whom tor (3.6 per cent) developed gas gangrene. Late in 1916 he treated
1,676 wounded men,? 33 of whom (1.9 per cent) developed gas gangrene. In October,
1918, Sieur and Mercier* reported that fewer than o.5 per cent of the wounded developed
gas gangrene in the advanced and intermediate zone. This was undoubtedly due to
improved hygienic conditions and character of the soil (non-fertilized). Lardennois‘
in 1916 reported 500 cases of gas bacillus infection with 15 per cent mortality; and Ivens®
in 1917, 460 cases with 9.5 per cent mortaity.
Regarding definite gas gangrene as distinguished from gas bacillus infection in general,
Gross, in 1916, listed ror cases with 56.5 per cent mortality, while Ivens, in 1917, reported
107 cases with a mortality of 26.4 per cent. It must be emphasized here, however, that of
the cases reported by Gross, those which were treated within twelve hours after the wound
was received had a mortality of only 10.9 per cent. This indicates more clearly than any
description could, the importance of early treatment.
Treatment.—The general principles include the following: detoxication
by serum; control of shock; the intravenous injection of sodium bicarbonate
for acidosis; the early and thorough removal of all injured tissues, infectious
agents and foreign bodies by surgical intervention, although it is not always
necessary to remove large areas of skin and subcutaneous tissue. All sutur-
ing is to be avoided; free drainage is to be instituted; the proper splints
applied; and Carrel-Dakin solution used. The question of amputation
depends on the condition of the patient, the extent of infection, its proximity
to the body and whether or not the infection can be controlled by conserva-
tive measures.
For the collapse symptoms hypodermic stimulants, hypodermoclysis,
intravenous injection of glucose solution (5 per cent), subcutaneous injections
of adrenalin and salt solution are indicated. In view of the hypothetical
assumption that the systemic manifestations represent the effects of acid
intoxication, subcutaneous soda solution (44 per cent) and intravenous
administration have been followed by definite results. Hypertonic solution of
salt intravenously injected is also recommended (Hercher, introducing
sodium chlorid 8.5, potassium chlorid 0.3, calcium chlorid 0.3 with water
up to 100).
Van Beuren gives the following general rules used for treatment of gas’ bacillus infection
during our recent war. First, operate as early as possible. Second, use nitrous oxid-
oxygen anesthesia if possible. Third, prepare the part with the minimum amount of delay
and trauma. Fourth, avoid tourniquets. Fifth, make incisions longitudinally and half
again as long as you think they need be, both in the skin and fascia. Sixth, leave as much
skin as you dare in your débridgement. Seventh, go between, rather than through, normal
muscles, and do not cut across them unless you have to (better a long separation between
two than a short cut across one). Eighth, however open the wound as thoroughly and
freely as you possibly can. Ninth, excise all torn, crushed, discolored, noncontractile
muscle, until you have left only that which is firm, of normal color, actively contractile, and
which bleeds readily. Tenth, make a careful and conscientious search for and remove all
loose bone and foreign bodies, especially clothing and blood clots. Eleventh, stop the
1 Gross, G.-Bull. de l’Acad. de med., Dec. 26, 1916, 76, 586.
2 Gross, G.-Bull. et mém. Soc. de chir. de Par., 1917, 43, 636.
8 Sieur and Mercier, Bull. de Acad. de méd., Oct. 29, 1918, 80, 394.
4Lardennois and Baumel, Presse méd., Nov. 16, 1916, 24, 500.
5 Ivens, Med. Press & Circular, 1917, 103, 12.
200 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
bleeding; leave the wound wide open and separate its walls with wet gauze, laid in, not
packed in. Twelfth, use Carrel-Dakin tubes, if you know they will be properly cared for,
otherwise omit them. Thirteenth, use plenty of dressings and make careful splint fixation
of the part. Fourteenth, do it all as rapidly as you possibly can.
We may divide the treatment into surgical treatment, treatment by
hyperemia, by oxygen insufflation, medical treatment, transfusion of blood,
and serum therapy.
Surgical Treatment.—In the mild cases of local gas phlegmon, wide and
extensive incision are the most reliable means for establishing a cure. The
incisions must be carried well into the healthy tissues, until bleeding muscle
is reached. ‘This is to be followed by loose tamponade drainage, the use of
Carrel-Dakin solution and splinting, to secure adequate repose of the parts.
When we can detect more extensive infiltration of the interstices of the muscle
with gas and edema; when the vascular sheaths are involved, and the process
is recognized in the discoloration of the skin, and subcutaneous emphysema—
the excision must be carried along such planes as seem to be involved, along
the vessel sheath and through the skin. The incisions through the skin are
best made in multiple fashion.
Where the affection is more virulent, and shows marked progressive
tendencies, more radical means are resorted to. So certain authors recom-
mend instead of the longitudinal incision (Fessler! and Friind?) transverse
incisions, which enable a more adequate and accurate investigation of the
muscle masses to be made. Indeed, in very bad cases, it may be necessary
to excise whole muscular territories.
When the gangrenous process threatens to invade the opposing groups of
muscles, to encircle the bone and to creep over the joint immediately above,
amputation is in order. The well developed gangrene of a portion of a limb
is also an indication. Should severe fractures through bullet wound (of the
long bones) complicate, amputation is also recommended. Even when the
gangrenous process is not as yet in evidence, but when the general symptoms
are severe, with rapid and weak pulse, threatening collapse, ablation of the
limb must be considered.
It is best to ablate in healthy tissues, at least beyond those macro-
scopically involved and beyond the edema, although cases have been reported
as cured where the amputation was very near and even through diseased
parts. In very extensive cases, exarticulation may be necessary. This
procedure is not so dangerous when done through the shoulder and gives
good operative results. A similar operation through the hip, however, is a
dangerous surgical procedure with a high mortality.
Lawson: believes that the best results can be obtained by treatment of the
subcutaneous tissues with nascent oxygen in the form of injections of neutral
hydrogen peroxide. Infiltration of the healthy tissues with oxygen above the
line of spreading gangrene is sufficient to check the advance of the infection,
and in the majority of cases, the limb may be saved. He believes that ampu-
tation of the limb for acute emphysematous gangrene is unnecessary, unless
all of the tissues are involved over an extensive area, thinking that high
amputation may prove fatal from shock.
Treatment with Hyperemia.—This includes active hyperemia and con-
gestive or obstructive (Stauung).
1 Fessler, Feldairztl. Beil. z. epee s med. Wchnschr., 1917, 10, 331.
2 Friind, Bruns’ Beitr.,1916, 98, 4
2 Birm. Med. Rev. aLO USS LXXVIL, D. G7.
MICROBIC GANGRENE 201
Obstructive Hyperemia.—Bier recommends the rhythmic method, claim-
ing good results. When the usual method is employed, 22 hours application
and 2 hours interruption are not recommended. Although these methods
have been well developed on the Continent and particularly in the Central
States, they have found but few adherents in America.
Oxygen Insufflation—Because of the danger of oxygen embolus, this
method has not won many supporters. It had been recommended in the
form of insufflation into the tissues. Intramuscular injection of 3 per cent
hydrogen peroxide has also been suggested with a fatal result (Borscher).
Local Medication.—Various types have been used, such as the washing
with peroxide, and Dakin’s solution. Charcoal has been used with a view to
combine with the aggressins formed by the bacteria. None of the local
methods of treatment have had worth-while results.
Blood Transfusion.—Both as a prophylactic measure before amputation
or after this procedure, blood transfusion is exceedingly valuable. It is
worthy of a trial for its beneficial effects in combatting the toxic results
of infection.
Serum Therapy.—For the elaboration of a dependable serum, it is
necessary to employ something that not only has an antitoxic function, but
also is anti-infectious, in the sense that it can inhibit the enormous multi-
plication of the organisms in this disease. The existence of both histogenic
and bacterial poisons, as a result of the action of the bacteria, makes it hard
to find an appropriate serum.
An antibacterial serum was prepared by the firm of Hoechst which is a polyvalent,
antibacterial, immune serum procured from horses. In the production of it, the Frankel-
Welch group, the gas edema group and the putrificus group were employed. It was given
a trial during the Great War in doses from 20-40 cc. Rumpel injected it locally, just
central to the wound; he also tried intravenous application. His results were considered
satisfactory in that the mortality was reduced. Anaphylactic symptoms appeared only in
a few cases. Aschoff compares a mortality of 43.9 per cent in the cases in which the
Hoechst serum was used, against a mortality of 68.7 per cent without any. Weinberg
and Seguin employed an antitoxic and bactericidal serum including the following group-
bacillus perfringens (Frinkel-Welch), sporogenes, cedematicus, vibrion septique and bacillus
hemolyticus (Weinberg and Seguin).}
Statistics on the efficacy of anti-gas bacillus serum are somewhat meagre, but are on the
whole favorable. Elser advises the following routine for serum treatment.
1. A prophylactic dose of polyvalent serum, given as early as possible after the receipt
of the wound, combined with tetanus antitoxin.
2. Bacteriologic examination of the wound and establishment of the presence of gas
bacillus infection and determination of the variety of the bacteria. The determination
can be made in about 24 hours.
3. Administration of the specific serum, either single or polyvalent or ‘‘ pooled,” accord-
ing as there are one or more gas formers found and also antistreptococcus serum.
Sacquepee? recommends the following procedure for differentiation to determine the
type of anaerobe present.
In each of four test tubes is placed 1 cc. of macerated gangrenous tissue and to three
tubes respectively is added 1 cc. of each of the three antiserums. After incubation for half
an hour the contents of each tube is injected respectively into one of four guinea pigs. The
one protected by the serum shows no reaction. The others die. They usually become sick
in from 6 to 12 hours.
The various reports generally agree that intravenous injection (while not always
possible) is to be preferred, in combination with deep muscular injection, proximal to, but
in the vicinity of the wound.
Dosage: 5-15,000 units of specific or pooled serum intravenously to be repeatedin 2
hours if no improvement occurs. At the same time, an equal amount is given intramus-
cularly in divided doses. This can be repeated in 24 hours, followed by daily injections.
1 Weinberg and Seguin, Miinchen med. Wchnschr., 1917, 152 and 848.
2 Sacquepee et de la Vergne, Bull. de |’Acad. de méd., 1919, 506.
202 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Anaphylactic reactions are rare. It is emphasized that sero-therapy is entirely auxil-
lary, and in no way replaces operative treatment of wounds. The time of application
should be as early as possible, since it is practically useless when the infection reaches the
stage of septicemia.
Gangrene Due to Pyogenic Bacteria.—The role of this type of organism
in causing tissue mortification has not been carefully studied so that we
can but dwell superficially on this theme. Enough is known, however, to
permit of the conclusion that streptococci of various types, and other organ-
isms when virulent, or in symbiosis, are able to cause extensive local tissue
disintegration in a direct fashion, or in a secondary or indirect way by virtue
of thrombosis induced locally in arteries and veins.
The direct alterations in some of the streptococcal forms are of a destruc-
tive type and are quite different from the usual purulent lesions. The skin
of the affected region may rapidly take on a yellowish, brownish or bronze
color, a significant appearance in these virulent infections.
The secondary gangrene of parts in or distal to the infected area, is often
of the dry type when digits are involved and due to a contiguous thrombotic
process in larger arteries and veins.
Dry gangrene of one or more phalanges may follow rapidly in the wake of
a severe infection of the palmar sheath, with or without infection of the
dorsum of the hand. Streptococcus hemolyticus is the more common offend-
ing agent. Dry gangrene of the fingers or toes may rapidly ensue, and is
probably due to thrombosis of the digital vessels at the base of the finger.
It is secondary in the sense that it is one of the complicating effects of the
infection on the larger source of blood supply. Therefore, it is not a necrosis
of tissue due to the direct action of the organisms as is the case with many of
the anaerobes. Extensive direct necrosis may here, too, be due to the bac-
terial influence.
The clinical course, which was well exemplified in one of the author’s
cases recently observed, may be briefly summarized as follows:
Severe infection apparently located in the palmar sheath of the index finger with
lymphangitis extending up to the elbow and above, and temperature of 104° for about one
day before the patient was seen by the author. Two small median incisions over the palmar
surface of the first and second phalanges liberated turbid fluid from the tendon sheath.
Another small incision over the dorsum within the zone of lymphangitis, permitted the
same type of fluid to escape. Within twenty-four hours following this incision, the lymph-
angitis had extended to the axilla, and the following condition of the hand required
further operative procedure. The dorsum was evidently the seat of an extensive strepto-
coccus infection, and the palmar infection had spread to about three quarters of an inch
farther down into the palm. The two distal phalanges of the fore-finger were bluish black
and gave all the signs and had all the appearance of an early stage of gangrene.
Multiple incisions were made over the dorsum of the hand, draining a large amount of
purulent fluid that had collected within twenty-four hours, and the palmar incision was
carried. three quarters of an inch farther down into the palm. By these incisions the infec-
tion was controlled, so that no further operative intervention was necessary. However,
the two distal phalanges became rapidly mummified.
Here we may assume that the streptococcus infection (streptococcus
hemolyticus in pure culture) was of such virulence as to cause contiguous
thrombosis in the digital arteries, and mortification of the two distal
phalanges.
GANGRENE COMPLICATING INFECTIOUS DISEASES 203
CHAPTER XXXV
GANGRENE COMPLICATING INFECTIOUS DISEASES
Typhoid Fever.—Recent authors (Klose!) have called attention to the
twofold causal elements that occasion vascular symptoms in the course
of typhoid fever, namely: The injury to the walls of the peripheral vessel, and
a central specific affection of the vasomotor center.
When the larger arteries are involved, thrombosis, hemorrhage and
gangrene occur; and the bacilli or their toxins may simply increase the
permeability of the capillary endothelium, and bring about edema and
transudates.
Hyaline thrombus formation resulting from parietal infectious injury
of the vessel wall, with stenosis of the vessels and localized circulatory distur-
bances are reported. Corresponding to these changes we encounter the com-
plication of typhoid fever, namely, hemorrhages into the various organs.
The larger arteries are described as containing foci of degeneration and
inflammation. Involvement of the cerebral arteries is reported in the litera-
ture (Jaffe?).
Gangrene of the peripheral parts of the extremity may be the issue.
External causes such as cold, and the chemical factors predispose to and
increase the severity of the gangrene. Necroses of the feet, fingers and
forearm, the genitals and nose have been reported. These were rather
common complications in the Great War, when toes were usually found
involved, although in certain cases, gangrene extended to the ankle or
higher. Sometimes it was symmetrical or multiple. Usually operative
intervention became necessary.
A prodromal stage is characterized by intense paraesthesiae and pain, and
sensory disturbances in the affected extremities. The pain may last for
weeks, and may be attended with pallor and a marmorated appearance of
the skin before gangrene appears. ‘The latter may attend the early part of
the clinical course, or after the temperature has attained the normal.
In infection with the paratyphus bacillus, mycotic aneurysms may develop.
When these are situated in the vessels of the extremities, circulatory dis-
turbances may result. Gangrene of the forearm was barely averted in a
case (Sick*) in which a mycotic aneurysm was located at the bifurcation of
the brachial artery.
It has been assumed that bacterial emboli entering the vasa vasorum are
responsible for the vascular lesions.
Gangrene in Recurrent Fever.—Symmetrical gangrene of the toes is one
of the complications of this affection. In some cases circulatory disturbances,
pain and cyanosis of the skin may precede the necroses. Perhaps in addition
to the action of the spirochetes, external factors such as cold may be con-
tributing causes.
For further consideration of gangrene complicating infectious diseases,
the reader is referred to Chap. LX XVI on Acute Arteritis.
1 Klose, Ergebn. d. Chir. u. Orth., 1921, 13, p. 74.
2 Jaffe, Med. Klin., 1918, nos. 9, 22, 23, 24.
3 Sick, Munchen. med. Wchnschr., 1918, p. 237.
204 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
CHAPTER XXXVI
INJURIES TO THE BLOOD VESSELS AND GANGRENE
The traumatic lesions of the blood vessels may be described as including
firstly, recent injuries; secondly, pseudo-aneurysms or that type which has
been described as pulsating hematomata; and thirdly, well developed
aneurysms.
Recent Injuries.—Statistics (Stich) taken from the Great War show wide
variations; but in the armies of the Central Powers from 40 to 45 per cent
of all injured, suffered vessel lesions. Not more than one-half of those who
received bullet wounds of the vessels arrived alive at the hospital stations.
Often spontaneous cessation of hemorrhage takes place, especially if of venous
origin. Injuries of the veins from bullet wounds are more common than
those of the arteries.
A knowledge of vein injuries is important, in that these may lead to remote
functional disturbances, even though the immediate effects do not seem to
be threatening. Indeed, the functional disturbances that follow may last
for years, while the cause thereof may be wholly over-looked.
Even bullet wounds of the arteries may cease to bleed spontaneously. If
these facts are taken into consideration, the incidence of vessel injury is in all
probability greater than statistics would show.
Bullet wounds of the peripheral arteries most frequently involve the
femoral and popliteal; wounds of the axillary and brachial arteries are some-
what less common.
Pathology.—The character of the vascular lesions would depend to a cer-
tain extent upon the character of the shot. Large grenade fragments or
shrapnel may occasion the severest tears. When the pieces are sharp the
vessels may be incised as if with a knife, and abundant bleeding ensue.
Tangential trauma may produce contused wounds and holes; or large vascu-
lar wounds may result with consequent retraction of the distal and proximal
ends of the artery. In the latter instance, bleeding may be but minimal.
If infection does not take place, thrombus formation and organization
follow. ‘The smaller vessels are usually torn through the action of infantry
bullets. In the larger vessels, the same shot causes extensive destruction, not
only by direct action, but by the secondary impact and penetration of con-
tiguous or nearby bony splinters. Circular and also slit-like orifices are
occasioned, the latter frequently being smaller than the caliber of the bullets.
The blunt forms of traumatism produce there types of injuries; (1)total
tearing with complete interruption of the continuity of the vessel; (2) partial
rupture with lateral injuries; and (3) rupture of the intima and media with
intact adventitia. Such lesions less frequently occur in the veins, but the
latter more often are injured in the neighborhood of comminuted fractures.
Injuries Due to Treatment.—Vascular injuries sometimes follow joint dis-
locations. More important are the. observations concerning injuries to
vessels in sequence of orthopedic attempts to correct position in old
dislocations.
The author recently had occasion to see a young woman in consultation, in whom the
femoral artery was torn in an attempt to correct an old ankylosed hip. Five days after the
injury, the greater part of the foot was in a state of gangrene; all the usual palpable arteries
of the extremity failed to beat, and there was an enormous hematoma occupying the
INJURIES TO THE BLOOD VESSELS AND GANGRENE 205
inguino-femoral region, with brawny sanguinous infiltration of a large part of the upper and
inner aspects of the thigh. Spontaneous cessation of the hemorrhage had occurred by the
pressure hematoma.
As many as 20 such observations are recorded by Ké@rte in dislocated shoulders.
Complete tears, as well as lateral holes, have been observed, and in 3 autopsies injuries of
the veins are reported. The factors responsible for the ruptures, were the employment of
excessive force, abnormal friability of the vessels, adhesions of the vessel sheath with the
ee bone or joint capsule or simultaneous fracture of the head of the bone (femur or
umerus).
Laceration of the blood vessels has been known to follow severe muscular
exertion. When brisement forcé for the treatment of ankyloses of the knee
joint, occasioned vessel rupture, gangrene of the extremity was a complica-
tion in 9 cases (Salzer?).
Gangrene of the lower extremities is a complication of severe general body
concussion and after burial or entombment under earth following explosive
shells that have penetrated into nearby earth. ‘The gangrene has often been
attributed to thrombosis of the vessels. In other cases, where the upper
extremities were also involved, the cause remained obscure, since the vessels
were found patent. Perhaps some of these eventualities are referable to a
traumatic vasomotor spasm (Chap. XCIII). When both artery and con-
tiguous vein are injured, a so-called arterio-venous aneurysm may develop.
Results of Recent Injury.—Partial injury of the vessel wall with laceration
of the inner layers, although unattended with hemorrhage, may lead to gan-
grene of the peripheral parts as a result of thrombosis and embolism.
Usually, however, hemorrhage is the first sign of vessel injury.
We may distinguish between internal and external hemorrhage depending
upon whether the blood appears ouside of the body, or not. The blood can
be extravasated into the tissues which it may destroy by compressive and
extensive forces, and form a spurious aneurysm.
The degree of hemorrhage depends upon the size of the vessel, and that
of the wound. If the blood does not find an exit externally, cessation of hem-
orrhage usually follows by reason of the pressure of the accumulating extrava-
sation; this may occur even without thrombosis. On the other hand, the
infiltration with blood may continue into the muscles of the thigh and gluteal
group until exitus occurs.
Bleeding from the veins is not as dangerous as the arterial, and more easily
arrested through compression bandages.
Another immediate sequence of injury to the veins is air embolus. This
may occur at operation, or especially as the result of bullet or war wounds.
Where the diagnosis can be made, the symptoms preceding death are pallor,
slight cyanosis, spasms of the facial muscles, sometimes opisthotonos and
cessation of respiration. A peculiar murmur through the vein wall is a signi-
ficant sign of the entry of air.
Thrombus formation in the vessels implicated in war wounds is not as
common as is supposed, at least as far as larger vessels are concerned. Borst?
believes that even larger tears and perforations may occur in vessels without
thrombus formation. Late thrombosis may occur in parietal or obturating
fashion, and then is said to bear some relation to secondary infection. As
pointed out in the Chapter on Thrombosis there is still much discussion as to
the réle of infection in the production of thrombosis. Stich reports extensive
thrombosis in larger arteries that he exposed because of the fear of secondary
hemorrhage in cases of bullet wound injuries.
1 Salzer, Wien. med. Wchnschr., 1884, No. 89. ; Aad
2 Borst, in Borchard-Schmieden, Lehrbuch d. Kriegs chirurgie, Barth. Leipzig, 1917.
206 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Where infection is associated with thrombosis as the result of blood
vessel injury, rapid extension of the thrombotic process not only in the
arteries, but in the veins may continue without interruption even into the
common iliac or inferior vena cava.t Where the thrombotic process is not
sufficiently extensive to cause gangrene, other grave sequelae may occur,
amongst which may be numerated the following: Recalcitrant edemas,
severe paresthesiz, and marked functional impairment of the limbs. :
When the circulatory symptoms are of milder degree, the patients com-
plain of a feeling of coldness, formication, and numbness. Compression
through extravasation of blood may cause symptoms without implication of
the larger arteries themselves, the hemorrhage ocurring from smaller vessels.
Spasm of the vasoconstrictors (Chap. XCIII) has also been observed
following bullet wounds in the neighborhood of large vessels. As an example
may be cited a case of Kroh.?
After an infantry wound of the inguinal region, a soldier complained of numbness and
formication in the foot. The femoral pulse above the bullet wound was barely perceptible.
The skin below the knee, inclusive of the toes, was yellowish white, cold, anemic, insensitive
to touch and to needle pricks up to the region of the upper calf. The pulse on the healthy
side was strong and full. A diagnosis of vasomotor spasm was made, and massage and
elevation were ordered. Nine hours later sensibility and pulses had returned to the normal.
In another case the same author demonstrated at operation that the vascular sheath
was infiltrated with blood, but not opened. When the femoral artery was exposed, its
caliber was about that of a knitting needle, but under the observation of the operator it
gradually returned to normal.
Complications.—The most frequent complications are nerve injury or
neuritis, pressure effects upon neighboring nerves or irritative phenomena.
In view of the proximity of nerves and larger arteries, it is comprehensible
that sensory disturbances are frequently associated with vessel injuries. The
proximity of the ulnar and median nerves to the brachial artery accounts for
the well known combination of vascular and nerve symptomatology. In
bullet wounds in this region, the following symptom-complex is not uncommon:
the extremity becomes cold and cyanotic, hyperhidrosis develops, and later
muscle atrophies and contractures, giving a picture not unlike that of ischemic
contracture.$
Some authors emphasize that actual organic implication of nerves is
altogether responsible for the vasomotor and contracture symptoms. On the
other hand, there are data available which suggest that the arterial lesions and
involvement of the periarterial sympathetic plexuses or nerves may give
similar clinical pictures (Chap. XCII).
Severe circulatory disturbances, usually of the upper extremities may
attend bullet wounds of large arteries and lead to ischemic contracture of the
muscles, without gangrene. Bier reports a number of cases in the upper
extremity, usually after injury to the brachialartery. The following example
may be quoted.
Bullet wound of the brachial artery of the right arm in a young lieutenant was followed
by severe contracture of the muscles of the forearm. About 6 years later the following was
the status: The musculature of the forearm was “stony” hard, and only slight motion was
possible in the stiff fingers, the wrist joint being ankylosed. The hand was cold, the sensa-
tion undisturbed, except in the ulnar territory, and the elbow joint mobile. The fingers
were in a position of marked flexion, and discolored bluish red; the peripheral pulses were
imperceptible.
1 See discussion of the stagnation thrombi associated with embolism when infection is
present, Chap. LXXXV.
2 Kroh, Bruns. Beitr. z. klin. Chir., 1917, 108, 61.
3 See case of embolism of the brachial artery operated upon by the author, in which such
symptoms developed, pp. 495, 496.
INJURIES TO THE BLOOD VESSELS AND GANGRENE 207
The lesions of ischemic degeneration following ligation of large or main
arteries of a member have been described (Leriche and Policard') as includ-
ing the following: In the marginal zones between regions poorly and ade-
quately supplied with blood (1) an absence of all inflammatory phenomena;
(2) characteristic changes in the small arteries and arterioles, namely, degen-
eration of the muscular elements of the media with conservation of the
-connective tissue.
In the ischemic territories the following muscle alterations are worthy
of emphasis: (1) a rapid degeneration of the muscle fibers that attains a
certain degree at which the process is held in statu quo over a long period of
time; (2) segmentation of muscle fibers in discs and the disappearance of
nuclei; (3) augmentation of the amount of fibrous connective interfibrillar
and interfascicular tissue, the nuclei here also being lost.
Injury of a Main Artery or Vein.—Wounds of large arteries give rise to
symptoms that vary according to whether there is a sufficiently large
wound to permit of the escape of the blood, or whether infiltration of the
deeper tissues with the escaping blood takes place, with the formation of a hema-
toma. When one of the chief vessels of an extremity is torn, the peripheral
portions of the limb, become pale, cold, somewhat insensitive to pain or
anesthetic. These manifestations may persist, or be evanescent. As a
rule, the collateral circulation becomes rapidly established, and it is only in
rare cases that gangrene follows an arterial injury, or wound, when the blood
can escape externally. However, when the tissues are infiltrated, and a large
hemorrhagic exudate is formed, gangrene is more frequently the issue.
Interesting and instructive observations could be made on the results of
injury of the femoral artery during the Great War. Only in some cases did
gangrene develop.
When there is an open wound-of the thigh involving the femoral artery or vein, lethal
bleeding takes place so rapidly that surgical aid rarely, if ever, comes into play. Where
the entering body is small and takes an oblique course, closure of the external wound may
take place, and by virtue of deep hemorrhage the collected masses of blood may by great
pressuré, bring about a cessation of the hemorrhage. Small holes in the femoral arteries
may heal spontaneously or lead to the development of traumatic aneurysm.
Late or secondary hemorrhages and secondary erosion of the vessel wall may lead to
grave consequences.
Sym ptoms.—The thigh is enormously swollen and tense. Large hematomata can spread
in the direction of the scrotum and perineum. Characteristic is the pulsation which when
it can be elicited over the hematoma, gives the picture of a pulsating hematoma. With this
there may be absence of the pulse in the dorsalis pedis and posterior tibial, circumstances
that make a diagnosis of injury of the femoral artery certain. However, the presence of
pulsation in the vessel does not necessarily indicate an intact femoral artery. Within a few
days a typical bruit can develop and this may be either systolic or systolic-diastolic, when
an arteriovenous aneurysm is present. :
Associated with the swelling are severe pain and paresthesiz, due either to injury tothe
nerves themselves or to their implication in the bloody exudate.
Secondary hemorrhages may take place through the bullet tract, and these are of grave
import.
Bes ndacy infection also may give concern, and may occur early within a few days or
late, even after a week.
1Teriche and Policard, Compt. rend. Hebd. de la Soc. de Biol., 1920, p. 415.
208 CIRCULATORY -AFFECTIONS OF THE EXTREMITIES
CHAPTER XXXVII
ANEURYSMS
Pseudo-aneurysms.—A false aneurysm or pulsating hematoma may result
from a condition in which an extravasation of blood remains in communica-
tion with an injured artery. Other appellations recently given to this condi-
tion are communicating or pulsating hematoma. By some authors this is
described as a transitional stage in the development of a traumatic aneurysm,
for in a few weeks the hematoma may become distinctly demarcated and
circumscribed against the surrounding healthy tissues, and become converted
into an aneurysm.
These pseudo-aneurysms or pulsating hematomata vary in size, depending
upon the caliber and situation of the injured vessel; also upon the size and the
form of the vascular wound, the initial treatment given, and the circumstances
attending the transportation of the patient. Thus, it has been observed
that relatively small vessels such as the radial artery give rise to hematomata
that are as large as those of subclavian origin. Pulsating hematomata are
usually larger in the case of arteries, than when a simultaneous injury of
artery and vein occurs.
Nor is there a constancy in the size of the hematoma. After cessation
of hemorrhage a shrinkage of the mass is observable due to resorption of
blood; or, by reason of increased pressure after exertion, constipation, or
other mechanical influences (sneezing, defecation) late hemorrhage into the
sac may occur with enlargement of the mass. Or, infection of the sac may
bring about similar changes in volume.
With the coagulation of the blood a stratified or onion-like deposition of
coagula takes place in the hematoma with white, red, and mixed thrombi.
Those masses that are in immediate apposition with the tissues become
organized first, and constitute the sac of the aneurysm, whereas the more
centrally situated contents are masses of cruor, blackish, reddish blood of
varying consistency. It is remarkable that the circulation may continue
in spite of the communicating thrombotic and cruor masses. Indeed, even
the peripheral pulses may be conserved.
Anatomically the pseudo-sac is made up of a thin fibrinous membrane,
composed of homogeneous fibrin enclosing leukocytes and red blood cor-
puscles. There is no endothelial lining in all of the recent cases.
Traumatic Aneurysms.—For a comprehension of the circulatory dis-
turbances of the extremities only the salient features of these types of aneu-
rysms and their réle in the production of vascular disturbances require
mention here. Further data with surgical bearing must be sought in the
surgical literature.
A traumatic aneurysm is produced by virtue of encapsulation of a pulsat-
ing hematoma. A distinction has been made between false and true aneu-
rysms. The former designation has been applied to aneurysms arising in
consequence of injuries to a normal vessel wall through dull or sharp force;
the latter has been referred to circumscribed or circumferential dilatation
of the vessel. A distinction has been made between two varieties; false
aneurysms in which there precedes a defect in the wall of the vessel, and true
aneurysms that are still lined with an attenuated and dilated wall. Some
authors would extend the term, aneurysm, so as to include all dilatations
TREATMENT OF INJURIES TO THE BLOOD VESSELS 209
irrespective of whether they develop spontaneously or after traumatic
lacerations.
_ The terms diffuse false aneurysm and circumscribed false aneurysm are found in the
literature descriptive of recent arterial injuries on the one hand, and older encapsulated
products on the other hand. Another appellative, encapsulated hematoma, either pulsat-
ing or non-pulsating has been suggested (Schum).
Symptoms.—Only those features concern us here that relate to the circu-
latory disturbances occasioned in the affected extremity. Referring briefly
to the general symptomatology, this may be summarized as follows: first,
tumor formation brought about by the presence of one or more partly or
completely organized blood sacs arising from the vessel; second, a pulsation
of this sac synchronous with the arterial pulse; third, a murmur synchronous
with the cardiac systole; fourth, circulatory disturbances in the peripheral
course of the artery and its branches with changes in the peripheral pulses;
fifth, manifestations due to implications of accompanying nerves (irritative
phenomena of the sensory fibers, paraesthesia pain, paralytic symptoms)
with involvement of either motor or sensory fibers; and sixth, contractures
implicating neighboring joints.
We shall dwell only upon those circulatory and neurogenic disturbances
that are germane to the subject matter in hand here.
Circulatory Symptoms.—The peripheral pulse may be felt beyond the site
of the aneurysm, or may be absent due to complete occlusion of the artery,
because of compression of the artery by a sac against non-yielding supports,
such as bone; or due to kinking of the arterial channel from overdistension
of the sac and the direction of its growth. When a pulse is present, it may be
diminished as compared with the healthy side.
Complications and Gangrene.—The most important of these is hemorrhage
which can occur externally or into the tissues, particularly in traumatic
aneurysms. Late secondary hemorrhage is not uncommon and a not in-
frequent cause of a lethal outcome. Indeed, it may occur from the first to the
fifth week, or after 2 months.
_ The symptoms of internal bleeding are the following: increasing pain in
the extremity, paraesthesia, swelling edema. As the result of the compressing
action of the hematoma, ischemic contractures, disturbances in the nutrition
of the whole extremity, and even gangrene may occur.
CHAPTER XXXVIII
TREATMENT OF INJURIES TO THE BLOOD VESSELS
In recent injuries of the blood vessels, our aim should be a two-fold one;
firstly, the prevention of the immediate danger of the loss of blood; and
secondly, the restoration of the circulation of the part.
The Control of Hemorrhage.—Little emphasis need be laid upon the
value of the Esmarch rubber tourniquet, for the prevention of hemorrhage
from an extremity. Occasionally, it is well to sew up a wound tightly when
bleeding occurs from regions inaccessible to an Esmarch or Martin bandage,
particularly on the battle field, when complete surgical equipment may not
be at hand. If the wound be too large, it may be tamponed very tightly and
the skin sutured over it, a pressure bandage being placed over the whole.
14
210 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
These are but temporary measures, and must give way to the permanent or
final control of the bleeding through other means.
Another method often suggested is the application of sterile gauze over
which compression is exerted through a solid unopened well rolled muslin
bandage. This is made to obliterate the arterial lumen through a compress-
ing force brought into play by a firmly applied superimposed rubber bandage.
Or, we may be constrained to leave artery forceps in the wound, under
certain circumstances on the battle field.
The Permanent Control of Hemorrhage.—The question whether a ligature
or suture of the vessel is indicated depends upon the size of the vessel, the
condition of the wound, the circumstances under which hemorrhage must be
controlled and the presence or absence of adequate surgical material and
equipment. During the Great War even some of the smaller arteries were
successfully sutured, when a lateral opening was present (radial artery, Stich).
Whenever we believe that the ligation of a vessel of moderate size will not
compromise the integrity of the peripheral parts, ligation may be carried out.
Given the proper circumstances, an absence of general or local infection,
and a patient who is in a condition for suture operation, the question of ade-
quacy of collateral circulation is an important one in determining whether
suture or ligature operation should be attempted.
For the investigation of the adequacy of collateral circulation a number of
tests have been employed, particularly the Mosckowicz test (Chap. X XIX).
This test may be carried out in the following modified manner.
Taking an injury of the femoral artery as an example, the limb is made ischemic either
through elevation, or better still, through the application of a rubber bandage, below the
point of injury. ‘Thereupon the femoral artery is compressed against the pubic bone until
all pulsation below disappears. The rubber bandage is taken off after about 2 minutes,
and the limb either kept at the horizontal or preferably depressed. If the collaterals are
adequate, a hyperemic reaction takes place up to the tips of the toes in spite of the continued
compression of the femoral artery. It must be remembered that it is good to control this
test by a similar one on the healthy extremity, and that the findings are only reliable if we
are certain that the artery is being properly obliterated by pressure above. The Lexer-
Coenen test (Chap. X XIX) also described by Henle and others may give valuable infor-
mation if it is positive, and the rapid almost pulsating arterial flow from the arterial stump
gives evidence of sufficient collateral circulation.
The Relation of Larger Arteries to Nutrition of the Part.—The effects of
ligation of the femoral artery have been variously estimated. According to
Wolff (1908) the following percentages were given for various larger arteries,
as to the incidence of gangrene of the lower extremity after ligation of
various large arteries. After ligation of the external iliac 50 per cent gangrene;
common femoral both above the profunda 25 per cent; popliteal 40.9 per cent;
femoral below the profunda 12.7 per cent. As for the upper extremities,
gangrene was noticed after ligation of the axillary artery in 15 per cent; sub-
clavian and brachial about 4.8 per cent.
Treves had already pointed out, years ago, the great risk attending liga-
tion of the common femoral artery. Observations during the late war,
however (Sencert) seem to indicate that ligature of the femoral artery is not
as dangerous to the vitality of the limb as is commonly believed. This
author ligated the femoral 11 times (in 3 the common femoral) with no case
of gangrene. Only where there was a large hematoma did gangrene occur
(g examples of the latter).
Heidrick reports that gangrene follows ligation of the femoral in 20.7 per
cent of the cases. This author is in accord with the view already expressed
TREATMENT OF INJURIES TO THE BLOOD VESSELS 211
that gangrene is more frequent following ligation below the origin of the
profunda than above.
It is important to take into consideration in any interpretation of the
consequences of ligation and injury as to the presence or absence of previous
arterial disease. Infection, trauma, secondary thrombosis all play a réle in
determining whether gangrene will take place or not.
It must be further remembered that while the skin may be adequately
nourished after ligation of a large vessel, this does not necessarily pertain
to the subsequent condition of the deeper tisssues. It is well known that
the musculature is much more susceptible to diminished blood supply than
the skin. Therefore, necrosis may take place after ligation, but leave the
integument intact. In this way can be explained the sequelae after ligation,
and complications that may occur weeks after the operation. Even ischemic
contractures have been reported.
Principles Underlying Surgical Treatment.—For details reference must
be made to surgical treatises and to the literature in this domain. Certain
basic facts and observations, however, that are relevant for an understanding
of the circulatory phenomena and conditions in the extremities merely need
be dwelt upon here.
It is now believed that ligation should be made at the point of injury,
and that both vessel stumps should be cared for. The older admonition
to treat and ligate the vessel at the site of predilection is fallacious advice,
since it can neither assure one against secondary hemorrhage, nor is it free
from the danger of gangrene. Only when the bleeding vessels cannot be
found nor sought for in view of the local condition of the wound, is the more
remote or indirect ligation permissible.
Ligation is only reliable in healthy tissue, so that it may be necessary to
dissect the artery for some distance, isolate it and tie in more healthy territory.
Ligation and Treatment of Aneurysms.—lIf a pulse beyond the aneurysm
is present, one can defer operation, while if the pulse is absent, extirpation
can be carried out without any fear of gangrene. -
Experience in the late war has taught us considerable regarding the time
necessary for the development of collateral circulation. Some authors
suggest waiting for several months, while others believe that in a period from
3 to 6 weeks adequate collateral circulation will have become established,
so that ligation of the artery can be done without danger. Early operation
after rupture of a blood vessel or formation of a traumatic aneurysm may be
dangerous, not only because of the absence of collateral supply, but also
because of the compressing effects of the hematoma, which may be expected
to become absorbed after sufficient delay. The danger to collaterals is thus
automatically and gradually removed.
Whenever ligation of an artery or extirpation of an aneurysm is done, it
is important to inspect the more peripheral parts of the extremity, as regards
the circulation, and to obtain a knowledge regarding the condition of the
collaterals. If the extremity is of good color after temporary compression
of the afferent artery (leading into an aneurysm) ligation can be carried
out without fear. If there is doubt, some authors advise small incision into
the periphery of the extremity, so as to determine whether bright blood, dark
blood or none is evacuated. If after from ro to 15 minutes of observation,
the extremity is still pale, or has a marmorated appearance, then we can
conclude that the collateral circulation is inadequate.
Furthermore, the data furnished by the Henie-Coenen collateral sign
(Chap. XXIX) are of importance. Considerable discussion has arisen as
212 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
to the advisability of simultaneous ligation of the accompanying large vein, .
when a large artery is ligated. In the case of arteriovenous aneurysms, this
matter requires no special decision. When suture is possible, both may be
conserved; if not, and extirpation has to be done, both have to be ligated.
When the vein, however, is intact, certain data on observations during the
Great War would point to the advisability of ligating the vein.
Thus Wolff! reports that after ligation of the femoral artery alone, there
were 20.7 per cent cases of gangrene, while if the vein also were ligated, only
8 per cent. In the case of the upper extremities, ligation of the arteries 7.8
per cent, ligation of both artery and vein—no cases of gangrene. Many
theories have been propounded regarding the explanation for this pheno-
menon. According to some, a disproportion between collateral afferent
supply and venous outflow is avoided by ligation of the vein. Johannessen?
published a case in which the lower extremities evidenced very poor circula-
tion after ligation of the femoral, edema and pain. After the vein was
ligated, 8 days subsequently, a continued improvement in circulation
occurred.
On the other hand, deleterious consequences have followed ligation of the
femoral vein. According to the statistics of Braun,’ the ligation of the
femoral vein alone, above the profunda produced gangrene in 2.8 per cent of
the cases.
Indeed, some authors advise against ligation of the femoral vein, because
of the likelihood of stasis. On the whole, although there are dissenting
voices, the majority of surgeons rather favor the simultaneous ligation of the
artery and the vein, with certain exceptions in the case of the lower
extremities. It is well in each and every case to decide this at the time of
operation, when by temporary arrest of the circulation of the vein, observa-
tions can be easily made as to whether the circulation is objectively improved
thereby.
Neurovascular Syndromes after Ligation of Large Arteries——There is a clinical complex
that either temporarily or permanently restricts the muscular activities, when impairment
of the circulation of a limb follows ligation of one of the larger arteries. It is not surprising
that a diagnosis of malingering is often made, for, while under the observation of the
physician, little is objectively in evidence. However, upon increased activity and work,
especially if the latter is excessive, and also under exposure to cold and moisture, circulatory
disturbances appear. These are coldness and blueness of the hands and feet, reduction in
the size of the pulses, rapidly developing edema, a sensation of numbness in the extremities,
and occasionally dull pain. When the limb is put at rest, both objective and subjective
manifestations appear.
It would seem, in light of experiences during the Great War, that reestablishment of the
circulation through suture of the artery involved would prevent the development of these
clinical syndromes. The favorable results obtained by von Haberer with arteriorrhaphy,
as compared with ligation, definitely demonstrated the advantages of the suture method.
Arteriorrhaphy.—Opinions are not in accord as to the value of vessel
suture after injury, some tending to the extreme that the method has little
or no useful sphere of application, while the other schools employ it even in the
presence of infection. It appears to the author that arteriorrhaphy, when
carried out by those sufficiently skilled and with careful technic, is an exceed-
ingly useful procedure that will receive more and more recognition, as the
experience of the surgeons in this work increases.
1 Wolff, Brun’s Beitr. z. klin. Chir., 58, 762.
2 Johannessen, Zentralbl. f. Chir., 45, 516.
* BraunwAtch Laskin shir 28.
THROM BO-ANGIITIS OBLITERANS—INTRODUCTION 213
The procedure is to be entertained in view of the following dangers of
ligation; firstly, the vascular and neurovascular remote consequences; and
secondly, the dangers of gangrene.
Certain authors report successes even in infected tissues, so that the
view oft accepted that scrupulously clean fields are essential, may have to
be rejected.
Among such instances may be mentioned the case of Danielsen! of suture of the axillary
artery in infected tissues. V. Haberer? described 7 cases of arterial suture with healing in
the presence of severe local infection; and Schoene? closed a longitudinal slit in the popliteal
aba in the presence of a gas phlegmon, with a pulsating posterior tibial artery (!) as a
result.
The danger of gangrene consequent upon suture is less than that follow-
ing ligation. The immediate reestablishment of circulation, however, after
suture does not preclude the possibility of late gangrene. Such has been
reported as taking place 2, 3 or 6 weeks after the operation, usually gradually
but in some instances suddenly. In such cases the outcome is due
to secondary thrombosis.
The mild circulatory disturbances that are most apt to occur after impaired
circulation due to arterial injury and ligation are less frequently observed
after suture, or in much milder form. These disturbances are the following:
a feeling of coldness, sometimes paresthesiz, sensations of heaviness, numb-
ness and formication. In some patients pain occurs after bodily exertion, or
a hard edema of the affected limb may ensue. It is the opinion of v. Haberer
and Stich that objective and subjective disturbances are usually absent in
those cases of arteriorrhaphy where the peripheral pulses were reestablished
after the operation. It has already been pointed out that peripheral pulses
may return weeks after arteriorrhaphy, due to the intervention of collaterals,
so that only the immediate restoration of the pulses can be regarded as an
evidence of a successful reestablishment of the arterial paths.
CHAPTER XXXIX
THROMBO-ANGIITIS OBLITERANS—INTRODUCTION
It seems strange that a primarily scientific study of the lesions of thrombo-
angiitis obliterans—later supplemented by clinical observations—should
have laid the foundation for a correct appreciation and classification of a
large number of affections involving the circulation of the extremities.
Indeed a careful consideration and investigation of all the basic anatomical
changes as well as the many clinical phenomena characteristic of thrombo-
angiltis obliterans, will do more in a practical way to fashion and shape our
concepts of the vasomotor and trophic neuroses and all allied organic affections
of the vessels of the limbs, than the study of any other single or group of
such diseases. And this is true because manifestations of almost all of the
morbid conditions in question are represented in this one interesting malady.
The medical student as well as the practitioner whose diagnostic apprecia-
tion of Raynaud’s disease, erythromelalgia, chronic acrocyanosis, athero-
‘1 Danielsen, Deutsch. Ztschr. f. Chir., No. 11, 40, 381.
2v. Haberer, Arch. f. klin. Chir., 108, H 4.
3 Schoene, Deutsch. Ztschr. f. Chir., 1918, 143, 84.
214 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
sclerotic vascular lesions, and thrombo-angiitis may still be obscure in spite
of reading of text books or of clinical experience, will find his doubts and
clinical obscurities remarkably clarified by an intensive study of the varied
manifestations and lesions of thrombo-angiitis obliterans. It is for this
reason, that the author has deemed it wise to indulge in a comprehensive dis-
cussion of its pathology, its latent and active symptoms.
CHAPTER: XL
THROMBO-ANGIITIS OBLITERANS—GENERAL CLINICAL
CONCEPT
Thrombo-angiitis obliterans! is a clinical and pathological entity which
has been, and is still, incorrectly called ‘‘endarteritis obliterans” by many
authors. The names, presenile, and juvenile gangrene have also been applied
to it.
At the onset, thrombo-angiitis obliterans is essentially an inflammatory
process, involving particularly the deeply situated and larger arteries and
veins of the lower and upper extremities. Almost immediately after the
inception of the lesion, there follows extensive occlusive thrombosis, that sub-
sequently gives way to a stage of healing or organization, the final result
being the complete closure of arteries and veins over a large extent of their
course by vascularized and canalized connective tissue. Although no
extensive study has been made of thrombo-angiitis in the vascular domain
outside of the extremities, the typical lesions have been observed by the
author: in the spermatic vessels, and according to Murphy, are said to occur
in the renal vessels.
Characteristic is the involvement of the superficial veins, of the lower and
upper extremities in the form of a migrating or thrombo- phlebitis in about 20 to
25 per cent of the cases. It is in this territory that the most thorough and
reliable investigations on pathology can be made, as the lesions in the vessels
then become accessible at the very onset of the malady before the effects of
organization and healing have confused the histological picture.
Clinical and Pathological Concept of Thrombo-angiitis.—The disease
manifests itself in most instances with indefinite pains in the sole of one foot
(usually the left) in the ankle, or in the toes, the patients being soon disturbed
in their walk by these symptoms, or by the sudden onset of cramp-like sensa-
tions in the calf or elsewhere in the leg (intermittent claudication). These feel-
ings make the patients take frequent rests, often inducing them to investigate
the condition of their limbs. Some take off their shoes and rub the part in the
hope of dispelling the pains or banishing the uncomfortable numbness of the
toes and feet; others say that the feet become cold and numb when the tem-
perature is low and the weather is inclement. After the lapse of weeks,
months or even years, evidences of trophic disturbances make their appearance.
Following the cutting of a nail, or without apparent cause, an abraded spot
or hemorrhagic bleb, a pustule, or a dry, dead patch of skin develops near the
_ | This name was suggested in 1908 by the author for this interesting and remarkable
disease and has been almost universally accepted in the United States.
THROMBO-ANGIITIS OBLITERANS—GENERAL CLINICAL CONCEPT PACT
tip of one of the toes or under a nail. Now the local pain becomes excruci-
ating during the night as well as day, so that some of the sufferers beg for
amputation of the affected part.
It is usually during the first attack of trophic disorder, but sometimes
when only intermittent claudication is present, that the physician or patient
notices another characteristic symptom, namely, a peculiar blush of the
toes and forepart of the foot, sometimes extending to the ankle or slightly above,
when the limb is in a pendent position (Plate IV). Upon allowing the limb
to hang down, the affected toe soon turns color. It assumes a bright red
hue which is seen to pass to the other toes and then up the back of the foot
Fic. 46.—Trophic lesions in thrombo-angiitis obliterans.
for a variable distance. This reddening is often termed rubor, or may be
called erythromelia. The elevated extremity on the contrary, rapidly
becomes blanched (ischemia). Sometimes the superficial ulcer will heal under
conservative treatment and the patient will either recover perfectly or his
symptoms will become chronic. At this period his limb may show the trophic
lesions and scars left by previous ulcers (Fig. 46). The dorsalis pedis and the
posterior tibial arteries usually fail to pulsate, and ischemia in the elevated
position and redness of ‘‘erythromelia”’ in the pendent position are regularly
216 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
elicited. Sooner or later, however, a patch of gangrene develops, the local
pain becomes intense, and amputation will be the issue.
Because of the striking condition of redness in the dependent position,
and because of the increase of local pain when the limb is hanging down, a
number of clinicians have been accustomed to diagnosticate ‘‘erythrome-
lalgia’’ in these patients. Some cases have been regarded as examples of
Raynaud’s disease, because in them the symptoms of blanching and cyanosis
of the parts were prominent features. Although resembling erythromelalgia
and Raynaud’s disease in a number of symptoms, the clinical picture of
thrombo-angiitis obliterans is so characteristic and definite, and the patho-
logical lesions so typical in this disease, that it constitutes a distinct clinical
entity.
A general concept of the disease could be briefly formulated in the follow-
ing terms. Imagine a patient seeking relief for acutely swollen superficial
veins of the lower or upper extremities, of sudden advent, and with all the
manifestations of an acute thrombo-phlebitis. Imagine this process involving
a considerable portion of the distal territory of the internal saphenous vein,
followed by abatement of symptoms, and consequent resolution or healing.
You will be in no doubt as to the general pathology nor as to the clinical
course of the condition, though your estimation of the etiology will in most
instances, at least be obscure.
Transfer this picture to the deeper vascular system, over the distribution
of the external and internal plantar arteries and veins, the dorsalis pedis,
anterior tibial, posterior tibial and the perineal arteries and veins, that is,
with lesions in territories where objective manifestations are absent—and
you will be depicting to yourself, what corresponds to our own conception of
the pathological process in the disease, thrombo-angiitis obliterans. So
here, too, we postulate, an acute inflammatory and thrombotic lesion, but one
involving deep arteries or veins, or both, as the initial stage of the pathological
anatomy. ;
Whereas, the patient afflicted with an“inflammatory and thrombotic
lesion of the superficial veins presents objective signs easy of recognition, the
patient suffering from thrombo-angiitis obliterans in its earlier stages may
offer no objective evidences suggestive of the true nature, or of the site of the
lesion. It is but in a very few cases that one is justified in ascribing certain
symptoms to the incipient stage of the disease. Severe, non-localizable
shooting pains in the calf or foot, attended with difficulty in walking, or,
possibly with tender calf muscles, with or without vasomotor symptoms and
coldness in the foot, with or without obliteration of the dorsalis pedis and
posterior tibial pulses, may be the only symptoms. It is only when we com-
pare the history with the future clinical course and pathology that we can
relegate such indefinite signs to the onset of the affection. In most instances,
however, the patient will not seek advice for such initial symptoms, either
because they are not sufficiently severe to require the attention of a physician,
or because they are incorrectly regarded as rheumatic in origin, possibly due
to trauma, cold, the presence of flat or weak foot, or because they are
explained on the basis of some other minor ailment.
Strange to say, patients afflicted with thrombo-angiitis obliterans may
present symptoms which differ in no way from those attending the thrombo-
phlebitis of the superficial veins, or so-called migrating phlebitis. These are
the cases of thrombo-angiitis obliterans in which an acute inflammatory
thrombosis involves smaller or larger!portions of the external or internal
saphenous vein, radial, ulnar, median cephalic or median basilic vein. Such
PEATE. LV
Erythromelia or Rubor in Thrombo angiitis Obliterans. (Buerger in Ochsner’s
“Surgery,” Vol. IV.)
THROM BO-ANGIITIS OBLITERANS—GENERAL CLINICAL CONCEPT 217
cases are the most instructive of all, for they are the ones which afford us
material for pathological study. Here the veins are accessible; portions can
be surgically removed when the lesions are in the acute inflammatory stage
and submitted to histological examination.
While the former type of cases is difficult to diagnose, the variety with
concomitant migrating phlebitis can be recognized by a study of the vein
lesions under the microscope. If the tissue be examined when the lesions are
still in the early inflammatory stage, before organization or healing has taken
place, certain characteristic and specific lesions can be identified, changes
which shall elsewhere be described as pathognomonic for thrombo-angiitis
obliterans.
Having learned that the incipient lesion of thrombo-angiitis obliterans is
an acute inflammatory one, involving the arterial and venous walls, we will
expect an occlusive thrombosis as the immediate sequence, and will not be
surprised to find that this stage gradually gives way to one of organization
and canalization, resulting in a healed product in which the vessel becomes
converted into a cord, more or less adherent to its surroundings, and in which
even the neighboring nerves may become agglutinated and enveloped in a
fibrotic vascular cord.
It is the interference with the circulatory conditions of the limbs brought
about by the extensive occlusive process that is responsible for most of the
clinical manifestations of thrombo-angiitis obliterans. So that it may be
correcily said that patients afflicted with thromb-angutis obliterans do not
usually suffer directly from the disease itself but from the disastrous occlusive
thrombosis which signalizes Nature’s method of healing a vascular lesion that
has long since disappeared.
From a study of the pathological material, and from a comparison of the
lesion with the clinical history, we must conclude that insidious or clinically
unrecognizable exacerbations of the lesion may occur from time to time, so
that the involvement of the vascular territory with the obliterative lesion is
a progressive one until the summit of the organized clot reaches the popliteal,
in rare cases the femoral or even the iliac arteries. It will not occasion
astonishment, therefore, that clinical manifestations, too, become more and
more serious as time goes on.
Nor must we be surprised if thrombo-angiitis obliterans simulates clinical
complexes brought about by arterial occlusion from other causes. Differen-
tiation from arteriosclerosis, endarteritic occlusion, and other thrombotic
conditions may at times be difficult. It is the fact that thrombo-angiitis __7/ pecan
obliterans occur in very young individuals in whom both the vis-a-tergo and
the cardiac power are adequate for compensation, and in whom the vascular
adaptability is elastic in its scope—it is this fact that accounts for the seem-
ingly almost inexplicable circumstance that gangrene occurs so late, or may
be absent, in spite of vast and extensive obliteration of arteries and veins.
It is to the development of the collateral circulation, therefore, that we owe,
in part at least, the production of a very peculiar, striking, and characteristic
clinical picture, recognizable even though manifestations of the acute stage
of the disease, or manifestations, such as migrating phlebitis are absent.
218 CIRCULATORY AFFECTIONS OF THEVEXT.REMTITIES
CHAPTER XLI
THROMBO-ANGIITIS OBLITERANS—ACUTE STAGE
More interesting than the study of the usual manifestations, due to
impaired circulation, is the investigation of those phenomena that are clin-
ically referable to the “‘acute stage,”’ that correspond to the acute inflamma-
tory invasion of the deep arteries and veins. As elsewhere pointed out,
when the patient seeks advice, he no longer suffers from the affection thrombo-
anglitis per se, but from the ‘‘healed stage” (in the pathological anatomical
sense) where the vessels have discarded their inflammatory products, have
become converted into hard fibrous cords, and are only in so far responsible
for the clinical picture, in that their function as conductors or vascular chan-
nels is completely in abeyance, the symptoms being altogether due to a “lack
of circulation” or a mechanical interference with the delivery of blood. A
diligent search for manifestations attributable to the attacks of deep thrombo-
angiitis or thrombo-phlebitis may find its reward in the discovery of treatment
or prophylaxis, available and applicable before extensive closure of vascular
channels has taken place. Such is the importance, then, of the recognition of
signs that may be interpreted as coincidental with the onset of acute lestons.
The Acute Symptoms.—These, as far as the author has been able
to detect, are lancinating pains in the legs, especially in the calf and foot,
cramp-like pains in the leg first interfering with walking, later requiring com-
plete rest, tenderness in the calf and along the anterior tibial region, simul-
taneously with, preceded by or unassociated with attacks of migrating
phlebitis. These manifestations may last for a variable time, are
unattended with trophic disorders, but accompanied by development of ische-
mia on elevation without or with evidences of disappearing pulses. When
the closure of the vessels is confined to the peroneal, and distal vessels such
as the plantar and peripheral distribution of the anterior tibial artery, and
even when a portion of the anterior tibial high up is involved, the posterior
tibial in its usual situation behind the malleolus and the dorsalis pedis may
be found pulsating.
The suddenness of the onset of pain in both legs with the absence of true
intermittent claudication at the incipiency of the trouble, with the slow
appearance of the usual signs, justifies the assumption that a period due to
“acute involvement of the deep vessels’’ was here exemplified in the clinical
examples at hand. Observed carefully from the stage where none of the
objective signs of thrombo-angiitis obliterans were associated with attacks of
pain in the calf and leg, up to the time when distinct manifestations could be
recognized, the following case permitted of the clinical separation into first a
stage of acute thrombo-angiitis obliterans, with symptoms referable to the
disease per se, and a second stage that of symptoms due to arterial obturation,
a period usually regarded as representative of the disease itself. (Cicatricial
stage; stage of mechanical hydrostatic and then trophic disorders.)
N.5S., male, Russian Hebrew, age 26, August 28, 1916, began eighteen weeks ago with
sudden severe cramp-like pain in the calf of the left leg radiating upward into the thigh.
This was treated as sciatica in one of the hospitals without improvement. Soon thereafter
a similar attack occurred in the right leg which made walking difficult. There were no
external noticeable changes to account for the trouble. Physical examination revealed no
ischemia, no rubor, none of the signs of thrombo-angiitis obliterans, other than doubtful
pulsation in the dorsalis pedes arteries.
THROM BO-ANGIITIS OBLITERANS—CHRONIC STAGE 219
December 11, 1916 (about three months of continued difficulty in walking) in the region
of the left calf, along the course of the peroneal and posterior tibial arteries, there was
marked tenderness; no change in the pulsations but ischemia now marked; so also reactionary
rubor with rather distinct cyanosis in the pendent position.
January 2, 1917. Now there is no doubt as to the absence of the dorsalis pedis in the
left leg. In short, first a stage of pain without further symptoms; second the development
of tenderness in the calf corresponding to the course of the vessels with some cyanosis in the
pendent position, and third, the development of ischemia, reactionary erythromelia and
pulseless dorsalis pedis artery.
Although in the main, it is a difficult matter to recognize the symptoms
that are referable to the acute process in the deep vessels, certain symptoms
have been noted in a number of cases, that were sufficiently suggestive to
warrant being interpreted as due to the deep thrombosis and inflammation.
M. P. gave a previous history of migrating phlebitis for which he was admitted to the
Mt. Sinai Hospital. On May 24, 1908, a physical examination was made by the author.
He had been in the hospital once before, on August 15, 1907, for phlebitis migrans. He was
again suffering from an attack of phlebitis now involving the saphenous vein and its tribu-
taries to the middle of the left leg, and also the ulnar vein near the left wrist. Now for four
days he had had paroxysmal attacks of deep pain in the right leg especially in the region of the
calf, not attributable to the superficial parts. Neither the dorsalis pedis nor the posterior
tibial artery could be felt pulsating. ‘These attacks were carefully observed. There was
no apparent cause for them; and it is more than likely that they were due to inflammatory
thromboses of the deep vessels, similar to those involving the superficial veins. The
gradual development of erythromelia and moderate ischemia in the elevated position, were
corroborative signs. Although the pain had disappeared after four days, the rubor
persisted.
The future course confirmed the suspicion of involvement of the deep vessels, since in
1909 trophic disturbances of both feet developed, and amputation of the right leg became
necessary; in rorr the left leg was also lost through amputation.
GHAP DER OXETT
THROMBO-ANGIITIS OBLITERANS—CHRONIC STAGE
It is only through a knowledge of the vicissitudinous paths followed by
the sufferer with this disease in his quest for a cure, and by a study of the
diversity of combinations that the usual manifestations may present, that a
comprehensive understanding of the mutations in the pathological process
and of the prognosis can be obtained. But a relatively few of the manifold
types will be mentioned here; the affection as it is associated with migrating
phlebitis (Chap. LVIII) and as it involves the upper extremities (Chap. LIX).
1. Cases without Trophic Lesions or Gangrene.—By these, we mean that
certain patients exhibit merely the usual subjective and objective manifes-
tations of impoverished circulation over years of clinical observations (2-10
yrs. or more), but may at any time thereafter be afflicted with ulcers or a
mortifying process. For years, with or without attacks of migrating phle-
bitis and intermittent claudication, chronic rubor develops, the foot is
distinctly blanched on elevation, the dorsalis pedis and posterior tibial
pulses are absent (sometimes the popliteal) but trophic disorders do not
appear. |
2. Cases of Exquisite Chronic Rubor, with dystrophic changes, loss of
merely one or more phalanges after 16 or more years of suffering (case D. B.),
220 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
deceive the prognostications of the clinician. After prodromal phlebitis of
either upper or lower extremities recurring for years, coldness, cyanosis and
pain with chronic rubor develop, so that a painful limp is established, a
phalanx or more may be lost, but the limb, except for slight edema, puffy
toes and angry red color, appears intact. This picture is analagous to that of
chronic pseudophthisis or chronic (vascular) atrophy with rubor described as
characteristic of arteriosclerotic vascular occlusion. In the former, however,
the age of the patient, the migrating phlebitis, the puffy toes, the swollen
rather than withered foot, are distinctive differential points (case D. B.
ChapsE VIII, p: 287):
3. Trophic Lesions the First Symptom.—As shall be pointed out elsewhere,
the disease may be present in a latent form in either or in both lower extremi-
ties, so that it may happen that the patient believes himself well until a
blister appears (big toe in case D. K.), the toe and foot become red and pain-
ful. Objectively, erythromelia is marked, the usual pulseless vessels are
demonstrable, a trophic ulcer has developed, and gangrene is imminent.
4. Cases of Short Duration (Acute and Subacute).—Although the usual
course of the disease is a chronic progressive one with a long prodromal period,
then the gradual development of trophic disorders and finally gangrene, there
are cases in which very rapid development of gangrene can take place. It is
barely possible that the initial symptoms are not noticed, their development
being insidious and too slight to warrant attention. Thus:
M. G., 35 years of age, Russian Jew, apparently well until four months before examina-
tion (June 30, 1909), noticed coldness of the left foot and then pain in the toes which rapidly
became so severe that it was necessary after some two months to go to bed. Now, four
months after the onset of the disease, the big toe of the left foot has become black, and the
tips of the fourth and fifth toes are also becoming mortified. At the time of examination
there were distinct evidences of gangrene of the fourth and fifth toes, absence of pulsation
in the dorsalis pedis and posterior tibial vessels, and the usual signs of thrombo-angiitis
obliterans. Within a few days amputation became necessary.
In short, within about four months the disease ran a complete course with
the loss of one limb.
5. Sudden Gangrene Simulating the Embolic Type.—Although the develop-
ment of gangrene is usually a slow process passing through the stages of
superficial necrosis, ulcer formation and then gangrene of one toe at a time, in
rarer instances after a period of the usual preliminary subjective manifestation,
upon cutting a nail or apparently without cause, extensive gangrene of several
or all the toes including the forepart of the foot may develop within a very
few days. Such a course would indicate that either a fresh accession of
thrombosis took place in many arteries with inadequate opportunities for the
establishment of collateral paths, or that an involvement of the popliteal
cut off the collaterals upon which the nourishment had previously depended.
When seen with gangrene well established, the clinical picture is confusing,
simulating mortification of embolic, thrombotic and arteriosclerotic processes.
6. Cases without Symptoms.—Very frequently the disease is overlooked by
the patient in one limb, whilst it is active in the other, or has existed for years in
one leg, remaining unnoticed until the advent of the more serious and distressing
manifestations calls his attention to the affection in the other limb. It is not
uncommon to find on examination of a case presenting the typical objective
phenomena in one extremity, that the other leg is the seat of the same disease,
physical examination revealing signs of extensive arterial obliteration and
signs of occlusion of many vessels. Other objective phenomena, too, warrant
the assumption of an insidious onset with subsidence of the acute lesions, and
the establishment of adequate collaterals. To cite a case:
THROM BO-ANGIITIS OBLITERANS—CHRONIC STAGE 221
M. P., the supposedly healthy leg evidences marked redness of the big toe and adjoining
region with some ischemia on elevation, and with the appearance of cyanotic patches over
the tips of the toes. Reactionary erythromelia is pronounced, being a phenomenon never
seen in a healthy leg.
The dorsalis pedis, posterior tibial and popliteal arteries are pulseless.
Comparing this type of involvement with that of the other leg in which the objective
manifestations were more pronounced, we find the following in the latter. First, marked
erythromelia even in the horizontal position varying in intensity, there being a play of colors
such as is seen in the vasomotor cases. Alternating rubor with patches of ischemia is seen,
the red color predominating. Second, the tumefied condition of the foot with the dis-
appearance of the normal irregularities. Third, the markedly cadaveric appearance on
elevation. Fourth, the very slow return of color on depressing the foot after previous
elevation. Fifth, the extreme descent below the horizontal necessary before any color
returns in the foot (small angle of circulatory sufficiency).
From this we may conclude: First, that both legs may be intensively
involved with thrombo-angiitis obliterans, one of them alone giving sub-
jective symptoms; secondly, that extensive obliteration of the vessels as
manifested by the absence of pulsations in the dorsalis pedis, posterior
tibial and popliteal arteries may occur without symptoms; and thirdly, that
certain physical signs, however, can be elicited, which will show that the leg
which gives marked clinical manifestations and is more recently affected is
the more profoundly implicated in the vascular occlusion. So also in the
following patient:
P. A. had four years of indefinite symptoms of rheumatism and pain in the ankle, worse
in cold weather. After a trauma of the dorsum of the right foot, an ulcer formed which
refused to heal. Somewhat later another ulcer appeared near the base of the little toe of
the same foot.
Physical examination showed the typical involvement of the right leg, erythromelia,
ischemia, absent pulsation of the posterior tibial, popliteal and dorsalis pedis arteries.
After a period of observation of about one month, edema developed and finally amputa-
tion became necessary, a Gritti being done with a successful result.
While in the hospital it was also seen that the left leg was involved in the same process,
although the patient did not know of this, the signs being marked reactionary erythromelia.
slight ischemia and absence of pulsation in the dorsalis pedis, popliteal and posterior tibial
arteries.
7. Cases with Intermittent Claudication Only.—These are the patients
who are apt to consult the orthopedist and run the gamut of mechanical
appliances for an affection in which the vessels are at fault. Careful physical
examination should elicit, in addition to pulseless vessels, some ischemia on
elevation, either chronic or at least reactionary rubor with other signs.
Or, closed vessels and intermittent claudication may make up the complex
for years, but sooner or later-ischemia and rubor are apt to develop, and then
the trophic lesion. As illustrated in one of the cases (I. M.) intermittent
claudication was the chief symptom for four years, with absent pulsation of
the dorsalis pedis and posterior tibial of the left leg, without erythromelia
or ischemia.
Or, after a period of intermittent claudication, the other phenomena
appear, many years being required for gangrene to set in.
M.L., aged 32, Russian Hebrew, examined on December 12, 1914. After about one
year of intermittent claudication the left leg showed marked redness, ischemia on elevation,
absence of dorsalis pedis, posterior tibial and popliteal pulsations, without any trophic
disorders. At the same time, the right leg was also involved, the main symptoms being
coldness of the big toe, cyanosis, absence of the dorsalis pedis and posterior tibial pulsations
without any other symptoms,
8. Cases with Intermittent Claudication and Migrating Phlebitis Only.—
Here the patient consults us for the pain on walking, the phlebitis not being
complained of, but a history of such is elicited on questioning.
222 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
D., January 29, 1915, aged 20, Russian Hebrew, began five years previously with pain
in the right calf and sole on walking. One year later he had migrating phlebitis along the
inner side of the right thigh; none since. For six months the left foot has been affected
with intermittent claudication, but not so severely as the right. No migrating phlebitis in
the left leg, no history of trophic disturbance.
Physical examination. In the horizontal position both feet look fairly normal; no
further evidence of phlebitis. Both femorals pulsate, the left posterior tibial pulsates, the
right does not. The right dorsalis pedis is absent, the left present. In the pendent posi-
tion erythromelia appears slowly but with moderate intensity over the whole of the right
foot and lower leg. No evidences of trophic disorder. In this position the blanching comes
on rapidly over the toes and the dorsum of the left foot. The ischemia in the left foot,
however, is only moderate, for, on pressure it is seen that some blood reaches the toes. On
elevation, after depression, the toes of the left foot lose the red rapidly, but develop only
slight ischemia. In the right leg, however, there is more ischemia, but not marked.
Summary.—This is a case in which the right limb alone was affected,
the symptom of intermittent claudication dominating, migrating phlebitis
having been present. After four years there was subjectively only inter-
mittent claudication, objectively, marked erythromelia, absent dorsalis
pedis, posterior tibial, slight ischemia, and no trophic disturbances. Here
was a very slowly progressing case with only slightly marked symptoms.
g. Cases Losing the Limb Last A ffected—Not infrequently the leg last
affected will be the first to require amputation. Among numerous instances
may be mentioned the following case.
A. P., with typical symptoms involving the right foot which began in May, 1906, witha
burning sensation on walking, would frequently have to go into a neighboring park on his
way home to take off his shoe and investigate the cause of the pain. ‘Then, during the
winter months came the feeling of coldness and soon a dark bluish black spot developed over
the base of the fifth toe. Finally, ten months after the onset of the trouble, and after cut-
ting a callus in the painful region, a sore developed which refused to heal. He was admitted
to the Mt. Sinai Hospital in April, 1907, where it was found that he had a trophic ulcer on
the outer border of the right foot near the head of the fifth metatarsal bone. There were
also the usual typical symptoms, ischemia on elevation and rubor in the dependent position,
the dorsalis pedis and posterior tibial arteries being pulseless.
In two months, however, the ulcer had healed and from then on the foot gave him no more
trouble.
In the meantime, however, the typical symptoms of thrombo-angiitis obliterans devel-
oped in the other leg, leading finally to amputation during the following year.
Not infrequently the disease exists in one of the limbs for months or years
without the knowledge of the patient, and is only discovered when symptoms
referable to the second leg are noticed by him. In such cases the process
is either developed insidiously or manifests itself simply by the presence of
intermittent claudication or difficulty in walking, finally coming to a stand-
still without the development of trophic disturbances or gangrene. In the
meantime the other limb is affected by more severe manifestations, ulcera-
tion and finally gangrene.
Such a case was J. G., aged 39, Austrian Hebrew who was seen November, 1908. Some
fifteen years ago he had been troubled with weakness of the legs and thighs on walking
and standing, also with indefinite pains which were only relieved by rest. These were
severe enough to incapacitate him for one year. He was apparently well until three months
ago, when a similar affection involved the right leg and then the foot became noticeably red
in the dependent position. Soon after an ulcer developed on the dorsum of the right foot
near the root of the fourth and fifth toes, which healed spontaneously, and then another
ulcer appeared on the right fifth toe.
The physical examination in February, 1909, revealed evidences of involvement of both
legs. The popliteal, dorsalis pedis and posterior tibial pulses of the right leg were absent,
and on the left the posterior tibial and dorsalis pedis were also negative. The right foot was
somewhat enlarged, tumefied, all the toes slightly thickened, a patch of gangrene being
observed on the outer aspect of the fifth toe; marked erythromelia, in the dependent posi-
tion, marked blanching on elevation. The left leg showed intense ischemia on elevation,
THROM BO-ANGIITIS OBLITERANS—CHRONIC STAGE 223
and upon depressing the leg after preliminary elevation marked compensatory erythromelia
most striking over the dorsum was noticed.
In short, we have here a case in which, except for the history of some
indefinite pain and intermittent claudication fifteen years previously, nothing
referable to the left leg could be elicited, although ischemia, erythromelia,
and absent pulsation were distinct evidences of the presence of the disease
in this limb.
On March 25th the right leg was amputated because of gangrene, the left
leg having in the interim again developed more active symptoms in the form
of marked redness and pain.
This was, therefore, a case of insidious development of the disease in one
leg and its spontaneous cure, the trouble lighting up in the other and lead-
ing to gangrene of the limb.
10. Cases with Chronic Course in One Limb, Acute Course in the Other.
The following is a typical example.
H. R., after having exposed both feet to cold suffered from “‘cramps” in both legs which
disappeared in a day or two (1897). A year later there was a recurrence of the pain. These
indefinite pains persisted for several years, until, in 1902 the typical symptoms of intermit-
tent claudication in the right leg came on, leading him to try various methods of treatment,
but without avail. Finally, about five years after the onset of the disease, prodromal
symptoms of gangrene or of trophic disturbances developed in the big toe of the right foot,
the toe becoming swollen and red, and trophic disorders showed themselves under the nail,
which was removed, leaving an angry red nail-bed which refused to heal. About the
same time the second toe also became affected in a similar way. In 1903 the toes were still
sore, but healed after several months of treatment. Then, after a period of remission of
three years (1906), trophic disorders developed again in the same place, namely, the big toe
of the right foot, the pain became very severe, and finally gangrene spread rapidly over all
the toes necessitating amputation.
In short, after a period of some nine years, initiated by pain referable
probably to the deep thrombosis, followed by intermittent claudication and
trophic disturbances, gangrene finally set in. It is noteworthy, however,
that several years elapsed between the first attack of trophic disorders and the
final onset of gangrene.
History of the Left Leg —In 1909 intermittent claudication of the leg, then pain and swell-
ing of the toes, bluish discoloration of their tips, the development of superficial ulceration
of the skin over the anterior part of the dorsum of the foot, gangrene of the fourth and big
toes, and marked edema of the foot.
In short, a rather acute case of eight weeks’ duration.
11. Relapsing cases may show vessels in which corresponding exacerba-
tions are found in the deep vessels, namely, more recent thromboses and even
‘“‘acute lesions’’ in the daughter or canalizing vessels. As a rule the free
intervals are shorter than in the following case.
A.L. presented a slow clinical course, there being a seven years’ history in a man 45 years
of age, with sudden onset of cramps in both legs, particularly the right, apparently followed
by cure of the left leg, there remaining at the time of examination only the absence of pos-
terior tibial pulsation on the left side as evidence of previous trouble.
After a period of seven years in which intermittent claudication was the chief symptom,
erythromelia and ischemia in the elevated position were to be elicited, absence of pulsation
in the posterior tibial and dorsalis pedis arteries, and marked diminution of the angle of
circulatory sufficiency. Then followed cyanotic discoloration of the big toe and gangrene.
Similarly, as evidencing the relapsing nature of the malady may be men-
tioned the following.
S. M. began with pain and coldness in the right big toe with blue discoloration in 1910,
and trouble with the second toe lasting from April, 1910, to September, 1912, at the age of
224 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
25, with complete recovery. Now (1913) recurrence of trouble in the big toe of the right
foot, swelling and gradual development of gangrene in the lower part of the thigh (total
duration about three years), leading to amputation August 21, 1913.
12. Cases with Lethal Outcome.—sSc extensive may the process be, that all the
extremities are involved. An atrophic condition of the upper extremities may
ensue from obliteration of the brachial artery.
I. L., male, aged 35, Russian Hebrew, in October, 1906, began ine intense pain in the
leftankle. In September, 1906, an ulcer on the dorsum of the foot was followed by progres-
sive gangrene requiring amputation October, 1906. Symptoms then developed in the right
leg which became markedly ischemic and extremely painful, so that the patient begged for
amputation which was done July 1, 1907, through the middle of the right leg. Neither
stump healed well, requiring reamputation, there being continued trophic ulcers over the
stumps of both legs in t909. On December 17, 1909, there was involvement of the right
hand, namely marked symptoms of scleroderma or sclerodactyly, atrophic fingers, with the
brachial artery palpable as a hard cord.
On April 25, ro11, the patient was readmitted to the hospital, and the left lower extrem-
ity was again amputated because of failure to heal. On May 25, the patient became lethar-
gic, drowsy, unable to answer questions, and ceased on May 30, rort.!
In short, this is a case in which both legs were amputated, the right upper
extremity showing symptoms of scleroderma, marked atrophy, leading to a
lethal outcome within a period of about five and one-half years.
13. Cases in the Young with Grave Prognosis.—Just why the disease when
it affects young men under the age of twenty-five should be apt to take a very
~ destructive course is difficult to explain. Many of the cases in the author’s
experience have lost one or both lower limbs within a very short time.
H. K., male, aged 27, Russian Hebrew, had been suffering since the age of seventeen with
pain in the left foot. In 1905 trophic disturbances appeared so that early in 1906 amputa-
tion became necessary, the leg being amputated five inches below the knee. Then in 1906
symptoms developed in the right leg, pain in the foot and in the big toe which persisted up
to the present time.
Physical examination April 2, 1908, showed a non-healed left stump with necrosis of the
bone; typical symptoms in the right leg, marked ischemia on elevation, erythromelia,
absent dorsalis pedis and posterior tibial, and trophic disorder of the big toe. On April 15,
the big toe was amputated, failed to heal, but amputation was refused.
So, also, is the following case—one of a youth in whom one would expect
collateral circulation to become established.
C. H., American, male, aged 25, had had vague symptoms for some years. Then
coldness of the left leg, and four or five months thereafter, discoloration of the forepart of
the left foot were noted. The heel, the big and fifth toes were painful, and trophic disturb-
ances of these toes with gangrene developed after about one and one-half years of definite
symptoms. The dorsalis pedis, posterior tibial and popliteal arteries of the left leg were
pulseless, as also the dorsalis pedis of the right leg.
Finally, in January, 1910, amputation took place. This was done eight inches below
the knee with a poor result, suppuration continuing, due to necrosis of the bone.
In short, within a period of two years both legs were affected in a boy
twenty-five years of age, leading to amputation of the left leg, the process
having been only slightly advanced in the right.
14. Cases of Long Duration without Trophic Lesions.—Because so many
years may elapse without manifestations of nutritive derangement of the
distal parts, the clinical picture devoid of this symptom should be recognized.
The author’s records show instances where eight to ten, and even fifteen years
had passed without ulceration or gangrene. ‘The following case may be cited.
B. H., Russian Hebrew, male, aged 47, seen October 19, 1910, began eight years ago
with pain on walking, intermittent claudication, one year later manifestations of migrating
1 This case because of its importance is discussed more fully on p. 372.
THROM BO-ANGIITIS OBLITERANS—CHRONIC STAGE 225
phlebitis, and for about one year the feet have been cold. Six years ago he noticed dis-
coloration of the feet.
On physical examination both feet were found to be involved with the typical symptoms,
erythromelia and ischemia, the left being more marked both as regards erythromelia and
ischemia, than the right. On the right, the dorsalis pedis and posterior tibial were pulse-
less; on the left, pulsation was absent in these vessels as well as in the popliteal.
Here is a case of long standing in which the trouble dated back farther
than the history would indicate, with involvement of both legs after an eight
years’ course, with development of all the typical symptoms up to the stage
in which ulceration was imminent.
15. Cases with All Extremities Involved.—Not unusual is it to note that
both upper extremities may participate in the process, although the de-
structive force of the vascular occlusion makes itself but slightly felt in the
upper limbs (Chap. LIX).
M. F., Russian Hebrew, aged 34, began at the age of thirty with pain in the right
foot. This was followed by numbness of the right hand. Six months ago symptoms
were observed in the left foot, such as coldness and pain on walking.
On physical examination it was found that the right hand and left leg were distinctly
involved, there being atrophy of the right hand and coldness of the fingers with a faint
radial pulse. The left foot showed evidences of involvement, rubor, coldness and absent
dorsalis pedis and posterior tibial.
Five years after the onset of symptoms in the left leg, the second toe became gangren-
ous. The foot was in a state of marked erythromelia, and the pulsations in the posterior
and anterior tibial arteries were absent. Gritti-Stokes amputation was done with good
result.
Eighteen months after the amputation of the left leg, the patient complained of intense
pain in the calf of the right leg accompanied by the formation of an ulcer on the foot. The
symptoms progressed and cons2rvative amputation was done below the knee. However,
owing to the persistence of an ulcer on the right stump for 6 months, Gritti-Stokes amputa-
tion was finally resorted to with complete abatement of all the symptoms.
Two years after the last amputation the patient gave evidences of involvement of the
left upper extremity, in the presence of pain and coldness of that part. The left radial pulse
was found imperceptible, the right barely palpable.
When last seen (September 8, 1922) the patient, who has been addicted to morphine
was free of all symptoms, the left radial pulse, however, being imperceptible.
16. Cases with Pain Only.—Recognition depending on objective signs are
amongst those usually undiagnosticated. ‘There are no trophic disorders.
The patients usually have been treated by an orthopedist, but the ischemia,
rubor and pulseless vessels should direct attention to the true nature of the
malady.
M. N., Russian Hebrew, aged 35, presented a picture of thrombo-angiitis obliterans
without trophic disturbances, simply marked ischemia, moderate erythromelia after a
period of indefinite pain which had been diagnosticated as due to flat foot. The arteries of
both legs failed to pulsate.
17. Cases without Trophic Disorder or Gangrene Requiring Amputation.—
There have been a number of cases in our experience, either with one or both
limbs affected, that suffered such agonizing pain for an extended period of
time, that they vehemently begged for amputation, which was carried out in
several instances. ‘The following may be cited as an example.
H. R., August 6, 1916, born in the United States, Hebrew, began to experience pain 16
months previously in the calf of the left leg, the pain extending downward over the entire
leg and foot, especially over the toes. The pain was severe, cramp-like in character,
intensified by walking, diagnosticated as due to flat feet. There was a history of migrating
phlebitis of both lower extremities a year previously.
Physical examination, August 6, 1916. The left foot was markedly cold and somewhat
smaller (atrophic) than the right, and in a state of chronic rubor, most marked in the
pendent position. On elevation there was intense pallor, on depression marked congestion
15
226 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
erythromelia, and rubor. None of the pulses, neither the dorsalis pedis nor posterior tibial
arteries were palpable.
Diagnosis. —Thrombo-angiitis obliterans without trophic disorder or gangrene.
The patient was kept under observation for some 12 days, and his supplication to have
the limb removed was finally acceded to.
At operation, August 18, 1916, amputation of the left leg (Gritti-Stokes), most of the
arteries were found closed, the popliteal also being filled with organized thrombus. The
popliteal veins were open.
18. Cases with All the Vessels Pulsating.—These will be described in
more detail under Borderline Cases (Chap. CIV). Clinical and pathological
investigations have demonstrated that an atypical clinical picture with
predominating vasomotor symptoms, or even the typical picture of thrombo-
angiitis obliterans may be produced, when the vascular lesions are confined
to the territory of the plantar or the digital vessels, with occasional involve-
ments of the distal parts of the dorsalis hallucis. The symptoms may begin
with vague pains in the feet to which little attention is paid, or coldness of
the toes. Later on this pain becomes severe, is referred to one or more toes,
and is followed by cyanosis or rubor, or a combination of both. Or, the pain
may be slight, and the coldness and cyanotic discoloration may be noteworthy.
In the latter case the clinical picture may simulate that of some of the vaso-
motor neuroses. When pain is marked, a diagnosis of incipient or
restricted vascular occlusion can be made with a fair degree of certainty.
M. C., Russian Hebrew, consulted me on the 7th of July, 1911. He was devoid of
symptoms until 2 weeks previously, when he suddenly began to experience pain in the
whole left foot. At first the pain was slight, but became gradually more and more severe.
After a week the toes became red without being preceded by any ischemia. Since then the
third toe has become blackish and ulcerated, and now the pain is intense by day and night.
Physical Examination.—Left foot shows discoloration of the third, fourth and fifth
toes, these being cyanotic. The fourth toe is reddened. On the inner side of the tip of
the middle toe there is a patch of superficial gangrene of the skin about the size of a ten cent
piece, the center being ulcerated. ‘The tip of the toe is very cyanotic, suggestive of impend-
ing gangrene. On elevation of the foot the visible veins become empty, the third, fourth
and fifth toes slightly bluish, but no distinct blanching can be elicited.
All of the vessels of both extremities pulsate normally.
Conclusion: Although an absolute positive diagnosis could not be made in
this case, since amputation was not done, a number of other similar cases
have shown conclusively that the clinical picture represented occlusive
thrombo-angiitis obliterans confined to the territory of the plantar and digital
arteries.
19. Cases with Marked Involvement of the Upper Extremities are discussed in
full elsewhere (Chap. LIX).
20. Cases with Migrating Phlebitis are of such importance as to warrant
special consideration later on (Chap. LVIII).
21. Cases in Females.—So rare is the disease in females, that doubt has been
cast on the possibility of its occurrence outside of the male sex. The author
has observed but 3 cases that were clinically indistinguishable from typical
thrombo-angiitis obliterans, but since amputation did not become necessary
in any of them, pathological confirmation is missing.
Raynaud’s syndrome in elderly women with arteriosclerotic vessels or
acrocyanosis may give confusing clinical combinations, that should be care-
fully differentiated from thrombo-angiitis obliterans.
A case that belongs clinically to thrombo-angiitis is the following.
M. D., female, American, seen February 2, 1912, parents Bavarian Jews, was always
perfectly well except for ‘‘sciatica”’ in October, 1911, possibly related to her present trouble.
About this time she had an attack of pain in the right thigh and foot which was so severe
THROM BO-ANGIITIS OBLITERANS—CHRONIC STAGE 227
that she was kept in bed for two weeks. The diagnosis was ‘‘sciatica” from which she
apparently recovered, but discomfort and even pain remained in the right sole and instep.
The right foot, too, seemed much colder than the left, not bluish but pale at times, always
appearing whiter than the left foot. After walking about one block, the pain would become
so intense that she had to stop and rest.
In short, an indefinite history of sciatica followed by pain in the foot, coldness, pallor and
intermittent claudication.
Physical examination, February 2, 1912, revealed the absence of the dorsalis pedis
pulse of the right foot, a doubtful posterior tibial, all the other vessels of both sides pulsat-
ing. On elevation the right foot showed moderate ischemia. Examination of the sensory
nerve condition was negative.
Diagnosis: A case of thrombo-angiitis obliterans with moderate erythromelia of the
right foot in the dependent position, ischemia on elevation, absent dorsalis pedis with a
history of pain in the foot, ankle and sole following sciatica.
The patient was not seen again until some four months later, when in June, 1912, the
following history was taken. Since the last examination she had been receiving hot air
treatment, which she believed caused a burn. An ulcer developed under the big toenail of
the right foot, the nail subsequently falling off. The nail-bed healed after four weeks.
About February 16, the foot became very bad, the toes looked almost black, so that in
March after several consultations with surgeons amputation was advised. The big toe
particularly seemed affected being bluish black, the bed of the nail having become gangren-
ous. Certain ointments were used, the symptoms gradually subsided, amputation was
refused, and healing took place.
June 10, 1912, physical examination of the right leg in the horizontal position showed
cyanosis of the big toe, with a deformed nail. There was slight erythromelia of the fore-
part of the foot in the dependent position, marked ischemia on elevation, especially over
the sole, less over the dorsum of the foot. A fairly marked reactionary erythromelia was
produced when the foot was returned to the horizontal, and absence of pulsation of the
dorsalis pedis and posterior tibial arteries was noted.
In short, since the last examination the patient developed trophic disorders which were
probably not at all related to the hot air treatment, and might have come on spontaneously ;
erythromelia had become more marked, as also ischemia, and the dorsalis pedis and pos-
terior tibial were definitely occluded.
The patient was again seen on January 4, 1913, when both feet were slightly cold with-
out evidences of atrophy. In the pendent position the right foot showed definite rubor.
On elevation both feet showed distinct blanching and there was distinct reactionary erythro-
melia of the right leg after elevation. The dorsalis pedis and posterior tibial arteries of the
right were not palpable, as well as the dorsalis pedis of the left foot.
Summary: January, 1913, although the process had not progressed much in the right
leg, the left leg also seemed now to be involved.
June 10, 1913, the patient said the right foot had become distinctly warmer, and she
considered herself much improved being able to get about much better. Physical examina-
tion showed the same condition of the pulses as at the last examination. The right foot
showed marked erythromelia, the left but slight, both evidencing distinct ischemia on
elevation.
The following case may be cited as another example of thrombo-angiitis
obliterans in a female. _
A. C., 38 years of age, began with pain in the calf of the right leg upon walking following
an attack of influenza 2 years ago. The right leg became swollen, but after 6 months the
cramps in the calf disappeared, the swelling, however, persisting accompanied by numbness
of all the toes. Eight months ago the right foot became cold, and the patient noticed a red
spot on the inner aspect of the right leg.
Physical examination reveals edema of the right foot and leg, more marked over the
ankle. The great toe is hemorrhagic, showing evidences of discoloration of the tip with
ecchymosis. ‘There is moderate erythromelia over the forepart of the right foot. Elevation
elicits considerable ischemia. Upon return to the horizontal position, the color does not
return for some time, rubor appearing first above the roots of the toes, the toes themselves
remaining ischemic and cyanotic.
The dorsalis pedis and posterior tibial pulses of the right foot are absent, those of the
left present.
In short, thrombo-angiitis obliterans in a female, with involvement of the
right lower extremity, the chief symptoms being erythromelia, ischemia and
absent pulsations.
228 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
22. Cases in Elderly Individuals will offer difficulty in differentiation from
sclerotic vascular diseases all the more so since the two conditions may co-exist
simultaneously, the latter usually engrafted upon the former when in
the silent, latent, or anatomically “healed” stage. Autopsy findings (Chap.
LXIII) have convinced the author that the arteries are particularly prone to
lesions of atherosclerosis, although the territories involved with thrombo-
angiitis obliterans may be least or not at all affected.
There is a series of cases in which the symptoms apparently become severe
after the age of forty. In these, a careful search into the history will reveal
the fact that there had been symptoms many years previously, and in all
probability the disease had come to a standstill. Therefore, in view of this
fact we must give a rather guarded prognosis in all cases of thrombo-angiitis
obliterans that apparently heal. Our experience with cases in young men
between twenty-five and forty years in whom complete cessation of all
manifestations takes place, confirms the diagnostic assumption of the previous
existence of the disease in some of the older arteriosclerotic individuals.
Pathological pictures afford the anatomic corroboration for the coincidental
occurrence of the two affections.
23. Cases with Apparent Healing or “‘Cure.’’—Clinical inactivity, abate-
ment of pain and intermittent claudication, improvement in ability to walk
and the absence of trophic lesions are interpreted by the patient as indicating
subsidence of the disease, usually in the words “‘my legs give me no more
trouble.”” That such a free interval is to be regarded under all circumstances
as of doubtful duration, experience has taught. An interruption by a repeti-
tion of the manifestations in the other limb is not uncommon as elsewhere
described.
In the period of clinical inactivity, however, the existence of the disease
should not escape our observation, since slight ischemia, or some rubor or
reactionary rubor, or a diminished angle of circulatory sufficiency and pulse-
less vessels can be demonstrated, these signs in varying combinations and
degree of intensity.
One of the most exquisite examples of apparently complete clinical cure
of a case in which trophic disorders had been present, and imminent gangrene
of one limb had impelled a surgeon to advise amputation, is afforded by the
following case.
J. R., Russian Hebrew, aged 32, consulted the author September 9, 1909 to ascertain his
condition, since his brother had the same disease and was developing gangrene. In 1894
(at the age of seventeen) he began to experience a peculiar cutting pain in the left calf on
walking a short distance, so that he had to drag the limb. This symptom (probably
intermittent claudication) persisted for about two years during which time he often could
not sleep at night because of the pain and burning in the toes. In 1896 the case was
diagnosticated as erythromelalgia, for at that time his leg was very red. The right leg, on the
other hand, at no time gave him any symptoms. Another surgeon about this time made the
diagnosis of flat foot and put the foot in a cast for two weeks. After the cast was taken off,
a sore developed on the inner side of the left ankle which refused to heal (decubitus?). In
spite of all the measures taken to bring about the healing of this ulcer, the wound was still
open one year after the removal of the cast. At that time, the symptoms were so intense
that he was advised to have the limb amputated, but refused, and a year later the wound
spontaneously closed with the use of ichthyol dressing, and gradually after this time (1898),
four years after the onset, all the symptoms left him, and he has been free from trouble ever
Since.
September 11, 1909, one year after the wound closed, he was examined by the author,
and all the vessels of both lower extremities, including the femorals, popliteals, posterior tibials
and dorsalis pedes were found pulseless. Both feet showed a very slight rubor in the pendent
position, but not of sufficient amount to be diagnosticated as erythromelia. Besides this,
there was distinct ischemia in the elevated position, but not at all marked. There were no
THROM BO-ANGIITIS OBLITERANS—CHRONIC STAGE 229
trophic disturbances, the patient complained of no pain, and considered himself perfectly
well. There was no intermittent claudication, nor any symptoms referable to the lower
extremities.
In short, we have here a case of typical thrombo-angiitis obliterans in the
left limb, spontaneously ‘‘cured”’ as far as symptoms are concerned, in spite
of the fact that extensive obliteration of vessels had occurred. ‘There seems
to be no question but that the disease must have been present in the right
limb also, although at no time did the patient discover any symptoms.
The following history is suggestive of the presence of lesions in one limb,
that however, spontaneously healed.
A. L. gave a history of cramps in the left leg as well as in the right, and on examination
seven years later marked symptoms of thrombo-angiitis were found in the right leg. In the
left, the only symptoms of the disease were the absence of pulsation of the posterior tibial
and at times cyanosis of the big toe in the dependent position. Therefore, all the symptoms
had subsided, these two signs being the only ones left indicative of previous trouble.
Some cases may go along for a year with the development of gangrene
of one toe and trophic disturbances, as well as all the usual symptoms, and
then spontaneously after hot air or postural treatment show complete
subsidence of all symptoms. Such a case was the following.
H. G. developed gangrene of the big toe after a year of the usual pains and intermittent
claudication (December, to1o). This gradually healed while he was treated in January,
1911, by the hot air method, and remained perfectly well under our observation for four
years, so that when the patient was seen in December, 1914, the left foot, although present-
ing a somewhat atrophic appearance, an absent dorsalis pedis and posterior tibial pulse, was
found otherwise in fairly good condition as far as circulation was concerned, and presented
no symptoms whatever. ;
Some of our cases were observed for several years, and although at times
there was slight exacerbation, many of them showed no tendency to marked
progression or to the development of gangrene, so that they could be regarded
as stationary or clinically “‘cured.” As,
A. G., was observed from November 27, 1908 to May 9, ro11. He had had a typical
history of intermittent claudication of the left leg, followed after two years by pain
in the region of a trophic lesion. ‘This spontaneously healed, and when the patient was seen
in 1908 there were definite evidences of involvement of both legs with a history of pain on
walking, coldness of the foot, thin condition of the foot, and numbness with occasional
whitening or pallor of the foot on walking. Although the patient was seen and carefully
examined some four or five times a year, no aggravation of his condition was noted, no ulcers
developed, and the case was regarded in 1g11 as being a stationary one, the cyanosis, the
pulseless vessels, the tendency to coldness and numbness of the feet persisting.
In short, we have here a proof of the fact that six years may elapse with-
out any marked destruction of parts, and without gangrene.
24. Arrested Stage or Temporary Healing in Thrombo-angitis Obliterans.
Surprising changes both for the worse and for the better are the impressive
features of the variegated clinical picture of thrombo-angiitis obliterans.
So, we occasionally are confronted with a stage of threatening gangrene
of the leg which limits itself and becomes restricted to the disintegration
of but a part of a phalanx or less. Or, one may observe the complex—
ischemia, rubor, pain and trophic disorders—all disappear with its subjective
symptoms, the patient believing himself cured as far as the previously
affected limb is concerned. When we encounter such cases during a period
of renewed morbid activities in the other extremity, the residual diagnostic
features such as atrophy and pulseless vessels can be appreciated and given
deserved consideration. Periods of remission, arrest of symptoms with
either none or very slight manifestations may last for years, but the possibility
230 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
and probability of an exacerbation leading to eventual loss of the limb must
be borne in mind, since such an issue is extremely common.
A good illustration of such subsidence and practically complete abate-
ment of circulatory disturbances is worthy of attentive contemplation to
aid in both diagnostic and prognostic conception of the malady. So we will
cite the case of
Typical thrombo-angiitis obliterans of the left leg, gangrene of toe, “ healing” or arrest and
disappearance of symptoms, followed by involvement of the right leg, four years after cessation,
relapse and extension of lesion in the left leg.
H. G., male, Hebrew (born in Turkey) age 39 years, examined December 10, 1910,
smoked fifteen Turkish cigarettes a day beginning at the age of fifteen. The diagnosis of
flat feet was made ten months ago when he had pain in the left calf, also the diagnosis of
‘“‘rheumatism.”’ He then used plates for the left foot. There was pain in the left calf on
walking three to four blocks. No history of migrating phlebitis could be elicited, and the
right leg was free of symptoms.
Five weeks ago there was pain in the left big toe, and four weeks ago redness. For the
past week a black spot had been seen on the outer side of the left big toe. Now the
patient has most pain in the big and second toes, particularly at night, sleeping only a
couple of hours.
Physical Examination.—December 10, rgr1o, the left foot is in a state of chronic ery-
thromelia, and the big toe shows a dry gangrenous patch on the outer side 1 cm. in diameter,
the rest of it being cyanotic.
The iliac, femoral and popliteal arteries of both legs were found pulsating, the posterior
tibial and dorsalis pedis pulses of the right leg palpable, those of the left not.
There was a moderate increase of the erythromelia in the pendent, moderate ischemia in
the elevated position.
On January 1, 1911, there was still an ulcer about one-half inch in diameter on the big
toe.
On March 14, 1914 the following history was obtained. Since early in 1g11 the left leg
had given him no more concern, and since the healing of the ulcer, all symptoms vanished.
For two months, however, the right leg had been troubling him with a sensation of pins in
the sole of the foot, so that he had to rest at every block, and when he walked the pain
ascended into the right calf. The right foot, too, had been discolored in the forepart.
Physical Examination (March, 1914).—The right foot is bluish red, the toes being most
involved. The dorsalis pedis and posterior tibial do not pulsate, the femoral does. The
left foot, which is now without symptoms, has a somewhat atrophic appearance, but is
negative except for the absent dorsalis pedis and posterior tibial pulses.
On elevation it is very evident that the circulation of the right foot 1s worse than that of the
left. ‘This can be seen particularly over the sole, where the right foot takes on a greenish
white appearance with the small toe cyanotic. If we press the other toes, those of the
right foot show very little blood, and that which is present is of a purplish tint, whereas
on pressing the toes of the left foot, considerable red color is in evidence. During the
period of elevation even the dorsum of the right foot became markedly blanched.
On putting the foot back in the horizontal position, the return of color is seen as a
mottling over the right foot, the toes being the last to regain their color.
In the pendent position ‘the return of blood in the right foot makes it intensely red, the
rubor extending somewhat above the ankle.
In short, four years after our first observation, the left foot was found (March 14, 1914)
in an arrested or temporarily healed state, the right previously normal, then actively
implicated in the disease.
October 27, 1914, the right foot has the intense red look and the puffy appearance of the
old chronic cases. In the pendent position, the erythromelia deepens rapidly and then
cyanosis comes on. The fourth toe, the distal phalanx of which is already separated, shows
a gangrenous area of skin. The fifth toe is completely absent and the foot is very cold.
The pain seems to be relieved in the pendent position.
When again seen on January 15, 1915, these notes were taken. The patient feels better
now, but still has intermittent claudication in the left leg, and pain between the third and
fourth toes of the right foot, where there is a patch of gangrene.
Both feet are in a state of chronic erythromelia, the right more marked than the left.
The right foot is somewhat enlarged, the toes slightly swollen, so also the dorsum. Where
the fifth toe spontaneously separated, the wound has healed. The site of the separation of
the terminal phalanges of the fourth toe of the right foot still shows a dry smooth patch.
In the horizontal position there is practically no erythromelia of the left foot, and only slight
of the right, but in the pendent position both feet show fairly marked erythromelia. It is
THROM BO-ANGIITIS OBLITERANS—CLINICAL PICTURE 231
noteworthy that the left foot shows this erythromelia although there are no trophic dis-
turbances. The dorsalis pedis and posterior tibial of both feet are pulseless. He has no
pain when at rest. On elevation there is marked blanching of the left foot, slight of the
right.
In brief, four years after establishment of the quiescent stage in the left foot, a fresh exacerba-
tion with recurrence of erythromelia, ischemia and pain.
25. Doubtful Cases.'—Such a group is but a clinical and arbitrary segrega-
tion of cases, the exact nature of which may seem questionable, at least
during a part of their clinical course. Because of the absence of pathog-
nomonic symptoms during the early stages of certain cases of thrombo-
angiitis obliterans, and because of the association of vasomotor symptoms
in others, enough data for any other than a presumptive diagnosis may fail
to be at hand. |
To divorce the following clinical complex altogether from thrombo-angiitis
obliterans and to make a symptomatic diagnosis of intermittent claudication
as has been done by Erb and others, would be tantamount to a relinquishment
of every desire to aim at a pathologic differentiation. Confronted with a
case of cramps or pain in the legs or feet on walking, without static cause,
without any history of migrating phlebitis, without either ischemia, rubor
or pulseless vessels, we may be allowed to suspect that thrombo-angiitis
obliterans is developing, and that it has as yet affected none other than those
arteries that are beyond the reach of palpation—e.g. the distal branches of
the anterior tibial and the plantars. To extend the designation of inter-
mittent claudication so as to denote a possible clinical and pathological
entity, would be subversive of all modern attempts to clarify clinical con-
cepts. For, intermittent claudication, as has been elsewhere lucidated,
should be restricted so as to indicate coordinate manifestations; that is, a
“symptomatic association,” and not a ‘“symptom complex,” when the latter
appellation is used as the equivalent of a morbid unity. So we may allow
such patients to constitute a group entitled ‘‘Thrombo-angiitis obliterans
with latent (larvata) or undeveloped physical signs.”’
This variety must not be confounded with that already alluded to, in
which a patient is unaware of the disease, that is, “‘ Thrombo-angiitis obliter-
ans without subjective symptoms.” For, in the latter no complaint is made,
whilst amongst the instances belonging here, the patient’s discomfort may be
great. It is merely an insufficiency of pathognomonic objective signs that
warrants this classification.
Amongst the various cases encountered are the following:
(a) Intermittent claudication only with absolutely no objective signs;
(b) Coldness and cyanosis of the toes, possibly with local pain; but the
physical signs of thrombo-angiitis obliterans absent.
CHAPTER XLII
THROMBO-ANGIITIS OBLITERANS—CLINICAL PICTURE
Classification.—F or purposes of clinical diagnosis it is useful to divide the
cases of thrombo-angiitis obliterans into four groups.
I. Typical thrombo-angiitis obliterans of the lower extremities.
1 Vide also Chap. CIV.
232 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
II. Thrombo-angiitis obliterans with associated thrombo-phlebitis or
migrating phlebitis.
III. Thrombo-angiitis obliterans with involvement of the upper extremi-
ties. |
IV. Thrombo-angiitis obliterans with secondary or complicating athero-
or arteriosclerosis.
It must be remembered, however, that this grouping is artificial, for
many cases may belong to one or more of these subdivisions at the same time.
Thus, cases in group I may be affected with migrating phlebitis, or may have
symptoms of thrombo-angiitis obliterans of the upper extremities. The
classification is helpful for description and study.
For purposes of treatment it is often useful to divide the cases according
to the stage of the development of symptoms at the time of clinical observa-
tion, into
1. The prodromal stage, that of intermittent claudication (sometimes
with migrating phlebitis).
2. The stage of trophic disorders and gangrene.
I. TYPICAL THROMBO-ANGIITIS OBLITERANS OF THE LOWER
EXTREMITIES.—The clinical picture varies considerably, depending upon
the duration of the disease when the patient is examined, the severity, the
effects of exposure, traumatism and complications. The following case
types may facilitate the recognition of the disease, although they must not
be considered as exhaustive. They should be recognized, since they are
in most instances but the prodromal manifestations of gangrene.
A brief exposition of some of the typical forms of onset (A) of the malady
in the lower extremities, and short summaries of some of the more usual
clinical pictures (B) as they are developed under our observation, may serve
to clarify our concepts of the effects of the morbid lesions in the vessels.
A. Forms of Onset. 1. Onset with Intermittent Claudication —This
symptom-complex need not be discussed in detail since it has been described
elsewhere. But allusion may be made to its importance as one of the first
manifestations of the disease. Very frequently it antedates by weeks,
months or years, the other symptoms—the rubor, the coldness, the cyanosis,
the blanching, the migrating phlebitis and trophic lesions. It may succeed
the attacks of phlebitis or the attacks of pain referable to the deep vessels.
And, it may be regarded as of such negligible character by the patient, as to
escape his notice, whenever more serious phenomena such as ulcers and
exquisite local pain in a toe render it comparatively insignificant. On the
whole, it is a sign of such distinctive character, as to be regarded as an
important and integral part of the clinical picture.
2. Onset with Symptoms Referable to the Deep Vessels (Acute Stage). —In a
number of cases there is a history of a rather sudden onset, with attacks of
severe pain in the calf of one of the legs, without demonstrable cause, and
attributed by the patient either to exposure to cold, or to severe exercises,
or, described as coming on without reason. In anumber of such cases symp-
toms of intermittent claudication developed somewhat later, but the history
of acute symptoms was so definite, that is seemed reasonable to conclude
that they bore some relation to the occurrence of thrombosis in the deep
vessels (Chap. XLI, p. 210).
Quite a number of cases describe the onset as being sudden, with pain in
the calf and foot made worse by walking. After a time, the acute symptoms
1 Chap. XXVI.
THROMBO-ANGIITIS OBLITERANS—CLINICAL PICTURE 233
give way to a recurring cramp or pain of moderate severity brought on by
walking (intermittent claudication). It is more than likely that in many of
these cases this acute onset marks the inflammatory stage of the disease in
the deep vessels and is followed by the stage of intermittent claudication,
where the pain is dependent upon circulatory deficiency.
It is quite a difficult matter in all cases to get a definite history of the onset
of the disease. If the hypothesis regarding the relationship between the
symptoms and the occurrence of the thrombosis of the deep vessels is correct,
namely, that certain attacks of cramp-like pain in the calves and in the legs
may accompany the real onset of the disease, we should be able to elicit such
a history in most of the cases. However, this is not possible. If we take
into consideration the type of cases with which we are dealing and the lack
of intelligence of some of the patients, their failure to properly estimate and
recall symptoms occurring many years back, will not be surprising.
Then, as for the symptoms which do not really belong and are really not
due to the onset of the pathological lesion, we may say that these also vary in
their incipiency. In some of the cases there is no question but that the disease
seems to begin with symptoms of intermittent claudication. In some others,
however, we were unable to obtain such a history, for the patients referred
their pain to the foot or to the toes, and particularly to those toes or that
toe which very soon becomes the seat of trophic disorder or gangrene. Ina
certain case there was a history of pain in the fifth toe of the right leg at the
very beginning of the disease. Two weeks later ulceration took place and at
the end of the month the toe was amputated for gangrene.
If we carefully analyze such a history, we cannot doubt but that the pain
complained of was that of the impending trophic disorders and gangrene.
It is more than likely that other manifestations had initiated the real begin-
ning of the disease, but had remained unnoticed.
3. Onset Overlooked, Trophic Lesions First Noted.—In the careless, ignorant
hyposensitive individual, the first indication of trouble may be the development
of an ulcer or even a patch of gangrene; or, exquisite pain in a toe, usually
the forerunner of serious nutritional disturbance is the first noticeable
manifestation.
Careful scrutiny of many of the histories demonstrates conclusively that
the onset of the disease is often overlooked. In some cases, we find that one
toe has been amputated, and in eliciting the history, we find that a sore had
developed many years ago without cause, leading to spontaneous gangrene
and finally amputation. Thus, in one case the history states distinctly
that fifteen years previously the big toe of the left foot was amputated for
spontaneous gangrene, the patient remembering no other symptom asso-
ciated with it other than the local pain.
4. Onset Overlooked until Second Leg Affected——In the chapter on the
Course of the Disease, the latency of the affection and the insidious manner in
which it may implicate one extremity, wholly unknown to the patient, have
been discussed. Here, it may be permissible to emphasize merely that a
medical examination should not disregard the following signs of arterial
involvement in a limb, that apparently gives the patient no concern; namely,
absent dorsalis pedis or posterior tibial pulses, with or without rubor or
ischemia, and coldness of a portion of the periphery or cyanosis. When
merely one pulseless vessel is the only apparent objective sign, careful
search for reactionary rubor and for ischemia after repeated and prolonged
elevation may be rewarded by positive findings sufficient to warrant the
diagnosis.
234 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
5. Onset with Coldness and Cyanosis.—The symptoms to which the prac-
titioner is wont to give too little heed are coldness and blueness of one or more
toes with or without pain. It is true, other manifestations wholly ignored by
the patient may precede, but it is for the signs of discomfort that the patient
seeks relief. If a routine examination according to the principles laid down
be followed, an early diagnosis may be made.
6. Onset with ‘Rheumatic Pains.’’—Pain described as such, when
referred to the ankle, the foot or the tibia, and when not typical of intermittent
claudication, is a symptom whose significance may be underestimated.
This dictum may be safely accepted, that in a young Hebrew, especially of
Russian or Polish origin, any persistent discomfort in the foot or leg justifies
careful investigation as to the integrity of the arteries of the limb, because of the
mantfold variations im the symptomatology.
B. Usual Clinical Pictures.—Some of the more common clinical manifes-
tations group themselves in our experience as follows:
1. Symptoms of intermittent claudication, namely, pain in the calf of
the leg or in the foot, made worse by exercise and walking, may last for a
variable period of time, and then distinct rubor or erythromelia develops,
the picture being a combination of these two chief symptoms.
2. Symptoms of intermittent claudication may predominate for long
periods, may remain unrecognized, but should be regarded with suspicion if
they are accompanied by blanching of the foot upon elevation, rubor upon
depresssion of the foot after elevation, and loss of pulsation in the dorsalis
pedis, possibly posterior tibial, or both, or even the popliteal arteries.
3. Symptoms of pain or intermittent claudication] may give way after a
variable time to trophic disturbances, ulcers, fissures, hemorrhagic blebs,
scaling of the skin, etc., but when these are present, the typical phenomena
elicited by physicial examination are regularly to be found.
4. Thrombo-angiitis obliterans may develop silently in one limb without
symptoms, indefinite signs of pain, indefinite intermittent claudication having
been present and having been unnoticed or undiagnosticated, being only
elicited when the patient seeks advice for characteristic symptoms of
thrombo-angiitis obliterans in the other limb. Physical examination will
reveal absence of pulses, in one or both limbs.
5. The symptoms of thrombo-angiitis obliterans may develop in
an orderly and typical sequence, namely: first, stage of indefinite pains or
intermittent claudication; second, stage of rubor or erythromelia, with absent
pulsations, and ischemia on elevation; third, a stage of trophic disorder;
finally, a stage of gangrene.
6. Cases may pass through any of these stages and the progress of the
disease may become arrested spontaneously, or with treatment. Those in
which the signs of intermittent claudication and pain alone have developed,
will regularly show upon examination the ischemia on elevation, or at least,
some reactionary erythromelia, absent pulse in at least one of the larger peri-
pheral vessels, such as the dorsalis pedis and posterior tibial, or often both.
When the disease comes to a standstill, the subjective symptoms disappear,
but the objective may persist for a long time, that is, the ischemia on eleva-
tion, the absent pulses and the erythromelia. In some of these, however,
even the ischemia and the reactionary erythromelia may become absent, the
pulseless :vessels alone remaining as indications of the disease. When ery-
thromelia becomes marked, it is likely to persist for a long time, even after
the disease is spontaneously arrested, or apparently cured by treatment.
THROM BO-ANGIITIS OBLITERANS—APPEARANCE OF THE LIMB 235
When trophic disorders develop, the pain is wont to become severe.
Ulcers may spontaneously heal; the pain may leave the patient; the inter-
mittent claudication may abate, the ischemia and erythromelia being the
last phenomena to disappear.
Those patients with gangrene who become spontaneously cured, pass
through the stages indicated above, the typical phases of mortification,
involving as a rule only small portions of a toe, or a toe, being followed by a
long period of convalescence, lasting months or even years, and resulting
finally in cure. In these, too, the pulseless vessels will tell the tale, erythro-
melia persisting for a long time.
7. The Chronic or Incurable Cases.—These are common, the disease in
most instances being a progressive one. The advent of the various stages,
although often delayed may be expected to develop. In the chronically
progressive type, amputation may become necessary, either in the stages of
trophic disorder, or gangrene. The pain may be so excruciating that sleep
is impossible, amputation finally being the last resort, even though the
lesions are merely those of ulceration with or without infection; or, the
control of pain in cases of gangrene may also be impossible, amputation being
the only method of obtaining relief.
8. Cases in which any of the above symptoms or complexes may affect
first one lower extremity, then the other, possibly abating in the extremity
first involved, and making more marked progress in the other. There
are cases in which one or both lower extremities are involved, and in the
further course of the disease one or both upper extremities also give mani-
festations of the same affection. These will be considered under the group—
Thrombo-angiitis Obliterans of the Upper Extremities.
g. Fulminating Cases.—Although the regular course of the disease is a
chronic, progressive one with a long prodromal period, there are cases
in which (according to the histories) very rapid development of gangrene can
take place. It is possible that the prodromal phenomena were unnoticed,
being of shght degree, or developing insidiously. In these patients coldness
of the foot and pain in the toes may be the first symptoms, leading rapidly to
areas of mortification.
CHAPTER XLIV
THROMBO-ANGIITIS OBLITERANS—APPEARANCE OF THE
LIMB
Since the special and more or less striking deviations in the appearance of
limbs affected with thrombo-angiitis obliterans are to be described sepa-
rately, there remains to be mentioned here only those general peculiari-
ties of color and conformation that cannot be classed into single categories,
but that are the result of a combination of factors, partly nutritional, partly
compensatory tissue growth, partly adaptation, and partly circulatory
derangement.
Leaving out of consideration, then, the appearance of the extremity when
it is discolored into marked pallor (ischemia), rubor (erythromelia, hypere-
mia), or cyanosis (asphyxia, lividity), when changed because it harbors
trophic ulcers and infections or gangrene, then there are still at hand
236 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
certain peculiarities that are the more or less characteristic products of the
many factors at play in this disease.
For our diagnostic purposes, it is true, our inspection should be concen-
trated first and foremost on the more striking alterations above reviewed;
but for special differentiation, even minor changes are of no mean import.
In the cases with but few symptoms, with pain or intermittent claudica-
tion predominating, there may be nothing worthy of note other than dys-
trophic alterations in the nails; or even these may be absent. When, how-
ever, rubor has existed for some time, and more particularly when trophic
lesions have been or are present, the gross appearance of the foot undergoes
distinct changes. ‘These vary in intensity and extent. It is very common to
not a peculiar thickening of the subcutaneous tissues that differs from edema
and that corresponds to chronic lesions under the skin. Through this the
normal markings as expressed by the prominence of the tendons and the
intervening furrows, may become diminished or effaced. The normal
displaceability and elasticity of the skin gives way to a more hide-like or
leathery-like texture, whilst the cutis itself, need not necessarily appear to
be thickened. ‘The toes in the territories that have suffered most marked
circulatory impoverishment may be enlarged, waxy in appearance, devoid
of wrinkles or furrows, and filled out as it were, in a manner that does not
yield to pressure, as does edema.
Alterations in the nails may be the sequence of trophic lesions in their
immediate neighborhood, as in the healed ulcerative lesions; or the nails—
especially of the fingers (Chap. LIX, p. 298) may become distorted, lifted off
the matrix and opaque, whilst the matrix becomes white, the cuticle retracting
so as to leave an exaggerated, enlarged, yellow white and dirty looking lunula.
Fissures over the soles, between the toes, near the margin of the nails, in
and near callouses, must not escape the watchful eye. For not only do these
give pain, but they may extend much deeper than we would suppose at first
glance, and further, may be but the harbingers of a serious menace
to the integrity of the part. For out of these, infections and gangren-
ous lesions are apt to develop.
Atrophic changes of the skin are more often symptomatic of the results of
marked atherosclerotic disease than of thrombo-angiitis obliterans. How-
ever, in that stage of chronic pseudophthisis or atrophy of the limb that occa-
sionally belongs here; or in some of the pseudo scleroderma lesions, or in the
vicinity of amputed limbs, striking atrophy is occasionally encountered.
A peculiar mottling of the skin of the distal parts, especially over the
digits seems to be the result of chronic circulatory disturbances. If one
compares this mottling of the diseased with the normal foot, one can appre-
ciate that it really represents an intensification of the normal venules, which,
by virtue of stasis, become permanently dilated. The mottling is produced
by streaks rather than by patches of discoloration and is brought out with
greatest intensity when the limb is held up for purposes of eliciting ischemia.
In some cases, hemorrhages take place with pigmentation, resulting in a
permanent brownish discoloration. The skin is apt to be thin over such areas
but when there is a combination of chronic enlargement of the toes, the
general puffiness may be obscured by mottling.
Atrophy of the leg, more rarely of the thigh, in varying degrees, is not
uncommon where the popliteal and femoral arteries have become closed.
This diminution of the girth of the calf is best appreciated with the patient
in the prone position, when the contrast in the size of the calf muscles is
noticeable.
THROMBO-ANGIITIS OBLITERANS—ISCHEMIA 237
CHAPTER XLV
THROMBO-ANGIITIS OBLITERANS—ISCHEMIA
Ischemia, blanching or whiteness of the peripheral parts, usually affects
the toes, feet and legs, and more infrequently is distributed over the
corresponding portions of the upper extremities. It may be considered as
of two distinct varieties, each having an essentially different cause. Irrespec-
tive of the source of immediate inducement, such as external or even internal
exciting factors, the blanching in thrombo-angiitis obliterans seems to have
two absolutely diverse modes of creation, so that we may speak of:
I. Mechanical or hydrostatic ischemia.
-II. Vasomotor ischemia.
I. MECHANICAL OR HYDROSTATIC ISCHEMIA
Pallor or ischemia is evoked by elevating the limb from the pendent
position to that extent which is incompatible with arterial influx into the vessels
and capillaries of the skin. ~With healthy arteries and adequate heart action
the normal arterial vis a tergo is adequate to deliver blood into the most:
peripheral parts of the foot, that is, into the tips of the digits, and lend and
conserve a pinkish normal blood tint in the distal skin areas. If in dorsal\
decubitus, the leg is raised to the vertical, any occlusive or obturating process |“?
in the chief arteries, makes such visible and customary color conserva-
tion impossible. Superadded to an abnormal diminution of blood supply
in such a position is a certain degree of depletion and evacuation in the
vascular system and one that conforms to the laws of gravity. In this sense,
therefore, we may speak of mechanical or hydrostatic ischemia in obstruc-
tive, occlusive, obturating or obliterating types of vascular disease of the
extremities.
Whilst vasomotor phenomena responsible for fugitive and transitory
patches or even extensive areas of local syncope may be associated and
contuse the clinicians’ concept of hydrostatic ischemia, a careful comparative
estimate of the phenomena, as they appear under various conditions, in
any case, will usually permit of definite differential recognition. A
knowledge of the coincidental occurrence of the two blanching phenomena is
a prerequisite for a comprehension, not only of thrombo-angiitis, but also
of the vasomotor and trophic neurosis so frequently confounded with it. A
few tests, and subjective or objective considerations should suffice to dis-
tinguish the two types of ischemia.
Mechanical or hydrostatic pallor should be studied in the following way:
Relative to
1. The situation of its appearance.
2. The angle of elevation that brings it forth.
3. The time that must elapse for its definite establishment.
4. Its extent.
5. The arc in which pallor persists. Its complement will be the residual
angle to which lowering of the limb must continue, for the restitution of a
normal or reactionary red color (Angle of Circulatory Sufficiency, Chap.
ATX).
238 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
6. The persistence of well localized areas of ischemia even after return
and reaction have been established by descent of the limb; especially when
the phenomenon can be reproduced in the same situation by subsequent
preliminary tests of elevation and depression.
From this summary it will be seen that the striking and distinctive feature
of this form of ischemia, is its dependence on, and variation with position of the
limb. By this it can at once be distinguished from the neurotic or vasomotor
type.
1. Situation of Its Appearance.—As the leg is elevated, pallor is seen to
replace the usual rubor that pendency brings on. The toes and then the
foot become abnormally pale, the veins flattened and depleted, the peripheral
digits often evidencing patches of cyanosis that may persist throughout the
period of elevation. The simultaneous blanching of the toes and foot,
possibly coupled with arteriovenous depletion throughout the leg, suggests
arterial occlusion of greater degree or greater inadequacy of the collateral
circulatory paths. Occasionally by irregular sequence, the pallor of the
foot may antecede that of the toes; one of these, usually the big toe, may
remain cyanotic and even the other toes may evidence a mottling or redness
due to intracutaneous hemorrhages; or, other variations may be noted.
Certain adventitious factors contribute to the difficulties attending the
correct estimate of the appearance of pallor. Thus, a continued cyanosis,
particularly in cold weather, or transitory vasomotor irritants exciting even
blanching in the pendent position, must not be confused with hydrostatic
conditions. For it is the latter alone that are of value in diagnosis of the
malady and in the appraisement of the degree of vascular obliteration. We
must await, therefore, altered circumstances, give aid by establishing a proper
environmental temperature state, and allow for psychic repose before making
a test for the appearance of ischemia.
Pallor on elevation may affect only a few of the toes at the outset (one,
two or more); or, there may be successive blanching of one after another
without orderly sequence, the intensive cyanosis and rubor being recalcitrant
and abolished with difficulty through action of gravity.
An extraordinary degree of blanching of a single toe, associated with
chronic cyanosis in the pendent position, warrants the suspicion that gangrene
or trophic disorder is imminent.
When the feet are very cold and apt to be cyanotic, as often occurs in
winter, a combination of rubor and cyanosis permits only very slow and
patchy replacement of color by yellowish white areas over the toes, until a
considerable time has elapsed.
2. The Angle of Elevation That Produces It.—Theoretically thisshouldbe .
but slightly greater than that at which reactionary rubor is called forth.
In truth, however, the two do not correspond, since, for a given time a
distinctly greater elevation is required to establish pallor, than the minimum
angle at which it still persists. Thus, if we have to elevate a limb to 170°
to evoke ischemia, we may find that pallor still exists when the leg is depressed
through a considerably larger arc than 10°. In a severe case with marked
circulatory impairment, it is not unusual to find ischemia established at 135°
or less, and continue for an indefinite time in the horizontal (90°). In
other instances pallor ensues almost at once on elevation to the bed level
(go° or horizontal).
When the degree of inducible blanching is doubtful or slight, a good
comparative estimate of the two limbs may be attained by resorting to one of
the following two methods; to,
THROM BO-ANGIITIS OBLITERANS—ISCHEMIA 239
(a) The repeated elevation and descension of the limb, two, three times or
oftener, with possibly, coincident production thereby of a reactionary rubor
during pendency, may evoke an ischemia otherwise concealed; or
(b) Careful observation of plantar aspect of the foot as it is raised and held
up, In varying positions with the patient prone and the leg flexed through
yee angles. Frequently distinct pallor is noticeable with the leg vertical
90°).
3. Time Interval for Its Establishment.—Employing approximately the
vertical (180° elevation) as a routine test, this generalization is acceptable,
that the more rapid the onset and completion of ischemia, the greater the
extent of vascular obturation. We must view both dorsal and plantar
surfaces of the foot, and even the leg with careful scrutiny and with adequate
but not too glaring illumination, for a dependable appraisal of this valuable
sign.
Where chronic cyanosis has set in, it may completely nullify the quanti-
tative value of this proof of circulatory disturbance. Under such circum-
stances we are, however, usually dealing with severe and extensive forms of
vascular obliteration.
Hemorrhagic infiltration of the skin and subcutaneous tissues, as also
pigmented areas, the products of previous disturbances, may give confusing
mixtures of colors that vitiate the general pallor that is to be expected.
A comparison of color phenomena displayed in the two legs will give
valuable information as to prognosis, since the more extensive involvement is
usually distinguished by more rapid evolution and greater distribution of the
ischemia.
4. Extent of Ischemia.—Usually, by virtue of the advanced condition
of vascular obliteration existing even at the first consultation, pallor on
elevation is apt to involve the whole of the foot and more or less of the distal
third, half or even two thirds, of the leg. Occasionally one toe alone, or
several of the toes will show definite blanching whilst an appreciable color
change is difficult to elicit elsewhere. It may, however, be persistently con-
fined to the same number of toes, this localization lasting for a variable time
yielding to more extensive blanching as the inadequacy of collateral, and
implication of additional arteries advances.
Where ischemia is well established in the horizontal position it is usually
limited in extent, rarely occupying a greater territory than the whole foot,
often restricted to one half of the foot or to some of the toes.
Careful continued and repeated observation over weeks and months may
reveal the striking fact, that ischemia may disappear, sometimes together
with the rubor and the trophic disturbances. These are the cases of arrested
symptoms and so-called ‘‘cures.”” In some of the quiescent cases all other
signs (except lack of pulsations) may disappear, but ischemia on elevation
will endure for years.
Per contra it is more usual to witness the reverse, namely, gradual increas-
ing intensity of blanching associated with progressiveness in the other
phenomena.
It is not uncommon to find seemingly inexplicable vagaries in the location
and intensity of the white patches, and also coincident lividity. The signifi-
cance may be better appreciated from a rehearsal of an instance such as the
following.
In case, M. S., after elevation of the leg, the pallor is admixed with patches of cyanosis
that almost look hemorrhagic. These are distributed over the big toes, being most promi-
nent over their plantar aspects. Complete ischemia is very hard to elicit because of the
240 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
persisting cyanotic areas although some look hemorrhagic. They can be proven to be foci
of stasis because blood can be dislodged by pressure converting them into pallid spots.
Not dissimilar lividity accompanies localities of imminent gangrene; but such do not become
pale.
Even after the induction of reactionary rubor which may begin over the ankle and spread
slowly over the dorsum and plantar aspects of the foot, a larger or smaller area of pallor
may remain either over the dorsum or the toes. Suddenly rubor may loom up in a distal
part, leaving here and there a mottling of white. The tip of the big toe may remain white
the longest, retaining a slight livid hue. Such a phenomenon is evidence of the poor circu-
lation in the big toe, especially when it is last to regain a pinkish tint. When it becomes
necessary to bring the leg to the pendent position to effect the latter, a valuable hint as to
the gravity of the prognosis in this locality is at hand.
5. Arc or Angle of Persistent Ischemia.—Since this is the complement of
the angle of circulatory sufficiency the phenomenon of blanching and its
behavior on depressing the leg after prior ascent, will merely be touched upon
here. Generally speaking, the greater the arc within which ischemia con-
tinues to remain in evidence the more extensive the arterial occlusion. A
limb that remains blanched in situations between 180° (vertical) and 70°
(20° below the horizontal) is one whose circulation is badly compromised.
More frequently reactionary rubor is perceptible before descent reaches the
horizontal. Although this angle cannot be estimated with mathematical
accuracy, an approximate appraisal will suffice as a good working guide.
This absence of precise delimitation between disappearance of ischemia and
reentrance of rubor, is responsible for the inaccuracy of the test. Thus pallor
over certain toes or even part of the foot may be difficult to dislodge and on the
other hand, rubor may develop in patches that alternate with recalcitrant
areas of pallor. If sufficient time be allowed to elapse, however, the reaction-
ary rubor will finally disappear and cause every vestige of ischemia to vanish.
6. The Obstinate Areas of Pallor—When one or more toes or areas, on
repeated examination fail to become red when the test for reactionary rubor
is made, and when such well localized spots of sanguinous depletion are visible
even at the horizontal or at an angle of greater depression, we then have
valuable evidence of marked local deficiency of circulation. Such areas are
apt to be the seat of gangrene, at no remote date. When there isa history of
spontaneous blanching in the same locality, or such discoloration after a walk
in the cold, or when the situation of the pain coincides with the distribution
of the pallor, strong corroborative testimony of impending gangrene or trophic
disorder is in our possession.
II. VASOMOTOR ISCHEMIA IN THROMBO-ANGIITIS OBLITERANS
Since local syncope is discussed elsewhere, and many of its striking features
defined in detail, it will be merely necessary here to allude to that perplexing
association of pallor of neurotic origin, with the multiform color manifesta-
tions of mechanical or hydrostatic causation. For, even in organic maladies
of the vessels where objective signs are eminently due to vascular obliteration,
a coincident display of vasomotor phenomena may create a confusing clinical
picture. A narration of the clinical manifestations alone will be attempted,
since the explanations of such occurrences are still too vague and unsatisfactory
to warrant argumentation. Suffice it to say here, that the implication of the
nerves, and the perivascular chronic inflammatory process so noteworthy in
thrombo-angiitis obliterans, may be responsible in part at least, for a loss of
normal vasomotor stability.
THROM BO-ANGIITIS OBLITERANS—ISCHEMIA 241
To what extent metabolites, or a vicarious functional implication of the
autonomic action of the capillaries and arterioles is responsible for these
phenomena, future investigation may help to clarify.!. Furthermore, it
has been the contention of a number of physiologists, that a vasomotor
constriction may be the sequence of ischemia alone whenever a part is arti-
ficially depleted of blood, just as a hyperemia is incident upon subsequent
filling of the emptied vascular channels. In conformity with this hypothesis,
a neurogenic reflex can play a réle whenever there is abnormal anemia or
plethora.
Too much emphasis cannot be laid on the fact, however, that most of the
objective symptoms regarded and described by many authors as of neurotic
foundation, are merely hydrostatic and compensatory phenomena; although,
it is true, independent vasomotor disturbances may be concomitant and clini-
cally mystifying in appearance.
Vasomotor ischemia in thrombo-angiitis obliterans seems to be especially
influenced by cold and exertion; it is independent of posture, since it may occur
in the horizontal and pendent positions as well as in the elevated. It differs,
too, from hydrostatic and mechanical ischemia in that it may come on with-
out apparent cause, alternate with rubor, and offer thus a variegated display
of color tints that stamps the phenomenon as the result of a neurotic agency.
Especially notable are such manifestations when they occur in cases of
thrombo-angiitis obliterans in which other objective pathognomonic signs
have not developed sufficiently to warrant a positive diagnosis.
Since these manifestations are frequently more pronounced in the early
stages of thrombo-angiitis obliterans than later in the course of the malady,
diagnostic uncertainty must necessarily exist in the minds of those not thor-
oughly conversant with the relative significance of the two types of ischemia.
An interesting example of the independent occurrence of the two varieties of
pallor may be worthy of consideration.
Vasomotor Phenomena in Only One Leg. Usual Clinical Course of Organic Vascular
Disease in Both——H. R. presented simultaneously striking vasomotor signs in the right, and
typical objective symptoms of thrombo-angiitis obliterans in the /eft. Later, whilst under
observation, the vasomotor phenomena gradually disappeared, the disease taking its usual
course in both extremities.
Thrombo-angiitis Obliterans Symptoms in the Left Leg, December, 1, 1908.—On taking
off the shoe the left foot appears markedly red; the dorsalis pedis, posterior tibial and popli-
teal arteries are pulseless; there is marked ischemia on elevation.
Vasomotor Signs in the Right.—At the same time the right foot was found blanched in
the pendent posture, cold, and patches of cyanosis appeared. All the vessels pulsate.
On December 24, the picture was still more striking. At this moment the progressive-
ness of the malady was noted by the disappearance of both posterior tibial and dorsalis pedis
pulses on the right.
Upon taking off the shoes and stockings and examining the lower extremities, the differ-
ence in color between the left and right foot is remarkable. On the left the swollen and
enlarged toes are of a deep red color, the hue extending up the dorsum of the foot is most
intense on the inner side of the foot and fades off gradually towards theankle. The right
foot is of a peculiar yellowish white color, the toes are most markedly blanched and are
nae smaller than on the left foot. (Angiospastic pallor of the right foot in pendent
position,
After the feet hang down for about five minutes their color changes. The color of the
left becomes admixed with a blue tint, which gives a livid appearance to the foot, the purple
color being particularly striking over the toes; here and there bright scarlet patches stand
out prominently between areas of cyanosis. ‘The right foot still retaining its more slender
appearance has become cyanotic, the distal phalanges being of a deep dusky purple unmixed
with any tinge of red, and the rest of the foot also shows a cyanotic hue but somewhat toned
by a pale ashy skin, which shines through in many places, After the right foot has
1 See Chap. VII concerning the independent action of capillaries and arterioles.
16
242 CIRCULAFORY AFFECTIONS OF THE EXTREMITIES
remained in the horizontal position for about five minutes, a little of the normal color
appears over the fourth and fifth toes, but the first three toes are still quite blue.
After cyanosis had set in, however, zschemia dependent on elevation could regularly be
demonstrated in the right foot—this being the noteworthy diagnostic point in favor of thrombo-
angittis obliterans.
March 1, 1909, amputation of the left leg. In November, 1908, the angiospastic condi-
tion in the right foot had disappeared, the popliteal artery no longer pulsated, the disease
evidently making progress.
January, 1919, amputation of the right leg; specimen showing typical lesions of thrombo-
angiitis obliterans.
Conclusions——A period of vasomotor disturbances as predominating objective sign
in the right leg; rapid development of thrombo-angiitis obliterans in the left with amputa-
tion; disappearance of vasomotor phenomena in right, followed by usual symptoms of
thrombo-angiitis obliterans.
A further discussion of this type of blanching is relegated to the chapter on
Vasomotor Symptoms in Thrombo-angiitis Obliterans.
Ischemia, an Index of Circulation.—We have elsewhere alluded to the
value of the angle of circulatory sufficiency as an approximate clinical
measure of the circulatory condition; and also to the fact that the obstructive
effects vary in inverse proportion to ‘the size of the angle (above the
horizontal) through which the limb must be elevated before pallor is estab-
lished. In acute exacerbation of any of the organic types of vascular occlu-
sion, when either by virtue of extension of the disease per se, or through
superadded accretion, bland or mechanical thrombosis, new vascular territories
become involved; these methods of circulatory appraisal become even more
reliable and valuable—for compensatory collateral paths (an otherwise
misleading factor) have not as yet become adequately established.
If cases of atherosclerotic disease of the arteries can be observed during
and after attacks of thrombosis, we can note subsequent improvement of the
circulation, not only by the usual signs, but also by estimating the altitude to
which elevation of the leg is necessary for the advent of the first signs of
blanching. Very frequently, ischemia is present even in the horizontal posi-
tion, shortly after thrombosis or embolism. As the limb improves, the leg
must be raised higher and higher to elicit the ischemia. [Early in the clinical
course of the embolic and thrombotic cases, a production of the blanching is
easy, for then a very slight raising of the limb above the horizontal i Is apt to
PIOCUCEME. ws
These observations apply also to other forms of organic vascular maladies
where obstructive conditions of the circulatory channels are at hand.
CHAPTER XLVI
THROMBO-ANGIITIS OBLITERANS—ERYTHROMELIA!
Erythromelia, Rubor, Hyperemia-—We may divide the rubor accompany-
ing this affection into (1) inflammatory, (2) non-inflammatory or intrinsic
rubor, and (3) the vasomotor.
Types of Rubor.—1. The inflammatory rubor or hyperemia hae requires
comment, in that it is associated with inflammatory processes, differing only
in so far from the reactive redness of the normal, that it is apt to be less
1 For other interpretations of erythromelia in the light of the findings of capillary
microscopy, the reader is referred to Chap. CVII.
2 This term must not be confounded with that of “‘erythromelie” proposed by Pick for
the disease, Idiopathic Atrophy of the Skin (see Chap. Scleroderma).
THROM BO-ANGIITIS OBLITERANS—ERYTHROM ELIA 243
intense in the neighborhood of trophic lesions than we would expect with
healthy vessels. Edema and lymphangitis are often coexistent lesions.
2. The intrinsic rubor or “erythromelia”’ (as the author has termed it)
seems to be due to compensatory dilatation of the superficial capillaries.
This manifestation has led to much confusion in the differential diagnosis
between erythromelalgia and thrombo-angiitis obliterans. It is a red blush
of varying degree or intensity, that usually begins in one of the toes (big toe
especially) and extends over all the toes for a variable distance up the dorsum
of the foot. It may be so slight as to necessitate comparative exposure of
both feet for its detection, or so marked as to partake of a crimson or vermil-
lion hue. Its appearance is enhanced in intensity and expedited in develop-
ing by allowing the limb to hang down, the color increasing gradually until it
attains its maximum, when a slightly cyanotic tint is wont to be admixed,
whilst the dorsal veins of the foot attain their maximum prominence.
When rubor is present in any position between the horizontal and the
pendent, when it is manifest at room temperature in these postures, we term
it chronic rubor or erythromelia in contradistinction to that rubor which is
induced after preliminary elevation of the limb. The advisability of making
so subtle a distinction will be made clear when the importance of the two
manifestations in diagnosis will be discussed.
Chronic rubor or erythromelia is an inherent, characteristic and unmistak-
able stigma of defective circulation in the deeper vessels and its chronicity
and dependence upon posture of the limb should at once differentiate it from
the rubor of vasomotor origin. It is not only influenced in intensity as the limb
is elevated or depressed, but suffers change secondarily through any circu-
latory alteration that may be transmitted to the deeper vascular channels.
As elevation of the limb empties the deeper channels, so also, will blood be
drawn from the superficial parts, both through evacuation by gravity, as.
well as by diminution of the supply. Variations in erythromelia upon
changes of position are greatest where the deep vessels are most extensively
diseased.
Mere elevation to the horizontal may decrease the redness considerably,
while lifting the limb towards the vertical causes its complete disappearance.
The position (angle or level) at which the hyperemic manifestations
appear is subject to variation. Sometimes rubor is apparent with the leg
elevated slightly above the horizontal, at the horizontal, or below this level.
It is evident that these types must correspond to different degrees of circu-
latory impairment, the vascular obliteration being doubtless most extensive
in the last type, or, per contra, the collaterals are least adequate.
Although erythromelia is a very constant symptom and usually appears
at some time during the course of the disease, it may be continuously pres-
ent in some, be absent in others, and in still other cases may persist for a
long time, disappearing completely when the symptoms have abated or the
limb is ina “‘cured state.’’ In two cases (S. and J. R.) erythromelia remained
for a considerable length of time, and then completely disappeared when
the limb was free from symptoms.
Reactionary or Induced Erythromelia.—With the limb held high for a time,
subsequent pendency is regularly followed by a reactionary or induced rubor
of much greater intensity. This phenomenon is closely analogous to the
hyperemic reaction that follows the application and removal of a constricting
bandage to an extremity. Since ischemia must precede its production, its
demonstrability indicates that a state of arterial occlusion or impaired circula-
tion must exist. For, without occluded vessels, the mere elevation of the limb
244 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
is ineffective in causing the requisite blanching. The importance of reactionary
or induced rubor in the recognition of obturated deep vessels can thus read-
ily be realized. In a routine examination of cases of suspected arterial
occlusion, the contingency of appreciably altering the degree of rubor by a pre-
liminary lifting of the limb must be considered. And it is always advis-
able, therefore, in order to gain a correct estimate of this symptom, to
examine the extremity first, in the dependent position (as the patient walks
into the office), second, in the horizontal position, third, in the elevated,
and finally, again in the pendent, when the reactionary or induced rubor will
be viewed.
Partly by reason of thermal constricting influences (vasomotor),
and partly for other reasons, it is not always feasible to demonstrate a very
noticeable reaction. In such cases, the procedure of elevating and depressing
the limb must be repeated two or more times, in sucha manner as to permit
ischemia of one minute duration to be followed by a reactionary period of
about three minutes or more. We will not infrequently be rewarded by thus
evoking a most exquisite rubor that seemingly could not be elicited at all.
Not only is this a valuable diagnostic sign in indicating the existence of
arterial occlusion, but may be utilized to differentiate between the relative
activity and extent of the obliterative process in the two limbs. Further-
more, it may be exhibited at a time when the chronic rubor is so slight as to
be doubtful. Fine distinctions, such as a color reaction in the horizontal
position in one limb, and in the position of complete pendency in the other,
with appearance over the leg before it reaches the toes and foot, are amongst
the variations encountered.
Reactionary erythromelia is frequently of value in the diagnosis of those
cases, in which, for a long time, there are no symptoms other than pulseless
vessels (possibly only the dorsalis pedis), and pain. In these, fairly marked
induced rubor may be present long before the characteristic chronic rubor
develops.
Thus, in one case H. F., absent dorsalis pedis and posterior tibial pulses, with reactionary
erythromelia were the only signs of thrombo-angiitis obliterans. Ischemia was doubtful.
Later on (June 11, 1910), a slight chronic erythromelia appeared. Under our own eyes
erythromelia developed, but for a long time we had to have recourse to the reactionary
rubor in making the diagnosis.
A careful scrutiny of the color changes accompanying the induced rubor
may lead to conclusions of diagnostic and prognostic importance.
With the advent of the reactionary eyrthromelia in certain cases, it is
very interesting to note how certain portions of the foot will remain white
longer than others. By digital compression of the hyperemic areas, the
rapidity of hyperemic return will show differences of circulatory activity in
various toes.
To cite an example:—In the case S. L., all of the toes and an inch and a half of the
dorsum remained white for 3 or 4 minutes, although the rest of the dorsum became very
red. The return of blood into the toes was not simultaneous, but the fourth and fifth
showed rubor, whereas the first, second and third remained white. Patches of white also
persisted over the dorsum. The big toe of the right foot remained white for a long time, and
the reactionary erythromelia existed much longer in the foot that was markedly affected
than in the other in which the symptoms were slight.
Other variable phenomena associated with induced rubor are of no mean
value in the acquisition of a general concept of the pathologic conditions at
hand. Evidences of inadequate circulation are notably enhanced by the
THROMBO-ANGIITIS OBLITERANS—ERYTHROMELIA 245
induction of this type of rubor. The observations in the following case
will illustrate.
In the case, M. S., the reactionary erythromelia begins to appear over the left ankle
extending slowly over the dorsum and plantar aspects, leaving a large and small area of
pallor over the dorsum and the toes for some time. Then it looms up at a more distal part,
leaving here and there a mottling of white. Remarkable, however, is the fact that the
tip of the big toe remains white longest, and with it there is an admixture of cyanosis. A
similar condition obtains in the right leg but not so marked. It is necessary to depress the
foot to obtain rubor of the big toe.
In short, here are phenomena expressive of the poor circulation in the big toe, since it is
the last to regain its circulation; and here is exemplification of the value of inducing rubor
to confirm signs that might be misinterpreted as of vasomotor origin. For, indeed, local-
ized syncope may occur even in organic obstructive arterial affections.
Cold and vasoconstriction from other causes may temporarily prevent
the demonstration of both chronic and induced rubor. So it may be neces-
sary either to warm the extremities affected or to artificially further the
dilatation of the superficial vessels by repeated changes of posture. The
latter is done by elevating the limb for 1 minute, so as to produce ischemia,
then to depress it for 2 minutes. Several changes of position will eventually
evoke a reactionary rubor that may be otherwise indefinitely postponed by
reason of vasoconstricting influences.
Duration of the Chronic Rubor.—When the postural treatment of the
author is successful in dispelling most of the symptoms, then we often note a
disappearance of the chronic erythromelia. Such disappearance of the
chronic rubor with a slight reactionary rubor, however, can be elicited even
when erythromelia is absent.
In short, the chronic rubor disappears before the reactionary. The
following case will exemplify.
J. K., 37 years of age, November 24, 1920, presented the typical history and physical
appearance of thrombo-angiitis obliterans involving both lower extremities, and the devel-
opment of an ulcer of the small toe, and another between the second and third toes of the
left foot. These have not healed.
A deep ulcerating fissure at the base of the little toe is observed, the foot in a state of
chronic rubor, the big toe slightly tumefied, and an ulcer over the small toe. The dorsalis
pedis and posterior tibial pulses are not perceptible. The postural treatment was
prescribed.
April 14, 1921, still marked rubor of the left leg and absent pulses of the right are
recorded.
October 24, 1921.—The chronic rubor has disappeared completely, but the dorsalis
pedis and posterior tibial arteries are still pulseless; postural treatment continued.
October 16, 1922.—Both feet have a normal appearance; disappearance of the chronic
rubor, but reactionary rubor can still be elicited, but of slight degree. His symptoms have
almost disappeared, demonstrating (1) the value of the postural treatment; (2) the dis-
appearance of the chronic rubor; and (3) the persistence of the reactionary erythromelia.
A similar change in the character of the rubor is not uncommonly noted
in the upper extremities, where, however, the restitution to a normal appear-
ance of the hand is more striking than in the case of the lower extremities.
The reactionary rubor persists long after the chronic rubor has disappeared.'
3. Vasomotor rubor may enhance an existing intrinsic or chronic rubor,
but more frequently is a patchy hyperemia of small extent interspersed with
areas of pallor. It may be reactive and follow that abnormal pallor of the
foot which is induced by cold. More data on vasomotor phenomena will
be given in Chap. LIV.
Significance of Rubor.—Whilst we do not expect a formal and definite
reciprocation between the dilatation of the superficial vessels and the quantita-
1 See p. 298, case R. L. if
—/
246 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
tive organic inroads on the deep circulatory channels, a partly abortive and
partly successful attempt is nevertheless made here by Nature to improve
the delivery of blood. This is accomplished, probably, by inhibition of
vasoconstrictor stimuli (or stimulation of vasodilators); but just how, it is
difficult to determine. In contrast with the establishment of the functionally
more potent deep collaterals (Chap. XII), this generalized tegumental
and subcutaneous vascular ectasia is but a vicarious attempt. Reasoning
a posteriori from the beneficial effects of the author’s postural treatment,? it
must be regarded as an index or partial measure of an accompanying enhance-
ment of vascular girth and patency in the deeper arteries.
In the “postural” procedure we call forth hyperemia by an artificial
sequence of changing positions. Knowing that induced rubor will follow
the preliminary blanching produced by elevation, we posit, therefore, that
such reactionary rubor—which is but a heightened erythromelia, and only
the external visible characteristics of which are perceived—is valuable, not
only through its amelioration of the skin circulation, but also because it may
be, and probably is, associated with similar angiectatic or expansive phe-
nomena in the muscular and other deep arterial branches.
A number of interesting phenomena attest the heightened vasomotor
instability of the vessels supplying the skin, when either chronic, induced
or both types of rubor become visible. Thus, the occurrence of irregularly
outlined and evanescent areas of pallor, interspersed amongst the general
redness that is evoked by elevating and then depressing the limb, is a mani-
festation of more severe impairment of circulation in the limited ischemic
area, or merely significant of a prolonged angiospasm. Setting aside the
former type which is evidence of chronically impoverished circulation for
consideration elsewhere,? let us appraise the importance of the observations
from which the vasomotor nature of the latter has been deduced.
We have already noted that when induced rubor is elicited, certain fugitive
spots or areas of pallor will outlast the general ischemic color, but will, after
a variable time, also be replaced by redness. What causes these pallid spots?
Why is the blanching so transitory?
Upon reflection it will be admitted that but three explanations are
applicable. Either there is a permanent narrowing of the arterioles and
capillaries of these parts that is more intensive than in the surrounding area;
or, the vis a tergo is insufficient to fill these as quickly as elsewhere; or a
vasoconstriction is present, which outlasts any such phenomena that may
have been present in the adjoining parts. Of these three different views,
the last seems to be the most plausible explanation.
Noteworthy and significant is the fact that the transitory type of persist-
ing ischemia does not affect exactly the same areas on all occasions, but
even during the same interview and examination, repeated tests for induced
erythromelia may bring forth varied pictures. Certainly, therefore, an
organic cause cannot be ascribed to the phenomenon.
Furthermore, it is not the most distant parts that are the seat of it, the
dorsum of the foot at points considerably removed from the tips of the toes
evincing it as frequently as the most peripheral parts. Therefore, an4 -
petent propelling force from behind is also not responsible. ~The bizarre \\——
colored appearance should, therefore, be attributed to an unstable nervous
mechanism.
1 Postural treatment is described on p. 380.
2 See Chap. XLV.
THROM BO-ANGIITIS OBLITERANS—ERYTHROMELIA 247
We believe that immediately on elevation of the leg and particularly
through prolongation of this position an arterial constriction may occur, as a
necessary functional and compensatory action. For, the diminished arterial
supply through the scant vascular channels and the reduced vis a tergo in
the distal parts, accounts for collapse of vessels when blood has to flow up
hill. A vasomotor constricting influence is the necessary sequence, though
its occurrence cannot be predicated for all cases. Depressing the limb, since
it causes a sudden inflow, should normally evoke a relaxation of the contracted
vessels. In fact this occurs in the areas that are the seat of reactionary rubor.
Pallid zones then, are those in which such vasodilatation is temporarily in
abeyance.
Where more or less permanent, identically situated ischemia, oft attended
with cyanosis, 1s a feature in the peripheral part of a digit, or other distal part
of the foot, organic vascular occlusion is usually the cause.
Explanation of Erythromelia.—An attempt was made by the author to
investigate clinically whether the dilatation of the capillaries and arterioles
producing chronic rubor was of paralytic nature. The induction of derma-
tographia suggests that in most cases, a true palsy of the capillary activity
does not exist. The observation that cases lose their chronic rubor when
they improve after the postural treatment, also speaks in favor of this
conclusion.
If we cause the red type of dermatographia (dermatographia rubra) in a
foot that is in a state of chronic rubor, and subsequently bring about ischemia
thereof by elevation, blanching of all of the skin is produced, the reacting
streaks showing slightly as very faint bluish red lines, or not at all. On
subsequent depression of the foot, it will be seen that the reactionary rubor
may appear first in the streaks of dermatographia and Jaéer in the immediately
surrounding areas. This would seem to warrant the conclusion that there
has been produced a distinct comparative alteration in the tone of the capil-
laries of the scratched areas, one that temporarily puts these into a state of
dilatation, whilst the surrounding parts yield to the reflexes gradually and
show belated dilatation in the pendent position of the limb. If complete
_ palsy of the capillaries were present, no such difference in time of response
should exist.
Whether the delayed rubor indicates belated reflex dilatation or slow
chemical response on the part of the capillaries, is an open question. At any
rate, the conclusion is warranted that the finer vessels are still able to respond,
and are not wholly inert and paralytic.
Can we satisfactorily account for the striking rubor so characteristic of
this affection, and of other obliterative arterial diseases? To state that it
is a compensatory phenomenon is merely an expression of a teleological view,
and an assignation of a distinctive attribute to the phenomenon. We can
obtain illuminating information on its modus operandi, however, by inten-
sive clinical and anatomical studies. From such, the author would offer
the following explanation.
We assume that with the exclusion of the normal major. circulatory
channels, although there is a generally diminished pressure, a relatively
larger amount of blood tends to remain in the superficial arterioles and
capillaries. This blood arrives through devious channels by circuitous
routes, and by virtue of the diminished ws a tergo must needs remain longer
in both arterioles and venules. In short, a sluggish circulation with stasis
is the result—an inference that receives confirmation in the fact that the
248 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
“expression test’? (compression of the skin) always indicates a tardy return
of blood into the integument.
Does not this stasis in the arterioles and capillaries exert an effect which
impresses itself upon, and evokes a response in the vasomotor innervation?
We must answer in the affirmative. For, although anatomical alterations
in the nerves accompanying the arteries (perineuritis) are concomitant lesions
of thrombo-angiitis obliterans, these alone cannot be responsible; this, because
rubor occasionally comes on rapidly after a sudden accession of thrombosis
in arteriosclerotic cases, where no perineural changes have been found.
Erythromelia may be of rapid advent, signalize, and be synchronous with other
evidences of an attack of acute thrombosis. In such, a neuro-anatomical and
pathological causal basis can be excluded, and we must expect alterations in
functional innervation as the creative grounds for the phenomenon.
With the limb pendent, the constant stasis in the arterioles and venules
then—whose existence is adequately corroborated by the color changes
elsewhere described—may be regarded as influential in producing a state of
chronic vasodilatation with partial exhaustion of the vasocontracting
mechanism. That complete paralysis of the constrictor power does not
occur, is proven by the occasional local syncope that goes with, and alter-
nates with rubor in certain cases, and by the circumscribed and limited
areas of pallor that outlast the generalized rubor, when the test for ischemia
and induced erythromelia is carried out, and by the response to dermato-
graphia occasionally elicited.
In short, we postulate a maladjustment, malfunction and instability of the
vasomotor mechanism, as the result of continued disturbance in the normal
intravascular pressure. What is more likely than relaxation of the normal
arterial tonus when the small vessels have lost the aid of the usual vis @
tergo in the propulsion of blood through the tissue and back through the veins?
Their muscular mechanism, just as in other viscera, may suffer; and they
may lapse into a state of chronic dilatation, which we have elsewhere regarded
as compensatory. In most instances however, their contractility is at least
partially conserved.
In erythromelia we presuppose an inhibition of the vasoconstrictor
impulses, incited, accompanied and aided by hydrostatic conditions. In the
usual ischemia on elevation or even in the horizontal position, we are dealing
merely with a hydrostatic phenomena, one of pure depletion; although (as
has been elsewhere pointed out) subsequent vasomotor contractions may
supervene, and prevent for a time at least a rapid refilling of the vessels when
the proper conditions of gravity (pendent position) are again restored
(neurogenic ischemic reflex).
In consonance with this conception, we predicate a division of the vaso-
motor phenomena into two types:—First, that of central origin (as in
Raynaud’s disease, erythromelalgia and the other vasomotor and trophic
neuroses), and secondly, an essentially peripheral form (thrombo-angiitis
obliterans, arteriosclerosis, and the other obstructive arterial diseases).
Whilst the deranging nerve impulses in the neurotic type emanate primarily
from the central nervous system, the aberrant vasomotor responses in the
organic vascular processes, owe their origin to abnormal impulses from the
periphery. Although this view is acceptable as applying generally, it must
be qualified in so far as it does not imply that centripetal stimuli play no réle
in inciting the unstable nerve mechanism of the vasomotor neurotic type, nor
that emotional, and other central agencies may be altogether impotent in
THROM BO-ANGIITIS OBLITERANS—ERYTHROMELIA 249
the organic arterial maladies. A more complete exposition of this subject
is to be found in Chap. LIV.
When we speak of compensatory dilatation, we unwittingly seem to
inject a teleological interpretation into effects whose origin may be wholly
passive. But for the student, such inferential thinking serves a good purpose
in emphasizing certain objective and therapeutically adaptable phases of the
phenomena; and, therefore, is wilfully allowed to be incorporated here.
If we were to attempt an explanation based on mechanical or hydrostatic
laws alone, we would err in not having taken into account the nerve mech-
anism, the autonomic action of the capillaries themselves,! and the possible
secondary paralytic and exhaustive influences occasioned by the unusual
obstructive impairment of circulation. Taking these forces into considera-
tion, it would seem that all do not participate to an equal degree, or else the
varied pictures, with or without fleeting vasomotor phenomena could not be
explained.
A detailed discussion of the réles of the numerous motivating and
determining elements is given in Chap. VII on Physiology of the Capillaries.
Here, we need but summarize our theories that superficial arterioles and capil-
laries may attain a more or less chronic state of dilatation as the result of
the following causes.
(1) Exhaustion of the vasoconstrictor mechanism of primarily mechanical
origin.
(2) Local action of metabolites or katabolic agents in a field of
impoverished nutrition.
(3) Action of specific toxins on the autonomic capillary regulatory func-
tions with paralysis of these.
1. The Exhaustion of the Vasoconstrictor Mechanism.—With more or
less constant collapse of, or diminution in the size of the arterioles and
capillaries, we would have to assume, according to the accepted views of
physiologists, that a chronic increased tonus in these vessels must be the
response. How long can this continue without yielding to that paralytic
stage which would objectively find its expression in the clinical state of
erythromelia? But that this cannot whooly account for the altered vascular
girth is demonstrated by the clinical phenomenon that with existing rubor,
vasomotor syncope, transitory, localized, fugitive, but nevertheless present,
may occasionally be conspicuous. How then could we reconcile an exhaus-
tive or paralytic state with one still capable of responding to a nerve mech-
anism?
Whilst seemingly diametrically opposed conditions, these are not so
diverse as they would appear at first glance, for, firstly, the vasomotor syncope
but rarely occurs when the hydrostatic factors are still at play, as in the
pendent position, and secondly, such fugitive neuromuscular activity as
angiospasm can be dispelled and actually exhausted by the clinical method
of inducing rubor already described (reactionary or induced erythromelia).
As for the first contention, we note that vasomotor syncope in the pendent
position is more apt to occur in those cases in which the disease has affected
but limited and shorter territories, as in the clinically early or little advanced
case; namely, in those in which exhaustion may be but partial and the vessels
are still amenable to nerve influences. And secondly, by passive exercises in
which the dynamics of hydrostatic and gravity nature are summoned into play,
an actual insufficiency and exhaustive state of the capillaries and arterioles can
1 Vide, also Chaps. XIII and LXXXVII.
250 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
be demonstrated. For, given that syncope of neurotic nature in thrombo-
angiitis obliterans which but occasionally qualifies the picture, its fleeting
nature can be readily recognized in the case in which the changing position
of the limb may cause it to disappear.
Nor must we interpret the absence of rubor in the horizontal position as an
argument in favor of retained vasoconstricting powers. For, in such position,
the force of the circulatory stream may be inadequate to force the blood
through the collaterals and into the capillaries. Unfortunately, the effects
of gravity must sometimes be called to aid in the production of rubor, so that
an additional mechanical factor is injected.
2. In consonance with the work of recent investigators, we must take into
account that the products of local metabolism are believed to be a potent
factor in producing dilatation of the smallest vessels. Are not metabolites
present in increased abundance in territories so badly nourished? Just
what part is played by the chemical influences is still a matter of conjecture.
That a vicious circle may be produced in areas (toes) that are in imminent
danger of gangrene, seems more than likely, for that stasis occurs is clinically
often demonstrable.
Perhaps this excessive stasis that leads to cyanosis is furthered by the
dilated condition of the capillaries.
Whilst it may seem paradoxical to recognize the possibility of chronic
dilatation of capillaries and venules, and to question the likelihood of a con-
tinued state of tonicity without exhaustion, more careful reflection will explain
this seeming inconsistency of thought. Whereas a state of dilatation,
passivity or inactivity can be comprehended as of unlimited duration, an active
constricted state, be it due to neuromuscular incitement (arterioles), or even
to an inherent contractile power of the cells themselves (capillaries) may
have its limitations in time, and yield to exhaustion.
3. Specific Toxins.—This last is purely theoretical and can hardly obtain
except in pregangrenous stages, for rubor is produced by diseases of diverse
pathogenesis. Whilst the hypothesis of the existence of such a poison in
thrombo-angiitis obliterans could be entertained for the acute stages of the
disease, the chronic obstructive stage with healed products in the vessels
should offer chemical substances not essentially different from those elabo-
rated as waste or by-products in the tissues in the other occlusive vascular
maladies (arteriosclerosis, bland thrombosis, healed syphilis with thrombosis,
etc.)!
CHAPTER XLVII
THROMBO-ANGIITIS OBLITERANS—CYANOSIS
As a manifestation of impaired circulation, this phenomenon varies
as to intensity, localization, and duration, and must be regarded as subject
to vasomotor influences, as well as to obstructive circulatory factors. With
this in mind, and with full cognizance of the influence of thermal and emo-
tional factors, its réle as a sign of thrombo-angiitis obliterans can be more
accurately appreciated.
1It may be of interest to note here that certain Russian observers believe that in the
course of intravascular thrombosis, a ferment or toxin is liberated that in itself can bring
about alterations in vasomotor function.
THROM BO-ANGIITIS OBLITERANS—CYANOSIS 201
Although subsidiary in importance to the rubor, it is frequently present
over one or more or all of the toes, and even over the whole foot, especially
when the latter is allowed to hang down for a considerable time. Then a cer-
tain amount of purplish discoloration is wont to be admixed with the rubor
that is so constantly present in this position.
In the elevated position of the limb, when blanching has already taken
place, multiple cyanotic areas are apt to remain, often more marked in the
toes whose circulation has been most impaired.
Cold has a decided influence in evoking and stabilizing an asphyctic state,
the rubor giving way to it particularly over the very peripheral parts. But
even under ordinary climatic conditions cyanosis of the toes is frequently
intermingled with the rubor. Thus, the tips of the toes may be cyanotic
whilst the dorsum shows marked hyperemia, and the plantar aspect of the
foot may evidence patches of bluish purple discoloration.
When considerable circulatory obstruction is present, cyanosis in the
dependent position may yield to ischemia in the horizontal or above the hori-
zontal, but patches of more or less permanent cyanosis tend to remain.
In many cases cyanosis of the big toe is rather suggestive of the presence
of the disease, and may be the only objective sign except for the absence of
pulsations. ‘That the diagnosis of thrombo-angiitis obliterans is warranted
on these manifestations alone, the future course has demonstrated as well as
the coincidental occurrence of the affection in the other leg where symptoms
may be pronounced.
Local chronic cyanosis when it is limited to one toe may precede gangrene of
that particular locality by months or even years. When it continues for a
considerable length of time, we must be guided in making our prognostication
as to the advent of gangrene by other signs, such as marked ischemia, a poor
angle of circulatory sufficiency, and extensive obliteration of vessels. The
persistence of localized and intense cyanosis, however, is always suggestive.
In such a case observed carefully for a year, the persistence of a more
pronounced cyanotic discoloration of the big toe of the right foot was noted,
the cyanotic color being much deeper in the big toe than elsewhere in the
foot. This sign was more or less constant for some ten months, when the
rubor was intense over the whole foot except for the deep asphyxia of the big
toe. After eleven months of almost constant cyanosis gangrene appeared.
Such chronic cyanosis when edema, coldness, and localized anesthesia are
superadded is no longer merely a sign of circulatory impairment, but augurs
that gangrene is imminent. Amputation (Gritti-Stokes) undertaken in such
cases has demonstrated extensive vascular occlusion involving even the
popliteal artery although one or more vessels (such as the anterior tibial)
may remain patent. It may be impossible even after careful anatomical
investigation to establish a causal basis for the chronic cyanosis.
In a review of the histories of one hundred cases, the author found that
seventy-one gave manifestations of asphyxia of one or more toes of either foot
at some time during the clinical course, although it was not a significant sign
at all. For, it is producible by a prolonged pendency even in the presence of
rubor and may precede and accompany the incipiency of gangrene. In
eighteen cases both extremities simultaneously showed cyanosis, a percentage
of bilateral involvement that might vary considerably and be much higher if
a longer period of observation had been undertaken.
But cyanosis as well as ischemia (and the two often coincidentally) may
be the expression of the concomitant action of mechanical as well as vaso-
252 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
motor causal factors. That this is true is evidenced by the observation, that
occasionally the forepart of the foot may be markedly asphyctic, remain so
for a considerable period of time (14 hour or more), and be irresponsive to
such vasodilating excitants as changing posture (elevation and consequent
depression) and heat. At other times, removed by but short intervals of
time, both ischemia and asphyxia in the same foot are less marked, more
evanescent and more readily abolished by the above mentioned means.
It is difficult to draw accurate conclusions as to the comparative impor-
tance of the ws a tergo, the hydrostatic and gravity elements, and the vaso-
motor influences in the determination of the intensity of local asphyxia.
Enough observations are at hand attesting to the participation of all of these
factors to varying extents. Perhaps most influential are the forces of gravity
and inadequate vs a tergo, that allow of the accumulation in the veins and
capillaries, and a certain degree of reflux of the poorly oxygenated blood.
Thus, we could explain the intensification of the cyanosis of the feet in the
pendent position, and the frequent disappearance of much of the asphyxia
in the horizontal and elevated postures. Vasomotor lability and the possi-
bility of venous spasm cannot be altogether excluded, however, as an occa-
sional causative or coincident and participating agent. For, while lividity
of the fingers may be noted in the hanging position of the arms where exten-
sive arterial obliteration is present, considerable or even exaggerated asphyxia
may persist on elevation, or even when the arms are in the horizontal posi-
tion. The venules probably do not empty themselves, partly because
arterial circulation is defective or almost in abeyance in these positions, and
also because of complicating venous spasm.!
An interesting case with marked cyanosis may be worthy of citation.
W. K. complains of pain in the feet at night and the inability to sleep. Walking is
difficult because of the swelling of the left big toe and stinging pain. Two years ago he
could not step on the sole of the right foot which was swollen. ‘The left big toe is now espe-
cially painful and made worse either by raising the foot or lowering it.
Physical examination.—In the pendent position the tips of the toes of both feet are cya-
notic, whilst the dorsal aspect of the toes shows rubor, more intense in the left than in the
right. The left foot is larger than the right, its forepart being slightly swollen and the veins
standing out more prominently. The sole of the right foot shows color changes, which are
more marked over the forepart and involve four toes. The latter show numerous cyanotic
patches, whilst the plantar aspect of the little toe is almost normal in color. When raised
to the horizontal the right foot becomes ischemic. All the toes of the left foot and the distal
half of the sole show marked cyanosis, but in a few minutes the purplish tint disappears,
leaving the sole and the toes ischemic, except for patches of permanent cyanosis. ‘The big
toe is tender to the touch, although without signs of trophic disturbance. The dorsum, too,
shows ischemia when the feet are in the horizontal position. Reactionary erythromelia of
both feet can be elicited. The dorsalis pedis, posterior tibial, and popliteal arteries of
both legs are absent.
Summary,—Intense cyanosis of the left foot, especially of the big toe; severe pain on
elevation of the legs, now also in the pendent position. The right leg, previously attacked,
is now in a latent stage.
Temperature conditions are not without influence in determining whether
cyanosis will predominate over the chronic rubor. Thus, in the case cited
below we quote from the notes taken on a cool and on a warm day, to demon-
strate the preponderance of cyanosis in colder weather.
Case D. B. male, on a cool day—the right foot has a violaceous red appearance, the
toes are livid, their tint composed of a mixture of deep bluish purple and bright red. Over
the dorsum there is a mottling of red and blue. A similar condition obtains in the left
foot with intensified cyanosis in certain areas, especially over the big and fourth toes. —
1 See DP. 300; Case Dao..0.
THROM BO-ANGIITIS OBLITERANS—CYANOSIS 253
On a warm day—the toes of both feet are bright red up to their roots. This color
deepens in the pendent position and is attended with increasing pain.
Pathogenesis of Cyanosis.—Cyanosis is perforce divisible into the types
produced by the following causes:
1. Venous obstruction.
2. Diminution of arterial vis @ tergo.
3. Vasomotor influences.
The most alluring explanation of the mode of production of cyanosis
when the limb hangs down—and one accepted and taught by numerous
clinicians—is that which presupposes obliterative disease of the veins as wholly
responsible. Although such lesions may be a factor in certain cases, numerous
pathological and clinical observations have demonstrated beyond per-
adventure that cyanosis of intense degree is compatible with patent veins.
When vasomotor influences may be discounted or excluded, the true cause
is to be found in the diminished pressure in the arterial system, which is
powerless to propel the blood with the usual rapidity into and through the
devious channels, stasis in the capillaries and veins being the consequence.
The truth of this assumption is demonstrable by the simple experiment of
reducing the requisite force for a prompt venous return. This may be done
by mere elevation of the limb from its situation of pendency to the horizontal
level, where the cyanosis will immediately diminish or vanish.
In some of the early cases' vasomotor instability is a decisive factor in the
production of cyanosis giving an unusual clinical picture; this is often associ-
ated with syncope, the whole making a confusing complex that antedates
the development of the pathognomonic composite of phenomena. Where
vasomotor action accounts for cyanosis, it is assumed by many that a spasm
of venules occurs, that is, vascular territories distal to the arterioles suffer
spasmodic contraction. Thus, in Raynaud’s disease even superficial veins,
large enough to be examined by the naked eye, have been actually seen to
contract in cases of local cyanosis, the asphyxia being thereby accentuated.
Even contraction of the arterioles alone after producing local syncope may
have as a natural sequence a superinduced cyanosis; and this by excluding
the cardiovascular force—the ws da tergo—so that stagnation in the veins is
to be expected.
When the technic will have become perfected and standardized, estimates
of capillary pressure may give valuable information concerning the influence
of diminished vis 4 tergo and the forces impeding the outflow of blood. Capil-
lary stagnation produced by the former mechanism should be associated with
low capillary pressure, and if by the latter, with high pressure. Dilatation of
capillaries alone could, by reason of the diminished velocity of the blood, be
followed by relative deoxygenation and cyanosis. This is the type that
succeeds the rubor when the limb has been allowed to hang down for a time.
In this position the vis a ¢ergo is insufficient to adequately accelerate the flow
upward through the venules and against the action of gravity. We would
not expect that the cyanosis of thrombo-angiitis obliterans developing on
rubor would be attended with an excessive capillary pressure, unless there is
coexisting vasomotor spasm of the venules during an attack of temporary
or fugitive vasomotor constriction. In such, spasm of the venules may occur.
Recent work suggests that through methods of estimating capillary
pressure, much valuable knowledge may be gleaned as to the nature of
1'Vide Chap. LIV.
254 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
asphyxia.! If increased pressure is found, spasm of the vessels may be
assumed, and so the participation of a. vasomotor factor is believed to occur.
Perhaps the comparative roles of the neurogenic and hydrostatic forces can
thus be differentiated, for the latter can be wilfully altered by the position of
the limb. So, the importance of such investigations, aside from a purely
academic interest, lies mainly therein, that hydrostatic or mechanical factors,
when of increasing importance, forecast an unfavorable outlook, and seem-
ingly incongruous vasomotor manifestations are of relatively little significance.
CHAPTER XLVIII
THROMBO-ANGIITIS OBLITERANS—EDEMA
A peculiar puffiness of the toes together with an effacement of the usual
irregularities of the dorsal aspect of the foot is often incorrectly ascribed to
edema alone. Although from the pathological standpoint a slight edema
pervades the tissues, there is also a chronic proliferative process in the sub-
cutaneous tissues of the toes that contributes to the picture. This more or
less permanent condition, which is so characteristic in the cases with intense
chronic erythromelia, may continue for years. The toes and the forepart
of the foot by reason of the disappearance of surface irregularities, acquire
an artificial appearance as if molded in wax.
A transitory inflammatory edema if slight, accompanying, and due to
the coexistence of trophic lesions such as ulcers and small patches of gangrene,
is not at all an unusual feature nor one that need give concern. But another
type of edema which is extensive and permanent is of great omen.
In a number of cases, most of which curiously enough belong to the severe
type of the disease in which the prognosis as to the integrity of the limb is
concerned, edema is a prominent feature. Days or weeks after the onset
of the trophic disturbances, the dorsum of the foot first begins to show signs
of extensive edema. This is unassociated with any phlegmonous process.
In a number of these cases the author was able to follow the course of this
phenomenon, and found that it often accompanied or preceded sudden
aggravation of the condition in cases in which amputation became necessary.
In one of these cases it was necessary to amputate within two weeks after
the onset of edema. Doubtless the edema itself, has a pernicious effect,
acting so as to further impede the circulation of the peripheral parts (in a
sort of vicious circle). It is apt to extend rapidly over the whole of the
foot, and even up to the ankle and leg.
There seems to be no doubt but that it has a bad influence upon the nutri-
tion of the limb. By compressing the small vessels the compensatory hypere-
mia is interfered with to a certain extent, and loses much of its efficiency in
the nourishment of the parts. A further untoward effect is its inclination to
increase the pain, which in these cases is already considerable in the neighbor-
hood of the trophic disturbances.
Pathological examination of the limbs in which marked edema is present
shows the absence of involvement of the veins in so many of the cases that
these could certainly not be held responsible, although it is possible that
1 See Briscoe, Loc. cit. Chap. VII.
THROMBO-ANGIITIS OBLITERANS—INTERMITTENT CLAUDICATION 255
veins proximal to the point of amputation were occluded. Indeed, a satis-
factory explanation for its production is difficult to find. It may be regarded
as being of inflammatory origin, as the result of a lymphatic inflammation,
although a suppurative process is certainly at hand in most of the cases in
which it is present.
Persistent Edema the Harbinger of Gangrene.—As already stated, in
thrombo-angiitis obliterans continued edema is exceedingly inauspicious.
When a manifestation of inevitable gangrene, it may usher in a state of
chronic cyanosis of the forepart of the foot, attended with marked coldness
and anesthesia, these constituting a group of phenomena characteristic of
one form of slowly developing gangrene. It is thus called, since weeks may
elapse before the unmistakable and classical external signs of tissue death
manifest themselves. The following case will illustrate.
M. K., male, Russian, aged 35 (January 6, 1917), had had an ulcer of one of the toes of
the right foot one year previously, and this healed slowly. For six months there were the
usual symptoms of intermittent claudication. Following the removal of a callous (?),
edema began to develop. This was soon attended with cyanosis; these signs with marked
frigidity and anesthesia of the forepart of the foot were the striking and enduring manifesta-
tions until amputation was done. None of the usual objective evidences of gangrene
appeared during a period of observation from January 6 to January 18. Nevertheless, the
pain and the persistent symptoms above mentioned attested to the assumption that the
peripheral parts had become gravely compromised. Amputation January 19—Gritti-
Stokes operation.
The specimen demonstrated an absence of purulent infiltration or marked necrosis, but
an intense ischemia of all the tissues, presaging inevitable tissue death. The popliteal and
posterior tibial arteries were completely closed.
CHAPTER XLIX
THROMBO-ANGIITIS OBLITERANS—INTERMITTENT
CLAUDICATION
Next to the palpable signs of arterial obliteration, namely, the absence of
pulses, this is perhaps one of the most constant features of the disease. In
a series of one hundred cases the author obtained a history of its occur-
rence seventy-eight times in one, forty-eight times in both lower extremities.
A story of cramp-like sensations in the calf or in the foot induced by walking,
and disappearing when at rest, may precede by weeks, months or years the
advent of other phenomena. When associated with vasomotor symptoms,
such as coldness, blanching of the foot, with patches of rubor alternating
with ischemic areas, or cyanosis, the typical syndrome of Erb is present.
However, as elsewhere pointed out, the descriptive appelation intermittent
claudication is incorrectly applied to this composite complex of sensory plus
vasomotor manifestations. The latter often occur in thrombo-angiitis obli-
terans and other obliterative vascular diseases, unassociated with the typical
pains and cramps induced by exertion. We prefer, therefore, to restrict the
designation of intermittent claudication to the sensory or sensory-motor
signs, acknowledging a certain amount of clinical interdependence of the
two varieties. Whilst it is true that exercise may simultaneously evoke
256 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
the characteristic pains and vasomotor changes, other excitants such as cold
and emotion may bring forth the vasomotor indications alone, unattended by
the typical cramps.
In some of the cases there is not only a history of intermittent claudica-
tion, but vasomotor and sensory symptoms accompanying. ‘The patients
describe one or both feet as becoming suddenly white half way up the foot
or as far as the ankle after walking one or two blocks. They experience
also a feeling of numbness or a “dead”’ feeling in the affected foot. There
may be no pain in the foot whatsoever, or there may be pain in the calf,
or the pain may be altogether absent. Some say that when they sit down
after this change in color, the foot turns red or blue, this being variable
whereas the whiteness is a more constant phenomenon. Or, ischemia alone,
or “‘coldness’’ may be induced by exertion.
Intermittent Claudication with Pulsating Arteries.—Symptoms of inter-
mittent claudication may attend apparently healthy arteries, if we accept
the pulsations in the pedal, crural and femoral arteries as a guide. But
one of the Jimbs may show advanced obliterative vascular disease, which
should be regarded as suggestive of the development of obstructive lesions.
We encounter cases in which one limb gives the symptoms of intermittent
claudication for months before the pulses become extinguished. The lesions
are probably of limited extent, and involve only the plantar or peroneal
arteries that are inaccessible to touch.!
Vasomotor Symptoms with Intermittent Claudication.—The prevalence
of vasomotor manifestations, notably coldness of the foot after walking with
numbness and pain in the calf of the leg, in some cases of thrombo-angiitis
obliterans has been responsible for much prejudication in the clinician’s con-
ception of intermittent claudication. Whilst coldness and pallor of the foot
may be accounted for on the basis of obstructive hydrostatic factors alone,
wherever intensive degrees of circulatory impediment are present, there are
equally marked examples of local ischemia and frigidity due to complicating
vasomotor influences. Both exertion and external temperature conditions
are influential in the production of pallor and coldness.
It would be erroneous to regard the so-called “intermittent claudication”
—pain in the legs and feet on walking with coldness and pallor of the peri-
pheral parts—as a morbid entity. For, it has been well attested and demon-
strated by the fact that most exquisite illustrations of such grouping of
clinical features are afforded by the disease thrombo-angiitis obliterans.
The term intermittent claudication, therefore, should be rejected as descrip-
tive of a disease and restricted to a combination of associated symptoms
observable in a number of different pathological processes. To amplify
and explain by actual case, the following history may be worthy of study.
Thrombo-anguitis Obliterans with Symptoms of the Sensory and Vasomotor
Type of Intermittent Claudication.
A. G., male, Russian, age 33 years, examined November 27, 1908, has been in this
country twenty-one years. Smokes six to seven cigarettesa day. He has not been at work
for about one year because of trouble with his legs that prevented walking. Illness began
three years ago with pain in the sole of the left foot on walking. For two years the pain in
the calf of the leg was associated with the othersymptoms. He would put his foot into cold
water and the pain in the foot would disappear. For two years he did not think it suffi-
ciently severe to consult a physician, until one year ago a physician told him that he
had rheumatism, for which he tried baths. The pain became worse, so that in October, 1907,
_ | We must not forget that seemingly authentic cases of neurogenic or angioneurotic
eae claudication have been reported (Westphal, Schlesinger, Oppenheim, Chap.
XXVI).
THROM BO-ANGIITIS OBLITERANS—INTERMITTENT CLAUDICATION 257
it was so severe that he could not walk at all. He would rub his toes, would suffer for hours
with severe pain in the fourth toe and just below the fourth and fifth toes. At that time
October, 1907, there was a little “‘sore”’ on the fourth toe. The pain was always worse at
night. His “sore” healed after several weeks. After that he noticed that the foot would
get pale and cold, and later would turn blue and red in the dependent position. Then last
January he went to another physician who gave him fourteen mercury inunctions, without
result. Then 35 injections of bichloride of mercury and potassium iodide were given with-
out improvement. In fact he got worse. On walking, he says that the instep feels dead, but
he has had no pain since the time he had his ulcers last summer. On walking, his left foot
feels peculiar: the ball of his foot falls asleep and he is not able to walk more than six or
seven blocks without stopping. After resting, “‘circulation returns” he thinks. No more
sores have developed. Now his foot turns pale when he goes out and when he takes his shoe
off ao jinds his foot white. Then, if exposed, the color returns. He feels better in warm
weather.
Chief complaint: Coldness of the left foot, and inability to walk because the foot
becomes numb.
Physical examination: The right dorsalis pedis does not pulsate; the posterior tibial
and popliteal are present. The left dorsalis pedis is absent; the posterior tibial and popli-
teal are good.
December 1, 1908: Thrombosis of veins of both legs, involving the territory of the
internal saphenous, is present. ‘The patient states that his left leg gives him more trouble
than the right.
Physical examination: The right dorsalis pedis is absent; the posterior tibial and popli-
teal pulses are present. The left dorsalis pedis and posterior tibial are absent; the popliteal
is present.
The left foot shows moderate erythromelia i in the dependent position. The angle of
circulatory sufficiency is about 110°.
Résumé: A case of temporary recovery, the left side being more involved than the right,
with both popliteals pulsating, and with a history of thromboses of the superficial veins on
both sides, probably involving tributaries of the internal saphenous veins.
F ebruary 27, 1909, physical examination: Both feet are cold to the touch. He says
that his feet are always numb; he cannot work. No changes in the pulse on the right side
are perceptible. The left dorsal pedis and posterior tibial are absent; the popliteal pulse
is doubtful or faint.
April 27, 1909: Patient says his left foot gets white at the instep as soon as he walks a
few blocks and the foot feels dead. Has no pain. When he sits down it turns blue. The
right foot is somewhat better, but also troubles him in the same way. He also has pain in
the back of the left knee. Upon examination the left foot is cold to the touch, the right
only slightly cold.
On allowing the feet to hang down for 5 minutes the left becomes dusky, the right
slightly blue, but there is no intense cyanosis. A peculiar brown pigmentation of the skin
of the extremities masks the real color. At times the left foot shows a slight degree of
erythromelia. No evidence of trophic disorder.
Summary: Obliteration of dorsalis pedis of both legs; with posterior tibial on the left,
with numbness and coldness as chief symptoms. No trophic disturbances.
October 21, 1909, complains of coldness of feet and he says they get stiff.
Physical examination: Both feet are cold to the touch, the left more than the right.
December 8, 1909: He complains mostly of coldness of both feet and both feet become
“dead”? when he walks. Theright foot troubles himnow. He has had no sores.
Physical examination: In dependent position, the left foot takes a dusky reddish purple
hue, the right also shows some slight cyanosis, with a tinge of red, the color extending a short
distance up the dorsum of the foot. Both feet are cold. The big toe of the left foot is
cyanotic. There seems to be more cyanosis of both feet than at last examination.
Cyanosis is more prominent than the redness; probably getting worse.
January 3, 1910: Color of both feet pretty normal. Remarkable change in appearance,
probably due to weather. Left, slight erythromelia. Right, still less.
, January 15, 1910: Left foot fair amount of erythromelia, and he complains of coldness
of foot.
February 20, 1910: Has “no feeling” in the feet. On examination left foot somewhat
more dusky than right, but no erythromelia of either. Right big toe somewhat red.
April 3, t910: He is getting worse. Left foot often gets red. Now it is cold and toes
have a reddish and bluish hue. As left is watched changes of color take place. After a few
minutes the redness spreads over the dorsum; it is admixed with blue but is not marked.
The right does not change color.
October 8, 1911: Still numb legs, ‘‘ without any feeling.”’ Color of both feet good, left
foot much colder than the right. Coldness beginning at the toes and goes up to the ankle
All7¢
258 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
on the left side, only to base of toes on the right side. Dependent position: Right almost
normal color, left gets slightly cyanotic and red. Vessels: Right, as at last examination;
left, also the popliteal and femoral pulses poor.
November 10, 1911: Does not feel well, feet get cold. .
On examination the left foot is slightly cyanotic, and the skin of the toes looks thin.
In the dependent position there is no true erythromelia; but slight increase of cyanosis is
noticeable on the left and very slight erythromelia.
Summary: Stationary and practically cured case with both dorsalis pedes closed, but
one posterior tibial open; and all the vessels higher up seem open. ‘The chief signs are
numbness and coldness of the feet, slight cyanosis and very slight erythromelia of the left. .
A case of thrombo-angiitis obliterans with varied vasomotor phenomena, and intermittent
claudication.
CHAPTER L
THROMBO-ANGIITIS OBLITERANS—PAIN
Thrombo-angiitis Obliterans without Pain.—Although pain is an almost
certain concomitant of the other characteristic manifestations of the disease,
it may be absent for a long period, or extensive obliteration of arteries may
be wholly divorced of it. And so the author has observed pulseless popliteal,
posterior tibial and dorsalis pedis arteries, with ischemia on elevation,
reactionary or chronic rubor, without any complaint or even a recollection
of the occurrence of pain on the part of the patient. Such are the latent or
insidious cases described elsewhere. When two limbs are simultaneously
affected, one may be free of pain, the other the seat of excruciating suffering.
Varieties of Pain.—The symptom of pain in thrombo-angiitis obliterans
has both diagnostic and prognostic significance. It is present in a variety
of different situations, and is occasioned by a number ,of diverse underlying
causes.
The degree of the pain is variable, not only in the stage where it is brought
on by walking, but also when initiated by the trophic disorders and gangrene.
In some there are distinct remissions with periods of comparative freedom, in
others the pain is constant. When it is severe, the patient may sit with his
leg bent at the knee holding the foot in his hand in an effort to obtain relief.
Pain may be so mild as to be a negligible component of the syndrome.
Or, it may be so distressing that the usual deterrent forces residing in the ego
and preventing us from stepping outside of the bounds of propriety are nulli-
fied or put into abeyance. When this occurs the patient falls a victim to
psychoses, or his mentality becomes almost completely unbalanced (see
Mental Symptoms). The pain is clinically diversified as follows.
1. Pain of intermittent claudication.
2. Pain of acute thrombo-angiitis obliterans.
(a) In the superficial veins (migratory phlebitis).
(6) In the deep vessels (acute stage of thrombo-angiitis).
. Pain with changing position.
. Pain of ischemia.
. Pain with chronic cyanosis and erythromelia.
. Continuous pain antedating gangrene or trophic lesions.
. Pain with trophic disorders (fissures, ulcers, etc.).
. Pain with infection.
Pain with gangrene.
Co om An BW
THROM BO-ANGIITIS OBLITERANS—PAIN 259
The pain may vary in situation, character, intensity, and relation to
movement and posture. Perhaps the most common is that already described
under Intermittent Claudication as a cramp-like and lancinating pain, or as an
ache in the calf, ankle, or throughout the leg. Besides this, however, there
are: (1) The vague deep seated pain attending the acute involvement of the
deeper vessels; (2) the local and diffuse pain of complicating migrating
phlebitis; (3) the pain associated with trophic disorders or gangrene.
- We have already referred elsewhere to that vague ache or pain which we
may attribute to the acute involvement of the deep seated vessels. To
what extent the pain originates in the vessel walls and how much the implica-
tion of contiguous nerve is responsible, is difficult to determine. Peculiar
“drawing’’ and aching sensations are described in the calf as occurring
independent of locomotion, and may be the premonitory signs of serious,
thrombotic invasion of the arteries. Sometimes these are of paroxysmal
nature, lasting for several hours (1-4), of spontaneous advent, independent
of motion and associated with tenderness to deep pressure. Such sensory
phenomena are attributable to migrating thrombotic lesions in the deep
vessels; they are not of ischemic or angiospastic nature.
Although the origin of the local pain of acute migrating phlebitis is
usually easy to recognize, the lesion may be so extensive! that the resultant
pain becomes correspondingly diffuse, ache-like and in part indistinguishable
from that which emanates from the deeper vessels.
But it is especially when any defect in the skin or infection occurs, that
a severe pain in the affected region (though not altogether confined to this)
may arise, persist and increase in intensity in a manner quite disproportionate
to the size of the lesion. A tiny fissure—one that usually is slow in healing—
- often suffices to give the patient sleepless nights. Small, insignificant ulcers
are frequently so excruciatingly sensitive and painful that until this observa-
tion is oft repeated in our clinical work, we are at a loss to reconcile the objec-
tive and subjective manifestations. Indeed, occasionally a patient will
request amputation of a limb even though the indolent non-healing ulcer
has in no sense objectively compromised the integrity of the part. And
furthermore, even after amputation of the leg there are many instances in
which the pain may persist for days, or even two to three weeks, or more.
The development of this condition of intense hyperesthesia may be coincident
with functional derangements in the centripetal sensory paths, possibly in
the cord itself, that persist even after the original afferent impulses have
ceased. Strange to say, however, the infiltration of the posterior tibial
nerve behind the malleolus may cause the pain to disappear in some cases;
but this is not true forall. It is also noteworthy that vasomotor phenomena
not uncommonly appear with or after the advent of the pain, seemingly in
some reciprocal relationship. As to whether the continuous sensory impulses
are at all responsible for the creation of vasolability through higher centers
is a matter worthy of further study.
The pain of intermittent claudication is described in detail under the
chapter on Intermittent Claudication. Attention is called here merely to
the method of differentiating this symptom from similar and coincident pain
due to other causes. When a patient who has discomfort, cramps or pain
“throughout the leg”’ or in the calf or ankle, or on walking, but also has had
acute attacks of pain independent of locomotion, the latter may under
certain circumstances be referable to recent active thrombosis in some of the
deep vascular territories of the leg.
1See fulminating cases, Chap. LVIII on Migrating Phlebitis.
260 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
The pendent position frequently intensifies the pain in the leg and foot,
and is described in some instances as coming on as soon as the patient gets
out of bed.
Because of conflicting statements, it is often difficult to draw definite
conclusions as to the influence of position. The history may reveal in the
case of one limb that the pain is increased in the pendent position and
aggravated by elevation in the case of the other.
Sequence of Various Types of Pain.—Most commonly a period of inter-
mittent claudication antedates the intense, more delimited pain. Such a
stage is often treated as ‘‘rheumatism”’ without relief to the patient. Then
follows a period of constantly increasing pain in one or more toes, which may
be designated as a tropho-prodromal' sign, since it usually forecasts the advent
of fissures, bullae or other trophic lesions and even gangrene. With the
onset of such lesions a marked increase in the intensity of the suffering can be
expected, the latter diminishing and even disappearing with the healing of
open wounds. Just prior to or after the cicatrization of such lesions there
may be a stage of vasomotor derangement. At this time coldness, pallor and
numbness, with their attendant discomforts, may modify the sensations
described as ‘‘pain”’ by the patient.
Continuous Pain in Toes.—When the patient begins to complain of
continuous distress and then of pain in one or more toes, the disease is usually
well developed, and the trophic type of lesions or even gangrene is to be
expected. Change in color of the affected toes to a distinct or angry red in
the pendent or horizontal position is then also} noted by the patient, except
in those more uncommon cases where the vasomotor blanching seems to
dominate in the clinical picture. A good illustration of the advent of the ,
constant type of pain is offered by the following case.
S. W., male, aged 37, began having pain in calf of left leg when walking but short distance
214 yearsago. A year and a half ago continuous pain in the left big toe set in, which subse-
quently spread to the second, third and fourth toes. In spite of a 4 week stay at a hospital,
the symptoms did not subside.
Seven weeks ago the same pain previously described in the left leg appeared in the right
leg, associated with discoloration of the toes and severe pain in the fifth toe. A fissure
appeared on the fifth toe because of which the nail was removed.
Four weeks ago the tip of the left big toe became very painful, a bleb appeared which
subsequently apparently healed, leaving the region of the nail very painful.
Physical examination: In the horizontal position the forepart of the left leg shows
moderate erythromelia, and there is moderate hyperemia over the greater part of the
dorsum. The big toe is swollen particularly over the outer part of its distal phalanx, and
there is an accumulation of serum under the nail.
In the horizontal position the right foot shows slight erythromelia. The fifth toe is
slightly swollen, and presents a fissure on its plantar aspect where the nail was removed.
In the dependent position both feet soon become angry red. In the elevated position
the color leaves the big toe of the left foot first, this toe becoming completely blanched
within a few seconds. Cyanotic patches are apparent over the second and third left toes,
and rapid blanching of the entire foot, with the exception of the cyanotic patches previously
described, takes place. The right foot, too, shows marked blanching in this position. The
patient complains of severe pain when the legs are elevated.
The external iliac and femoral arteries of both lower extremities pulsate; the right popli-
teal is present, the left absent as also both posterior tibials and dorsalis pedes.
Tenderness.—This would seem to be an almost inexplicable phenomenon
in many cases and at certain stages of the disease. In its most exquisite
form it accompanies trophic disorders of rather limited extent, when these
manifest themselves as ulcers or deep fissures near the tip of the toe, especially
near or at the nail bed.
1 The word is coined to denote that which is a harbinger of trophic disturbances.
THROM BO-ANGIITIS OBLITERANS—COLDNESS 261
Its existence bespeaks the presence of one of the following conditions:
(1) migrating phlebitis; (2) the acute involvement of the deep vessels (deep
tenderness); (3) chronic cyanosis, or more or less chronic ischemia of the toe
whose nourishment is most impaired (impending or imminent gangrene);
(4) trophic lesions (fissures and ulcers); and (5) gangrene.
CHAPTER LI
THROMBO-ANGIITIS OBLITERANS—COLDNESS:
Coldness of one or more toes or fingers is a common complaint, and,
according to the anamneses and records of physical examination, its advent
is influenced by a number of different factors. These are exposure to cold or
inclement weather, washing in cold water, walking, and morerarely, emotional
strain (vasomotor) frequently described by the patient as ‘‘excitement.”’
Just as in the case of the ischemia, rubor and cyanosis, so also here sub-
jective and even objective diminution of temperature is produced either by
(A) neurotic (vasomotor) causes, or (B) by abnormal mechanical or hydro-
static agencies.
A. Neurotic Types. (1) Transitory Vasomotor Coldness—After a pro-
dromal stage of intermittent claudication, ‘‘coldness and numbness” of one
or both feet may be the striking features in the clinical picture. When pro-
voked by walking there ensues the syndrome dignified into a morbid entity
by Erb. Ifthe sensory and vasomotor symptoms—that is, the cramps, pains,
the pallor and coldness of the parts be alone taken into consideration, “‘inter-
mittent claudication” will be diagnosticated, whilst, in truth, we will have at
hand manifestations of a pathological and clinical unity—thrombo-angiitis
obliterans.?
(2) Prolonged Vasomotor and Hydrostatic Coldness (with Ischemia).—When
coldness with or without ischemia in the horizontal position is protracted,
we are dealing with a stage in which vasomotor influences exert a pro-
longed effect on the superficial capillaries and arterioles—an influence
quite out of proportion in intensity to the degree of organic circulatory inter-
ference. Thus, when a patient complains that the toes and foot have been cold
(and possibly white) for some time, although not through twenty-four hours of
the day, and the sensation is regularly evoked by the horizontal posture as
also by exposure to cold, we must differentiate between coldness and pallor
due to hydrostatic influences alone—lack of adequate distribution of blood—
and that partially motivated by vasomotor activities. Because clinical and
pathological observations have shown that coldness and pallor in the hori-
zontal do not go hand in hand, in a given case, with the extent of intra-
vascular obstruction, but that both manifestations may disappear as more
and more arterial territory becomes obturated, the réle and significance of
complicating and associated neurotic agencies becomes clear and comprehensible.
1 Because of the intimate association of coldness and ischemia, the description of these
two manifestations must needs overlap, so that the two chapters are best studied together.
2 For an excellent illustration of the symptoms here mentioned refer to Chap. XLIX,
Intermittent Claudication; also see Chap. XX VI.
262 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
We assume that by virtue of an excessive lability of the vasomotor mech-
anism in some cases, the partial circulatory depletion (partial ischemia)
occasioned by elevation of the limb to the horizontal is sufficient to elicit
disproportionate vasoconstricting response, extending to and implicating
particularly the superficial capillaries and arterioles. We have contended
and attempted to explain elsewhere! that a neurotic reaction is induced by
raising the leg ninety degrees above the horizontal.
So, by a combination of two wholly diverse mechanisms, subjective and
objective phenomena described as “coldness and whiteness or pallor” are
brought into being.
When coldness and pallor occupy but a relatively short period of the
clinical history and vanish either completely or in part with progressive
aggravation of the pathologic lesions, we are justified in assuming other than
merely obstructive agencies as responsible.
It is well, therefore, to attempt to differentiate in making a physical
examination between the réle of mere elevation of the extremity, or insuffi-
cient blood supply from the vasomotor influences. Such power of appraise-
ment can be gained by experience.
Another set of hypotheses may be applicable here, too, as previously
offered in explanation of other vasomotor phenomena; namely, the local
influence of metabolites,? (or possibly specific vessel toxins), and the inherent
independent functional activity of the capillaries and venules themselves.* If
such additional factors be accepted, it is clear that the regulation of the periph-
eral circulation in the extremities (as also in organs) is necessarily
exceedingly complicated and not always divisible into its several causal
influences.
B. Coldness Directly Attributable to Vascular Occlusion.—This, too, may
be subjectively or objectively demonstrable. The variations in normal suscep-
tibility to the feeling of ‘‘cold”’ of the extremities, in individuals whose cardiac
and vascular systems are apparently normal, is a matter of common—
knowledge. So here, too, the neurogenic and emotional factors cannot be
excluded and their presence may obscure an otherwise clear reciprocity
between arterial disease and thermic conditions. A certain restraint, there-
fore, must be exercised in the interpretation of “‘coldness”’ both of subjective
and objective varieties. Some patients with but limited invasion of arterial
territories describe ‘‘coldness’’ as an annoying and persisting complaint;
whilst others rarely notice it—except under special climatic conditions
—even though the arteries are extensively compromised. Where a limited
part of the foot, such as one or more toes, are continuously cold, often pain-
fully so, over a protracted period, and objective signs correspond, the pheno-
menon is of grave import and often initiates a trophic disorder or gangrenous
lesion.
Although a certain degree of coldness is common to most of the cases, there
is a kind of frigidity that accompanies the severe types of gangrene. In some
of these cases where sudden and extensive gangrene may take place, not only
the foot, but also a quarter, a third, or a half of the leg will be intensely
cold, so that we almost fear that an occlusive thrombosis has occurred.
Objectively we should examine all cases of suspected organic obstructive
vascular disease of the extremities by a comparative method of palpation,
both as to differences in the warmth of the corresponding extremity, and in
1 Chaps. XLV and LIV.
2 Chap. VII.
3 See Chaps. CVII and CVIII; also group 5, p. 578.
THROM BO-ANGIITIS OBLITERANS—ARTERIAL PULSATION 263
the temperature at different levels. It is a good procedure to pass the palm
of the examining hand slowly from the knee (first in front, then behind)
towards the foot, noting the degree of warmth or cold, and the upper limit
of the zone of frigidity, if such be present. Then each toe should be
separately tested and compared with the others of the same foot as well as
with those of the other foot.
Perhaps one of the most valuable objective methods of roughly appraising
the quantitative influx of blood into the lower extremities, is a search for this
level of distinct lowering of temperature. To this end, we first eliminate those
factors that may lead to fallacious interpretation, to wit: the effects of imme-
diately prior exposure to cold and vasomotor instability. Then, by passing
the warm palm of the observer’s hand in close contact with the extremity from
above downward, and by a comparison with the other side, changes as well as
definite coldness at certain levels will be appreciated. Similar methods are
applicable to the upper extremity.
As a test for the response of the circulation to special circumstances, such
as exercise, thermic influences, etc., the search for the degree and level of
coldness is also of some value. Single observations, however, must be dis-
carded as insufficient and unreliable; repeated ones may throw some light on
the prognosis.
CHAPTER? LIL
THROMBO-ANGIITIS OBLITERANS—ARTERIAL PULSATION
A. Absent Pulses.—As an indication of organic arterial disease, a lack of
beat in the dorsalis pedis, posterior tibial, popliteal, and femoral arteries is a
most reliable sign. In thrombo-angiitis obliterans, a malady that usually
comes to our notice after advanced inroads on the integrity of the arterial
and even venous distribution of the extremities have occurred, an absence of
at least the dorsalis pedis and posterior tibial pulses is to be expected. The
occlusion begins for the most part in the peripheral arteries, in the plantars,
dorsalis pedis and their larger branches, and it is not long ere the expansile
activities of these vessels cease. However, the variations in the intensity
and site of the pathological alterations are sufficiently great to make us cogni-
zant of the incidence of a stage or clinical period in which no tangible evidence
of arterial obliteration is at hand.
Arterial Pulsation in Certain Early Cases.—Although we must concede
the diagnostic value of lack of pulsation in thrombo-angiitis obliterans,
normal arterial beats are demonstrable even in the peripheral vessels (that is,
dorsalis pedis and posterior tibial) in some of the “‘early”’ cases. It is not
only theoretically possible, but has been proven beyond peradventure by
clinical and pathological observations, that a number of the other char-
acteristic objective phenomena of thrombo-angiitis obliterans may ante-
date by weeks or months the disappearance of either the dorsalis pedis or
posterior tibial pulses. Thus the following sequence of events in a certain
case will illustrate.
(1) At the first examination the vessels are found pulsating; ischemia and
erythromelia absent.
264 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
(2) A period of pain in the calf of the leg with tenderness and some cyanosis
in the pendent position, the vessels still pulsating.
(3) The development of marked ischemia on elevation, pain persisting, and
still no change in the pulses.
(4) Finally, the disappearance of the pulses.
Again, in other early cases, with the accessible arteries beating, the
absence of corresponding pulsations in the other leg, with other symptoms,
should arouse our diagnostic suspicions. Or, the existence of a solitary sign,
such as ischemia on elevation with or without a history of intermittent claudi-
cation or migrating phlebitis, is incontrovertible evidence of the advent of
further trouble and of the coincident involvement of arteries beyond the pale
of examination by palpation. If we follow carefully the clinical course of such
early cases, we will note a progressive disappearance of the pulses, usually in
the following sequence—the dorsalis pedis, then the posterior tibial, and then
the popliteal. In what period of time this may occur is illustrated by the
following case.
H. R., age 32, Russian Hebrew, first examined by the author on August 17, 1908, had
had pain in the toes of the left foot 5 years previously; then cramps in the legs up to the
knees on walking, over most of the subsequent period. A few weeks before examination he
was treated for “‘phlebitis” of the right leg, that had existed for almost 5 months.
August 17, 1908, right leg: AJl the vessels pulsate but vasomotor phenomena are present
as also ischemia on elevation. ‘The left leg shows absence of pulses in the dorsalis pedis and
posterior tibial, marked erythromelia, ischemia on elevation—a typical example of thrombo-
anglitis obliterans.
December 1, 1908, persisting vasomotor phenomena in the right leg—vessels still pulsate.
February and March, 1908, the dorsalis pedis and posterior tibial arteries of the right foot
no longer pulsate. Left foot—beginning trophic disorder of the big toe; gangrene to be
expected.
March 1, 1909, amputation of the left leg.
June, 1909, marked disturbances in the right foot on allowing weight to rest on it, and
burning pain in the foot when he walks a short distance with the aid of crutches (thus the
typical thrombo-angiitis obliterans symptoms are now well developed in the right leg
appearing pari passu with the extension of the obliterative process as estimated by investi-
gation of the pulses).
In this instance the disappearance of the dorsalis pedis and posterior tibial
pulses within a period of 7 months was coincidental with the transformation of
a case of exquisite vasomotor symptoms, into one with the usual attributes of
true thrombo-angiitis obliterans. Other signs, however, synchronous with
the neurotic manifestations, made the diagnosis of organic arterial occlusion
acceptable, even at the first examination.
Pulsation Absent in All Arteries of a Limb.—While it is tempting to
prognosticate a severe clinical course when arterial] occlusion over vast
extent is objectively demonstrable, experience teaches that symptoms may
be absent or slight, with obturation of all the accessible vessels of the lower extremi-
ties‘ including the external iliac artery.2, So we note a group which may
be described under the above caption. Here belong:
(a) Cases without symptoms.
(b) Cases with minimal or insignificant symptoms.
(c) Cases with one or both limbs compromised early and lost.
(a) Cases without symptoms, demonstrate the insidious onset and develop-
1For brevity the words “of the extremity” being implied and self-understood, are
frequently omitted in the text.
2It may be recalled here that absent or imperceptible pulsations are not, accurately
speaking, identical with obturated vessels (Chap. XXIV).
THROM BO-ANGIITIS OBLITERANS—ARTERIAL PULSATION 265
ment of the disease and the apparent unimportance of multiple pulseless
vessels. Such cases, however, are rare and are candidates, as it were, for
immediate conversion of a dormant into an intensely active and severe
clinical course upon the least insult. An instance of this type has been
recounted in Chap. XLII, p. 220.
(b) Cases with Insignificant Symptoms——The absence of many pulses
does not imply that we are more apt to find trophic derangements. Indeed,
where there is a paucity of manifestations extensive arterial obliteration is one
of the striking features in thrombo-angiitis obliterans, as well as in arterio-
sclerosis. Many of the ‘“‘latent cases” and those examples where only one of
two affected lower extremities is complained of, evidence lack of pulsation in
both arteries of the foot, in the popliteal or even the femoral. Where clinical
proofs of disease are apparent, these may be minimal, often represented
merely by intermittent claudication, frigidity of the foot in cold weather,
possibly with attendant attacks of migrating phlebitis; but trophic derange-
ments and gangrene may be absent. The following excerpt from an illustra-
tive case merits brief citation.
Obliterated dorsalis pedis, posterior tibial, popliteal and femoral arteries
without trophic disorders.
A. G., 42 years of age, Austrian Hebrew, on February 12, 1909 gives a history of having
had trouble in the right foot and leg for about 22 years, difficulty on walking and pain.
Until 1 year ago, however, this was not sufficient to give him any concern; but for the last
11 months the pain has been so marked over the inner side of the ankle after walking, that
he is trying to obtain relief by means of arch supporters. In addition he has noticed nod-
ules in the skin. Six weeks ago such a red nodule appeared under the skin at about the
middle of the right leg. He can go no farther than 1 or 2 blocks at a time.
Physical examination: The right leg is distinctly paler than the left, but there is no
chronic erythromelia. All the vessels of the left leg pulsate. On the right side, however,
the dorsalis pedis, posterior tibial, popliteal and femoral arteries do not pulsate; the external
iliac beat is only faint. On elevation the right leg blanches distinctly.
During December, 1909, and January, 1910, while under observation, he had recurrent
Bee of migrating phlebitis involving the region of the right calf and the inner side of the
ankle.
A typical case, then, of thrombo-angiitis obliterans combined with migrating phlebitis,
and without any trophic disturbances in spite of the very extensive vascular occlusion, all of
the usual pulses being imperceptible, except a very faint beat in the external iliac artery.
On close observation of many cases with perceptible beats in certain or
all of the usual situations, the advent of extinction of the pulse can be
demonstrated.
H. R. showed an absence of the posterior tibial and dorsalis pedis pulses of the left leg
(the limb more markedly affected), whereas the same vessels of the right leg were beating
strongly (August, 1908). In December, 1908, the dorsalis pedis beat of the right foot could
no longer be elicited. Later in the month the posterior tibial pulse was also absent. In
June, 19009, the popliteal, too, became imperceptible. Therefore, within 1 year (about
10 months) all three pulses, posterior tibial, popliteal and dorsalis pedis disappeared in the
right limb.
Intermittent claudication and possibly a “sore” over one toe which may
heal, may be the only manifestations. Thus, the following is an example.
B. B.,! aged 34 years, Russian Hebrew, when examined June 17, 1909, gave a typical
history of migrating phlebitis with trouble in the right leg for 8 years, and in the left leg for
3. years. For 2 years, intermittent claudication in the left leg had been present, and in
January of this year a small sore appeared at the tip of the left big toe. His chief complaint
was ‘“‘trouble” with the other leg, and except for some coldness and numbness of the left
foot, this extremity gives him little concern.
1See Chap. LVIII, p. 286.
266 CIRCULATORY AFFECTIONS. OF THE EXTREMITIES
Objectively the signs of thrombo-angiitis obliterans of both lower extremities are strik-
ing, and the femoral, popliteal, posterior tibial and dorsalis pedis of the left leg fail to
pulsate.
(c) Cases with One or Both Limbs Compromised Early and Lost.—It may
be called to mind here—for it will be elsewhere described im extenso and
illustrated by clinical example—that there is an acute fulminating thrombo-
arteritis and phlebitis involving the deep vessels, as well as of the superficial.!
The invasion of a large vascular territory may take place within a brief time,
contrary to the general rule.
B. Pulses Present.—Valuable as the positive finding of imperceptible
pulse may be, the existence of pulsations throughout all of the usually
palpable arteries of the lower extremities may not preclude the presence
of thrombo-angiitis obliterans or other obliterative or occlusive vascular
affection. Occlusion of certain vascular territories may escape our diagnostic
means of interpretation; and we must have recourse to other concomitant,
complicating signs and complexes for diagnostic conclusions, when the affec-
tion is restricted to the confines of these. Such regions are the peroneal,
digital, and plantar arteries.
Of the many bizarre pictures that thrombo-angiitis obliterans affords,
the following apropos of the above observation, may be cited.
Thrombo-angiitis Obliterans with Pulsating Arteries.
M. R., Russian, male, aged 40, when seen November 24, 1908, stated that 6 years ago he
had ‘‘rheumatism” of both feet, with pain becoming progressively worse in the toes and
most marked in cold weather. The pain was finally alleviated by heat and disappeared
until 2 years ago, when it recurred most intensely in the middle toe of the left foot. After
the application of a carbolic solution, spontaneous gangrene of this member occurred,
necessitating amputation.
Although gangrene of the fourth toe of the right foot presented itself 1 year ago, this
disappeared leaving trophic disturbances of the nail. One month ago there were trophic
disturbances of the middle toe of the right foot and small toe of the left. He further stated
that both feet had been red since 2 years.
Physical examination: Slight cyanosis of the left small toe, amputation of the third,
otherwise the left foot appears normal. There is marked cyanosis of all the toes of the
right foot, most intense in the third.
Upon elevation, slight ischemia of both feet can be elicited.
In the dependent position there is intense cyanosis of both legs, admixed with patches
of red; exquisite pain in this position.
Vessels: Both dorsalis pedes, posterior tibials, and femorals pulsate strongly, the popli-
teals are weak.
November, 1908, amputation of the right middle toe for gangrene. December 29, 1908,
returned to hospital because of gangrene of the left little toe.
Physical examination: Bleb over little toe of left foot, filled with pus, erythromelia of
rest of toe; remaining toes normal; no cyanosis in dependent position.
January 4, 1909, disarticulation of left little toe for gangrene.
January 15, outer half of dorsum of left foot slightly reddened.
January 20, still erythromelia of the left foot, no cyanosis in the dependent position,
ischemia on elevation.
Evidently since November, 1908, ischemia on elevation has developed, a significant
evidence of organic vascular lesion.
March 21, 1909, on allowing feet to hang, they soon become cyanotic, the blue discolora-
tion being admixed with patches of erythema; soles of both feet pinkish in color; all vessels
pulsate.
C. Pulsations Disappearing under Observation.—Were it possible to
keep cases confined to bed for many months under daily observation, the
manner of invasion of new vascular territories particularly in more or less
approachable sites could be well studied, and valuable information acquired.
This is particularly true as applied to that portion of the posterior tibial
1 See p..3 72), Case 1 Lev also p.v207,,Case din the
THROMBO-ANGIITIS OBLITERANS—ARTERIAL PULSATION 267
artery that pulsates behind the internal tibial malleolus. We shall refer
elsewhere to what the histories have conveyed in this matter.
Certain interesting data relative to time and advance of the disease, and
to the significance of added vascular involvement in the symptomatology,
could be derived from a less continuous but frequent study of cases over long
periods of time (several years).
The Severity of the Symptoms Corresponding to Arterial Occlusion.—
While this caption emphasizes a truism which is applicable in many cases,
it needs qualification in two different senses. For, we have learned firstly,
that extensive arterial occlusion may be adequately compensated for by
collaterals and have no subjective concomitants (Chap. XLII) and
secondly, that the presence of pulsation in certain vessels may be associated
with widespread obturation in many distal and concealed channels. Thus,
a patent posterior tibial is not significant if the plantar, dorsalis pedis,
dorsalis hallucis and possibly also the peroneal arteries are closed.
Importance of the Popliteal Pulse-—The disappearance of the popliteal
may correspond to aggravation of symptoms. So, in a case (D. B.) the
course may be summarized as follows: 3
D. B. in 1896, had migrating phlebitis over the left thigh; 1899, phlebitis over right calf.
In 1904, migrating phlebitis in left antecubital region involving the median cephalic vein
and one of the anterior ulnar veins. A specimen removed for microscopic examination
showed acute inflammatory lesions that were not correctly interpreted at that time, but
after subsequent studies by the author, the lesions were recognized as being those of the
acute phase of thrombo-angiitis obliterans. At the same time the patient had prodromal
pains in the ankle of the left foot with some cyanosis in the pendent position.
In January, 1907, the posterior tibial, and dorsalis pedis arteries of both feet did not
beat, both popliteals did.
February, 1907, symptoms, especially referable to the upper extremities were noted,
some pain on walking and rubor of the left foot.
In December, 1907, the usual symptoms of thrombo-angiitis obliterans in both legs.
January 3, 1908, both posterior tibials pulseless, both popliteals beat strongly.
February 7, 1908, right popliteal pulse strong; left diminished.
September 7, 1908, right popliteal pulse has disappeared, with this, distinct aggravation
im condition of right leg and more pain.
November 19, 1908, pulsations the same, left popliteal still present. Up to early in
1908 the left feg was distinctly worse, the right popliteal pulse better than the left. Since
then there was marked intensification of symptoms on the right side with absence of the
popliteal pulse. In both feet there are rubor and cyanosis with ischemia on elevation.
April to June, t909—ulcers of both feet; condition of both aggravated and all of the
pulses except the femorals and iliacs, are now absent.
Almost simultaneous loss of the popliteal pulse with increase in the
severity of the symptoms, followed by gangrence and amputation is
Illustrated by the following case.
S. S., February 5, 1910, migrating phlebitis 1908, 1 year ago intermittent claudication.
February 6, 1910, evident involvement of both lower extremities, dorsalis pedis and
posterior tibial arteries pulseless, all others patent.
March 20, 1910, aggravation of condition in both legs.
January 3, 10911, right foot looks somewhat withered, simulating sclerodactyly, a dead
patch of skin over the big toe, right popliteal pulse now absent.
January 28, 1911, Gritti-Stokes amputation (right).
Disappearance of Pulses Compatible with Arrested Symptoms.—To conclude
that progressive arterial occlusion should correspond with an exaggeration in
the extent and degree of the complaints, would be a universally warrantable
assumption, were it not for the occurrence of the following two types of
clinical complexes, first the dormant obliterative process without subjective
signs, and second, the inverse type in which “apparent healing”’ with cessa-
268 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
tion of subjective phenomena or even regression of objective manifestations
may take place.
The cases exemplifying the loss of pulsation unattended with subjective
and objective alterations perceptible to the patient have been described on
p. 220,6. They seemingly invalidate and nullify the deductions derivable
from the presence of pulseless vessels. Our ability to elicit other coincident
signs of which the patient is unaware fortifies the diagnostic value of the silent
vessels. Such indications elsewhere alluded to, are notably ischemia on
elevation, chronic or induced rubor and possibly the demonstration of a
diminished angle of circulatory sufficiency.
To illustrate the two opposed dicta, we may cite in brief the salient facts of
the following history, showing:
1st, that pulses disappear pari passu with progressive sensory and circu-
latory manifestations; and
and, that they are absent while symptoms regress and the latent or
arrested stage is being developed.
M. C., aged 24 years, with the usual prodromal symptoms, when examined March 18,
1908, gave these physical signs; left leg in a state of erythromelia, dorsalis pedis absent,
all other pulses present; right leg shows doubtful ischemia, all vessels beating.
November, 1909, the left leg ‘‘cured” as far as the subjective manifestations are con-
cerned, but erythromelia persists; dorsalis pedis pulse absent, posterior tibial very faint.
The right leg now gives him trouble, intermittent claudication and a trophic ulcer over
the big toe are present. ‘The dorsalis pedis and the posterior tibial arteries do not beat.
February 12, 1910, under conservative treatment the gangrenous area on the right big
toe has practically healed, and the dorsalis pedis and posterior tibial arteries of both legs
are pulseless. No symptoms on the left, objectively erythromelia is present.
Epicrisis—Closure of two vessels of the right, one of the left leg, while under observa-
tion, with aggravation of symptoms in the former, improvement in the latter.
Such antagonistic clinical states when viewed in relation to advancing
vascular obturation, can only signify and emphasize that the state of the
collateral paths plays just as important a réle in symptomatology as the quanti-
tative circulatory impediment.
Sequence of Loss of Pulsation.—A careful search for the inception of the
occlusive process in the pulsating arteries discloses the following as the usual
chronological sequence in loss of beat: first, in the dorsalis pedis, then in the
posterior tibial and popliteal, and finally, in the femoral and external iliac
artery (the latter being but rarely affected). No inflexible rule, however, is
applicable, since the closure of the posterior tibial artery behind the malleolus
may antedate loss of pulsation in the dorsalis pedis, an indication, too, of
prior and more extensive disease in the plantar distribution.
The advance of the lesion may occur so rapidly that within 1 year or less,
all the pulses of one extremity may be missing, although symptoms may be
moderate and gangrene absent.
J. A., February 26, 1907, case with intense blanching of the right foot on exposure to cold
and on walking, began 1 year before with sudden attack of inability to walk, there being no
definite localization of the pain, which was referred to the whole leg (an acute attack of
thrombo-angiitis obliterans’), All of the usual vessels of the right leg are pulseless; the
big toe is pale, the others slightly cyanotic.
If a patient be kept long enough under observation, the dorsalis pedis or
posterior tibial pulses, or both, may be observed to become extinguished.
Occasionally, other symptoms such as intermittent claudication may pre-
cede the loss of certain pulses. For, intermittent claudication may depend
on the closure of deep arteries beyond the realm of diagnostic palpation.
THROMBO-ANGIITIS OBLITERANS—ARTERIAL PULSATION 269
Intermittent claudication may appear before the advent of erythromelia. The
following case will illustrate:—
F. K., Russian Hebrew, 24 years of age, November 5, 1907, had evidently been troubled
mostly with the big toe of the left foot; and amputation became necessary. ‘There was,
however, a distinct history of pain in the right calf. On physical examination the right
dorsalis pedis pulse was distinctly palpable, although the left was not palpable. May 27,
1908, the beat in the dorsalis pedis of the right leg disappeared. The intermittent claudica-
tion antedated the disappearance of the pulses by a considerable period.
Relation of Pulsation and Clinical Duration—So capricious are the
exacerbations of this disease, that no conclusions as to the age of the process
should be drawn from mere clinical observations alone. The extremity
affected for many years may show fewer pulseless vessels, and be in better con-
dition than the other in which symptoms have been noted but recently.
B. B., after symptoms in the right leg for 8 years, with the left implicated for 3 years,
demonstrated clinically a more extensive disease of the latter when none of the pulses could
be elicited, while a good femoral beat was present in the other extremity. The other object-
ive and physical phenomena, too, gave testimony to the more grave vascular impairment
of the left in a smaller angle of circulatory sufficiency and more marked ischemia.
Pulsation and the Angle of Cirulatory Sufficiency—The number of pul-
sating vessels is not always in harmony with adequacy of circulation, nor
is it in consonance with the angle of circulatory sufficiency. Thus, this
may be less than go°—and evidence of marked impairment—and still the
popliteal and other arteries may be pulsating. In other patients, however,
where we find both legs involved, the palpable extent of vascular obliteration
corresponds fairly well with the intensity of the other signs. So, erythro-
melia and ischemia may be most marked on the side where all three vessels of
the leg and foot are found pulseless. In one case (B. H.) 3 vessels were pulse-
less on the left side and 2 on the right, with a corresponding development of
the symptoms.
D. Pulses of the Upper Extremities——A more detailed record of the
involvement of the radial and ulnar arteries will be found in the chapter on
_the Upper Extremities in Thrombo-angiitis Obliterans. Here we will simply
allude to certain peculiarities in the relationship between evidences of arterial
obturation and symptomatology.
The radial pulse may vanish during the period of clinical observation
without any other clinical signs referable to such closure.*
The radial pulse may become extinct simultaneously with the manifes-
tation of an acute thrombo-arteritis and periarteritis; but there may be no
other symptoms save those referable to the local alteration in the recently
oecluded and inflamed vessel.
Vasomotor symptoms may antedate the disappearance of the radial pulse,
in which case differentiation from the vasomotor neuroses may be difficult or
almost impossible. The unilateral appearance (asymmetrical) of the affec-
tion speaks in favor of thrombo-angiitis obliterans.
A further discussion of this phase of the subject wil! be found in Chap.
LIX.
E. Return of Pulsation.—Observers report return of pulsation in arteries
that had been seemingly obstructed; and, in personal communications from
clinicians, this fact has been made note of. That pulsation cannot return in
an artery, that is completely closed through the lesions of thrombo-angiitis
obliterans, we are convinced from the pathological changes. However,
iGase Ja Ay Pp: 205:
270 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
dissection of numerous amputated limbs has given a clue as to the possible
cause of the reported reestablishment of the dorsalis pedis and anterior
tibial pulses, and it is these vessels in which the observation has been most
frequently made. A glance at Figs. 47 and 56c will demonstrate how
Fic. 47.—Representation of the patency of certain vascular territories in thrombo-
angiitis obliterans, and its possible effect on the perceptibility of the pulses.
sections of the anterior tibial or dorsalis pedis artery in their palpable por-
tions may remain patent, whilst the central more proximal parts may be
partly or completely occluded. In such cases the artery is more or less
collapsed, or allows a small amount of blood to trickle through, or the
circulatory force therein is insufficient to produce a beat. With increasing
and improving circulation through collateral paths, pulsation may become
reestablished, the blood flowing through devious channels in uninvolved
territory.
CHAPTER LIII
THROMBO-ANGIITIS OBLITERANS—MENTAL SYMPTOMS
The gloomy outlook in this malady has become so well known to a certain
class of the population in many of our! big cities, that the dread of the conse-
quences surpasses even the fear of the necessary attendant endurances.
Thus, amongst the more highly educated (including physicians), temporary
neuroses are not uncommon, often aroused by fancied or simulating manifes-
tations in the extremities. When one or the other of the subjective symp-
toms of thrombo-angiitis obliterans persists, and when no adequate causal
explanation is forthcoming, even in the absence of closed vessels or the char-
acteristic objective signs, we should regard the case as a suspect, although
allaying the patient’s apprehensions as much as we can.
The patients who have run the gamut of many distressing lesions, severe
intermittent claudication, exceedingly painful toes with or without ischemia
1 United States.
THROM BO-ANGIITIS OBLITERANS—VASOMOTOR SYMPTOMS 271
or cyanosis, severe and even excruciating local pain, associated with fissures,
ulcers and gangrene, with inability to walk, possibly with the experience of
single or multiple amputations of parts of one or more limbs—in these it is
not surprising that with increasing calamitous happenings and constant
attention to their ills, the afflicted should retire into their subjective world,
where the intolerability of their own physical status is paramount.
A haggard look, the staring eyes, the trunk bent with arms clasping and
embracing the knee and leg of the affected part, is a striking and well known
picture. Or, the- foot is held tenaciously, the sole or dorsum rubbed and
stroked in fruitless unavailing attempts to mitigate the intensity of the pain.
So distressing can the symptoms be, that it is little wonder that intense
mental depression is common. The pain, the disability, the threat of
gangrene aroused by a knowledge of the fate of fellows in distress, so pervades
every thought and action of certain cases as to cause complete demoraliza-
tion, and in a few instances has led to attempts at suicide. One of the
author’s cases successfully accomplished this with illuminating gas; another
cut his throat with a razor whilst in the hospital, the enormous gash miracu-
lously avoiding the jugulars.
The author had just made rounds, was called back and was able to save
the patient by immediate suture of the parts, including the transversely
cut larynx, and by the introduction of a tracheotomy tube.
CHAP] ERSLLV
THROMBO-ANGIITIS OBLITERANS—VASOMOTOR SYMPTOMS
What with the perplexing nature of the fleeting pains of the prodromal
acute stage, what with the long doubtful period of intermittent claudication
that is so often underestimated or regarded as ‘“‘rheumatic’’ or orthostatic,
and, what with the confusing objective phenomena due to nervous agencies,
it is little wonder that thrombo-angiitis obliterans is so often mistaken for
other maladies. The attendant vasomotor disturbances, especially when such
objectively dominate the clinical picture, may add no negligible onus to the
clinician’s diagnostic task. Although in thrombo-angiitis obliterans the
paroxysmal nature of such symptoms is less marked or absent, the coexist-
ence of other neuroses less frequent, the response to emotional influences not
so striking, there still remain sufficient points of resemblance to account for
the difficulties of differentiation.
Vasomotor phenomena may occur independently, unaccompanied by the
usual hydrostatic and mechanical color changes, at a time when even the
vessels pulsate, may be superimposed, as it were, or be a coincidental manifes-
tation in a well developed clinical picture of this disease. Both upper and
lower extremities may be affected.
It is in the cases of involvement of both lower extremities but with vaso-
motor disturbances confined to one of them, that opportunity for compara-
tive study of the confusing phenomena is afforded. The limb in the more
advanced stage is usually indubitably stigmatized as the seat of arterial
occlusion by the ischemia on elevation, chronic erythromelia and pulseless
vessels. The other limb may be markedly blanched even in the pendent posi-
272 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
tion—an evidence of vasomotor influence. Such pallor may give way to
intense cyanosis admixed with areas of an ashen color in which vestiges of
blanching can be discerned. No rubor develops in this position of the limb.
The blanching and cyanosis are independent of posture. Persistent syncope
of short duration followed by cyanosis, uninfluenced by position is one of the
characteristic types of vasomotor derangement.
Walking and cold exert a distinct influence in the incitement of neurotic
vascular manifestations, and the phenomena thus brought forth, have, when
coupled with the “cramps and pains”’ in the legs, been described by Erb and
designated as “intermittent claudication.”’ We have alluded elsewhere to
the advantages of segregating the sensory! group—which we shall call
symptoms of “intermittent claudication”—from that of vasomotor insta-
bility, since the two are not necessarily interrelated, mutually dependent nor
coexistent.
Referring, here, only to the vasomotor symptoms, it must be recorded
that transitory or even prolonged syncope may result from either walking or
exposure to cold in a given case, or from either one of these instrumentalities
alone. A striking pallor may persist in the pendent position offering a
marked contrast to the usual hyperemia in this posture, or to the other leg
if that is also the seat of the malady. ‘The blanching may occupy the whole
or part of the foot, may spare some of the toes and may be associated with
patches of cyanosis, the affected area usually presenting a distinct reduction
in temperature.
Patients at times will notice very early in the disease that the foot changes
color. They will say that it has a tendency to become pale in cold weather
and remain so; in the dependent position, they complain of marked redness
and often blueness, and at times of coldness. This is a rather constant .
description in many of the histories. Very often these manifestations give
way to the development of intense local pain in one of the toes with the sub-
sequent appearance of trophic disturbances. Again in some cases, irrespective
of temperature conditions, syncope and coldness seem to be brought forth
on exertion or merely on locomotion, the story being “when I go out my
foot becomes pale; when I take my shoe off, I find it has turned white.”
To illustrate by a case:
M. N. examined November 24, 1914. ‘The right foot is very pale, even in the pendent
position, except for the little toe which is red. When he walks, he says the little toe also
becomes white. On pressing the toes, the tips become cyanotic. ‘The foot is very cold;
there are no ulcers and no edema.
After walking about for a while the right foot again shows signs of vasomotor distur-
bance, but instead of pallor there is a mottling of red and white, there being patches of white
at the base and over the dorsum of some of the toes, the greater portion of the dorsum
of the foot being red. At the same time the plantar surfaces of all the toes have a cadaveric
hue. The right dorsalis pedis and posterior tibial are pulseless; left dorsalis pedis absent,
but posterior tibial present.
While an abnormal color may repeatedly afford an unchanging picture
under similar circumstances, the vasomotor disturbances occasionally exhibit
a variegation with kaleidoscopic mottlings of tints of yellowish white, red,
purple and blue. Fugitive pallor may yield to a marmorated combination
of patches of red and white, these in turn being replaced by cyanotic and
pallid areas. Or finally, unless a more or less persistent cyanosis ensue, all
play of colors will cease and reactionary rubor will terminate the ephemeral
phenomena.
1 The sensory group has been described in Chap. XLIX on Intermittent Claudication.
THROM BO-ANGIITIS OBLITERANS—VASOMOTOR SYMPTOMS 273
Besides the demonstration of one or more pulseless vessels (if such are
present), and ischemia on elevation, an important and valuable method for
the recognition of the vasomotor symptoms is the possibility of eliciting the
phenomenon of reactionary erythromelia. When in doubt, given a case with
syncope either of spontaneous or induced advent, or with alternating pallor
and cyanosis, or pallor and patches of red, repeated elevation and depression
of the leg may dispel all these neurotic displays and produce a distinct and
continued rubor in the pendent or even in the horizontal position.
Vasomotor Mantfestations May Merely Occupy the Early Clinical Stages of
the Malady.—Thus, in reviewing the history of a characteristic case (H. R.)
we find that at a time when the left leg showed all the typical symptoms with
rubor, the right presented none of these except ischemia on elevation. On
the other hand, there were vasomotor symptoms in the latter, namely,
cyanosis, a blanched condition of the foot when the shoe was taken off (par-
ticularly in cold weather), cyanotic patches at the tips of the toes, and cold-
ness. This complex was observed on several occasions.
Notes taken December 1 1908 read: On taking off the left shoe, the foot is fairly red, the
right is slightly blanched, but all the vessels of the right leg pulsate. However, ischemia
could be elicited on elevation, an evidence of arterial occlusion.
If we compare the limb exhibiting vasomotor symptoms with the other
that is the seat of a more advanced process, we will note that the former is
not swollen, the toes not tumefied, rubor absent and the color yellowish white;
or, the toes may be markedly blanched, particularly if they have been exposed
to cold. In the dependent position, also, a difference is seen in the two
limbs. The one that combines the early stage of thrombo-angiitis obliterans
with vasomotor symptoms, shows cyanosis after the leg has been hanging
down, the distal phalanges or phalanx being of a deep dusky purple; the
color may be unmixed with any tinge of red, and the rest of the foot also may
show a cyanotic hue; a pale, ashen skin in many places modifies the picture.
However, rubor is absent. This condition may change in such a leg, so
that when the leg is examined 1o or 11 months later (in the case H. R. 11
months later), the appearance may have completely changed, the usual
typical signs, marked erythromelia together with or without cyanosis being
in evidence.
A study of the case H. R. threw no light on the reason for the marked vasomotor symp-
toms in the right leg. They persisted fora long time. They were present August 17, 1908,
and even November, 1909, at a time when there developed deep cyanosis of the big toe
due to impending gangrene, and the rest of the foot had a slightly bluish color. The dorsum
of the foot still exhibited occasional fugitive areas of unexplicable syncope.
Syncope or Ischemia after Exertion While the typical picture of inter-
mittent claudication is characterized by the predominance of sensory mani-
festations sometimes with attendant pallor of the foot and coldness, the
vasomotor symptoms may exist alone and be evoked by the same form and
degree of exertion as ordinarily excites sensory responses. One limb may
be striking because of coldness, the other because of pallor, pain being absent
in both. The following case will illustrate.
Thrombo-angiitis Obliterans with Migrating Phlebitis, Syncope and Coldness
of the Feet after Exertion.
I. B., Russian, 33 years of age, typical case of thrombo-angiitis obliterans with migrating
phlebitis states that the right foot becomes white and cold, sometimes pink after walking.
The left foot also becomes cold and tires easily; the pallor of the right foot is striking, the
left slightly cyanotic.
18
274 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Evidences of Altered Vasomotor Function.—Many as are the clinical
phenomena illustrative of the peculiar instability of the peripheral vaso-
motor apparatus, still further evidence thereof is obtainable through simple
clinical tests. Vagaries in vasomotor function,’ it is true, may modify and
impair the uniformity of the demonstrable phenomena; nevertheless, certain
essentially reliable reactions are wont to follow these motivating factors—(rz)
elevation of the limb; (2) thermic influences (cold); (3) mechanical irritation
(dermatographic reactions) ; and (4) exercise.
It has already been shown that all of these may evoke not only immediate,
but unduly prolonged vasoconstriction of the capillaries and arterioles.
The vasodilating mechanism may be activated on the other hand through
such forces as these: Establishment of preliminary ischemia by elevation of
the leg with consequent refilling of the peripheral vascular branches in the pen-
dent position (reactionary rubor); temporary compression of the femoral
artery (3 to 5 minutes); or application of a constricting bandage at the root of
the limb. Less effective means of evoking vasodilatation is the application
of external heat and diathermy.
If we examine and compare the healthy and affected lower extremities in
the horizontal position, we may demonstrate that where there are obstructed
arteries, normal red dermatographic reactions are usually substituted by
excessive and persistent pallor; that is, a reversal in the sense of vasocon-
striction takes place over an unusually large zone. The test is thus carried
out: The femoral artery is compressed for 3 minutes; this is followed by
tardy and imperfect fading out of the existing chronic rubor of the foot
(vide Chap. XII, p. 84, paradoxical rubor and ischemia). If then a
number of scratches be forcibly made over the foot during this period of
arrested circulation, and the femoral artery be then released, an abnormal
persistence of pallor in and around the irritated zone will be noted. An
ischemic area of considerable size will be in striking contrast to the general
reactionary and intensive rubor of the rest of the foot.
Quite different will be the reactions of the healthy extremity. Firstly,
the ischemia of the foot will be more intensive and of more rapid advent after
the artery is compressed. ‘This paradoxical ischemia on the healthy side has
been referred to in the Chapter on Collateral Circulation; it is an evidence of
the lack of development of substituting by-paths where the arteries are patent.
No such dermatographia alba is here evoked; but the scratches soon attain
the normal hyperemia.
Such are some of the demonstrable evidence of altered vasomotility in the
affected territories. To certain excitants an unusually hypersensitive vaso-
constricting mechanism is set into motion; to others, vasodilatation.
Amongst the former agents belong depletion and ischemia (consequent upon
elevation of the part), cold, mechanical irritation, and exercise. Whatever
tends to produce a plenum, however, such as the pendent position, sets the
dilating mechanism into activity. The reactionary rubor in the foot after
compressing the femoral artery is much more pronounced and of more
rapid advent on the side of the obstructed arteries—another sign of altered
vasomotility.
In explanation of vasomotor lability may be mentioned Kravkof? on the effect of throm-
bosis on the vasomotor functions. He states that: “In the coagulation of blood certain
protein-forming amines are formed, possessing vasoconstrictor powers, and therefore the
vasoconstrictor effect of the serum may be ascribed, not to adrenalin, but to these protein-
forming amines.”’
1 For vasoneurosis attending arteriosclerotic disease, see p. 578, paragraph s.
2 Oppel, Gangreena Arteriitica Suprarenalis, Lancet, July 15, 1922, p. 116.
THROM BO-ANGIITIS OBLITERANS—OSSEOUS CHANGES 275
CHAPTER LV
THROMBO-ANGIITIS OBLITERANS—OSSEOUS CHANGES
Rather characteristic of thrombo-angiitis obliterans is the absence of bone
absorption of the terminal phalanges. A differential diagnostic point is
thus at hand that may serve to distinguish it from Raynaud’s disease and
sclerodactyly. However, in one case, very marked diffuse bone absorption
Fic. 48.—General rarefication of the osseous tissue with absence of absorption of the distal
ends or terminal phalanges in thrombo-angiitis obliterans.
was noted, involving the lower end of the radius and ulna, all of the carpal bones,
the bases of the metacarpal, as well as the shafts of the phalanges. The
radiogram is depicted in Fig. 48.1 Rarefication of the osseous tissue due
to impaired circulation and obliteration of the radial and ulnar arteries was
1See section Involvement of the Upper Extremities in Thrombo-angiitis Obliterans
(Chap. LIX).
276 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
apparently responsible here. But the characteristic disappearance of terminal
portions of the phalanges was absent.!
Secondary destructive osseous alterations, defects, erosions and necroses,
may occur as the result of trophic disorders, gangrene and infection. But
these are lesions common to other forms of gangrene, and defective circu-
lation plus infection.
A diffuse atrophy of bones due to disuse is also no more pathognomic
than those just mentioned; it may be expected in those in whom one or more
extremities have been extensively involved or not employed on locomotion for
a long time.
A differentiation from the bony changes in the nerve or anesthetic type of
lepra will be clarified by a reference to Chap. XIV, p. 94.
CHAPTER LVI
THROMBO-ANGIITIS OBLITERANS—STATISTICAL DATA
Although in the light of more recent experiences certain modifications of
the following data may become necessary, they may be taken as indicating
average findings in a series of 100 cases collected for special investigation in the
year 1916. Over 500 cases have come under the notice of the author, but a
careful statistical review has not been made since 1916.
Of roo consecutive cases reviewed, there were 100 Hebrews; of 400 other
cases observed, 1o Gentiles.
There were 76 of Russian birth, 17 of Austrian birth, 3 Americans (of
foreign extraction), 2 Roumanians, 1 German, and 1 Turk.
The sex incidence was 99 males, 1 female; among the other 400 cases, how-
ever, 2 additional females were studied.
The division of 100 cases in whom there were 171 lower extremities involved
was as follows: both lower extremities in 71 cases, the right only in 7 cases, and
the left only in 22 cases, the preponderance of the left over the right being
noteworthy. In other words, the majority of cases of thrombo-angiitis
obliterans, if followed for a sufficiently long period of time, will show the
lesion in both lower extremities.
Of the upper extremities, which are less frequently involved, 30 arms
were affected in 21 cases; both arms in g cases, the right only in 5, and the left
only in 7, again demonstrating a slight increase of the left over the right.
The cases with involvement of both upper and lower extremities (21)
revealed involvement of both upper and both lower extremities in 8 cases, 2
lower and 1 upper in 10 cases, 2 upper and 1 lower in 1 case, and 1 upper and 1
lower in 2 cases.
Although the age at the onset of the disease varied considerably, ranging
from 17 years to 56, the average age was 32 years,5 months. These figures,
however, are much too high, since it is very difficult to estimate the exact
age at which the disease began, because of the insidious nature of the onset,
and the fact that the onset is overlooked in many cases.
The advent of gangrene, which in some instances ushered in the disease,
occurred in others from 1 year and 8 months after the first symptom was
1 See Chap. XCIX, Raynaud’s Disease.
THROM BO-ANGIITIS OBLITERANS—ETIOLOGY 277
noted, to 12 years after the onset. Amputation was carried out in 52 cases
of the 100.
In some cases the gangrene set in within a short time or almost simulta-
neously with the apparent onset, the longest period being 12 years after the
beginning of the complaint.
Doubtless in many of the cases amputation became necessary at some
later date, when they were no longer under observation, so that an estimate
of 75 per cent or 80 per cent would not be too high.
A similar disease is described as occurring not infrequently amongst the Japanese.
Koyano collected 120 cases during the years 1900 to 1921, and gives the following deductions.
Most of the cases occur in young males between the ages of 20 and 40, usually in the labor-
ing classes. Inadequate and poor diet, and local exposure to wet and cold are given as
factors in etiology. Most of the cases were moderate smokers. ‘The lower extremities were
most frequently affected. The pulses were extinct in the following order, dorsalis pedis,
anterior and posterior tibial, popliteal, and lastly the femoral. About two-thirds of the cases
on admission to the hospital had already lost the right and left popliteal pulses. The blood
viscosity was somewhat high, 5.16 in the average case (Koyano); blood sugar normal,'as
well as cholesterol. The Wassermann test was usually negative. The Japanese laud con-
siderably the hypodermic injections of Ringer’s solution (Mayesima-Koga), attributing its
efficacy (?) to its power to diminish the viscosity of the blood. ‘The same author was able
to find the “acute” lesions in but one case, and therefore is surprised at the relative
frequency of the characteristic findings amongst the cases observed in the United States.
Evidently the migrating phlebitis was either overlooked or it is rarely associated in the
disease of the Japanese.
CHAPTER LVII
THROMBO-ANGIITIS OBLITERANS—ETIOLOGY
The cause of the pathological process in thrombo-angiitis obliterans has
not yet been definitely established. By his studies of the clinical aspect
and pathology of the disease, the author has established the following facts.
That the disease zs not an endarteritis obliterans; that it is an occlusive
thrombotic process involving the deep arteries and veins of the upper and
lower extremities, or the superficial veins; that the early stages of the dis-
ease manifest themselves in an inflammatory lesion which shows a specific
and characteristic morphological picture, while in the process of healing;
and that in the early or acute stage, certain purulent foci make their appear-
ance that would suggest a microbial agent or infectious causative factor.
No organism, however, has a yet been demonstrated, even in the superficial
veins, when these are in the stage of acute inflammation.
Syphilis has been regarded by some as a possible cause, but a study of
the histories and of the Wassermann tests in more than 30 cases? has shown
that lues is not responsible.
It is a striking circumstance that of a series of 500 cases, the author found
only 3 cases in women, and in these patients no amputation was performed,
so that the diagnosis was made on clinical signs alone. Furthermore, it is
interesting that but 4 cases out of 500 did not belong to the Semitic race.
1 Some of the more intelligent Russian immigrants have called the author’s attention to
this factor; but this is irreconcilable with the development of the malady in cases in affluent
circumstances since birth.
2 Buerger and Kaliski, Med. Rec., Oct. 15, gto.
278 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Tobacco is probably a predisposing factor, and may be regarded at least
as causing some alteration in the vessels that makes them liable to the attacks
of inflammation and thrombosis. Most of the cases are heavy smokers,
although smoking was denied in 1 per cent of the author’s cases.
Here, more especially than in any of the organs or tissues of the body,
must we seek not only for predisposing moments, but also for the agency
that directly motivates the inflammatory thrombotic lesion. The conducive
factor can certainly not be held wholly accountable. Unwarrantable are
inferential hypotheses that would attribute an essential rdéle to mere con-
tributory forces. It is immaterial whether these be ontogenetic (individual-
istic traits) or phylogenetic (Hebrew races), acquired (as thermic cold),
traumatic (after cutting nail, etc.), inebriant or chemical intoxicants (nico-
tine, ergot, toxins of typhus).
An understanding of the histological alterations in the vessels could limit
the promulgation of hypotheses or etiology that are of purely theoretical
nature.
Predisposition to Thrombosis.—Wf a bland thrombosis without inflamma-
tory process occurred here, we could perhaps have greater confidence in
those hypotheses that seek a special thrombophilic tendency in explanation
of the extensive obturating process. Although a certain chemical predisposi-
tion of the intima or a diminished metabolism in the vascular,wall (Zurhelle?)
cannot be excluded from the realm of possibility and may lend to the blood a
tendency to clot iz loco, it is more likely that the determining factor is that
sum of chemical and toxic moments that are set into activity pari passu with
the incidence of the inflammatory lesion.
From time to time most interesting explanations are given by various
authors and commentators of the cause of this malady, and often individual
predisposing factors are dignified by the appellation “exciting cause.’’ ‘Thus,
hyperglycemia, or an increased sugar content of the blood, and dyscra-
sias of endocrine origin have been suggested as causative factors (W. Meyer).
But we must not forget that enough clinical and pathological data are at
hand to furnish us with a reliable concept as to what is here actually influen-
tial in producing the changes in the vascular system. It is known that the
arteries and veins, par excellence, furnish examples of tissue complexes
requiring several factors for production of pathological alterations. And,
strange to say, one or another of these factors (that are merely predisposing
agents) are apt to be singled out and heralded as the true cause. When
the author’s pathological studies revealed that certain specific histological,
architectural alterations in the vessels were characteristic of the disease
thrombo-angiitis obliterans, it was not presumptious to conclude that
a special exciting agent, be it a toxin or organism, must play a rdéle here, in
addition to the many other conducive circumstances that may play larger or
smaller parts. For how else can we explain the occurrence of the unique or
specific alterations that are found nowhere else in thrombotic processes and
are a pathognomonic for thrombo-angiitis obliterans, just as the peculiar
pathological pictures of tuberculosis are attributable to the tubercle bacillus,
and the changes seen in the glands of Hodgkin’s disease are doubtless the
reactions to special agents.
Reverting to the peculiar reaction of arteries and ‘veins, one may empha-
size the fact that more than one factor must be invoked in the case of these
peculiar tissue changes. Thus, stasis, locomotion, dependency of the limbs,
1 Zurhelle, Zentralbl. f. Gynec., 1908, No. 43.
THROM BO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS 279
activity of circulation, vis a tergo, tobacco, age, sex, and thermal influences
—all these play greater or lesser roles in determining thrombotic and athero-
matous occlusion.
As for tobacco, its influence has been recognized for many years. Erb,
long ago, in papers written subsequent to his publications on intermittent
claudication, attributed extensive atherosclerotic conditions ot the lower
extremities, in the main, to the influence of ¢obacco. Just how far the absorp-
tion of tobacco poisons is responsible for the degenerative changes in the
arterial walls cannot be determined accurately, but that it may be safely
regarded as a predisposing cause, no one will venture to deny. So also in
thrombo-angiitis obliterans, it is possible that the use of tobacco may render
the vessels more susceptible to special agents, be they toxic or infectious, but
that tobacco is the only and exciting cause is exceedingly doubtful and highly
improbable.
Cases of migrating phlebitis in patients who are heavy smokers occur not
infrequently. In these, the territory of the saphenous vein becomes
gradually occluded, and the differential diagnosis between migrating phlebitis
of the “bland type” and migrating phlebitis associated with thrombo-angiitis
obliterans must be made. If we exsect a portion of the vein in thrombo-
phlebitis of the bland type, we find, it is true, slight changes in the media,
but an occlusive thrombus that presents none of the characteristic lesions.
In such cases we are dealing with a bland thrombosis in vessels that are
damaged by various influences, tobacco, or other causes. In thrombo-
angiitis, however, when migrating phlebitis occurs, certain specific architectural
changes can regularly be diagnosticated and found under the microscope. An
infectious agent is in all probability, responsible for the “‘acute”’ or earliest
lesions. The evidences in favor of this view are discussed at length else-
where.! It is of some interest to note that persistent leukocytosis has been
observed in the early stages of this malady (Thomas?). Ina case of extensive
vascular occlusion of doubtful origin’ (obliterating thrombo-arteritis, possibly
thrombo-angiitis obliterans) leukocytosis was present for a number of months.
That something else must call forth or evoke such remarkable architectural
complexes seems unquestionably true.
CHAP TERSDVITI
THROMBO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS
There is no phenomenon of more importance in elucidating the true nature
of the pathology of thrombo-angiitis obliterans than the characteristic
thrombo-phlebitis or “‘migrating phlebitis’? of this disease. The asso-
ciation of thrombosis of superficial veins of the upper and lower extremities
with other evidences of obliteration of the larger arteries occurs in a
sufficiently large number of cases to make the affection of the veins almost
pathognomonic.
‘Pathology of the Acute Stage, Chap. LXI.
2 Thomas, Am. Jour. Med. Sc., 165, Jan., 1923, p. 86.
+P ard, Case G..G.
280 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Those interested in a more intensive and comprehensive study of this
disease will find a critical review of the clinical history of such cases of great
value.
For the sake of clearness the cases of thrombo-angiitis obliterans attended
with thrombo-phlebitis or migrating phlebitis may be divided into seven
different groups. (1) Cases of thrombo-phlebitis without symptoms. (2)
Thrombo-phlebitis with symptoms of limited veininvolvement. (3) Migrat-
ing phlebitis causing the patient to seek treatment. (4) Cases in which both
the migrating phlebitis and thrombo-angiitis obliterans play equally important
roles in the symptom-complex. (5) Migrating phlebitis involving both the
upper and lower extremities. (6) Extensive migrating phlebitis of the
chronic fulminating variety associated with a similar process in the deep and
femoral veins; and (7) migrating phlebitis with a long prodromal phase,
evidences of deep arterial involvement being lacking over an extended period
of time.
I. THROMBO-PHLEBITIS WITHOUT SYMPTOMS
There are patients who have no knowledge of the occurrence of any
trouble in the veins of the leg, but in whose amputated limbs extensive old,
or old and recent thrombo-phlebitis of the internal saphenous or its tributaries
is discovered. Such a case was J. C., who could recall nothing referable to a
disturbance in the superficial veins. Study of the vessels revealed old occlu-
sion of a large part of the saphena by virtue of a thrombotic process, and some
areas of more recent thrombo-phlebitis. Sometimes an augmented streak
corresponding to the course of the internal saphenous with induration under
it, may be a definite evidence of a healed thrombotic lesion in the
corresponding vein.
Case rt. J. C.,45 years, Russian Hebrew, admitted May 18, 1908; has eight children
(all well); gives a rather typical history of vascular disease of both lower extremities,
resulting in amputation of the left leg at the knee. Four years ago he had “‘rheumatism”’
of the right leg with pain in the sole of the foot and redness of the toes lasting eight months.
Since then it has not troubled him. ‘The left leg, however, began to hurt him last summer;
he could not walk a block without taking a rest. His big toe became “sore” recently,
and now the pain in the foot is constant. He is told that the big toe is becoming gangre-
nous, and that his leg should be amputated, which he gladly permits.
With the observation just cited, no new clinical facts are adduced, but
certain similarities between the thrombotic lesions of the saphenous vein,
as seen under the microscope, and the changes characteristic of the closed
deep vessels were deemed sufficiently suggestive to warrant the suspicion
that here, in the superficial veins, a new territory for the process “ thrombo-
angiitis obliterans” had been found.
II. THROMBO-PHLEBITIS WITH SYMPTOMS OF LIMITED VEIN
INVOLVEMENT
A more interesting group is represented in those patients who come to us
with active thrombo-phlebitis and periphlebitic manifestations. Here and
there along the course of the internal or external saphenous vein, alterations
in the skin and subcutaneous tissues occur. These are in the form of small,
erythematous, slightly indurated patches, about a centimeter in diameter,
and tender to the touch. Were it not for the concomitant phenomena refer-
able to the tributaries of the saphenous or the trunk itself, the nature of these
cutaneous nodosities would have remained obscure. With the appearance
THROM BO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS 281
of these, however, or at other times in the course of the disease, cord-like
thickenings of portions of the long saphenous, with or without adhesion to
the skin, are frequently observed. As examples let us briefly tell the story
of Cases 2 and 3 in Group II.
Case 2. S.S., 30 years old, Russian Hebrew, admitted July 8, 1907; father of one child;
has been suffering for four years with ‘‘ weak legs;’’ for two years there has been pain in his
left foot. About one and one-half years ago the second toe became gangrenous and was
removed. Last winter his attention was directed to the blueness of the toes; it was difficult
to keep the left foot warm. For a couple of years he has noticed that “red spots’? come and go
along the inner and outer side of the shin bone. ‘They area little painful and disappear with-
out treatment. Now he seeks advice because the little toe looks as if it were going to die off.
Amputation just above the middle of the leg.
Diagnosis.—A typical case of thrombo-angiitis obliterans with gangrene of the little toe
of the left leg and cutaneous nodosities along the course of the internal saphenous vein from
the ankle up to the region of the tubercle of the tibia; probably closure of a part of the
saphenous vein.
The study of the vessels of the amputated leg showed extensive occlusion of the posterior
tibial, anterior tibial, peroneal, and plantar arteries (thrombo-angiitis obliterans). The
long saphenous vein was filled for the most part with old organized tissue of a type indis-
tinguishable from that seen in the deep vessels, and some of its tributaries were closed by
more recent obturating masses. ‘The cutaneous nodules correspond to the distribution of
the finer tributaries, but inasmuch as they had almost completely disappeared at the time of
operation, no histological examinations were made.
As representative of the occurrence of migrating thrombo-phlebitis of
the long saphenous and of erythematous nodosities in the same patient, let us
cite Case 3, who observed and related quite accurately how the painful
“hard cords” developed.
Case 3. F.S., 37 years old, Russian Hebrew, father of two healthy children, April 13,
1909; says that he remembers having had peculiar pains in the soles of both feet on walking
a few blocks for the last three or four years. About four months ago the big toe began to
trouble him, but even before that he noticed hard cords along the inner side of the leg. Since
then the nail of the big toe came off, leaving a raw wound which refuses to heal. The long,
hard strands come and go; sometimes they are seen high up on the leg; at others, three or
four inches above the ankle. Besides this there are lumps farther back on the inner side of the
leg. Patient does not return for treatment, so that the further course of the disease is
unknown.
On physical examination the usual signs of thrombo-angiitis were found, with a trophic
ulcer of the big toe. There were no evidences of recent thrombosis of the long saphenous
other than one hard node four inches above the ankle; evidently the last attack of thrombo-
phlebitis had subsided. ‘The other leg showed somewhat less advanced symptoms of the
disease.
Here, then, we are dealing with a case in which both the patient’s
narrative and ocular evidence point to the association of superficial and
deep thromboses.
III. MIGRATING PHLEBITIS CAUSING THE PATIENT TO SEEK TREATMENT
When the attacks of migrating phlebitis make their appearance early in
the history of the case, and when the attendant discomfort and pain are
sufficiently great, then the symptoms belonging to the true, deep-rooted
affection—thrombo-angiitis obliterans—are sometimes wholly ignored by the
patient and remain undiscovered by the physician. Medical advice is
sought only for the “lumps” and “hard, tender strands” or “‘cords”’ that
are oftentimes so disturbing. Such observations are of no mean importance
in diagnosis, since they have taught the author fo seek for the early subjective
and objective signs of thrombo-angiitis in every patient in whom there are spon-
taneous and unaccountable attacks of inflammation of superficial veins. Let us
282 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
see what we can learn, then, from Group III, in which migrating phlebitis
causes the patient to seek treatment.
Case 4. E. B., 36 years old, Austrian Hebrew, consulted me on January 17, 1909, with
the history of having had stinging sensations on the inner side of the right leg, low down,
some three months previously. A few days after the onset of this trouble he could feel a
long, thickened ‘‘lump” behind the shin bone, a short distance above the ankle. Soon after
this, another swelling, not unlike a “‘hard cord,” appeared somewhat higher up on the leg,
was very tender, and was succeeded not many days later by a third somewhat shorter
strand.
Upon close questioning he admitted that although he seeks relief from the symptoms
mentioned, he has been annoyed for almost a month before the beginning of the present
seen by frequent cramp-like pains in the calf of the right leg upon walking a few (five or
six) blocks.
Physical examination, January 17, 1909, revealed induration of the tissues about the
saphenous vein, from the ankle to the upper fourth of the leg. The distal portion presents
a cord-like thickening, with scarcely any inflammatory signs. Higher up, however, the
skin is adherent to the deeper hardened area, and is exceedingly tender to the touch.
The dorsalis pedis and posterior tibial arteries of both legs are pulseless; the femorals and
popliteals can easily be felt to beat. The big toe of the right foot has a cyanotic hue.
Course.—January 31, his phlebitis was found much improved; his right big toe often
hurts him, and his foot easily gets ‘“‘cold”’ and “tired.”
Two months later, March, 1909, no evidences of the old thrombo-phlebitis can be found.
The big toe of the right foot still shows a peculiar bluish discoloration, and the absence of
pulsation in the vessels is the same as before. There are no trophic disorders; the most
striking phenenomon is the vasomotor disturbance in the big toe.
In short, we have here an exquisite example of a combination of early
manifestations of thrombo-angiitis obliterans (pain on walking, evidences of
disturbed ciculation), with attacks of thrombo-phlebitis in the territory of
one of the saphenous veins.
Whereas pathologic proof of the correctness of the diagnosis—thrombo-
angiitis obliterans—is lacking in the last case, the history of another patient
will be given in whom there were similar symptoms, and in whose amputated
limb and exsected veins ample material for anatomical investigation was
found.
Case 5. M. K., 44 years, Russian Hebrew, father of three healthy children, was
admitted to the hospital on December 8, 1908. His limbs never troubled him until
about a year ago, when he felt the presence of tender spots on the inner side of the right foot.
Soon other hard “lumps” and “cords” appeared, some of these in the neighborhood of the
ankle, others higher up on the leg. After two months these disappeared, only to recur after
a very short interval. Since then he has never been absolutely free from peculiar “‘ painful
spots,’ and now, on admission, he still has signs of some of them. About three months
after the onset of these symptoms he experienced pain in the big toe, especially on walking.
This has become gradually worse, so that he has been unable to get about properly for
almost two months. Of late he has often had cramps in the calf and instep of the right leg
after walking for a short distance. His chief complaint, however, is the painful condition of
the inner side of his right leg.
Physical examination showed evidences of circulatory disturbance in the right lower
extremity. Both the dorsalis pedis artery and the posterior tibial were pulseless, although
pulsation of both the femoral and popliteal arteries could be easily detected.
Over the inner border of the right foot there is a red streak about one-half inch in length.
This corresponds to a tender indurated mass which thins out and is lost as it is traced
upward. A short distance below the middle of the leg the upper end of a hard cord can be
palpated. This extends down behind the border of the tibia for more than two inches, is
adherent to the skin, somewhat nodulated, and marks the center of an area of hypersensi-
tive, swollen, turgid skin. There are no trophic disturbances. Diagnosis—thrombo-
angiitis, and thrombo-phlebitis of the internal saphenous and some of its tributaries.
On December 15, 1908, a portion of the thrombosed saphenous was removed for patho-
logical examination.
On December 26, 1908, the physical examination was recorded as follows: In the hori-
zontal position the right foot has a light shade of red; this is most marked over the big toe,
and fades off towards the ankle. In the web between the third and fourth toes there is a
THROMBO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS 283
superficial ulcer. On the inner side of the foot, almost two inches from the internal malleo-
lus, there is a hard, cord-like nodule which is adherent to the skin. Behind the tibia there
is a scar left after removal of a portion of the saphenous vein. The saphenous vein can no
longer be felt.
On elevation of the foot, blanching sets in rapidly and pain becomes intense. The
pendent foot turns very red (marked erythromelia).
Further Course.—February 15, 1909, the pain in the foot has been getting steadily
worse, and the fourth toe is beginning to turn black. On the 23d of February amputation
at the knee was done, at the request of the patient, for early gangrene of the fourth toe.
The prognostication that was made clinically in regard to the condition of
the long saphenous vein was confirmed by pathological examination of the limb
for, practically the whole of the main trunk of this vessel was found converted
into a fibrous cord, the result of an old thrombotic lesion, similar to that found
in the deep vessels. As for the arteries, the plantars, peroneal, posterior
tibial, and lowermost portion of the popliteal were completely occluded by the
brownish organized tissue usually encountered in the disease under con-
sideration, whilst the deep veins were patent throughout.
Stated succinctly the case is one of thrombo-angiitis obliterans, in which
the symptoms manifested themselves first in the form of migrating phlebitis
that has persisted almost the whole of the years’ course of the disease. The
thrombotic lesion has affected the right leg and is associated with the develop-
ment of typical symptoms of thrombo-angiitis. At the end of the year some
of the deep vessels are closed, for there is absence of pulsation in the dorsalis
pedis and posterior tibial. For a long time there are no trophic distur-
bances, but finally in the thirteenth and fourteenth months of the disease,
ulcers develop and dry gangrene of one toe leads to amputation of the limb.
When the migrating phlebitis is a prodromal manifestation of the disease,
thrombo-angiitis obliterans, or, if it marks a relapse in an apparently healed
case, no phenomena referable to obliteration of the deep vessels may be obtain-
able. In such instances the excision of the affected superficial vein, followed
by microscopic examination, will frequently reveal the typical pathognomonic
lesions upon which a correct diagnosis may be based.
Case 6. H. P., 42 years, Russian Hebrew, seeks advice for a hard lump in back of the
left leg on November 15, 1912. Twenty years ago the tip of the big toe of the right foot
was removed in Russia, ostensibly for frost-bite. Since then (the exact date being unknown)
the second toe of the same foot was also ablated. Save for these affections, no symptoms
referable to the extremities can be recalled by the patient.
Physical examination shows a small thrombosed nodule, apparently associated with a
varicose vein, over the calf of the left leg. In the vicinity there are small nodules, seemingly
connected with tributaries of the external saphenous. There are no evidences of closure
of the peripheral vessels.
Histological examination of the excised nodule, December 7, revealed the typical lesions
of thrombo-angiitis obliterans.
Summary.—We have here, then, a case in which the history of the loss of two toes points
to the existence of an old-standing thrombo-angiitis obliterans, the disease having become
spontaneously cured. Recently there have developed evidences of involvement of super-
ficial veins, the histological studies corroborating the diagnosis.
Another striking instance of the cases in which the thrombo-angiitis
obliterans symptoms are masked and not noticed by the patient, and where the
patient seeks advice because of migrating phlebitis, is presented by the
following case:
Case 7. J. W., Russian Hebrew, consulted the author in November, ro11, because of
red lumps in the left leg, and indefinite pains. He thinks he had syphilis 16 years ago, and
that the lumps now present are due to this disease. The present trouble dates back about
six weeks. ;
Physical examination shows a number of nodules of the usual type over the outer and
posterior aspects of the left leg, and along the course of the internal saphenous vein.
284 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
On November 26, one of these nodules was removed for microscopic examination.
Pathological examination shows the typical lesions of thrombo-angiitis obliterans in the
early stages, typical giant cells, and miliary foci. Wassermann reaction on the 26th of
November was negative.
December 4, some of the nodules had disappeared completely. The internal saphenous
vein can be felt as a hard cord one-half way up the leg.
February 16, 1912, a fresh nodule has appeared above the Achilles tendon, another over
the left calf, still another over the outer side of the leg above the external malleolus.
The dorsalis pedis and posterior tibial vessels of the right leg pulsate. The dorsalis
pedis of the left does not pulsate. The posterior tibial pulsates very faintly.
We may cite as exemplifying cases of this group, the following history.
Case 8. B.C., 39 years, Russian Hebrew, seeks advice on account of pain in the left
leg, which came on about four months ago. ‘This seems to be associated with a nodule on
the inner side of the middle of the tibia, and a similar nodule somewhat lower down. Three
weeks ago another lump appeared on the outer aspect of the right leg. He has no pain on
walking, and none of the symptoms of thrombo-angiitis obliterans.
Physical examination, December, 1911; several typical phlebitic nodules over the inner
aspect of the left leg. The internal saphenous vein, from a point just above the ankle up
to the upper fifth of the leg, can be felt as a hard cord. Anteriorly, three inches above the
ankle there are two fused nodules in a somewhat reddened skin.
The dorsalis pedis and posterior tibial arteries are not felt in the left leg. The posterior
tibial pulse of the right leg is also imperceptible, though the dorsalis pedis pulsates faintly.
There is no erythromelia, but moderate ischemia on elevation of both limbs.
In short, we have here a case in which the symptoms of migrating phlebitis are promi-
pit the pulseless vessels and slight ischemia being the only evidences of thrombo-angiitis
obliterans.
On December 5 one of the nodules was removed from the left leg for microscopic
examination.
December 16. The phlebitis is extending from the region of the excised nodule in the
upper part of the leg, and a distinctly tender cord, some 234 inches long can be felt along the
course of the saphenous.
December 22. The nodules in the right leg have almost disappeared.
Still more interesting and instructive are those cases in which the disease
of the superficial vessels affects both legs and one or both thighs.
IV. BOTH MIGRATING PHLEBITIS AND THROMBO-ANGIITIS PLAY
EQUALLY IMPORTANT ROLES IN THE SYMPTOM-COMPLEX
The following case will illustrate this variety. The patient could be
observed for almost a year, the progression of the obstructive changes in
the deep vessels could be closely followed by proper interpretation of the
varying circulatory phenomena in the leg, and many of the attacks of
thrombo-phlebitis in the territory of at least one saphenous vein could be
recorded.
Case 9. H.R., 32 years, Russian Hebrew, August 9, 1908, has been suffering for five
years. At first it was a burning sensation in the toes of the left foot that gave him most
concern, but later on he was troubled more by his inability to walk distances on account of
the.sudden advent of attacks of pain that were felt from the toes upward almost to the knee.
In cold weather he seems to be in poorest condition, for then his toes get cold and blue, and
walking is very difficult. Although this has been going on for years, he has not found it
necessary to consult a physician until something else in his right Jeg began to engage his
attention. ;
For the last five months long “streaks” or “swollen places” would come and go over
the inner side of the right leg, behind the shin bone. ‘These are often very painful. A week
ago a physician told him that he had “‘phlebitis.”’ :
Physical examination on August 17, 1908. The vessels of the right leg pulsate, but the
left posterior tibial and dorsalis pedis cannot be felt.
The right leg shows a tender cord with some edema around it, extending from the ankle
almost to the tibial tubercle. This corresponds to the long saphenous. Erythromelia is
THROMBO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS 285
definite on the left side, there are no trophic disturbances, and the circulation of the right
leg is fairly good. ;
From now on aggravation of his subjective condition went hand in hand with the
advancing lesions in the vessels. That an increase in the extent of vascular occlusion took
place from this time on could be easily deduced from clinical observation.
On December 1, 1908, the following was recorded: The right foot looks pale (evidence
of the beginning of circulatory disturbances). After a short time it becomes slightly cya-
notic. If looks cadaveric when raised for a short time. There is no erythromelia. The
dorsalis pedis does not pulsate. A tributary of the long saphenous about two inches long
can be palpated as a tender cord along the lower inner aspect of the right thigh; the skin
over itis reddened. There are two nodosities in and under the skin below and to the inner
side of the tubercle of the tibia. The left leg shows marked erythromelia; blanching in the
elevated position is extreme; the popliteal is open, but the dorsalis pedis and posterior tibial
arteries cannot be felt. There are no ulcers or other signs of trophic disorder.
The steady advance of the occlusive process in the deep vessels is well
illustrated by the findings on December 1, 1908. In August all the vessels
of the right lower extremity pulsated in normal fashion; now, in December,
the dorsalis pedis is occluded. Corresponding with this there is a new symp-
tom, the blanching of the foot. How remarkable that the disease of the
deep vessels on the right side should be so closely associated with the attack
of migrating phlebitis, the latter first attacking the saphenous in the leg, and
now appearing in the thigh! We have evidences of chronicity in the affection
of the superficial veins, and as regards the deep lesion, we have been able to
watch its gradual development both by its effect on the palpable arteries and
by the clinical manifestations it has produced.
On January 31 the big toe of the left foot was swollen and red; the nail was coming off.
Immediately upon removing his shoe, the right foot had a very white color, but soon
cyanotic patches mingled with the pallor all over the foot, especially in the region of the big
toe. The pain in the left foot was now excruciating and he consented to an amputation
with scarcely any reluctance. The left leg was amputated at the upper fourth.
Examination of the vessels of the amputated limb showed occlusion of the following
arteries: Dorsalis pedis, peroneal, plantars, and posterior tibial. The anterior tibial artery
was open throughout most of its course. A large part of the long saphenous vein was found
occluded by an organizing thrombotic process.
Diagnosis.—Thrombo-angiitis obliterans.
In short, this patient presents the following features of interest: (1)
Migrating thrombo-phlebitis of both saphenous veins; (2) involvement of the
same vein in its course through the thigh; (3) associated progressive and
synchronous development of the thrombosis in the superficial and deep vessels
of the right lower extremity; and (4) absence of any cause for the lesion of
the superficial vessels.
Case1zr. W. T., 26 years, Russian Hebrew, admitted July 10, 1909.
In April, 1907, he was treated for gangrene of the third toe of the left foot. Three
months before admission to the hospital he had been suffering with pain in the left calf and
foot. During the previous winter i 906) the left foot did not seem to be normal, so that he
sought the advice of an orthopedist, who gave him the usual treatment for flat feet. Lat-
terly, he has had severe pain in the calf, and shortly before admission gangrene of the third
toe setin. He had an amputation performed on the 27th of May, 1907, the left leg having
been ablated at its upper third.
At that time pathological studies revealed the usual changes that are seen with thrombo-
angiitis obliterans. The dorsalis pedis, posterior tibial, the greater portion of the peroneal
and plantar arteries were closed.
Present Status (1909).—Since discharge, June 27, 1907, until eight months ago, he seemed
to be doing well. About this time (8 months ago) he noticed the appearance of red streaks
and nodules on the inner side of the right thigh. After a few days these would disappear
and new ones would appear in their stead, either higher up on the thigh, or near the knee.
They caused a peculiar pricking sensation, and some were tender and painful. Lately, he
has been able to walk no more than two hundred steps without resting.
286 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
The external manifestations on the roth of July, 1909, were as follows:
A healed amputation scar in the left leg. In the dependent position there is marked
erythromelia of the right leg. Neither the dorsalis pedis nor the posterior tibial can be felt
to pulsate. On the inner side of the thigh, near its middle, there is a sensitive strand, which
corresponds to the thrombosed saphenous vein. On the outer side there are a number of
hard, indurated, reddened nodules. Over the inner side of the dorsum of the foot there are
similar nodules and strands.
Diagnosis.—Migrating phlebitis and thrombo-angiitis obliterans.
In short, the history of this case reveals the following: Thrombo-angiitis
obliterans first involving the left lower extremity, leading to amputation;
insidious development of the same disease in the right lower extremity, with
extensive thrombosis of the superficial veins of the thigh and leg.
From the consideration of the data thus far presented it would appear that
the internal saphenous vein is the site of predilection for that peculiar lesion
which is termed a migrating phlebitis. In July, 1904, the author had the
opportunity of studying a case in which the veins of the upper extremity,
too, were involved. Since then several additional patients with a similar
distribution of the lesions have come under observation.
V. MIGRATING PHLEBITIS OR THROMBO-PHLEBITIS INVOLVING BOTH
UPPER AND LOWER EXTREMITIES
In three out of four of these patients the disease has reached that stage of
chronicity in which the suffering is almost constant and in which the limbs
may be regarded as irretrievably lost. For there are cases that become “cured”’
as far as symptoms are concerned. And by “cured” in this sense we do not
mean to imply that the pulseless dorsalis pedis, posterior tibial, or both,
begin to beat again, but rather that, in spite of closed vessels, an adequate
collateral circulation has become established, as evidenced both by the
absence of the typical manifestations of impaired circulation, and by the
patient’s improved subjective state. These three patients per contra had the
‘“‘severe’’ form of the disease, even though the issue, gangrene, was delayed
far beyond our expectations.
Case 11. B. B., 34 years, Russian Hebrew, married, has no children; operator for
eleven years. His malady began eight years ago, when he first experienced pain in the right
calf on walking. He would be compelled to rest after walking four or five blocks. At about
the same time he often noticed that there were long “‘hard cords” and “‘reddened lumps”’
over the front of both forearms (anteriorly) and over both legs. "These would come and go,
appear with provocation, now in an arm, now in a leg. The lumps were always small,
pea-sized or slightly larger, and could be felt for two or three days.
He always felt better during the summer months. The nodules in the legs were present
almost every winter for the first five years. Six years ago there was a “‘bad attack,” in. the
course of which there were (‘“‘Adern’’) “‘veins” or “nodules” behind and above the right
ankle. Then again, about three years ago, there was a repetition of this trouble. Nodosi-
ties formed behind the shin bone on the inner side of the right leg (region of saphenous) and
the pain kept him abed for almost ten weeks.
Thus, up to this time he complained of the following: Pain in the right calf on walking
two to four blocks, painful nodules and cords, and cramps in the toes and sole of the right
foot at night.
For two years the left leg has given him concern; the condition is practically the same as
that of the right. Last winter, January, 1909, there were ‘‘sores”—one at the tip of the
big toe of the left leg, and another at the end of the little toe of the right. He feels best
when his legs hang down (a variation from the usual statement); but even in this position
the toes often feel ‘‘dead.”” In the same way his fingers get ““numb” in winter; he thinks
that there is no blood in them.
Physical Examination.—In the right leg the toes have a tense, reddened appearance,
the second and third being discolored most, the little toe having a cyanotic hue. Just behind °
THROMBO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS 287
the nail on the plantar surface there is a deep fissure, the tips of which are adherent. Slight
pressure brings forth a ‘drop of pus from the bottom of the wound. ‘The erythromelia is
marked over the dorsum of the foot, as well as over the sole. Ischemiain the elevated
position is intense; this posture excites severe pain. The femoral artery pulsates; the
popliteal, posterior tibial, and dorsalis pedis cannot be felt.
The left leg is similarly affected; the rubor is deeper and the toes are more swollen.
There is a trophic ulcer at the tip of the big toe. The ischemia, too, is of a greater degree.
All the vessels (femoral included) fail to pulsate.
Summary.—This is a case which, according to the story, combines
thrombo-angiitis obliterans with migrating phlebitis of both upper and lower
extremities.
One of the most instructive cases of this series is a patient in whom the
attacks of inflammation and thrombosis of superficial veins dominated the
clinical course for years before the symptoms characteristic of thrombo-angiitis
obliterans came into evidence.
Case 12. D. B., 35 years, Russian Hebrew, first seen by the author July 16, 1904
He had been treated in the hospital eight years previously for ‘“‘ phlebitis” of the right
leg; a portion (5 inches) of a large vein was diseased at that time, and the history states that
the process was ‘‘migrating,’’ moving up and down the thigh. He says that this trouble
lasted off and on for two years. In 1903 there were “lumps” in and under the skin of
the right leg, and then, three months later, in the left leg. Such swellings would last a
week, develop into hard ‘‘tender spots”’ with a covering of red skin, and on one occasion
three such spots appeared on the left arm, in front of and just below the elbow.
Physical examination, July, 1904. In the left antecubital region there is a thickened,
slightly reddened cord about two inches long. Another is situated on the ulnar aspect of
the same forearm, near the elbow. ‘The right forearm presents a similar vein about three
inches from the elbow; the skin is not reddened. On the inner side of the right cubital
space a subcutaneous adherent nodule can be felt; it is very tender. ‘There are several
such nodules in the right calf and smaller ones over the left shin bone. No edema, but
slight cyanosis of both legs in the pendent position. i. It was found that
the disease involves the deep arteries and veins of both the lower and upper
extremities, commencing by preference in the vessels of the foot, such as the
dorsalis pedis and plantars and their larger branches, ascending so as to
sometimes close even the iliacs and aorta. Clinical and pathological data led
to the assumption that the progression of the thrombotic process takes place rather
in‘ attacks or sudden exacerbations than by a gradual ascent; that larger or
smaller territories of the deep vessels become suddenly closed, just as the
saphenous veins are wont to be thrombosed and inflamed from other causes—
in other words, that the process is a migrating thrombosis of the deep vessels
comparable to the migrating phelbitis of the extremities.
A cursory study would lead one astray as to the significance of the most
common lesions seen in the arteries and veins, for it would fail to reveal the
fact that there are two distinct phases in the pathology of the disease. The
lesion most commonly encountered is but the result of the organization of
thrombi, and of importance only in so far as it is productive of the pictures
that may be confused with endarteritis obliterans. More interesting and
more valuable for investigation is the “‘acute stage,” or earliest lesion, that
occurs simultaneously with, or shortly after the onset of the thrombosis.
THROM BO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS 293
This early stage was found by the author in the deep vessels of but two of the
amputated limbs. In these certain specific morphological alterations were
encountered, whose meaning was not understood at that time. Thesé histo-
logical changes appeared to be characteristic of the disease, thrombo-angiitis
obliterans, not having been met with in vessels thrombosed through other
causes. The regularity of the occurrence of the typical lesions aroused the
suspicion that here was a specific morphological alteration, due to a specific
cause.
In short, whereas the usual changes in most of the vessels of an amputated
limb represent the healed stage of the disease, that in which a fibrous mass
containing canalizing vessels has taken the place of the original clot, there is
another early or acute stage of the disease which alone is of value in throwing
light upon the true nature of the process. It is only at this particular period
in the history of the pathological process that the media is diffusely infiltrated
with leukocytes, and that the lumen is filled with red clot, in which certain
typical miliary giant-cell foci! make their appearance. It is these foci that
lend a characteristic appearance to the thrombotic lesion of thrombo-angiitis
obliterans.
When these lesions were first referred to in 1908 their significance was
not understood, although the suspicion was already aroused at that time
that they were specific for the disease and probably represented a peculiar
reaction on the part of the tissues to some toxin or organism. Itseemed clear,
too, that it would be a difficult matter to obtain an adequate amount of mate-
rial from the deep vessels for the study of the acute stage of the disease. It was
here that we had to pause in our deductions, when we were fortunate enough
to encounter a most interesting fact, that the superficial or subcutaneous
veins of the upper and lower extremities may also be affected by the disease,
thrombo-angiitis obliterans. Thus, in 1909, the association of migrating
phlebitis of the subcutaneous veins of the extremities was noted in eleven
cases. From a study of the clinical history of the cases, and of the histology
of the affected subcutaneous veins exsected during various stages of the
disease, the following conclusions were drawn:
1. The disease thrombo-angiitis obliterans is often associated with
thrombo-phlebitis of superficial veins of the arms and legs.
2. Certain peculiar cutaneous nodosities are characteristic manifesta-
tions in many cases.
3. The disease of the superficial veins may be subsidiary or it may
dominate the clinical picture. Objective signs referable to these vessels
should be regarded as extremely suspicious marks of the synchronous develop-
ment of thrombo-angiitis obliterans, in the form of pulseless vessels, erythro-
melia, blanching of the leg in elevated posture, cold and blue toes, pain in the
calf of the leg brought on by walking, and other typical phenomena.
4. Migrating thrombo-phlebitis may give no symptoms, the signs refer-
able to the deep vessels being of most importance.
5. Patients may suffer at one time from migrating thrombo-phlebitis,
at another from the progress of the occlusive change in the deeper
vessels.
6. Certain cases suggest the possibility that attacks of trouble in surface
veins may occur simultaneously with similar exacerbations of disease in
deep vessels of another limb.
1 Buerger, Mitteilungen aus den Grenzgebieten der Medizin und Chirurgie, 21 Band,
1919; also Am. Jour. Med. Sci., October, 1908; and Surg., Gyn. & Obst., Nov., 1914.
294 CIRCULATORY AFFECTIONS OF. THE EXTREMITIES
7. The morbid process resulting in the production of cutaneous nodosities
and thrombosed superficial veins is independent of varicosities, of infection,
or of ttophic disorders in the territory which they drain.
8. The vessels of the upper extremity may be affected by the lesion
thrombo-angiitis obliterans.
9g. Thrombo-phlebitis in the arm and forearm should arouse suspicion
as regards involvement of the deep vessels of the legs.
to. Further studies should be directed towards solving the relationship
between the two thrombotic lesions. Perhaps excision of nodules and veins
early in the disease, exploratory incision for inquiry into the condition of the
deep vessels, and bacteriological and serum investigations along the proper
lines will do much to enlighten us in our interpretation of this most puzzling
symptom-complex. Although absolute proof is lacking, it seems more than
probable that the same determining causative factor is responsible for the
lesions of both the superficial and deep vessels.
Up to the year 1922 it was possible to gather data on additional cases in
which the superficial veins were involved which increased the number of
exsected veins up to thirty-five. In these, both the acute and healed stages
of the disease were found. From a consideration of the pathological pictures
the conclusion was reached that the specific characteristic lesion of thrombo-
angiitis obliterans may affect the deep as well as the superficial vessels; that it
is in the veins that we shall have to look to find material for investigation of
the causative agent; and that not{only do the superficial veins present the
typical miliary giant-cell foci, but they also demonstrate that these foci are
a later stage, or attempt at organization of purulent foci. In other words,
the finding of miliary pus foci in the subcutaneous veins as precursors of the
typical giant-cell foci was noted in a sufficient number of instances to warrant
the conclusion that this lesion represents the acute stage of the disease, and
suggested, too, that the thrombotic process may be caused by the presence of
some organism, virus, or specific toxin.
CHAPTER LIX
THROMBO-ANGIITIS OBLITERANS—INVOLVEMENT OF THE
UPPER EXTREMITIES
In about 500 cases of thrombo-angiitis obliterans observed from 1909
to 1922, the author was able to watch the course of this remarkable disease
through all its clinical stages. Many of the cases were followed from
five to fourteen years, and the presence of interesting mutations in the
symptomatology could be recorded. It was found that in a certain number
of the patients the upper extremities are involved, although it is- usually
believed that only the lower extremities are affected.
Early Symptoms of Involvement of the Upper Extremities.— Coldness and
a feeling of numbness and deadness of the fingers may be the first symptoms
in one or both hands simultaneously, trophic disturbances soon following.
Patients describe these as being sores at the tips of the fingers that are exceed-
ingly painful, that are sometimes followed by suppuration gradually healing,
leaving retracted scars near the nail at the tips of the affected fingers. Pallor
THROM BO-ANGIITIS OBLITERANS—UPPER EXTREMITIES 295
of one or more fingers in cold weather is also mentioned by patients as a
striking symptom.
Objectively, when seen several months after the onset of the symptoms,
the picture of early involvement without gangrene and without trophic lesions
is the following. The hands may show rubor and this is associated with cold-
ness of the tips of the fingers. This combination of diminution of
temperature with the usual objective manifestations of heat is paradoxical
but characteristic of thrombo-angiitis obliterans. The tips of the fingers
may be slightly cyanotic or a cyanotic hue over the proximal portion of the
nail bed is present.
The retracted sores at the tips of the fingers are apt to lie in whitened
thinned-out skin, and although completely healed, are exceedingly sensitive
to the touch.
With these manifestations the radial pulse may be absent in one or both
hands. The circulatory manifestations do not bear the same relationship to
posture as in the lower extremities, for ischemia may be absent on elevation,
or if present, may be very slight.
In some cases the incipiency of this affection in either the ulnar or radial
arteries manifests itself in the coldness of one or more fingers only, and on
examination one of these two arteries may be closed, one or two fingers
distinctly cold, with a tendency to pallor. If an Esmarch be applied to the
arm, the differences in circulation between the affected fingers and the others
can be made more evident, for the reactionary hyperemia will be sluggish
in appearing in the territory of impaired circulation.
A survey!of many histories shows that the upper extremities may be
clinically involved in the following ways: (I) without subjective symptoms;
(II) with vasomotor symptoms predominating; (III) with lesions simulating
the results of neurogenic disturbances; (IV) with trophic disturbances alone;
(V) with trophic and vasomotor phenomena; (VI) with gangrene of slight
extent; (VII) with extensive gangrene threatening the viability of the
extremity; (VIII) with extensive atrophy of the hand and forearm; (IX)
with changes simulating scleroderma and sclerodactyly; and (X) cases with
acute arteritis of portions of the radial or ulnar artery (migrating arteritis).
I. Thrombo-angiitis Obliterans of the Upper Extremities without
Symptoms.—Just as in thrombo-angiitis of the lower extremities, there are
cases in which the radial or ulnar artery, or both, become gradually closed
without the patient’s experiencing any noticeable symptoms. In some
instances, absence of pulsation was discovered during a routine physical
examination; in others, where symptoms were present in the lower extremities
investigation of the radial and ulnar vessels had demonstrated their occlusion.
J. A., male, aged forty years, Russian, began to have trouble in the right leg ten years
ago (1904), pain coming on during walking, subsiding when at rest. Gangrene of the little
and of the big toes developed, leading to amputation of the left leg at its middle in 1906.
Since 1908, similar symptoms involved the left leg, and the first and second toes became
ulcerated, also requiring amputation. During the period of clinical observation the right
radial pulse gradually disappeared, although no vasomotor or trophic manifestations could
be elicited on examination. The patient was lost sight of so that the further course could
not be followed.
The symptoms of Raynaud’s disease, too, may be closely mimicked, as
in the following cases:
II. Cases in Which Vasomotor Phenomena Preponderate.—Such an
instance is described in the following history, where, after about ten years of
migrating phlebitis, and the usual circulatory disturbances of the lower
296 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
extremities, distinct evidences of involvement of the vessels of the arm and
hand supervened.
The following history denotes an instance of remarkably striking vaso-
motor manifestations that are either part of the thrombo-angiitis obliterans
syndrome or coincident with it. When we are confronted with neurotic
manifestations suggestive of chronic acroasphyxia as here, a long period of
clinical observation may be required in order to determine accurately whether
two types of vascular disorder, neurogenic and organic obstructive are not
simultaneously represented. Certain it is that vasomotor phenomena may
accompany thrombo-angiitis obliterans as a part of the latter’s symptom-
complex.
J. V., male, aged thirty-four years, Russian, admitted to the hospital December 17,
1907, says that three and a half years previously he noticed that his fingers were cold
but not blue. The following winter the same symptoms returned, but, in addition, the
skin of the tip of the right middle finger became dry and a “‘wound” spontaneously
developed. For the past two years his hands would get blue, cold, and numb on exposure
to cold, their natural color returning ina warmroom. There was never any pallor. A
sort of ‘‘sticking”’ pain in the finger tips would regularly accompany the state of blueness.
Physical examination, December 17, 1907. Both hands are deeply cyanotic up to the
wrist, and very cold. During the examination bright red or crimson colored spots can be
seen to appear in the dorsum and palm. Over the back of the hand these red blotches
become very distinct and do not shade off into the blue areas. The two distal phalanges
remain deep blue. If the hands be observed for a still longer time (five minutes) the red
color becomes paler and is mottled with a yellowish pink; at times a totally different and
much lighter shade, variegated with red and blue, will completely replace the deep colors
first noted. In the palm the red areas are not so apparent, but they also give way at times
to the lighter shades. The terminal phalanges of the ring fingers are enlarged, those of the
middle fingers somewhat less so. When the hands are held above the head for two or more
minutes the redness disappears, a pale sickly purple remaining. The radials and brachials
pulsate well.
In the lower extremity a similar picture is present, but there are evidences of obliteration
of the vessels. The right dorsalis pedis cannot be felt, although palpated on many occasions
from December 17, 1907, to January 20, 1908. In the left dorsalis pedis there is fair pulsa-
tion. ‘There is ischemia in the elevated position of the legs, as evidence of the impaired
vascular supply, and bespeaking the presence of the lesion, thrombo-angiitis.
If such an exquisite example of vasomotor disturbance can belong to a
case of thrombo-angiitis obliterans, there is little wonder that confusion should
exist in the differentiation of the symptoms due to neurogenic and organic
vascular affections.
A. B., male, aged thirty-one years, Russian, noticed the appearance of small hard lumps
under and in the skin of the calf of both legs in 1904 (ten years ago). They were painful,
lasted for a few days or a week or more, and would then disappear (migrating phlebitis).
For three years similar lumps and strands would come and go over the lower and inner side
of the right thigh. About seven years ago he began to experience cramp-like pain in the
right foot and calf of the leg on walking. Later the right foot became ‘‘cold.” An ulcer
developed on the third toe and showed no tendency to heal.
For seven years he has been suffering with similar symptoms in both legs and feet, the
typical symptoms of pulseless vessels, erythromelia, ischemia in the elevated position, and
gangrene of several toes being present. He now (1914) has already lost four toes of the left
foot and two of the right.
Four months ago his right hand began to trouble him. In cold weather it would become
very pale, particularly the little finger. On warming the hand, color would gradually
return. Of late, however, the tip of the little finger has been bluish for days at a time,
although excessive heat seems to bring back a normal color.
Physical examination, May 6, 1914. The radial and ulnar arteries of both sides pulsate
distinctly. Both hands perspire profusely, and are somewhat cold. The tip of the little
finger of the right hand is cyanotic and deeply discolored over its palmar aspect. Pressure
over this part elicits some pain. Roentgen-ray examination of the hand is negative.
THROM BO-ANGIITIS OBLITERANS—UPPER EXTREMITIES 297
On July 31, 1914, patient says that the little finger and thumb of the right hand feel cold.
Scales form on the tip of the little finger, and when these separate, leave a healed depression.
He has no pain.
Physical examination shows that both the little finger and the thumb are distinctly cold
to the touch, the coldness extending to the base of the fingers. The other hand and fingers
are warm. ‘The radial and ulnar arteries pulsate well. On elevation there is no appre-
ciable change in the color of the fingers.
In short we have an example of thrombo-angiitis in which vasomotor
symptoms initiate the onset of the disease in the upper extremities. Previous
experience warrants the assumption that we may either expect a complete
cessation of the symptoms in the hands, if adequate collaterals be established,
or progressive occlusion of vessels until the radial and ulnar arteries become
obliterated or until gangrene ensues.
III. Cases with Lesions Simulating Neurogenic Disturbances.—The
following picture was characteristic in certain of the cases in which thrombo-
Fic. 49.—Atrophic and dystrophic changes in the fingers and nails in thrombo-angiitis
obliterans.
angiitis obliterans of the lower extremities had already been present for a
long time, necessitating amputation of one of the lower extremities.
All the fingers of the affected hand are tumefied and have an exaggerated
conical appearance due to relative abnormal increase of the girth of the prox-
imal portion of the fingers. The general swelling is such as to obliterate all
of the normal furrows and markings. ‘The texture and color of the skin also
are altered in that portions of the skin, particularly about the nails, have a
glossy appearance. The integument (Fi ig. 49) appears stretched over swollen
subcutaneous tissues, and the color, too, is peculiar in that there is a diffuse
reddening of the distal digits. There seems to be a subungual trophic distur-
bance manifesting itself by discoloration of the nails. As aresult, thelunulais
298 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
increased in size to four or five times the normal. One or more of the fingers
may show the absence of the distal portion of the last phalanx, and depressed
scars, at the bottom of which a necrotic section of the bone may protrude.
The palmar aspect of the hand and fingers shows a general tumefaction
and reddening. Both the radial and ulnar arteries usually fail to pulsate.
In addition to the objective manifestations, there may be limitation of
motion in most of the phalanges.
In the case described below, the employment of hot baths, intermittent
compression of the brachial artery was followed by rapid diminution of the
edema and intensity of the rubor, and by improvement in the temperature of
the fingers.
In rare cases there are atrophic changes in the bones of the hand associ-
ated with articular changes that do not show any evidence in the X-ray, but
lead to ankylosis. The bone lesions differ from sclerodactyly in that there is
no change in the terminal phalanges even though defects in the soft parts may
occur. The most marked lesions in the bones are absorption and rarefica-
tion of the radius and ulna and carpal bones, of the bases of the metacarpal
bones, and of some of the phalanges.
The history in one of the typical cases was as follows:
R. L. was observed from July 23, 1912, till March, 1921. In January, 1912, he was
twenty-nine years of age, with the usual symptoms of thrombo-angiitis obliterans of the left
lower extremity, with the typical erythromelia, and absence of dorsalis pedis and posterior
tibial pulsation. ‘The process was progressive; on the 8th of March, 1918, it had advanced
so as to involve both extremities. ‘There had been ulcerations of the toes of both feet.
The right leg was amputated in 1918. March 17, 1912 he consulted me because
of severe pain in the right hand radiating to the wrist, and because of the discoloration of the
nails and of the fingers. He says that the first sign of trouble in the right hand, was the
absence of the radial pulse, which he felt repeatedly, having a good knowledge of the signi-
ficance of pulsation, and fearing that the right hand might be involved. About eight
months ago, spontaneous gangrene of the tip of the ring finger of the right hand occurred,
and following this the other fingers became swollen and reddened.
May 5, 1921, rubor still present, but rather diminished. The opaque portion of the nail
is greater than before.
The disappearance of such marked symptoms 18 months later is worthy of note;
Oct. 26, 1922, remarkable improvement in the condition of the right hand, the chronic
rubor having disappeared. The fingers have taken on a more healthy appearance, the only
evidences of disturbance being the retracted scar at the tip of the ring finger of the right
hand where a piece of bone had separated; and the somewhat atrophic condition of the skin.
The right brachial artery can be felt beating in its upper part, but its pulse is imperceptible
below the middle of the arm, although it is easily palpated. The left brachial artery can be
felt all the way down. Just as remarkable as the disappearance of the chronic erythromelia
and the normality of the nails and nail-beds, is the freedom of motion in the interphalangeal
joints, in which the fixation 18 months previously seemed sufficiently advanced to threaten
chronic ankylosis of the joints.
This pseudo-ankylosis appears at first sight to be due to joint involvement.
However, it was observed to disappear in the following case, as the vaso-
motor and trophic disturbances gradually improved. Perhaps the fixation
isfof the nature of those sympathetic contractures that the French authors
attribute to derangements of the periarterial sympathetic. The extensive
obliteration of the radial and brachial arteries with the periarteritis that
accompanies would seem to substantiate such a theory, although such con-
tractures and fixations are but rarely observed.?
Another striking instance of the association of vasomotor symptoms and
trophic lesions is the following:
1 see Chans..LAX XVI xX Cliand Cy.
THROM BO-ANGIITIS OBLITERANS—UPPER EXTREMITIES 299
A. W., 24 years, a Russian Hebrew, had thrombo-angiitis obliterans of both legs,
necessitating amputation of the right leg.
November 8, 1922. For some weeks there has been pain in the fingers of the right hand,
coldness, varying discoloration of the fingers, and an ulcer developed at the tip of the ring
finger.
Physical Examination.—The right hand has a peculiar variegated appearance due to the
difference of color in the various parts of the fingers, and the abnormal appearance of the
nails of the second, third and fourth digits.
Color changes take place while wnder observation, in that parts of the fingers are deeply
cyanotic, and other parts have a more scarlet hue; still other areas have a yellowish ashen
tint. Over the tip of the fourth finger, near the nail-bed, there is necrosis of the skin and
an accumulation of fluid under the adjacent skin, the whole region being deeply cyanotic.
All the fingers are slightly swollen.
The radial and ulnar arteries do not pulsate, but the brachial artery can be felt down to
the elbow. The pulses of the left hand are normal.
The texture of the nails is entirely changed, being completely whitened and having the
appearance of celluloid or sea shell, this due to an opacity that does not permit the matrix
to shine through. They seem abnormally convex and prominent.
IV. Cases with Trophic Disorders Only.—In some patients, distinctive
signs of an affection of the upper extremities manifest themselves as trophic
disturbances not extensive enough to lead to gangrene. The disease may be
wholly overlooked by the patient and, when the lesion has healed, it may be
subsequently referred to by him as a slight “sore” or “ulcer”? developing
without cause. Were it not for the presence of the disease in the lower
extremities and for the changes in the radial pulse the nature of the trophic
disorders would be difficult of solution.
T. S., aged thirty-one years, Russian, consulted me in May, 1914, because of the
condition of his left foot. Three and a half years previously he experienced pain in the sole
of the left foot on walking and was treated for rheumatism. Two years after the onset a sore
developed between the fourth and fifth toes of the left foot and another one on the tip of the
big toe of this foot. Since then the foot became red and the little toe gangrenous, falling
off about a year ago. About this time his right leg began to trouble him, the symptoms
being pain in the calf on walking.
Two and a half months ago there developed a spontaneous ulcer over the middle
phalanx of the right hand, not accompanied by any evidence of inflammation, hardly pain-
ful, and not brought about by any injury. He was treated for this for about eight weeks,
when the wound healed.
Physical examination, May, 1914. Over the middle phalanx of the right hand there is
an irregularly shaped scar, about 8 mm. in length and 4 mm. in width, evidently the site of
the old healed lesion. The right radial pulse is not perceptible.
We have here a typical case of thrombo-angiitis of the lower extremities,
first involving the left then the right lower extremity, and three years later
manifesting itself also in the hand, with trophic disturbances and oblitera-
tion of the radial artery.
V. Cases with Trophic and Vasomotor Phenomena.— It is rather charac-
teristic of the symptomatology of the disease as it affects the upper extremi-
ties that manifestations are frequently overlooked by the patient, until
definite objective signs, such as trophic ulcers, make their appearance. The
almost inexplicable development of such phenomena may lead to careful
examination on the part of the physician, and to the detection of the absence
of the radial or ulnar pulse, or even the brachial. The chronological
sequence of events in a number of these cases is the following:
(1) Symptoms of thrombo-angiitis obliterans of the lower extremities,
with or without amputation of one extremity, or ulcers of both, overa period.
(2) A stage of involvement of the upper extremities with ulcers, and
disappearance of the pulses in this territory.
300 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
(3) A chronic period with more or less permanency of symptoms both
in the lower and upper extremities, a condition of vasomotor lability and
impaired circulation of the hand being a striking development.
S. S. S., 37 years, born in Russia, consulted me on the roth of September, 1922, witha
history of having had an amputation of the left leg, and complaining now of pain in the right
foot, inability to walk, ulcers of the big and little toes, coldness, discoloration of the foot;
also of numbness of the tips of the fingers of both hands, and a chronic fissure or ulcer on
the middle finger of the right hand.
Six years ago he began to experience pain in the left foot, and phlebitis was recognized.
In 1918 a diagnosis of occlusion of the blood vessels of the left leg was made. After the
removal of a callous a wound developed, which did not heal, and the foot became progress-
ively worse. He was treated until September, 1920, when amputation of the left leg had
to be performed.
In October, 1921, the right foot began to annoy him, and shortly thereafter ulcers
developed over the big and little toes of the right foot. In January, 1922, the big toe
became bluish and the wound was still not healed. Then improvement occurred, but
another ulcer developed 3 weeks ago on another toe, and the foot became very painful.
The History of the Upper Extremities——As far as he knows there were no symptoms
referable to the upper extremities until January, 1922, when ulcers developed at the tips of
the second and third fingers of the left hand. Since then, however, both hands became
numb and cold, and bluish discoloration has been regularly noted in cold weather; latterly
even at room temperature. Within the last 2 weeks he complained of numbness of the
right hand. However, as far back as January, 1922, he was told that the ulnar and radial
pulses of both hands were not palpable.
In short, an old history of thrombo-angiitis obliterans of both lower extremities followed
by the development of ulcers on the tips of the second and third fingers, closure of both
ulnars and radials having already been present, when the ulcers appeared.
Physical Examination.—On the left there is a stump, amputation having been performed
above the knee. The right leg is in a condition of intense erythromelia, both the dorsalis
pedis, posterior tibial and popliteal pulses being absent. The right and left femorals pul-
sate. The coldness of the foot extends up almost to the ankle.
The Upper Extremities——The tips of all the fingers are markedly cyanotic, particularly
those of the left. The lividity extends almost to the bases of the first phalanges over the
volar aspect of the left hand, and not quite so far centrally on the dorsal aspect. The
cyanosis is less marked on the right. ‘The fingers are cold, as far as 1 inch beyond the meta-
carpal phalangeal joints on the left, and up to the metacarpal phalangeal joints of the right
hand. Both ulnars, both radial, and the right brachial arteries do not pulsate. The left
brachial pulse is small.
On elevation of the hands there is a moderate degree of blanching, but the cyanosis is
exaggerated in this position. The tips of the index and middle fingers of the right hand
show cicatrices and retracted fissures near the nails. Similar, but less marked lesions are
present in the same situation in the left hand. Both hands show marked reactionary
rubor after preliminary elevation, especially the right hand.
Comments.—It is rather noteworthy that in spite of the extensive obliterac
tion of the arteries of the upper extremities here, such minimal trophi-
disturbances should have developed. As contrasted with the appearances
of the lower extremities in such cases, and as well illustrated in this case, the
intense cyanosis may characterize the upper extremities, whilst a marked
degree of rubor is present in the foot or feet. That vasomotor phenomena
play a rdle in producing the exaggerated lividity, seems evident, for
variations in the degree of asphyxia frequently occur, and much of it may
disappear and give way to reactionary erythromelia when the arms are
elevated and depressed secondarily for a number of times. Whether a
venous spasm plays a rdéle is worthy of investigation. The intensive
asphyxia of the hands in some of these cases might lead to the tentative
diagnosis of chronic acroasphyxia, if careful attention is not given to
palpation of the pulses.
VI. Cases with Gangrene of Slight Extent.—Not a small number of the
patients that suffer with occlusion of the vessels of the upper extremities
come to us with a history of having had pain in the tip of one of the fingers
THROM BO-ANGIITIS OBLITERANS—UPPER EXTREMITIES 301
for a considerable time. This is followed by a change in the color of the skin,
usually reddening of the tips of the fingers, as if they were inflamed. Later
there develops a sore or the skin changes color and becomes gangrenous,
usually at the tip of a finger, although the lateral margin of the finger may
be first affected.
_ M.S.,aged forty-seven years, Russian, was admitted on June 25, 1907, giving the follow-
ing history: About eight or nine months ago he noticed that the fourth toe of the left foot
was cold, blue, and painful. About four months ago the pain became so severe that he
consulted a physician, who told him that an infection had taken place. Since this time a
sore developed under the nail and the nail-bed became black.
Fic. 50.—Gangrene of the tip of the index finger.
Physical examination showed complete gangrene of the distal half of the fourth toe of the
left foot, absence of pulsation in the dorsalis pedis artery, an area of superficial gangrene of
the skin on the dorsum of the foot, intense erythromelia (hyperemia of the foot) in the
dependent position, and marked ischemia in the elevated position. June 28, 1907, amputa-
tion was done through the tarsometatarsal articulation. On July 5, re-amputation was
done through the middle third of the leg, the wound healing slowly.
In ror1o the disease began to involve the right leg in the same typical manner, leading
also to dry gangrene of the fourth toe. When examined in March the popliteal, posterior
tibial, and dorsalis pedis of the right leg could not be felt.
In short we have a typical case of thrombo-angiitis obliterans, first involving the left
popes ce tiemity leading to gangrene, amputation, and some three years later involving the
right leg.
im March, 1914, I again saw the patient, who now complains of symptoms in the left
hand.
March 18, t914. For several months he has had pain in the tip of the left index finger
and lately the finger has changed color becoming withered and glossy.
Physical examination shows an ulcer at the tip of the left index finger, the live skin above
it atrophied and glossy, the hand somewhat smaller than the other, and the fourth finger of
the same hand distinctly shrunken. The radial pulse of this hand cannot be felt (Fig.:50).
302 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
We are evidently dealing here with a case in which some seven years after
the onset of the disease in the lower extremities, the left upper extremity
became attacked, as evidenced by ulceration and trophic disturbances.
An interesting group is formed by those patients in whom trophic distur-
bances and gangrene are the salient features. These are the cases so often
confused with Raynaud’s disease. The lower extremities are regularly
involved at some time or other, and it is, therefore, necessary to watch
carefully for the advent of the typical symptoms in these, so that a correct
interpretation of the phenomena in the fingers and hands may be made... The
following two histories will well illustrate.
VII. More Extensive Gangrene.—The gangrene is usually of very limited
extent and confined to the tips of the fingers. However, it may progress
so as to involve the whole of several fingers and be accompanied by such
signs of circulatory impoverishment as to arouse the fear that the hand or
forearm may be lost.
A. K., male, aged twenty-seven years, Russian, was admitted to Mt. Sinai Hospital,
January 4, 1908. About two years previously he had had severe pain in the middle
finger of the right hand. The finger became cold, at times very blue, and extremely
painful. These symptoms persisted for about two months, when he was told to have the
nail removed. Shortly after this was done the tip of the finger became dry and black.
After several months the terminal phalanx separated spontaneously, but a wound remained
which refused to heal.
For about two months his left hand has been affected, there being excruciating pain in
the middle finger of the left hand, and -the fourth finger of the right hand also being
somewhat painful. He thinks that the tip of the middle finger of the left hand first became
dark blue or purple, and lately has become dry and black.
Physical examination, January 4, 1906, shows that the distal phalanx of the middle
finger of the right hand is absent, the tip of the fourth finger of the left hand showing a small
patch of dry gangrene and there is beginning gangrene of the distal phalanx of the middle
finger.
Somewhat more than a year later, February 24, 1907, he was again admitted to the
hospital, presenting evidences of thrombo-angiitis of the left foot. The second toe of the
left foot had been ulcerated for about three months, and gradually all the toes of that foot,
except the fourth, became involved in the same process.
Physical examination, February 24, 1907. Left foot: On the dorsal and plantar sur-
faces of the great toe there are ulcers. A similar condition is found at the tip of the second
toe and on the plantar and dorsal surfaces of the fifth toe. The skin about the ulcer is
sloughing and shows no tendency to heal.
The right foot is negative. The right hand shows an absence of the terminal phalanx
of the third finger. Both hands are cyanosed.
March 22. Amputation of the toe. Wound does not heal.
May 17. Re-amputation through the leg.
Physical examination, May 20, 1907. The left radial pulse is absent and the artery
appears to be converted into a hard cord. In the right radial artery a very faint pulse is
perceptible. The brachial artery seems to be much thickened, although the pulsation is
good. Ever since amputation of the left leg was done, the stump was painful, discolored,
bluish, presenting a wound that failed to heal. Finally, on January 2, 1909, the patient
consented to re-amputation. The author performed the Gritti-Stokes amputation, the
stump healing kindly.
January 3, 1909. ‘The tip of the little finger of the right hand presented a small spot
of gangrene about 1cm.in diameter. The distal phalanx of the third finger isabsent. The
nail of the fourth finger is deformed and thickened. In the dependent position the fingers
become cyanotic, with a slight increase in the normal red color. The left hand is normal
as regards color, but the nail of the middle finger as well as the tip are very much deformed.
The right radial artery is felt as a cord, and no pulse can be detected; the ulnar artery is
also pulseless; the brachial pulse is poor. The left radial artery is faint, the ulnar cannot
be felt, the brachial also is poor. In the elevated position the right hand becomes some-
what paler than the left, but neither becomes very much blanched.
Lower extremity: The stump is in good condition. The right foot shows evidences of
development of thrombo-angiitis, the dorsalis pedis and posterior tibial arteries being
absent, and there are other evidences of involvement of that leg.
THROM BO-ANGIITIS OBLITERANS—UPPER EXTREMITIES 303
December 30. The fifth finger of the right hand presents an ulcer at the tip, the result
of the separation of a gangrenous patch. He says that he has had pain in that finger for
about three months, and that gangrene set in about three weeks ago.
February, 1910. The trophic disturbances, involving the little finger of the right hand
seem to be progressive. The tip of the finger shows advancing gangrene, the rest of the
finger is swollen and red. In the dependent position the third and fourth fingers become
‘intensely red and slightly cyanotic. Left hand: Here there has been no progression of
the symptoms.
February 2, 1910. ‘The little finger of the right hand was amputated (Fig. 51).
Fic. 51.—Necrosis of the tip of the middle finger of the left hand; results of amputation
of the fingers of the right.
This is a good illustration of those cases of thrombo-angiitis obliterans
in which the symptoms first make their appearance in the upper extremities,
are initiated by pain, and followed by trophic disturbances and gangrene.
In this case the terminal phalanx of the middle finger and the whole of the
little finger of the right hand were lost. During the evolution of these
symptoms the disease attacked the left leg, where even greater progress
was made than in the upper extremities, amputation being the outcome.
Pathological examination of the vessels of the amputated left limb showed
the usual lesions of thrombo-angiitis obliterans.
VIII. Atrophy and Gangrene.—It is rare that gangrene of the fingers
and hand becomes so extensive as to warrant amputation of the forearm or
arm. In neglected cases with secondary infection, however, such may be
the issue. Interesting, indeed, is the occurrence of extensive gangrene of
one upper extremity and atrophy of the other as results of the vascular
obliterative process in the following case.
S. A., male, Russian, examined March 23, 1905, records a typical history of thrombo-
angiitis obliterans of the left lower extremity, finally leading to gangrene, for which the leg
was amputated August, 1903, and re-amputated September 5, 1903, at the knee.
304 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Eight weeks before admission there appeared symptoms referable to the same disease
of the right lower extremity, an ulcer appearing at the inner side of the right heel. On
March 21, 1905, the right leg was amputated for advancing gangrene of the right foot.
March 10, to10. I found evidence of the involvement of the left upper extremity.
He says that he has had trouble in his left arm and in the fingers and forearm for several
months, there having been pain in the fingers, followed by swelling and redness. Thena
bleb appeared at the tip of the index finger, which was incised by a physician. Shortly
after this the wound became much worse and sloughing took place. About the same time a
black spot appeared over the back of the middle finger. Neither middle nor index finger
has improved, and it is for these that he seeks relief.
After admission the gangrene rapidly spread, the pain becoming excruciating, and the
forearm was amputated through its upper fourth.
The ablated forearm (Fig. 52) showed complete occlusion of both radial and ulnar
arteries. The typical lesions of thrombo-angiitis obliterans were present.
Fic. 52.—Amputated arm (photographed after fixation) showing extensive gangrene
of index finger.
Four years later, April, 1914, the patient was again admitted in a condition of stupor.
The notes taken read as follows: “ Both legs and the left arm have been amputated. Speech
is incoherent and there are evidences either of some cerebral lesion or of an arterial lesion
in the brain. The condition of the right hand is of particular interest. Nowhere is there
any evidence of ulcer or gangrene. The skin of the right hand is dry and atrophic. The
jingers have a tapering appearance. The skin has lost its elasticity, the subcutaneous tissues
have withered, and neither the radial nor the ulnar arteries are palpable. ‘The brachial artery,
too, gives but the slightest impression of the presence of pulsation.” :
Here, then, is a case in which two distinct clinical pictures were evolved
in the course of the obliterative vascular disease, one exhibiting gangrene of
THROM BO-ANGIITIS OBLITERANS—UPPER EXTREMITIES 305
an upper and two lower extremities, and the other demonstrating the unusual
phenomenon of extreme atrophy of both hand and forearm.
IX. Cases Simulating Scleroderma and Sclerodactyly.— Perhaps most
interesting of all are those cases in which the vascular occlusion has led,
by virtue of the effects of malnutrition, to a condition of dystrophy, the clin-
ical picture being akin to that of sclerodactyly. In fact we have had occasion
to observe a most pronounced example of this manifestation in a patient in
whom the diagnosis of scleroderma was made by expert dermatologists.
I. L., aged thirty-five years, was admitted on October 1, 1906, with a typical history of
thrombo-angiitis obliterans of the left leg. There was absence of pulsation in the dorsalis
pedis and complete gangrene of the second toe, necessitating amputation of the leg. Patho-
logical examination of the vessels of the amputated leg showed the typical lesions of
thrombo-angiitis obliterans.
June 29, 1907. He was again admitted to the hospital, complaining of intense pain in
the right leg which showed the symptoms of ischemia on elevation, redness in the dependent
position, but no evidence of trophic disorder or gangrene. The patient begged that the
limb be taken off, and the right leg was, therefore, ablated through the middle third.
Pathological examinations showed here, too, the typical lesions of thrombo-angiitis
obliterans.
December 17, 1909. He entered the hospital complaining of trouble with his right hand
and arm. For several months he has been unable to use it properly, the muscles having
become stiffened. He thinks, too, that a marked diminution of the size of the hand and
arm has taken place.
On physical examination the picture presented by the right arm is striking. The fingers
have the typical appearance of the skin in scleroderma. Motion of the distal phalangeal
joints is markedly impaired in extent. The skin is atrophic and dry and the circumference
of the fingers of the right hand is distinctly diminished. Both the radial and brachial
pulses are absent. The brachial artery can be felt as a hard cord, and can be traced as far
as the axilla. In the axilla there is a distinct pulse.
The left hand shows no trophic disturbances, no ulcers, but the radial and ulnar pulses
are absent. The brachial pulse is fairly good.
X. Cases with Acute Arteritis of Portions of the Radial or Ulnar Artery
(Migrating Arteritis)—Just as a single or limited number of tributaries
of the veins of the forearm may be the seat of an acute thrombo-phlebitis,
and antedate the signs of the deep seated process by months or years, so also
restricted portions of the radial or ulnar artery may be come suddenly acutely
inflamed, adherent and thrombosed. An interesting example where that
portion of the course of the radial artery immediately above the wrist was
involved, is the following.
H. S., Russian, male, 38 years old, complained of burning pain in the thumb, index and
middle fingers of the right hand, also of swelling and reddening over the course of the radial
artery for the past 4 months. There were no symptoms in any of the other extremities.
Upon physical examination the right radial artery could be felt as a thickened cord,
and occluded up to a point 234 inches above the wrist. There was no ischemia, and the
radial pulse was absent.
The specimen of the right radial artery after resection showed the following.
Pathological examination: There was intensive periarteritis and marked thickening of
the vascular sheath and overlying fascia. When the latter was opened over the groove
director, the radial artery was firmly adherent and could only be liberated with difficulty.
About 34% inches were removed. The lower end did not bleed on section, and showed the
typical lesions of rather advanced thrombo-angiitis obliterans in the brownish stage. The
upper end of the clot was darkish red, lying in a contracted but patent vessel 144 inches above
the wrist. ‘There must have been another thrombotic lesion higher up, since bleeding did
not occur. It is, therefore, permissible to call the process a migrating one. The absence of
pulsation in the patent portion was doubtlessly due to a similar occlusive process centrally
situated.
Microscopic examination confirmed the diagnosis.
Another instance of thrombo-arteritis involving the radial and ulnar
arteries of the right forearm, and a portion of the left radial artery, is illumin-
20
306 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
ating in demonstrating the close relationship between the advent of
circulatory disturbances and tenderness along the course of the right radial
artery.
T. G. H., American Gentile, 45 years of age, states that 8 years ago he had had symp-
toms of intermittent claudication of the right leg, followed by similar symptoms of the left.
The history suggests that there had been migrating phlebitis of the lower extremities.
Ulceration of the right big toe 5 years ago; subsequently similar symptoms in the left foot,
and gangrene of both; 2 years ago amputation of both legs at the upper fourth. Three and
one-half months ago there developed numbness of the tips of the fingers of the right hand,
with tenderness and vague pain along the course of the right radial artery from the wrist
to the upper fourth of the forearm, with disappearance of the right radial pulse 1 month
after the onset of the symptoms. The right ulnar artery disappeared almost simultan-
eously with the right radial.
Physical examination, January 22, 1923: The fingers of the right hand are colder than
those of the left; the radial and ulnar pulses absent; moderate ischemia on elevation,
marked reactionary rubor; tenderness along the lower half of the right radial artery. The
left radial artery is absent at the wrist, the ulnar pulsates; vasomotor instability of the right
hand.
GOARTERSIOXS
THROMBO-ANGIITIS OBLITERANS—ASSOCIATED
ARTERIOSCLEROSIS
The clinical picture of thrombo-angiitis obliterans becomes confused
when it is complicated with arteriosclerosis. In most of the cases the patient
must have had either the insidious or silent form of thrombo-angiitis obliterans
which developed gradually with only an indefinite history of intermittent
claudication. ‘These are followed by spontaneous cure so far as evidences of
impaired circulation are concerned. Later, between the ages of 50 and 65
or even older, either because of the gradual occlusion of the collateral vessels
by the atherosclerotic process, or by virtue of a recent thrombosis com-
plicating the arterioslcerosis in the popliteal artery or higher, the symp-
toms of insufficient circulation return, often very rapidly, and gangrene may
result. In such patients we are apt to find not only pulseless vessels on the
affected side, but also in the limb which shows no symptoms.
Or, more rarely do we find thrombo-angiitis obliterans developing rather
late as far as can be determined by the anamnesis; then a period of temporary
recovery, followed later on by recurrence of the symptoms in arteries markedly
sclerosed or calcified.
The pathological investigation of the arteries in such cases has demon-
strated two lesions side by side, that of the arteriosclerosis with its degenera-
tive sequelae, and that of thrombo-angiitis obliterans (Fig. 124).
Occasionally we encounter the precocious development of arteriosclerotic
patches in arteries that are the seat of thrombo-angiitis. We need not
wonder at this circumstance, since it is not uncommon to find marked
atherosclerosis in relatively young individuals in whom thrombo-angiitis is
never a complication. Nevertheless it must be admitted that a predis-
position to vascular disease (vascular mediocrity or inferiority) as it mani-
fests itself in certain cases, seems to express itself both in a susceptibility
to thrombotic lesions as well as to degenerative ones. Certain it is that
the autopsy findings in cases of thrombo-angiitis show that the more centrally
THROM BO-ANGIITIS OBLITERANS—PATHOLOGY 307
situated arteries do develop a tendency to atherosclerotic lesions even though
the arteries of the extremities show but little sclerosis.
For diagnostic and pathological data the reader is referred to the chapters
on Arteriosclerosis, Pathology, and Diagnosis of Thrombo-angiitis Obliterans.
Clinically these cases fall into the following groups:
1. Cases with undiscovered thrombo-angiitis that had been present during
the early years of maturity (from the ages of 20 to 40), but in which vague
aches in the limbs, difficulty in walking, and similar symptoms, were insuffi-
cient to lead to a diagnosis. In these patients the disease remained in an
arrested or non-progressive state.
2. Cases in which such a latent period as above described is followed by
a moderate degree of arteriosclerotic change in the arteries of the extremities
as the individual grows older.
3. Cases in which the latent thrombo-angiitis is followed by intensive
arteriosclerosis.
4. Cases in which either relapsing thrombo-angiitis or bland thrombosis
in arteriosclerotic vessels leads to gangrene in elderly individuals.
CHAPTER LXI
THROMBO-ANGIITIS OBLITERANS—PATHOLOGY
Thrombo-angiitis obliterans has been previously described by the Germans
under the name ‘“‘Spontan-Gangran” and “Endarteritis Obliterans.”” In
1879, von Winiwarter published the results of the pathological findings in
one case, and reported on obliteration of practically all of the arteries of the
leg by reason of a chronic proliferative process due, in his opinion, to a new
growth of tissue from the intima. He, therefore, proposed a new name for this
condition, namely, ‘“‘ Endarteritis Obliterans.”
This theory has been accepted by most authors, and even to-day, itis to
be found in many text books. Somewhat later, Wilonski pronounced the
opinion that the essential change in the vessel walls was due to a multipli-
cation of the elastic fibers, and proposed the name “‘ Arteritis Elastica”’ for
the condition. Perhaps the most important contributions are those of Weiss
and Zoege von Manteuffel, because these authors placed an entirely new inter-
pretation upon the pathological findings. Basing his paper upon the studies
of his assistant, Weiss, von Manteuffel suggests that the extensive occlusion
of the vessels in this disease is dependent upon a primary arteriosclerosis;
that the obliterative process commences in the popliteal artery, where it owes
its inception to the formation of a parietal white thrombus; and that by
virtue of a gradual extension of the parietal thrombus downward, followed by
organization, a picture resembling an obliterative endarteritis is produced.
In his cases the veins did not seem to be involvedin the process. Von
Manteuffel comes to the conclusion that the thrombosis is due to desquama-
tion of endothelial cells, and that this occurs where the intima shows most
advanced lesions of arteriosclerosis, namely, somewhere in the popliteal artery.
In 1908 the author pointed out that the name, endarteritis obliterans, as
applied to the clinical picture just described, should be discarded, since the
occlusive lesion is a thrombotic one, affecting arteries as well as veins of the
(
308 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
extremities, and that it is independent of athero- or arteriosclerosis. He
proposed the name, thrombo-angiitis obliterans, which has now found almost
universal adoption in English speaking countries.
Investigations! which included a thorough pathological and histological
study of the vessels in 45 amputated lower extremities, 1 upper extremity,
and 25 pieces of superficial veins resected and exsected from the lower and
upper extremitites during attacks of so-called migrating phlebitis, have demon-
strated that when the patient comes to the physician for observation, the
larger arteries and often the larger veins, are completely obliterated.
LEV Dz.
RJZEISTE DN.
RUBENSTEIN.
LEVDIZ.
Fic. 53.—Schematic drawing showing the extent of occlusion in the arteries of the lower
extremities in thrombo-angiitis obliterans. The cross lines represent the points at which
amputation was done, I indicating the first amputation; II, reamputation. The anterior
vessels are shown above; the posterior, below. The dotted lines indicate that the vessels
were not examined. The four sets will be referred to in the text as 53 a, b, c, d, from left
touwrignt.
In the Figs. 53, 54, 55, 56, 57, 58 and 59 a schematic representation of the
extent of occlusion in the larger vessels of 29 amputated lower extremities is
1 Buerger, Am. Jour. Med. Sc., Oct., 1908. Proc. New York Path. Soc., Feb. and
March, 1908. Int. Clin., III, roth series, 1909. Jour. Med. Res., Nov., 1914, X XI, No. 2.
Amy; Jour..Med.Sc:; Feb., 1015, p. 210.
THROM BO-ANGIITIS OBLITERANS—PATHOLOGY 309
shown. Examinations were conducted below the horizontal lines indicated
in the drawings, and if a second amputation was performed, again in the region
between two horizontal lines.
A very extensive obliterative process was found inFig. 53a where all of the
larger vessels from the beginning of the popliteal downward, were completely
SUCHOPP.
Licutinsrrr,
EEG
rosEsirs. “GOOIT)
UTT.RAN
Fic. 54.—Schematic representation of extent of occlusion in thrombo-angiitis obliterans;
referred to as a, b, c, d, e from left to right in the text.
obliterated. In Fig. 53b upper part of the anterior tibial artery was open
as depicted, although the posterior tibial and plantars were obturated. The
sharp lower end of a thrombus is seen in the upper peroneal artery in Fig.
53¢, this being the only one of the larger arteries to remain intact.
~ Popliteal thrombosis with patent peroneal and upper posterior tibial
arteries, is exemplified in Figs. 54a and 5s5c. In Fig. 54b and c the upper
extent of the process was detected in each case. More complete involve-
ment of the posterior tibial and popliteal arteries was presented by other
cases Figs. 54e, 55a and 5oc—d.
The thrombotic lesion in the popliteal may extend down into the anterior
tibial, ending abruptly a short distance below the aperture in the interosseous
membrane (Figs. 56a and 57a), leaving certain portions of the anterior tibial
open.
310 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Sometimes the posterior vessels except for the plantars are unaffected
(Fig. 57c) and then again we meet those in which the anterior vessels are
almost free, except for their most distal branches. Completely patent
anterior tibial arteries are shown in Figs. 58a and 0; partly open in 58c and d.
Where the vessels are dotted, their course was not thoroughly examined.
As a rule, the plantar vessels, dorsalis pedis and many of its branches,
anterior tibial, posterior tibial, peroneal, and sometimes the popliteal are
already completely closed, although any one or more of these vessels may
eee
x
7
tae Try
Pe
——
Ww
POLLATSCHEK.
PINXEL.
MORRISON
Fic. 55.—Schematic representation of extent of occlusion in thrombo-angiitis obliterans,
(a, b, c, d from left to right).
escape. One or both the venae comites may partake of the same lesion.
The obturating tissue is, for the most part representative of, or indicative of a
healed lesion, or the end-stage of a process, whose incipiency is marked by
an acute inflammation of the vessel wall, with consecutive, red, occlusive
thrombosis of the affected vessel. It is only in rare instances that the early
stages of the vascular lesion are found in the deep vessels, but in superficial
veins, when they are affected with the lesion migrating or thrombo-phlebitis,
the early or acute stage of the disease can be studied.
THROM BO-ANGIITIS OBLITERANS—PATHOLOGY oll
The author has observed what he terms the acute lesions of the disease in
territories other than the vessels of the extremities, namely, im the spermatic
artery, in the veins of the spermatic cord; and old lesions in one of the branches
of the gastric artery in a case of ulcer of the stomach.
Gross Pathology.—The deep vessels of the amputated legs regularly show
an extensive obliteration of the larger arteries and veins. Besides this, there
are two other lesions which vary greatly in their intensity, namely, the peri-
CoHiat. ROTLAR
Fic. 56.—Schematic representation of extent of occlusion in thrombo-angiitis obliterans,
(a, b, c, d from left to right).
arteritis and the arteriosclerosis. The appearance of the vessels on gross
section depends upon the age of the occluding process. Usually the vessel
is seen to be filled with a grayish or yellowish mass that can be distinctly
differentiated from the annular wall of the vessel, and that appears to be
pierced at one or a number of points by an extremely fine opening, through
which a minute drop of blood can be squeezed. Such obturating tissue is
firm in consistency, and does not at all resemble the crescentic or semilunar
occluding masses typical of arteriosclerosis. The vessel itself is usually con-
312 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
tracted, so that its wall appears somewhat thickened. This picture is char-
acteristic of arteries or veins which are the seat of a very old obliterative
process, and is to be found most frequently in the peripheral portions of; the
vessels, although at times this type of lesion may extend throughout the whole
length of the vessel, from the dorsalis hallucis into the popliteal artery.
apes ee
SE
=a
are,
,
vee ge oh
WOSCHOWITZ. ‘
Vee
{
\
\
\
\
1 /
eon
I
MOSCHOWITZ,
ANGILOVITZ.
Fic. 57.—-Schematic representation of extent of occlusion in thrombo-angiitis obliterans,
(a, b, c from left to right).
As we trace certain of the obliterated arteries or veins upward, we are apt
Frequently
to meet with a change in the character of the obturating tissue.
it becomes softer, more brownish in color, and terminates abruptly in
the lumen of an apparently normal vessel; at other times the brownish tissue
gives way to soft reddish masses which are evidently the results of recent
In some cases this thrombotic process occupies large portions
thrombosis.
of the vessel’s course; in others, it is of short extent and terminates in a long
cone of recent thrombus.
THROMBO-ANGIITIS OBLITERANS—PATHOLOGY ole
The veins share equally with the arteries in the lesion of occlusion. In
some cases the veins are more extensively involved than the arteries, and this
is particularly true of the collaterals of the posterior tibial, which are often
closed when the anterior tibial veins are open. As for the arteries, we usually
find an obliteration of a part or the whole of the anterior tibial, of the dorsalis
pedis, and dorsalis hallucis, an occlusion of the posterior tibial and plantar
SHHNSAL.
ARYA! SHOEN EX.
SHEISAL.
Fic. 58.—Schematic representation of extent of occlusion in thrombo-angiitis obliterans,
(a, 6, c, d from left to right).
vessels, with or without involvement of the peroneal. Sometimes the
anterior tibial is practically normal in its upper half or upper two thirds.
More rarely a large portion of the dorsalis pedis is open, with the beginning of
the occlusion in the upper part of this vessel or in the lower part of the
anterior tibial.
Besides the lesion of occlusion there are two other striking changes,
namely, a certain amount of arteriosclerotic thickening and periarteritis.
Arteriosclerosis is absent in the younger cases; when present, it is never pro-
nounced, except in those rare instances in which the patient has suffered from
the disease for many years, and has reached the age of 4o or more. Asarule,
314 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
we note but a very slight degree of whitening or thickening of the intima, here
and there, in the patent portions of the vessels. In a very few cases small
atheromatous patches are present.
A much more interesting and more important change is the fibrotic thick-
ening of tissues immediately about the vessels. Wherever the vessels are
occluded, there is apt to be an agglutinative process which binds together the
artery and its collateral veins, and sometimes also the accompanying nerve,
PERLN AV
Fic. 59.—Schematic representation of extent of occlusion in thrombo-angiitis obliterans,
(a, b, c, d from left to right).
so that liberation of the individual vessels by dissection is difficult. The
adhesive condition is due to fibrous tissue growth, and varies considerably in
its amount. ‘The periarterial fibrosis varies, sometimes being almost absent,
at other times so great, that isolation of the vessels or nerves becomes impossi-
ble, and the vascular structures make up one dense rigid cord.
Histo-pathology.—The lesions may be considered in two stages, first, the
healed or organized stage, and second, the acute or incipient stage of throm-
bosis. Between the earliest alterations in the deep arteries and veins, and
THROMBO-ANGIITIS OBLITERANS—PATHOLOGY ole
Fic. 60.—‘‘Old”’ occlusion of the fenestrated or cribriform type; large canalizing vessels in
fairly dense connective tissue filling the lumen of an artery.
Fic. 61.—Elastic tissue formation about the canalizing vessel; a picture that can be
mistaken for endarteritis obliterans.
316 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
superficial veins, and the finished product, there are a large number of
intermediate pictures that illustrate the metamorphosis of the obturating
clot into the intravascular cicatrix.
1. Healed or Organized Stage —The most common lesion is a total oblitera-
tion of the lumina of arteries and veins by connective tissue (Fig. 60). His-
tologically this may be extremely varied in the general appearance, but each
picture can be interpreted correctly as having its origin in the lesion of occlu-
Fic. 62.—Absence of elastic tissue in thrombo-angiitis obliterans (orcein stain). The
umen is filled with old organized clot; no elastic tissue production; below, elastic tissue is in
arteriosclerotic plaque.
sive thrombosis. This obturating connective tissue usually harbord
numerous small vessels, pigment containing hemosiderin, and a fair amounn
of connective tissue cells. The canalizing vessels, when they become dilateel
form smaller or larger sinuses, giving the fenestrated or cribriform lesion
seen on microscopic section of the vessels, or when the canalizing vessel
becomes eccentrically placed, and sufficiently large, this sinus is responsible
for the appearances which have been incorrectly interpreted as the product
of an endarteritis obliterans (Fig. 61). |
Elastic tissue stains demonstrate characteristic differences between this
process and arteriosclerosis. Thus, the region of the organized clot is almost
completely free from elastic tissue (Fig. 62). The small amount which is
present, is concentrically disposed about the new-formed vessels (Fig. 115).
The abundant elastic tissue formation in the arteriosclerotic plaques is well
seen in Fig. 63.
THROM BO-ANGIITIS OBLITERANS—PATHOLOGY ol7
Still more suggestive and instructive is the finding of various stages of the
disease in different members of the same vessel sheath. Thus, in Fig. 64 a
large artery affords a view of the old lesion, as well as one of its venae comites.
Another accompanying vein, however, is in the “‘acute”’ stage of the disease,
a smaller venule or satellite being in the intermediary stage, where certain
“miliary giant cell foci” make their appearance. Such pictures not only
reveal the thrombotic nature of the disease, but also present an argument in
favor of the following two assumptions: that the disease begins with an inflam-
Fic. 63.—Obliterating arteriosclerotic process (orcein). The greater part of the lumen
is occluded by tissue arising from the intima, and containing the typical elastic tissue found
in arteriosclerosis; the small triangular clear area in the left part of the lumen contains a
recent thrombus.
matory lesion attended with occlusive thrombosis, and that it affects the arteries
and veins in a sort of relapsing fashion, very much in the same manner as in the
veins in migrating phlebitis.
The termination of the occluding tissue in arteries and veins is often seen
in the form of a rounded, convex projection looking upward (cephalad), and
lying in practically healthy vessel wall (Fig. 65). At other times, the
old occluding tissue is capped by an additional clot which rises in pyramidal
fashion ending by a long tapering extremity.
2. The Acute or Specific Lesion—The early lesions are so characteristic
histologically that their appearances are practically specific for thrombo-
angiitis obliterans and may permit the pathologist to make a diagnosis of
the disease. They are rarely to be seen in the deep vessels, for the reason
that patients do not allow amputation until the disease has lasted for months
or years. However, they can be well studied when these are the seat of the
318 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
typical migrating phlebitis, and have been shown by the author to be
identical with the acute lesions in the deep vessels.
The earliest changes appear to be the usual evidences of an acute inflamma-
tory process involving all the coats of the vessel. The media, adventitia
and perivascular tissues are infiltrated with polynuclear leukocytes and the
Fic. 64.—Various stages of occlusion in thrombo-angiitis obliterans; above, a vein;
just below it, artery in healed fibrotic stage of occlusion; below, two veins; the larger
recently occluded (acute stage) and the smaller satellite in the intermediate thrombotic
stage with giant cells.
lumen of the vessel is completely filled with red clot. In the peripheral
portions of the clot, larger or smaller foci of leukocytes (purulent foci) begin
to form, whose growth occurs by virtue of immigration of leukocytes (Fig. 66).
Certain peculiar giant cell foci develop (Fig. 67), which are characteristic.
They contain giant cells, endothelioid or angioblasts and numerous broken-
down leukocytes. These foci then undergo connective tissue replacement.
The giant cells gradually disappear, numerous small vessels are formed, the
THROM BO-.ANGIITIS OBLITERANS—PATHOLOGY 319
Fic. 65.—Thrombi in apparently healthy vessels. Upper figure: Conical type of clot,
there being an accretion or stagnation red clot, over the old obturating organized clot.
Lower figure: Rounded extremity of the older type of clot ending in apparently healthy
vessels.
Fic. 66.—Acute lesion in internal saphenous vein; on the right, purulent focus; on the left
remaining crescentic portion of lumen filled with organizing clot. (Giemsa stain,)
320 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
final product being a fibrous nodule containing vessels andsome pigment. In
the rest of the occluding clot, the organizing process is somewhat different,
resembling that which characterizes the organization of blood clot in other
thromboses.
‘
Fic. 67.—High power appearance of characteristic ‘‘miliary giant cell’’ focus in thrombo-
angiitis obliterans.
In short, the lesions in thrombo-angiitis obliterans are in chronological
order, an acute inflammatory lesion with occlusive thrombosis, the forma-
tion of miliary giant cell foci, the stage of organization or healing, with the
disappearance of the miliary giant cell foci, the organization and canaliza-
tion of the clot, the disappearance of the inflammatory products, and the
development of fibrotic tissue in the adventitia that binds together the
artery, vein and nerves.
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 321
CHAPTER LXIT
THROMBO-ANGIITIS OBLITERANS—MORE DETAILED HISTO-
PATHOLOGY
For the student of pathology, a more comprehensive account than is
needful for the clinician may be of value. More detailed knowledge carries
with it the foundation for a correct interpretation of other occlusive arterial
lesions. We have only dwelt upon the essential alterations in the previous
chapter. Here, we shall discuss at greater length, (1) the acute lesions in the
superficial veins; (2) the acute lesions in the deep vessels; (3) the intermediary
stages of organization, and (4) cicatrical, ‘‘healed,” or completely organized
stage.
The Acute Stage of the Disease.—In superficial veins it has already been
pointed out that the superficial, that is, the cutaneous and subcutaneous
Fic. 68.—Infiltration of the media (below) in a vein and migration of leukocytes into the
purulent focus (above).
veins, offered the best material for the study of the earliest or acute lesions
of thrombo-angiitis. The site of predilection for this thrombophlebitis
seems to be somewhere in the lower half of the territory of the internal
saphenous vein, although the external saphenous, saphenous of the thigh,
median basilic, median cephalic veins of the forearm and foot may also be
21
322 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
attacked. Clinically two types of affection manifest themselves, either as
indurated strands or cords one-half to two, three, or four inches in length or
as small nodosities. Both of these are the expression of an acute thrombo-
phlebitis, with marked perivascular inflammatory infiltration; in the first
case, in and about larger veins, in the second, involving minute venules or
cutaneous tributaries.
Fic. 69.—Normal organization of red clot on the right, the periphery of a purulent focus
on the left. In the former new capillary growth, in the latter compressed concentric layers
of angioblasts (endothelioid), and giant cell formation.
Even in the cases of migrating phlebitis it is not an easy matter to procure
material in the proper stage of the disease. It is seldom that the patient
will consult us at the very onset of the phlebitis, and it is even rarer to be
able to acquire the veins by extirpation at this time. And that is why
many of our biopsies were disappointing, yielding lesions already in the
stage of healing and connective tissue organization. On the other hand, these
difficulties were of advantage in that we were enabled to obtain veins showing
many stages of the process and could then synthetize the individual findings
into a composite picture of the evolution of the disease.
The general impression obtained from a cursory examination of many
sections of the affected veins is that we are dealing with an acute inflammation
of the vessel wall, invasion of the media with polynuclear leucocytes, marked
reaction on the part of the adventitia, and perivascular connective tissue,
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 323
and an obturating thrombosis, which practically always leads to complete
closure of the lumen. In the clot which is for the most part red, but also
contains platelet areas and fibrin, there appear either the typical “miliary.
giant cell” areas, or the precursors of these, collections of polynuclear leuco-
cytes arranged in veritable miliary abscesses.
For an elucidation of the nature of the pathological process and of its
metamorphosis into the stages just preceding the healed connective tissue
product, it may be best to refer to photomicrographs selected from many
hundreds of sections. In these we will attempt to show that an inflammatory
Fic. 70.—Greater magnification of Fig. 72; at 2 o’clock the miliary focus; the giant cells
at’‘o.-and 10.0 clock:
phlebitis and periphlebitis (or arteritis and periarteritis) are the initial lesions,
synchronous with the phenomenon of complete vascular occlusion by clot;
that in the proper evolution of this disease, healing is the rule, in so far as the
products of the inflammatory stage disappear, and give way to fibrous tissue;
that in the course of this healing, certain characteristic pictures are evolved—
such as the miliary giant cell foci—whose raison @ étre can easily be explained;
and, finally, that the peculiar architecture of the anatomical framework, its
specificity for thrombo-angiitis, and its purulent foci, all favor the assumption
that some specific agent, parasitic or bacterial, is responsible for the disease.
Of all the pictures, that depicted in Fig. 66 and taken from a portion of the
saphenous vein is the most instructive, for it bears testimony to the presence
324 ~ CIRCULATORY AFFECTIONS OF THE EXTREMITIES
of an inflammatory lesion. Here we see a vessel filled with clot, a portion of it
undergoing organization in the normal fashion, the rest occupied by a focus
of polynuclear leucocytes. Were it not for the rapid changes in the clot,
such findings would doubtless have been more frequent amongst the many
vessels examined. But it takes only a very short time for the process of
organization to completely metamorphose these purulent areas, and develop
the more usual pictures containing miliary giant cell foci.
Fic. 71.—Acute stage in superficial vein; at 5 o’clock miliary abscess; rest of lumen filled
with red clot, in process of ‘‘bland’’ or normal type of organization.
Such aggregations of cells are not due to fortuitous grouping of the white
blood corpuscles, for they not only contain more leukocytes than could
have issued from the intravascular blood stream, but can be seen to owe their
existence to immigration of cells by way of the media (Fig. 68). Elsewhere,
the lumen may be ocupied by red clot, in which the typical normal process of
organization is going on pari passu with certain atypical changes in the pus
focus (Fig. 69), alterations that lead to the production of the specific pictures
previously described.
In the media as well as in the adventitia the evidences of inflammation are
manifested by intense infiltration with leukocytes (Figs. 68, 70 and 71), which
seems to be more marked in the superficial (subcutaneous and cutaneous
veins), than in the deep vessels. Then the fixed cells multiply. Later the
cellular elements diminish in number, and even disappear, being replaced in
the media by new vessels, in the adventitia by new formed fibrous tissue.
THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHLOGY B20
Fic. 72.—Acute lesion in vein; on the right, the vein is seen in cross section; on the left,
a tributary is cut longitudinally and shows an older process.
Fic. 73.—High! power of Fig. 70; the margin of the inflammatory focus is seen on the
right; the bland type of organization on the left with the giant cells at the margin.
326 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
In Fig. 72 there is a beautiful example of a vein with the acute lesions.
Section has been so made that the vessel (on the right) is cut transversely,
and on the left either strikes the same longitudinally as it makes a sharp bend,
or possibly goes through a large tributary. The purulent focus is well depicted
(at 2 o’clock) on the right, with the giant cells clearly defined. Where the
section passes in a more longitudinal direction and partly tangentially
through the media, it reveals much older obturating tissue in a solid organized
form, the inflammatory process in the wall of the vein having disappeared.
Fic. 74.—High power of a portion of Fig. 71; acute stage illustrating giant cell develop-
ment, and aberrant ingrowth of angioblasts.
The same vessel seen at another level and reproduced in Fig. 70 will
clearly illustrate some of the finer details of these distinctive inflammatory
responses. ‘To the left where the clot is in part of bland variety (red portion)
organizing capillaries can be seen. ‘The intense cellular infiltration of all of
the coats of the vein and especially the inner layers of the media is made
apparent. ‘The margin of a miliary purulent focus, the giant cells and the
adjacent area of “‘bland’’! organization are brought better to view in the high
power photograph reproduced in Fig. 73.
Returning to a consideration of the occluding tissue, the two different
portions merit separate discussion. In the red portion of the clot we see an
1 Refers to normal and_non-specific type of organization.
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 327
Fic. 76.—High power of Fig. 75; purulent focus with large giant cells; breaking down of
leukocytes illustrated.
328 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
orderly penetration of capillary sprouts, the angioblasts forming new capil-
laries (Fig. 69), just as occurs elsewhere in the organization of thrombi, in
thrombosis of arteriosclerotic vessels, in the accretion clots capping the
“specific” clots of thrombo-angiitis, or in any clot in which suppuration is
absent. ‘These areas of organization may occupy a crescentic portion of the
lumen (Fig. 71) when there is a single purulent focus, or may constitute
various parts of the clot if several miliary abscesses are present.
If we carefully study the transition of these typically organized zones
into the purulent foci, we shall learn why and how the giant cells are formed,
and will be able to explain the development of the later stages of the pus foci
Fic. 77.—Giant cell formation in thrombus filling posterior tibial artery, angioblasts
directly traceable into these cells.
—the miliary giant cell foci. As the angioblasts approach a purulent focus,
the cells arrange themselves in compressed, concentrically disposed layers
(Fig. 74), penetrate the pus foci in a wayward fashion, or form giant cells,
never showing a tendency to orderly invasion, nor any ability to form vas-
cular sprouts (Figs. 71 and 74). The giant cells must be regarded as abortive
attempts on the part of the angioblasts to produce new vessels.
A scrutiny of Fig. 74 will demonstrate how the angioblasts became impo-
tent, as it were, at the periphery of purulent focus, some cells becoming merely
distorted and unable to enter the leukocytic area at all, others passing in for
a short distance, or proliferating 77 loco into a giant cell.
ea oY
a
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 329
Figures 75 and 76 illustrate the same phenomena, the giant cell formation
at the periphery of the infectious focus; and in the high power picture (Fig.
73) there is clearly indicated the contrast between normal purposeful vessel
formation in the red clot and the bizarre formation at the edge of and in the
purulent focus. In Fig. 77, taken from a posterior tibial artery, the abortive
growth of angioblasts is also illustrated.
Fic. 78.—Acute lesion taken from the clot of a vein; the greater portion of the area is
occupied by polynuclear leukocytes; about the periphery of the purulent focus there are
numerous giant cells.
Even more striking than in the last sections is the demonstration of these
facts in Figs. 71 and 74, where a vein in the “‘acute” stage also contains a
normally organized crescentic zone and one large miliary abscess. The
angioblasts can here also be discerned passing into and forming giant cells
and wandering in irregular, erring fashion amongst the leukocytes.
The muscle fibers are usually widely separated by the invading cellular
elements, which are for the most part polynuclear and endothelial leukocytes.
But where the process has existed for a long time, a large number of new
formed capillaries still further increase the tissues that separate the muscle
fibers. These vessels can be traced into the adventitia, which is also consider-
ably increased in thickness, and the fatty tissue in the immediate neighbor-
hood, as in the older specimens, has become more dense and replaced by
connective tissue. Even the adjacent nerve fibers show thickening of their
perineural connective tissue and are surrounded by mononuclear leukocytes
in collections of varying size.
300 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
To pass in review all the kaleidoscopic appearances that mark the transi-
tion of these characteristic foci into the final, healed connective tissue product
would be a work of supererogation, for the selected photomicrographs now to
be shown will suffice to make our argument clear. Unable, then, to organize
the pus foci, the angioblasts proliferate at the periphery of these. As the
leukocytes disintegrate (Figs. 76, 78, 79 and 80) and the toxic products are
absorbed, the atypical distorted angioblasts—now looking like typical
‘“endothelioid” cells— together with the giant cells, gradually replace the
she
Fic. 79.—Acute lesions; miliary focus in which the process of organization is quite
advanced, the clear space showing the residual, broken-down polynuclear leukocytes.
Below there are a number of giant cells, and surrounding the clear space numerous endothe-
lioid or angioblast cells.
leukocytes from the periphery toward the center, a picture resulting that
closely resembles miliary tubercles (Figs. 80 and 81). In the center of such
areas are broken down leukocytes and pyknotic nuclei. No organisms have
been demonstrable. Still later even the disintegrated nuclei (Fig. 80) dis-
appear, the giant cells atrophy somewhat and a nodule is produced completely
made up of the altered angioblasts (endothelioid) and giant cells (Fig. 82).
Although the giant cells may persist for a long time, this tissue is finally
converted into the fibrillar variety, into which new vessels do penetrate
(Fig. 83). The rapidity with which this conversion may take place is readily
understood when those specimens are studied in which, side by side, in
contiguous tributaries, the older and early process can be followed.
THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY sal
Fic. 80.—Old giant cell focus going on to healing; very few leukocytes remain.
CIRCULATORY AFFECTIONS OF THE EXTREMITIES
332
Fic. 81.—Miliary giant cell focus resembling tuberculosis in obturating clot found in
vein of the forearm.
valves of the vein; above and on the
’
Below and on the right side
left, organization well advanced, tuberculoid focus retaining its characteristic appearance,
THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY Sou
Fic. 82.—Later stage in ‘‘acute lesion,’ simulating miliary tubercle; endothelioid cells
and giant cells surrounding focus of disintegrating leukocytes.
Fic. 83.—Vascularization (in the middle), proliferation of angioblasts and connective tissue
around the purulent focus (above); older tissue below.
334 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
The Specific Lesion in the Deep Vessels.—If we turn to a consideration of
the vessels in which the earliest lesions were best represented, we will be
apprised of the interesting circumstance that the morphological alterations
are such as apparently occur. only in this disease. Certain foci containing
giant cells, endothelioid cells, leukocytes and disintegrated nuclei are found
lying usually in the periphery of a red or mixed clot. These areas strikingly
resemble tubercles, and, in our experience, have been regularly diagnosticated
as such by the uninitiated.
Fic. 84.—Acute lesion in a large artery. The middle coat is infiltrated with leukocytes,
the clot showing miliary foci.
The Acute Lesion in the Deep Vessels.—It was possible to study these in
the arteries and veins of three amputated lower extremities, where extensive,
acute, inflammatory alterations were present in the popliteal, posterior
tibial, and peroneal arteries and veins.
In one of the posterior tibial vessels of large caliber depicted in Fig. 84
the distribution of at least two purulent miliary foci in the obturating clot,
and the diffuse inflammatory infiltration of the walls of the vessel are clearly
represented. Under greater magnification the intensity of the cellular
invasion and proliferation between the muscle fibers of the vessel wall can
be well seen in Fig. 85, where the giant cells can also be discerned in the
obturating thrombus.
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 330
Fic. 85.—Acute lesion in posterior tibial artery. On the left a portion of the media,
and on the right a portion of the inammatory clot areshown. Fibers of the media on the
left are separated by inflammatory cells (leukocytes). On the right there are miliary
inflammatory foci with giant cells in the clot.
Fic. 86.—Acute lesion in deep artery.
336 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fic. 87.—Acute lesion; a portion of a clot in an artery showing the acute lesion of
thrombo-angiitis obliterans, At I or 2 o’clock the dark area is made up of fibrin; above and
to the left,giant cells.
Fic. 88.—Early stage ina deep vein. The media is infiltrated with leukocytes, the lumen
is filled with clot, in the periphery of which there are miliary giant cell foci.
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY ool
In a still larger posterior tibial vessel there is less dispersion of the muscle
fibers of the media, but the clot itself shows an exquisite illustration of the
grouping of the miliary foci along its periphery (Fig. 86).
The formation of the giant cells can be studied in the deep vessels as well
as in the superficial veins. An illuminating picture is one found ina posterior
tibial artery, where the purulent focus almost came in contact with the inner
wall of the vessel. In Fig. 77 the angioblasts can be seen migrating into the
focus, and pass imperceptibly over into a syncytial body whose termina-
tion is a giant cell. Some of the later stages of organization in, and in the
neighborhood of the miliary abscesses where the giant cells are taking on
their older forms are illustrated in Fig. 87.
The disposition of a number of miliary foci in a deep vein is shown in Fig.
88, and the crowding together of the specific elements and reactive response
into one section of the clot are exemplified in Fig. 80.
Fic. 89.—Peculiar disposition of giant cells in clot.
The Intermediate Stage of Healing.—Only a very few examples of the
types of tissue evolved in the organization of the clot can be offered as examples
here. Characteristic in the earlier stages are the multiplicity of cells, the
large amount of pigment, the diffuse distribution of the small capillaries
interspersed with blood pigment. Later there develops a relative preponder-
ance of young connective tissue with consecutive dilatation of some of the
canalizing capillaries, and the development of elastic tissue around the new-
formed vessels part passu with increasing age. Depending partly upon the
shape and character of the clot, the fortuitous grouping of the canalizing
vessels, the eccentric disposition of some clots, the retraction of these from
the vessel walls, larger or small sinuses may be developed. ‘These give the
obturating tissue a fenestrated appearance, or make it semilunar on cross-
section. ‘The latter pictures can be confused with endarteritis obliterans,
when organization is complete.
22
338 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
In Fig. 90 the rich cellular substitution of the clot, the interspersed capil-
laries, and the dark areas of blood pigment are the active response which has
for its purpose the obliteration of the clot with connective tissue. The
character of the cells is also shown in Fig. 91, where only a part of the organ-
izing tissue has been reproduced.
Some of the later pictures with the enlarging blood vessels, the disappear-
ance of many of the cells and the increase of young connective tissue can be
studied in Fig. 92.
Fic. 90.—Intermediate stage of organization; on the left a portion of the media and the
internal elastica; on the right, the cellular obturating tissue.
The formation of larger spaces or sinuses is depicted in Figs. 93 and 94.
In the former organization is complete, only a part of the vessel wall being
shown. On therighta portion of the occluding tissue with its smaller and larger
vessels, its capillaries obliterated by connective tissues, and two sinuses of
moderate size are not unusual appearances (Fig. 93). A higher magnifi-
cation of the tissue in another case, (Fig. 94) shows that these sinuses may
occasionally be lined with endothelium and filled with blood. Later, how-
ever, their walls are fortified by the deposition of elastic fibers.
The “Healed” or Old Stage.—For a thorough comprehension of the
pathology as it presents itself in most of the vessels obtainable from
an amputated limb— the ‘‘old” or “healed” stage is the most instructive.
The most common lesion is a total obliteration of the lumina of arteries
and veins by vascular connective tissue. A study of the development
of this connective tissue shows that the end product may be extremely varied
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 339
Fic. 91.—Cellular intermediate stage of the organizing process.
340 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
FIG. 92.—High power picture of one variety of end result in the process of organization of
the clot, the vessels and pigment being striking features.
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 341
Fic. 93.—Fenestrated occluding tissue on the right with two large sinuses; on the left
a part of the middle coat with the fluted internal elastic membrane running from above
downward.
342 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fic. 94.—A type of obturating tissues enclosing a large blood sinus and smaller capil-
laries. The internal elastic membrane on the left is partly disorganized and well preserved
on the right below.
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 343
in its general appearance, but that each picture can be interpreted
correctly as having its origin in the lesion of occlusive thrombosis. Thus
the vessels may be filled with connective tissue harboring numerous small
vessels, much pigment containing hemosiderin, with a fair amount of con-
nective tissue cells; or, the cellular elements and vessels may be but sparsely
represented, dense sclerotic fibrous tissue with but an occasional sinus pre-
dominating.
Another interesting variant of the terminal stages of occlusion and one
which is more apt to affect the smaller arteries (such as the dorsalis pedis and
dorsalis hallucis) is reproduced in Fig. 95. Here the new vessel formation in
Fic. 95.—Old healed stage in small artery, artery converted into a’cord containing dense
fibrous tissue and vessels.
the organized clot is striking, and the vascularization of the media can be
wellseen. The penetration of the media by new vessels and the proliferation
of the small vessels in this coat have been described elsewhere, and need only
be mentioned here as evidence of the attempt at organization of the clot and
of the establishment of a supplementary circulation.
The occlusion of the popliteal artery by the completely organized tissue
in which every vestige of inflammatory product has been resorbed, a multi-
tude of canalizing channels only remaining, is portrayed in Fig. 96. In
contrast to this a very small artery may also be completely obliterated into a
cord of bizarre appearance, because the canalizing vessels have become so
markedly hypertrophied (Fig. 95).
344 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fic. 96.—Popliteal artery occluded by vascularized connective tissue, Pigment, small
vessels, and capillaries being features.
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 345
Fic. 97.—Old type of organized clot showing cicatricial contraction of the connective
tissue, and occlusion and compression of the cellular elements, also secondary thickening of
the intima.
346 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
With increasing age, changes in the intima may occur that show themselves
as diffuse thickening, and the vessels contract about the obturating tissue,
the latter becoming more and more firm (Fig. 97).. This cicatrization may
go on to such an extent as to give confusing products, in that the hypertrophy
of the intima may lead to erroneous interpretation. The contraction of the
obturating tissue mass, the enlargement of the intimal layers and the diffuse
fibrosis about the vessels extending well into the fatty tissues about the arteries
can be studied in Fig. 98.
4
Fic. 98.—Contracted type of closed artery. The lumen is narrowed and filled with
fibrotic tissue. The intima shows hyaline degeneration and is thickened following the
thrombotic process.
In the older stages in which there is but a sparse distribution of the cells in
the cicatrizing mass, the veins are apt to show less contraction than the arteries.
So in a vein shown in Fig. gg, the irregular sinuses that canalize the occluding
mass are in sharp contrast to the more rigid and contracted process in the
cribriform arterial sections shown in Fig. too.
Again in the artery in Fig. ror, where a central lumen is simulated by a
narrow canalizing channel, the retraction of the internal elastica with
corresponding constriction of the artery is well shown. Fig. 102 is an interest-
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 347
Fic. ro0o.—Old or healed type of lesion with large canalizing vessels.
348 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
FIG. 101.—Obliterating tissue, old variety in dorsalis pedis, can be mistaken for ‘‘endarter-
itis;’’ old connective tissue, canalization; only slight vascularization of media.
Fic. 102.—‘‘Old’”’ occlusion in artery simulating ‘‘endarteritis obliterans;’’ eccentric-
ally situated large canalizing vessel (below) crowding rest of tissue to one side (above in
illustration).
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY o49
Fic. 103.—Lesions of the media in medium sized arteries; many capillaries with or
without slight perivascular lymphoid infiltration in the media; penetration ot the internal
elastic lamina by vessels which enter rather old typical occluding tissue.
Fic. 104.—Longitudinal section of an artery containing termination of organized clot;
to the left the arterial walls are normal, collapsed and in contact; to the right, occluding
tissue.
300 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
ing illustration of an eccentrically placed canalized channel that crowds the
organized clot into the small crescentic mass on the right and is an example of
the formation of pictures that can be mistaken for endarteritis obliterans.
The change that is left in the media in the healed stage, besides connec-
tive tissue infiltration and atrophy, is the diffuse invasion with new formed
vessels (Fig. 103). Although this process is most pronounced in thrombo-
angiitis obliterans, it can be also observed in atherosclerotic processes,
whenever secondary thrombosis occurs, or whenever there is marked degenera-
ation, calcification or bone formation in the walls.
Fic. 105.—Termination of the red clot ina vein. It is adherent at 3 o'clock, and in the
media at this site there is inflammatory infiltration.
Terminations of the Occluding Tissue.—Studying some of the termina-
tions of the occluding tissue in arteries and veins, we not infrequently
encounter a rounded convex projection looking upward (cephalad), abruptly
ending the obturating plug, and often lying in and just below an apparently
healthy vessel wall (Fig. 65). At other times the old occluding tissue seems
capped by a more recent pyramidal or tapering clot, which appears grossly
and microscopically to be deposited by mere accretion (stagnation clot).
When we view the former type, as illustrated in the longitudinal section
(Fig. 104), we can well understand the nature of the pathological change.
Here there can be no doubt as to the thrombotic nature of the process.
The accretion or stagnation clots, on the other hand (Figs. 105, 106, and
107), present a somewhat different picture, not varying from that of throm-
bosis and organization induced by other causes.
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY dol
Fic. 106.—Bland termination of accretion clot in vein with healthy wall. (See Fig. 105.)
302 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fic. 107.—Termination of clot in an artery the seat of atherosclerotic disease; good
example of associated lesions.
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY B05
In Fig. 104 the rounded termination of the obturating mass is seen lying
in a vessel cut longitudinally, and whose walls are collapsed just beyond the
organized clot. The latter presents the usual picture of the old stage with
connective tissue vessels and pigment. A parietal termination in a vein is
seen in Fig. 108.
The accretion clot may be either abruptly separated from the specific,
Or may pass imperceptibly into it. When the latter is the case, the tapering
termination may be found adherent to the wall in places, and it is there that
evidences of the inflammatory nature of the process may still be present.
In Fig. 1o5 such infiltration of the media and intima is seen where the clot is
Fic. 108.—Termination of obturating tissue in a vein in parietal form.
attached. If the media be infiltrated with migrating and polynuclear
cells, we may conclude that the specific inflammatory process has extended
into and emerges imperceptibly into the accretion clot. If the organizing
process is the typical bland one, no such reaction in the media can be noted.
Fig. 106 shows sections made somewhat nearer the apex of the clot, the
vessel being absolutely healthy in this region.
When such a termination occurs over an atherosclerotic or thickened
intima, confusing pictures may result after organization has taken place
(Fig.*107).
In rare instances terminations of the clot may adhere in a parietal fashion
to the walls of the vessels, as shown in the vein in Fig. 108.
23
304 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
The Pathology of the Relapsing Lesion.—Not only is the process a migrat-
ing one both in arteries and veins, but all of the constituents of a sheath may
not be simultaneously affected. An old advanced lesion may be found in an
artery or vein, an acute lesion in contiguous vessels. The finding of various
stages of the disease in different members of the same vessel sheath is exceed-
ingly instructive. This is well illustrated in Fig. 64.
Thus in Fig. tog a large artery affords a view of the old lesion, as well as
one of its venae comites. Another accompanying vein, however, is in the
“acute” stage (Fig. 110) of the disease, a smaller venule or satellite being in
Fic. 109.—Old sclerotic occluding tissue in thrombo-angiitis obliterans; a high power
magnification of this vessel being reproduced. (See Fig. 64.)
the intermediary stage, where certain “miliary giant cell foci’? make their
appearance (Fig. 111). Such pictures not only reveal the thrombotic nature
of the disease, but also present an argument in favor of the following two
assumptions: that the disease begins with an inflammatory lesion attended
with occlusive thrombosis, and that it affects the arteries and veins in a sort
of relapsing fashion, similar to that which occurs in the veins in migrating
phlebitis.
Recurrences are found also in the deep vessels. In the popliteal vessel
seen in Fig. 112, evidences of thromboses are found. The whole artery was
doubtlessly affected by the acute process a long time since, for the lumen was
filled with the old type of organized tissue, many capillaries and large blood
sinuses, and thick walled canalizing vessels. One of these daughter canalizing
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 300
Fic. 110.—Acute stage in another of the veins seen in Fig. 64.
306 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fic.4111.—Miliary foci in an acutely inflamed vein in same sheath with preceding. (See
Fig. 64.)
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY O07
Fic. 112.—Relapsing acute stage in an artery already occluded and in the old stage
on the left, giant cell focus.
Fic. 113.—High power of Fig. 112.
398 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
arteries shows the acute process within its walls, and a miliary giant cell
focus. A high power view of this focus is seen in Fig. 113. ‘Thus the com-
bination of an old healed lesion with a recent superimposed acute inflamma-
tory one in a daughter canalizing vessel is beautifully shown.
A similar instance of combined old and recent lesion in the peroneal
artery is depicted in Fig. 114. Here the crescentic mass to the left in the
picture shows the healed connective tissue stage, and in the eccentric lumen
that is left, recent thrombosis, acute inflammation, and miliary giant cell foci
are present,
peripheral portion of the obturating tissue is composed of vascularized connective tissue.
On the right, the greater portion of the lumen, however, is occupied by a more recent clot
with miliary foci.
The Elastic Tissue in Thrombo-angiitis Obliterans—What information
can be obtained from a study of specimens stained for elastic tissue?
Characteristic of the early stages of the metamorphosis of the obturating
clot is the absence of elastic tissue, and also the absence of the excessive
reduplication of the internal elastic layer so characteristic of arteriosclerotic
processes. As the canalizing vessels become older, however, new formed
elastic tissue disposes itself about them (Fig. 115) in concentric layers. The
scant development of the elastic tissue in a popliteal artery completely filled
with organized clot is seen in Figs. 116 and 117, where but the faintest indica-
tion of new elastic fibers is seen about some of the canalizing vessels. Where,
however, there are small complicating plaques of arteriosclerosis, there the
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 309
Fic. 115.—Elastic-tissue stain of section of vessel shown in Fig. ror.
360 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fic. 116.-—Occluding tissue devoid of elastic fibers in the popliteal artery.
THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 361
Fic. 117.—Elastic tissue but sparsely represented about the vessels of the occluding tissue
in a vein,
362 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fig. 118.—Absence of elastic tissue in the clot; small atherosclerotic patch below in the
intima of the artery.
Fic. 119.—New lumen found in organized clot in vein simulating endarteritis obliterans
(elastic tissue stain).
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 363
corresponding hyperplasia and duplication of elastic lamina take place
(Fig. 118).
Serial sections stained with the elastic tissue method demonstrate clearly
that the occasional pseudo-lumina (Fig. 119) found in arteries of thrombo-
angiitis obliterans are but expanded or eccentrically placed canalizing sinuses
which divide up into subsidiary branches and are traceable (Fig. 120) into
numerous smaller canalizing vessels at different levels.
Fic. 120.—Septum formation due to the eccentric position of the two large canalizing
sinuses,
In Fig. 120 the elastic. tissue disposed about the two sinuses separated
by a septum stamps these as new formations. Elsewhere they are found to
divide into smaller canalizing vessels.
Other sections, such as are seen in Figs. 121 and 122, further demonstrate
the new formation of elastica about a canalizing vessel.
Where, however, the lesion is one of long duration (years), a secondary
thickening of the intima takes place with corresponding proliferation of
elastic fibers that must not be confused with arteriosclerotic processes
(Fig. 123).
True atherosclerotic plaques in which the elastic fibers are disposed more
or less parallel with the internal elastica lamina and encroaching upon the
lumen of the vessel may occur, for the two diseases may be associated. This
is seen in Fig. 124, where such an atherosclerotic plaque occupies the cres-
centic portion of the right part of the lumen, whilst the occluding mass of
thrombo-angiitis obliterans completes the recess left.
364 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fic. 122.—Perivascular disposition of new elastic fibers in the occluding organized clot.
TH ROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 365
Fic. 123.—Relative absence of elastic fibers in the organized clot; secondary hyperplasia
of the intimal elastica in the artery below.
366 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fic. 124.—Old type of occlusion at site of an arteriosclerotic plaque on the right.
THROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 367
Fic. 125.—Elastic tissue stain showing old lesion in arteries and vene comites; also
picture in vein simulating endarteritis obliterans; on the left and right, arteries; in the
middle two veins, the left with small, the right of the two with a large canalizing channel.
Fic. 126.—Fibrosis of perivascular tissues binding the two vessels above together;
endarteritis and endophlebitis here simulated.
368 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Of great value is a study of those sections that include a number of the
larger obliterated vessels, as is seen in Figs. 125 and 126. Many of these
will exemplify the secondary sclerotic intimal changes! that occur long
after the occlusion has taken place; and further, they will demonstrate the
fibrosis that binds the arteries and veins together, being the sequel of an
inflammatory process extending from the adventitia. Fig. 126 shows
beautifully how the two vessels on the right are encased in a dense fibrous
sheath, whilst the large canalizing lumina suggests endarteritis obliterans
rather than thrombo-angiitis obliterans. No wonder then that these lesions
should so long have been misinterpreted.
CHAPTER LXIII
THROMBO-ANGIITIS OBLITERANS—PATHOLOGY IN LETHAL
CASES
The autopsy material studies by the author was obtained from cases that
died after amputation or from other causes. In the former, exitus was due
either to pulmonary embolism, embolism of the mesenteric arteries, or to
accidental causes.
Little is known regarding the participation of arteries other than those
of the extremities in the characteristic process. The author has observed
the “old type” of occlusion in the spermatic artery; and in a branch of the
gastric artery leading to a callous ulcer of the stomach. Since but a small
amount of material was at hand, it would be audacious to assert positively
that the lesion was identical with that of thrombo-angiitis. However,
recently the typical ‘‘acute” lesions were found in the spermatic vessels of
the cord.
In a young man who consulted the author for a subacute enlargement of the testis,
epididymis and cord, the diagnosis of tuberculosis or thrombosis of the vessels of the cord
was made. Orchidectomy yielded an interesting specimen in which most of the veins
(spermatic) of the cord and tributaries about the testis, were thrombosed. Microscopic
examination revealed the typical ‘‘acute lesions”’ in many of the vessels.
The literature is practically devoid of reliable information on this point,
so that autopsy material is highly desirable for enlightenment. But few
data could be gathered since only 3 autopsies? were done on the cases under
the author’s observation. Great care must be exercised in interpreting the
significance of the endarterial lesions evidenced by necropsy, since years had
elapsed in 2 of the cases since the amputations of the lower extremities had
been performed, during which time intercurrent affections, atherosclerosis
and secondary thromboses could play a réle in producing the final anatomical
and pathological results. Because of the paucity of such records in the
literature, however, it may be valuable to give in detail these findings, even
though a final and authoritative interpretation of their importance and
meaning may not be permissible from the meager data at hand.
1 See also similar alterations in the veins.
2 Autopsy material and findings in an additional case, in which the fatal outcome was
accidental and due to hemorrhage in the wound were put at the author’s disposal through
the courtesy of the Pathological Laboratory, Mt. Sinai Hospital.
THROM BO-ANGIITIS OBLITERANS—PATHOLOGY IN LETHAL CASES 369
The fact that in the autopsy material at our disposal, the lesions of
thrombo-angiitis obliterans were confined to the vessels of the extremities,
might lead to much speculation and critical query. It would seem that local
predisposing factors must needs be requisite for the special susceptibility of
these vascular territories. In the present state of our knowledge we think
it unwise to attempt to give explanations for all of the many seemingly
inexplicable circumstances that surround this interesting malady. That the
arterial channels affected by thrombo-angiitis become, or are inherently pre-
disposed to atherosclerotic changes as well, seems proven both by autopsy
material as well as through our studies of the amputated limbs. Where
reamputation is done years after the more distal part of the limb has already
been removed, more marked atherosclerosis is found. Or, when the second
lower extremity requires amputation years after the first, atherosclerotic
changes may be found that were absent during the earlier years of life; they
may be slight or marked in degree.
The fatal termination in some of the cases may be accidental, dependent
on the cardiovascular system, or may be preceded by a state of malnutrition
and asthenia occasionally observed in cases of extensive atherosclerotic
disease that have already lost both lower extremities.
The following grouping is now permissible in consonance with the author’s
experience: (1) the fatal cases in which death may be attributed to the
operation, or some sequela of the disease itself (accidental); or (2) cases with
asthenia and slow termination, possibly with cerebral arterial involvement.
1. Accidental Exitus.—As accidental we would designate the lethal out-
come in cases that die from cardiac failure after operation, from hemor-
rhage or from pulmonary embolism. ‘The author has personal records of but
2 cases of embolism with fatal termination after Gritti-Stokes amputation.
In one there was pulmonary embolism with sudden exitus, in the other,
mesenteric thrombosis or embolism. Cases collected elsewhere! afford
instances of accidental complications and death, such as fatality from hemor-
rhage at the site of the ablation. In one such instance the autopsy material
studied by the author again confirmed previous observations in the finding of
atherosclerosis of some of the larger vessels and in the absence of the thrombo-
angiitis process outside of the peripheral territories.
Case 1. Thrombo-angiitis; precocious atherosclerosis; coronary artery
disease; sudden exitus.
F. K., male, aged 24, when admitted November 5, 1907, stated that 1 year ago he had
severe pain in the left big toe; this recurred 2 weeks ago, and has grown progressively worse;
the foot is swollen, red, and tender; for the past 2 days the big toe has become bluish in
color; intermittent cramp-like pains in the calf of the right leg have also been experienced.
On physical examination the left foot is seen to be very edematous up to the ankle;
pepnernces of the big toe and cyanotic discoloration; slight erythromelia of the toes of the
an ‘Sil 6, 1907, incision and drainage of cellulitis of left foot; Nov. 8, amputation of left
big toe for gangrene; Dec. 10, left dorsalis pedis pulse absent, right present. Because of the
failure on the part of the wound to heal, amputation at the left knee was resorted to, May 8,
oe examinations May 27, 1908, revealed absence of right dorsalis pedis and posterior
tibial beats, and slight ischemia of the right foot upon elevation; July 15, still absent right
dorsalis pedis and posterior tibial pulses, but good pulsation in the right popliteal artery;
ulceration of the left stump; Aug. 20, absent left popliteal, only faint popliteal right, and
pain in the right foot and calf.
On physical examination Jan. 23, 1909, there was marked erythromelia of the entire
right foot, edema of the first and second toes, which were also in a state of trophic distur-
1 Studied with the permission of Drs. Mandlebaum and Libman of the Pathological
Department, Mt. Sinai Hospital, N. Y. C.
24
370 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
bance. March 1, 1909, amputation of the right leg at the middle third for impending
gangrene.
The patient was lost sight of until May 2, 1911, when he returned to the hospital because
of the presence of a painful sinus on the right stump which*had persisted for 3 months.
Both femoral pulses were good at this time, but ¢he right popliteal had completely disap-
peared. Because of the pain and ulceration, Gritti-Stokes amputation of the right thigh
was performed May 29, and, although the patient had engaged in conversation with the
nurse following the operation, was shortly afterwards found dead.
Histologic examination of the vessels from the right and left legs established the diag-
nosis of thrombo-angiitis obliterans.
Autopsy Diagnosis: Thrombo-angiitis obliterans atherosclerosis of the coronary arteries,
interstitial myocarditis.
Heart—Rather smaller than normal; tricuspid orifice about normal, tricuspid
flaps show no thickening; right ventricle outflow tract dilated, wall very thin
measuring about 2 tog mm. Pulmonary valves show no abnormality; few fatty plaques
at the origin of the pulmonary artery; left auricle endocardium somewhat whitened;
mitral valve shows distinct thickening at its edges; left ventricle dilated; heart muscle very
brown, measures 8 mm. in thickness and throughout it yellowish areas of degeneration can
be seen, some of which look fatty and other areas of a more or less circumscribed fibrosis
Such lesions can only be found in the wall of the left ventricle, and not in that of the right;
left coronary artery is normal for about 1.5 cm. from its origin, when the main branch
running down to supply the left ventricle is found to be more or less filled by fibrous, yellow-
ish white substance, which is adherent to the wall and divides the lumen of the vessel into
two very small parts (recanalization?). This fibrous process in the lumen of the vessel can
be traced down for about 3 cm., when the vessel is lost. The right coronary artery and
veins Show no such change. At the point of origin of the right coronary artery there is an
atherosclerotic plaque on the right posterior sinus of Valsalva, which encroaches upon the
lumen of the orifice of the right coronary to such an extent as to very markedly obstruct it;
in fact, the orifice is only pin-point in size. There are numerous pin-head and slightly
larger atherosclerotic patches scattered diffusely beneath the intima.
Lungs—Both lungs show very dense adhesions at the apices and along the posterior
border.
Liver—About normal in size, dark reddish brown in color.
Spleen—About one and a half times normal size, shows the presence of 2 depressions
beneath the cortex, which on section are found to be healed infarcts, and consist of fibrous
tissue containing some yellowish pigment; capsule slightly thickened and has a few adhe-
sions scattered over it. On section, the organ is of a bright red color, very soft and the
Malpighian bodies stand out prominently; splenic vessels show no changes.
Kidneys—About normal in size; capsules strip easily. ‘The cortex shows a few smaller
and larger reddish depressions, evidently healed infarcts. On section, the cortex and
medulla of normal proportions, markings fairly distinct.
Microscopic examination of the coronary arteries presents the typical
picture of arteriosclerosis. In short, marked lesions of atherosclerosis in
the coronary arteries, but nowhere any evidences of thrombo-angiitis
obliterans in the vessels examined.
Case 2. Thrombo-angittis; extensive atherosclerosis; bland thrombosis in
aorta, celiac axis, superior mesenteric arteries; exitus.
In the case B. D., aged 21, male, a typical Gritti-Stokes amputation of the left thigh
was done July 19, 1916, and the usual lesions of thrombo-angiitis obliterans found in the
vessels of the extremity, even at the site of ablation in the popliteal artery. July 21, the
patient complained of intense pain in the abdomen, and there was marked rigidity of
the abdominal wall. Per rectum a boggy mass could be felt, and the patient was in great
distress because of the pain and distension. ‘The diagnosis of mesenteric thrombosis was
established, and at operation July 22, gangrenous gut was revealed; exitus.
Author’s notes on viewing autopsy July 24, 1916: Extensive thrombosis of the cceliac
axis and of the superior mesenteric artery; gangrenous gut; the femoral artery and external
iliac on the side of the amputation, about 1)4 inches above Poupart’s ligament thrombosed.
In the external iliac there is a stagnation or accretion thrombus descending to meet the top
of the old thrombus; in the femoral or possibly the distal part is an extension from the old
clot in the femoral (accretion and stagnation).
In the aorta, mural thrombi some extending into the cceliac axis and the superior mesen-
teric; numerous infarcts in the spleen, in the kidneys, and infarctions of the heart.
THROM BO-ANGIITIS OBLITERANS—PATHOLOGY IN LETHAL CASES 371
Autopsy July 22—Body is that of a young adult male; no icterus or petechiz; moderate
rigor mortis. Left leg has been amputated above knee; surgical incision through right
rectus muscle.
Heart—on the anterior surface of the right auricle, near the base, milk-spot the size of
a five cent piece; right heart moderately dilated; the tricuspid and pulmonary orifices
normal; mitral shows few small yellowish, atheromatous patches. In the inner leaflet of
the posterior wall of the outflow tract, near the aortic orifice, is an irregular, grayish patch
which, upon section, appears to be diffuse scarring. Another similar patch is found in the
muscularis near the apex. Coronary vessels show very marked atheroma; entire intima
presents numerous raised patches. Here and there, however, are small button-like eleva-
tions due to nodules in the media of the vessels over which the intima appears perfectly
normal.
Aorta—elasticity normal; entire intima studded with irregular, yellowish, atheromatous
patches (ordinary atherosclerosis). In the upper part of the arch near the origin of the
great vessels are two button-like patches, about 2 cm. in diameter. On section, these are
situated in the media and consist of dense fibrous tissue, the intima and adventitia cover-
ing them not being involved. The fatty atheromatous changes in the intima extend all the
way down the thoracic and abdominal aorta on its posterior wall, also on the posterior wall
near the site of the cceliac axis, is a thickening of the intima similar to that described in
the aortic arch, which has apparently ulcerated into the lumen. ‘The base of the ragged
ulcer is covered by a layer of blood platelet thrombus. About 1 inch below this, also on the
posterior wall of the vessel, is a still larger patch which is ulcerated. The base of the ulcer
is also covered with blood platelet thrombus which extends down into the common iliac
artery, occluding it completely at about 114 inches from the bifurcation. The left common
iliac artery is closed by red thrombus. In the upper portions of the femoral artery, how-
ever, the thrombus again becomes blood platelet in type, and on the posterior wall of the
femoral artery is a marked fibrous thickening, apparently disease of the vessel. The supe-
rior mesenteric artery is closed at the beginning by a blood platelet thrombus, lower down
by a red thrombus. The mesenteric vein is filled with red thrombus. One of the main
branches of the splenic artery is also filled with a blood platelet thrombus.
Liver—moderately enlarged, cloudy parenchyma.
Spleen—about 114 times its normal size; center portion presents a large, firm, yellowish,.
anemic infarct similar to the infarct seen in subacute bacterial endocarditis.
Kidneys—normal in size, capsules strip with some difficulty, surface smooth; intense:
congestion of the parenchyma.
Adrenals and pancreas—negative.
Gastro-intestinal tract—intense congestion of. the serosa of the stomach and small
intestines; complete gangrene of the terminal 4 feet of ilium.
Microscopic examination of the superior mesenteric, common iliac,
femoral, external iliac, abdominal and thoracic aorta showed the typical
lesions of arteriosclerosis with varying degrees of thrombosis (parietal and
occlusive) of the mechanical type; nowhere lesions of thrombo-angiitis,
obliterans. ,
2. Cases with Slow Termination.—Just as in certain cases extensive:
aortic thrombosis was found, so here the mental condition antedating exitus
would suggest the possibility of thrombosis of bland or specific (thrombo-
anglitis) type in the territory of the cerebral vessels. Such a case is the
following.
Case 3. Amputation of both lower extremities and one upper; duration of
disease 10 years; exitus with cerebral symptoms.
S. A., aged 35, male (see Chapter on Thrombo-angiitis Obliterans of the Upper Extremi-
ties), when examined August 11, 1903, reported trouble in the left foot, 3 years previously.
Since then there were attacks of pain in both feet.
For the past 2 days (Aug. 11) the left foot has been painful, particularly at night, so:
that now he is unable to stand. His clinical course may be divided into four stages;.
(x) gangrene of the left leg; (2) gangrene of the right leg; (3) gangrene of the left forearm;
and (4) cerebral symptoms leading gradually to exitus.
1. Amputation of the Left Leg —Examination reveals early signs of gangrene of the great
toe of the left foot. Aug. 11, 1903, amputation of left leg; Aug. 15 to Sept. 2, no tendency
to heal, sloughing marked; Sept. 5, reamputation through the knee; Sept. 22, again necrosis
of the flaps; Oct. 3, reamputation through the middle of the thigh. A thrombus 4 inches
in length was extracted from the femoral artery; Oct. 24, wound healed.
a0 fhe CIRCULATORY AFFECTIONS OF THE EXTREMITIES
2. Amputation of the Right Leg.—March 23, 1905, says he has been suffering for 8 weeks
with pain in the right foot. An ulcer developed on the inner side of the heel, and recently
this region has become black.
Examination reveals a gangrenous area over the right heel; March 31, 1905, amputation
through the upper third of the right leg; March 15, 1907, because of recurrence of gangrene
in right stump, reamputation through lower third of thigh; June 13, 1907, patient insists
upon leaving hospital, although bare bone with suppurating sinuses can be still detected.
3. Amputation of Left Forearm.—Ma rch, 1910, says that since 6 weeks has had severe
pain in index and middle fingers, which gradually became swollen and red; after the incision
of a bleb at the tip of the index finger, gangrene of index and middle fingers set in. Notes
made March 14, 1907, called attention to the absence of the left radial pulse and cyanosis
of the hand. March, 1910, amputation through forearm for gangrene.
4. Exitus with Cerebral Symptoms.—April 14, 1914, patient admitted to hospital in
stuporous condition. There had been no apoplexy and no signs of palsy. Physical examin-
ation—patient incoherent in speech; talks in mumbling unintelligible manner; pupils are
equal and react to light; right upper lid is ptosed; right radial pulse absent (the left forearm
has been amputated); left thigh stump contains a sinus; from the right stump dead bone
protrudes; April 24, 1914, condition unchanged; April 29, temporal pulse weak; marked
asthenia; exitus.
Case 4. Amputation of both lower extremities for thrombo-anguitis obliterans;
obliteration of the brachial arteries with a clinical semblance of scleroderma and
sclerodactyly, lethal outcome, autopsy showing thrombosis of a portion of the aorta.
I. L., male, aged 35 years, examined Oct. 3, 1906, said he had always been well. Ten
months ago he began to experience pain in the left ankle shooting into the toes (acute stage
of the disease in the deep vessels, plantars and posterior tibial behind the ankle?). At first
this was intermittent but soon became constant. He became progressively worse so that
he was then confined to his bed for several months because of the pain. He was in the
hospital a few months previously when amputation was suggested, which was refused.
About 1 month ago the toes of the left foot became dark in color, exceedingly painful and
then an ulcer developed on the dorsum.
Physical examination: A rather poorly nourished man; good radial pulsations. The left
foot is the seat of gangrene involving the second toe, which is black. The other toes are
deeply cyanotic, partly anesthetic. Near the root of the second toe on the dorsum there is
a sloughing ulcer the size of a quarter, at whose base a tendon is exposed. ‘The dorsalis
pedis pulse is absent. Lymphangitis extends upwards to the mid-calf. The popliteal and
femoral arteries pulsate.
Oct. 3, 1906, osteoplastic amputation of the left leg through the mid-calf region. Necro-
sis of the flaps and bone, with healing, Nov. 17, after removal of dead bone and sloughing
skin.
Pathological examination of the occluded vessels showed the typical lesions of thrombo-
angiitis obliterans.
In June, 1907, the pain in the right leg became so intense, that although gangrene had not
occurred, the patient begged for amputation of this leg too. Therefore, July 1, 1907, an
osteoplastic amputation was done, but because of unsatisfactory healing reamputation
had to be resorted to, July 15, 1907.
Pathological examination of the obliterated arteries showed both the old and acute
lesions of thrombo-angiitis obliterans. The posterior tibial contained miliary giant cell foc
characteristic of the disease.
Dec., 1909. The patient says that he had a “sore” on the outer surface of the left
stump about 1 year ago. He had no pain in the stump until 1 year ago, when a painful
wound developed that took 3 months to heal. Three months ago pain in the right stumpi
set in; at the tip a sore developed which refused to heal, and became gradually worse.
Physical examination, Dec. 15, 1909: This reveals swelling of the entire right stump.
Posteriorly in the flap there is an ulcer the size of a dollar with gangrenous margin. The
whole stump up to the upper border of the patella is discolored; has a purplish reddish hue.
In the elevated position there is a fair amount of ischemia. The left stump shows marked
erythromelia, otherwise negative. Both femorals and popliteals fail to pulsate.
On December 17, 1909, the patient stated that he had had trouble with his right hand
for several months. He has noticed ‘‘swellings” along the front and inner aspects of the
arm, forearm and hand. The use of his hand has become impaired, the hand has become
thinner, and the skin relatively thicker and dryer.
On physical examination of the right hand it is seen that all the fingers look like those of
sclerodactyly; movement of the distal joints is diminished. ‘The skin is atrophic, dry, and
the circumference of each finger is considerably less than that of the fingers of the left hand.
THROM BO-ANGIITIS OBLITERANS—PATHOLOGY IN LETHAL CASES 373
No radial or brachial pulse is palpable; the brachial artery can be felt asa hard cord. An
axillary pulse can be obtained.
Examination of the vessels of the left hand reveals absent radial and ulnar pulsations,
fairly good brachial pulse. There are no trophic disturbances.
Neither femoral pulse is obtainable.
X-ray examination of the hands, Dec. 23, 1909, shows atrophy of all the bones.
The patient was readmitted to the hospital April 11, 1911, complaining of pain in the
left stump; the condition of the hands unimproved.
April 26, reamputation of the left stump for ulceration and sloughing. The femoral
artery and vein were found occluded. May 2, skin flaps blue and poorly nourished;
May 5, no union of external half of wound, union of inner half incomplete, tissues appear
necrotic. May 25, during the past few days the patient has become more lethargic;
temperature ranges from 100 to 102.5°; tongue dry, cracked; patient unable to answer
questions, drowsy; left stump necrotic; May 30, patient considerably weaker and comatose,
exitus.
Autopsy Diagnosis: Thrombo-angiitis Obliterans, Thrombosis of Abdominal Aorta.—
General—body is that of a rather emaciated man, marked rigor mortis, both lower limbs
amputated through the thighs.
Heart—rather smaller than normal; subpericardial fat slightly increased in amount.
Tricuspid valve admits 4 fingers, and tricuspid flaps are normal. Right ventricle is widely
dilated; muscle quite brownish and extremely thin. Some invasion of the muscle by sub-
pericardial fat. Pulmonary valve shows no abnormality; no signs of atherosclerosis in the
pulmonary artery; left ventricle endocardium somewhat whitened. Mitral orifice admits
3 fingers easily; mitral flaps very slightly thickened; left ventricular muscle brown and of
about normal thickness; avenue of outflow widely thickened. Aortic valve shows slight
fenestration and thickening of the corpora Arantii, corresponding to about the third
degree of atherosclerotic process.
The aorta elasticity is normal; a few, small, fatty areas in the intima around the orifice
of the anterior coronary artery; a few very slight fatty plaques in the intima of both
coronaries.
Aorta—from the arch down to the level of the superior mesenteric is of normal thickness
and elasticity, and shows only a very few, small, yellow, fatty areas in the intima. The
vertebral branches come off regularly. The cceliac axis and its branches show not the
slightest thickening, similarly with the superior mesenteric, but beginning just below
the origin of the latter, is a fusiform expansion of the aorta about 3 cm. long, 2.5 cm. wide
and 2 cm. thick. Below this the nature of its continuation is doubtful because the aorta
has been torn off just above the bifurcation, but, although the swelling tapers downward,
it probably was continued into the iliacs.
Around the swelling of the aorta is dense fibrous tissue (periarteritis). On cutting
through the center of the fusiform swelling the aorta is found to be filled with a mass of
what appears to be organizing thrombus. The vessel wall itself appears even thinner than
normally. The mass of tissue in the lumen is firmly adherent to the wall of the vessel.
The part on the periphery of the mass and immediately adjacent to the intima is firm and
yellowish in color, whereas the central part is of a cherry red color and much softer. Just
to one side of the center the material is a deep red, very soft and resembles more closely
rather fresh clot. When the aorta is opened down to the beginning of this process and
when the mass within the lumen is viewed from above downward it is seen to bdgin o.5
cm. below the origin of the superior mesenteric artery, here being entirely parietal and
adherent to the intima of the anterior half of the vessel wall. The vessel is completely
closed about 2 cm. below the origin of the superior mesenteric artery, but as has just been
said, it sends up a parietal tongue-like process which is adherent to the anterior half of the
wall. This tongue-like process is of a deep pink color, firm in consistency and densely
adherent to the vessel. The two renal arteries are given off above the level where the
aorta is completely occluded, and from the portion of the aorta which contains the
parietal mass. The left renal appears normal and is perfectly free of clot, but the right
renal contains at least for 7 mm. from the point of origin (which is all the vessel that is on
the specimen), a parietal mass which is firm in consistency, pinkish grey in color, semi-
translucent. It is about 1 mm. in thickness, and runs completely around the entire cir-
cumference of the vessel, narrowing the lumen to a diameter of 2 mm.
Liver, pancreas and intestines negative.
Right kidney—shows evidence of parenchymatous degeneration, striations poorly
marked. Renal artery and vein show no changes whatever.
Left kidney—cortex about 14 normal thickness and the markings extremely faint;
peripelvic fat increased in amount. Near the upper pole of the organ and situated about 0.5
cm. beneath the surface is a multilocular cavity containing greenish pus, the walls of which
are smooth and consist of fibrous tissue, in some places being 2 mm. thick.
374 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Microscopic Examination.—This showed none of the typical lesions of
thrombo-angiitis obliterans in the aorta or renal vessels. The lesions were
those of recent thrombosis with bland type of organization and arteriosclerosis.
CHAPTER LXIV
THROMBO-ANGIITIS OBLITERANS—DIAGNOSIS
Much to the confusion of our diagnostic concepts of the circulatory
affections, individual and combinations of manifestations loom up and enter
into the clinical field under extremely varied disguises.
Thus, pain on walking may be associated with blanching of the feet; or,
spontaneous vasomotor ischemia may be followed by rubor and cyanosis—
both types occurring in thrombo-angiitis obliterans, and mimicking
Raynaud’s disease.
Chronic rubor and pain, a combination common in thrombo-angiitis
obliterans and atherosclerotic vascular occlusion may simulate erythrome-
lalgia.
The chronic atrophies and the indurated skin sometimes accompanying
advanced lesions of thrombo-angiitis obliterans may be mistaken for
scleroderma and sclerodactyly.
The transmutations and kaleidoscopic nature of the dominant features
of thrombo-angiitis are in singular contrast with the more stable clinical
symptoms of the vasomotor neuroses.
Thrombo-angiitis obliterans must be diagnosticated from, first, lesions
of other organic vascular diseases of the extremities, second, cases of neuro-
pathic or neurogenic vascular disorder of the extremities. In the first group
belong athero- and arteriosclerotic gangrene, endarteritis obliterans, embolic
and thrombotic gangrene. In the second group belong Raynaud’s disease,
erythromelalgia, acro-paresthesia, multiple neurotic gangrene, scleroderma,
sclerodactyly, and chronic acro-asphyxia. A careful clinical study of
thrombo-angiitis obliterans will dissipate all doubt as to the possibility of
separating this disease, as a clinical entity, from the other types of organic
vascular disease, as well as from all those neurogenic varieties of vasomotor
and trophic disorders that may be clinically confounded with it.
Characteristic for thrombo-angiitis obliterans are the following groups of
symptoms: (1) the disappearance of the pulses, particularly the dorsalis pedis,
posterior tibial, and popliteal, more rarely the femoral, radial and ulnar; (2)
the development of typical manifestations of impaired circulation, to wit:
Blanching of the lower extremities when these are elevated above the horizon-
tal, hyperemia (rubor or erythromelia) or reddening of the foot in the depen-
dent position during certain stages of the disease, and trophic disturbances,
such as impaired growth of the toe nails, slightly atrophic condition of the
skin, ulcers, and gangrene; (3) true vasomotor phenomena of transitory
nature, such as alternating syncope, rubor, coldness apparently independent
of those chronic changes that have been cited above, and that are distinctly
traceable to the occluded condition of the arteries and veins; (4) the
symptoms of pain, either in the form of intermittent claudication (pain in the
calf of the leg or in the foot on walking with cessation when the limb is at
THROM BO-ANGIITIS OBLITERANS—DIAGNOSIS o790
rest) or the severe pain that is associated with the advent of trophic distur-
bances, especially with ulcers and patches of gangrene; (5) the slow course of
the disease, symptoms of intermittent claudication or pain, preceding the
development of trophic disturbances for months and years; (6) the fact that
about 99 per cent of the cases occur in Polish, Galician or Russian Hebrews,
and that almost always young males between the ages of twenty and thirty
are taken with this disease; (7) the onset of symptoms in the lower extremi-
ties, one of the legs being first affected; (8) the comparative infrequency of
involvement of the upper extremities; (9) the association of a peculiar type of
migrating phlebitis in the territory of the external or internal saphenous, less
frequently in the larger veins of the upper extremities, characteristic in about
20 per cent of the cases; (10) the slow but steadily progressive course, leading
in a large majority of the cases to amputation of at least one limb, not infre-
quently of both lower extremities, and in rarer instances to amputation of one
of the upper extremities as well.
For the clinical diagnosis of thrombo-angiitis we must depend upon (tr)
the racial (Hebrew) and sex (male) predilection; (2) the early involvement of
the lower extremities; (3) the early symptoms of pain or intermittent claudi-
cation; (4) the presence of migrating phlebitis; (5) the evidence of pulseless
vessels; (6) the presence of blanching of the extremity in the elevated position;
(7) the existence of rubor in the dependent position; (8) the relation of the
hyperemic phenomena to posture; (9) the absence of simultaneous, symmetrical
involvement; and (10) the slow, progressive chronic course terminating in
gangrene.
Differential diagnosis between thrombo-angittis obliterans and the vaso-
motor neuroses: Were it not for the fact that certain symptoms, closely
resembling typical vasomotor phenomena, may persist for weeks and years in
this disease, confusion with the true neurogenic vasomotor process would
scarcely ever arise. The chronic condition of redness in thrombo-angiitis
obliterans can be explained as due to dilatation of the superficial capillaries,
this being a compensatory phenomenon making for an adjustment of the
impaired circulation. This chronic redness or rubor may be mistaken for
erythromelalgia, or for the rubor of Raynaud’s disease. The fact that it is
associated with other evidences of closed vessels and the other characteristic
features above mentioned, together with the circumstance that the redness
disappears at once upon elevating the extremity, will make the recognition
of its nature possible.
For the recognition of thrombo-angiitis of the upper extremities, it is well
to separate the cases in which vasomotor symptoms predominate, from
those in which the symptoms in the lower extremities are well marked; and
also, to distinguish those in which we are compelled to investigate very care-
fully in order to elicit evidences of vascular occlusion.
The symptoms simulating Raynaud’s disease and acro-asphyxia are cyan-
osis of the finger tips, coldness of the fingers with or without trophic distur-
bances, and alternating cyanosis and rubor, involving the fingers or the whole
hand. Rather characteristic in the symptomatology of thrombo-angiitis is
the apparent dependency of the vasomotor symptoms upon variations in
temperature, the chronicity of the manifestations, the absence of pain in some
of the cases, and the absence of paroxysmal nature of the attacks so character-
istic in Raynaud’s disease.
When we turn to those patients in whom the trophic disturbances seem to
be unassociated. with evidence of vasoconstriction and vasodilatation we note
that there is merely a history of the development of a spontaneous ulcer of the
376 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
fingers. It seems more than likely that in many of these the history of the
absence of the vasomotor phenomena would be found unreliable if it were
possible to observe the cases throughout the whole course of the disease.
Future observations will probably support my belief that here, too, some mani-
festations of deranged vasomotility do occur.
When we consider the largest group, namely, that in which gangrene of
small or greater extent develops, we find that some cases may be mistaken for
simple paronychia. Others claim that the development of a gangrenous
patch or of the felon was preceded for a long time by distressing pains in the
tips of one or more fingers. ‘The vasomotor symptoms may be absent or the
cyanosis and redness may be quite striking. The following sequence of
symptoms may be observed and is interesting, because pain and trophic
disturbances alone are complained of. The onset is marked by severe pain
in the tip of a finger. This is superseded by atrophic changes in the skin,
the development of a dry, hard patch, mortification, and also formation of an
ulcer. In still other cases the similarity with Raynaud’s disease is even more
marked, for the symptoms are pain, cyanosis, rapidly followed by gangrene.
More rarely do we meet with those interesting examples of the effects of
arterial occlusion in which the development of intense atrophy of a hand or
limb or the production of the typical picture of scleroderma and sclerodactyly
is the significant feature of the clinical picture.
The differential diagnosis of this condition from the vasomotor neuroses
may however be difficult in the cases in which we cannot exclude the associa-
tion of the two diseases. It will be noted that where coldness and cyanosis
are complained of, a distinct dependency on temperature or other environ-
mental condition can often be elicited or that pain is absent. ‘The presence
of vessel changes and the history of the involvement of a lower extemity at
once clear up the diagnosis.
Where trophic changes alone are present, the absence of symptoms refer-
able to the central nervous system speaks decidedly against nerve lesions.
The relation of the vasomotor symptoms to the position of the limb will in
other cases be of value in explaining the nature of the symptoms.
How can we explain the occurrence of true vasomotor phenomena such as
do not seem to owe their existence to the mechanical effects of impaired
circulation? The blanched appearance that is a sequence of an obstructive
condition of the arteries, and which can be demonstrated by elevation of the
leg, and in bad cases can even be elicited in the horizontal position, is a phe-
nomenon easily explicable on the theory that the avenues of arterial supply
are cut off through extensive obturation of the arteries. Many clinical and
experimental observations have been gathered that speak in favor of this
view. So also is the rubor not a true vasomotor phenomenon, but a sign of
chronic vasodilatation of the superficial capillaries and is compensatory in
nature. The part played by the vasomotor mechanism in its production is
discussed in Chap. XLVI.
On the other hand, veritable symptoms of disturbed vasomotility can be
associated with thrombo-angiitis obliterans. ‘That these should occur is
not surprising when we call to mind that not only have intense and extensive
destructive, pathological alterations taken place in the most important arteries
of a limb, but that the accompanying nerves are frequently bound down by
a dense mass of cicatricial tissue and have undergone severe fibrotic changes.
Although the mechanism of the irritative and exhaustive vasomotor
phenomena is not clear, the total disorganization of the vascular innervation
in many of the cases would seem to afford some basis for the possibility of the
THROM BO-ANGIITIS OBLITERANS—DIAGNOSIS 377
‘“‘vasomotor’’ in nature.
occurrence of the disturbances which we call
Other theories are discussed elsewhere.!
Where signs of thrombo-angiitis of the lower extremities are unquestion-
ably present, and where evidences of vascular occlusion in the upper extremi-
ties are lacking, although these are the site of disturbed vasomotor innervation,
we may for a long time be unable to rule out the possibility of the
simultaneous occurrence of two different diseases.
In addition to this more or less chronic or permanent sign of deranged
circulatory function in thrombo-angiitis other phenomena which are truly
vasomotor in nature may frequently be associated; and, it is these that must
be differentiated from similar phenomena accompanying Raynaud’s disease,
erythromelalgia, scleroderma, sclerodacytly, and acrocyanosis.
In order that a differential diagnosis may be clearly presented,
let us briefly recapitulate the typical course of a case of Raynaud’s disease.
The latter is an affection whose pathology has not as yet been definitely deter-
mined, the lesion doubtlessly residing somewhere in the central nervous
system. Its clinical characteristics may thus besummed up: Somewhere in
the peripheral portions of the body (so-called acra) there occurs more or less
severe pain not confined to distinct nerve territory, usually affecting sym-
metrical parts, attacks of vasomotor disturbance being part of the syndrome.
These latter are (1) syncope, asphyxia, or local rubor, and (2) severe trophic
disturbances, usually in the form of gangrene of the parts first affected with
symptoms. ‘The course is an intermittent one, for there may be completely
free intervals; but in some instances, evidences of disturbed vasomotility may
persist. ‘The disease may consume itself in one attack or several attacks may
occur in succession. Objectively, sensory disturbances are usually absent,
as well as paralysis, although other evidences of disturbed vasomotor inner-
vation, such as aphasia, hemoglobinuria, arthropathy, may occur. Usually
neuropathic individuals are affected. The organic vascular changes, as well
as the lesions of the nervous system, reported as occurring in some of the
cases, have doubtless no causative relation with the disease.
It is true that there are still some who cling tenaciously to the theory that
some lesions of the peripheral arteries may account for the symptoms of Ray-
naud’s disease. In support of this view, certain anatomical findings have
been cited as strong arguments by those who believe that a definite
anatomical lesion in the peripheral vessels is irresistible testimony
against pure hypothesis. A careful analysis of the cases in question, as made
by Cassirer, shows that reported organic alterations in the vessels will
not suffice to explain the symptoms any more satisfactorily than the theory of
a central nerve affection of the sympathetic system. Whereas in thrombo-
angiitis obliterans the territory manifesting symptoms, corresponds to that
containing the diseased vessels, we find that no such relation exists where
vascular lesions are associated with Raynaud’s disease.
In Raynaud’s disease we will note the following features: A sudden onset
of the first stage of local syncope or regionary ischemia involving usually the
fingers, more rarely the toes, and occasionally the margins of the ears or the
tip of the nose with coldness and blanching; associated sensory phenomena,
paresthesia, and pain; a comparatively short duration of the vasomotor and
sensory manifestations, their intermittent character with return to normal
between the attacks; the symptoms of local asphyxia attended with local
depression of temperature and swelling of the parts involved; the disappearance
1 Chap. LXXXVI, also Chap. LIV.
378 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
of the asphyxia with substitution of reactive hyperemia and a third stage of
dry gangrene. Characteristic for this disease as well as for the cases of sclero-
derma and sclerodactyly is the striking atrophy of the ends of the distal
phalanges. The changes in the bones can be well demonstrated by Roentgen-
ray examination, atrophy and disappearance of large portions of the end-
phalanges being distinctive and diagnostic features. In our own experience
the alterations in the bones could be detected early in the disease, probably
developing simultaneously with the other trophic disturbances.
The differentiation of true scleroderma from thrombo-angiitis will be rarely
difficult to make. In scleroderma and sclerodactyly the first stage with hard
edema is characteristic and never simulated by cases of organic vascular *
disease. ‘The second indurative stage may, however, be almost exactly repro-
duced by other affections. The form ofscleroderma known as “‘sclerodactyly”
because of attendant alterations in the deeper tissues, may not be unlike
thrombo-angiitis. Roentgen-ray examination of the hand in sclerodactyly
offers the most valuable means of differentiating the two diseases. The
phalanges will very early show atrophic changes and disappearance
of the terminal portions in scleroderma, sclerodactyly, and Raynaud’s
disease, while the bones, although somewhat rarefied, will be seen to conserve
their outlines throughout the course of the disease, thrombo-angiitis obliterans,
until they are disturbed by the effects of gangrene.
So far as our experience permits us to judge, symptoms of scleroderma
occur only late in thrombo-angiitis when other signs of vascular occlusion have
already become well developed. The recognition of the condition will then
depend upon the absence of pulsation in the larger peripheral vessels, the
presence of gangrene (or the history of such a condition) and of the other typical
signs of obliterated arteries and veins.
It is most probable that in Raynaud’s disease and the related affections the
seat of the pathological process is to be sought in the vegetative system, that
is, somewhere in the vasomotor apparatus. Nor are we likely to be rewarded
in a search for any organic change. The frequent return to a normal con-
dition, observed clinically, also speaks against the likelihood of morphological
or chemical alterations in the nervous system.
Whereas in thrombo-angiitis obliterans a definite and specific morpho-
logical change in the arteries and veins is responsible for the varied phenomena
in the superficial capillaries, in Raynaud’s and allied diseases, the vasomotor
and trophic disturbances are the outcome of irritative and exhaustive proc-
esses of the sympathetic nervous system.
CHAPTER LXy
THROMBO-ANGIITIS OBLITERANS—TREATMENT
It must be remembered that we have as yet no treatment for the acute
stage of the disease in the sense of a procedure that has specific effect on the
acute inflammatory process in the arterial and venous walls. Nor have we
any prophylaxis against the disease. Whether salvarsan injections or drugs
of similar action or other bactericidal agents may be of value, we cannot as
yet determine, in view of a too limited experience. Certain it is, that when
THROMBO-ANGIITIS OBLITERANS—TREATMENT 379
we speak of treatment of the disease, we are in truth referring to therapeusis
of the consequences of the “healed stage” and not of the morbid process per
se. With this qualification, therefore, we may proceed to the discussion of
what is known regarding the care of the many effects of the resultant
impaired circulation.
The treatment should vary according to the stage of the disease, the
presence of migrating phlebitis, trophic disorders and gangrene. Since the
methods recommended for atherosclerotic cases often apply here, it is well to
read the two chapters in this connection.
PROPHYLACTIC TREATMENT
If we accept the theory that the process is one induced by some infectious
agent in arteries that exhibit a certain predisposition to disease, it is quite
evident along what avenues future investigations of preventitive nature
should be directed. In all susceptible individuals then (racial proclivity,
etc.) both the predisposing forces and the inroads of the specific type of
noxious agent are subjects of concern.
To combat the former, all the usual stresses of mechanical or chemical
nature that produce arterial inferiority (excessive exercise, exposure, certain
foods, tobacco, etc.) must be avoided. As for the latter, however, we are
still at a loss for either a preventitive serum or medicament.
It would not be paradoxical to state that the only efficacious treatment
of this disease is one of pure prophylaxis. For even with the most careful
scrutiny and search for evidences of arterial involvement, we are usually
unable to recognize the existence of the disease before arteries and veins
over considerable territory are already irremediably damaged. It is per-
haps only in those cases where a period of migrating phlebitis ushers in the
malady and precedes the involvement of the deep vessels by months or years,
that there is given us a period during which experimental work of preventi-
tive therapeutic nature can be applied.
As soon as signs of obstructive vascular lesions are diagnosticated, even
before the advent of destructive alterations in the peripheral tissues, great
stress should be laid on the importance of diminishing the functional demands
on the local circulation. The agencies that are likely to disturb the fine
balance between the tissue requirements and the permanently defective
circulation, are the following: Prolonged standing, walking, compressing
forces that produce local anemia, such as tight shoes, bands, etc.; exposure
to cold with its sequence—ischemia of the parts (or to cold and moisture);
mechanical insults that produce clean wounds or infections and thus call
forth the need of an enhanced circulatory activity. In short, the locomotor
apparatus must be spared as much as possible for its adaptive or accommo-
dative powers are greatly reduced in this condition.
Treatment of Pain.—Clinical experiments have been carried out by the
author and others with a view to blocking the afferent nerve paths. The
Foerster posterior root section! has not found aceptance because of the
magnitude of the operation. Silbert? recently reports complete relief of
pain in 3 cases after the injection of absolute alcohol, care being exercised
not to infiltrate adjacent tissues. Anesthesia of the sole of the foot with
relief of pain is said to result immediately. Because of the occurrence of
1 Elsberg, Case observed by author.
2 Silbert, Jour. Am. Med. Assn., Nov. 18, 1922, 79, 1765
380 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
late palsies and trophic ulcerations the author does not recommend this
method.
II, CONSERVATIVE TREATMENT
When the disease is well developed, distinct intermittent claudication being
present and fairly marked pain with or without trophic disorders, it is
advisable that the patient remain in bed for several weeks or even longer, or
at least that walking and standing be completely interdicted. Therapeutic
measures should be directed towards the conservation of warmth, enchance-
ment of the circulation, the prevention of traumatism, and the treatment of
local conditions, trophic disorders or gangrene, when these supervene.
A. Methods of Enhancing the Circulation. 1. The Postural Method.—
The author has suggested that certain passive exercises may be of value in
inducing hyperemia or rubor in the affected limb, and therefore, thera-
peutically beneficial in increasing the blood supply.
This method is the logical therapeutic outcome of the author’s method of
diagnosticating impairment of circulation of the lower extermities, in that it
uses the phenomenon of induced rubor, or induced hyperemia in a therapeutic .
way. If the method be carried out daily for a sufficiently long period, it
is of greater value in improving the circulatory conditions and in increasing
the blood supply, than any of the other mechanical or thermal means that are
at our disposal.
The procedure is as follows: The affected limb is elevated with the patient
lying in bed, to from 60° or go° above the horizontal, being allowed to rest
upon a support for from 30 seconds to 3 minutes, the period of time being the
minimum amount of time necessary to produce blanching or ischemia. Assoon
as blanching is established, the patient allows the foot to hang down over the
edge of the bed for from 2 to 5 minutes, until reactionary hyperemia or rubor
sets in, the total period of time being about 1 minute longer than that necessary
to establish a good red color. The limb is then placed in the horizontal
position for about 3 to 5 minutes, during which time an electric heating pad
or a hot water bag is applied, care being taken to prevent the occurrence of a
burn. The placing of the limb in these three successive positions constitutes
a cycle, the duration of which is usually from 6 to ro minutes. These cycles
are repeated over a period of about one hour, some 6 to 7 cycles constituting
a séance.
The number of séances cannot be categorically stated but should vary
with the case. In a general way they should occupy at least 6 to 7 hours a
day, that is every alternate hour during the daytime. During the hours of
rest, heat is applied continuously in the form of an electric pad, hot water
bag, hot air apparatus, or electric lamp.
In the opinion of the author, this method does far more to improve the
circulation than either the application of superheated air (so-called baking
treatment), or the diathermic treatment.
The length of time of its application may require modification according
to the manner in which the procedure is borne. In some cases pain induced
by elevation may necessitate a diminution in the period of elevation.
It is not possible to lay down hard and fast rules as to the exact application
of this method in any given case. Its employment should be varied accord-
ing to the requirement of each and every clinical stage, and the patient’s
response. A more detailed discussion will be found in the chapter on Arterio-
sclerotic Gangrene.
THROM BO-ANGIITIS OBLITERANS—TREATMENT 381
2. Heat.—For the cases of thrombo-angiitis obliterans, as well as arterio-
sclerosis, it is best to exclude the foot from the hot air treatment, when it is
the seat of trophic disorders or gangrene. Heat may be applied either by
means of an electric thermophore, by a hot-air apparatus, or an incandescent
apparatus containing one or more incandescent lamps, or a single strong
electric lamp with reflector. The temperature should not be raised higher
than 120° F. at the first treatment, and gradually increased to 150° and 180°,
but never more than 200° F. Heat is applied as high as the middle of
the thigh, for about one-half hour. In the presence of migrating phlebitis
this treatment is not well borne. Whenever gangrene is present, the
gangrenous part is left covered with a dressing but not included in the
apparatus.
The frequency of the heat treatments is to be varied in accordance with
the reaction and the exact condition of the affected limb. It cannot be
emphasized too strongly, however, that occasional applications (once or
even twice in 24 hours) are of little therapeutic value, and that treatment over
prolonged periods of time is necessary to obtain beneficial results.
3. Diathermic Treatment.—This is an excellent method of obtaining the
effects of heat upon the deeper parts, and is particularly applicable to the
early cases, especially those in which intermittent claudication is the most
marked symptom, and in those patients in whom ambulatory treatment must
be carried out. In the presence of inflammation, migrating phlebitis, ulcers
or gangrene, it does not seem to be well borne or beneficial. The séances
should last from twenty to twenty-five minutes.
The patient will feel the development of the heat in the region of the
ankle, where the effects of warmth can be demonstrated by the touch.
Subjectively, there is in addition to the feeling of heat, a dull ache which
should not be allowed to become marked. Pain is a sign for diminishing the
strength of the current.
Some authors claim success in the treatment of thrombo-angiitis oblite-
_rans by the diathermic method, which H. Wolf employs as follows.
The patient sits on a chair with each foot in a basin of warm salt water.
Each basin is connected with one of the poles of the diathermic apparatus.
This can be done simply by putting an electrical plate electrode with con-
necting wires into the water. ‘The current is then turned on and increased
according to the sensation of the patient, usually to about 700 M.A. The
patient is allowed to increase and decrease the amount of current at will, so
as to avoid excessive current strength. If it is desired to concentrate the
current in the toes, a block of wood is placed under the heel so that it stands
above the water. The current is then forced through the toes mainly, and
the effect is stronger. The duration of treatment is from 25 to 30 minutes.
The frequency depends upon the reaction. With the occurrence of inflamma-
tion or phlebitis, the treatment is discontinued. After subsidence of such
complications, the treatment may be resumed and given daily.
4. Many attempts have been made to improve the circulation through the
subcutaneous or intravenous injection of solutions that might diminish the
viscosity of the blood. So Koga! employed Ringer’s solution. Ginsberg?
and Steel? have suggested sodium citrate intravenously. Others (Meyer)
have claimed beneficial results after flushing the intestinal tract daily with
1 Koga, Deut. Zeitschr. f. Chir., 1913, p. 371.
2 Ginsberg, Am. Jour. Med. Sc., (Sept.), 1917, 154, 320.
3 Steel, Jour. Am. Med. Assn. (Feb. 12), 1921, 76, 420.
4 Meyer, Jour. Am. Med. Assn. (Oct. 19), 1918, 1268.
382 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
8 to ro quarts of Ringer’s solution through a duodenal tube, this supple-
mented by several daily subcutaneous injections of this solution. The
belief that beneficial results follow intravenous administration of sodium
citrate solution seems hardly warranted.
5. Intermittent Compression of the Main Arteries—An exceedingly tedious
but sometimes valuable method of inducing reactionary rubor and further- |
ing the development of collateral circulation is intermittent compression or
digital obliteration of the brachial or femoral arteries, when these are patent.
The circulation in these vessels is made to cease by pressure of one or more
fingers; the brachial artery being easily accessible at its beginning, the femoral *
just below Poupart’s ligament. Where the facilities are at hand, the artery
may be controlled for one minute and the circulation allowed to return for
five minutes, this being repeated over a period of an hour. Such séances
should alternate with those of the postural method and hot air treatment.!
B. Internal Medication.— Mercury may be given in some cases in smaller
injections when syphilis is suspected, although it does not seem to have any
material effect upon the disease. Nitro-glycerin and iodides may be adminis-
tered under certain circumstances, although their effects are of questionable
value.
C. Local Treatment.—Trophic ulcers must be treated on general surgical
principles, the combatting of the severe pain attending these being the most
difficult part of the treatment. An ointment containing 5 per cent novocain,
and ro per cent orthoform or anesthesin in lanolin and glycerin is sometimes
beneficial in allaying local pain due to trophic disorders. The continuous
saline bath or repeated baths alternating with the postural exercises is a
valuable adjuvant in aiding healing.
III. OPERATIVE TREATMENT
Ligation of the Femoral Vein.—Lilienthal has suggested the ligation of the femoral vein
as of some value in enhancing the circulation. He claims that in some cases of sudden
gangrene healing may take place after conservative treatment, such as removal of a toe
alone, and that frequently a lower amputation will be more apt to be successful after
ligation of a vein. The author cannot subscribe to this view.
Arteriovenous Anastomosis.—This has been suggested by Wieting
with a view to reversing the circulation, the femoral artery and femoral vein
being anastomosed in such a manner that the vein will receive the arterial
blood. Wieting and others have reported successful results, cures of impend-
ing gangrene and restoration of circulation. Experimental work, however,
(Stetten) would tend to show that it is practically impossible to transform
the veins into arteries by anastomosis, and clinical reports do not justify
us in recommending this method either is the presence of gangrene, or in
threatened gangrene. Involvement of the veins in thrombo-angiitis
obliterans, both superficial and deep, with obliteration in a larger percentage
of the cases, makes it unlikely that improvement of circulation could occur —
by deflecting the arterial current into the veins.
1Tt is interesting to note that an apparatus for mechanically producing intermittent
Bier’s venous hyperemia was used in Germany during the Great War, in order to combat
infection in limbs infected with the gas bacillus. The compressing cuff is distended by
pressure from an oxygen tank, and a mechanical timing interrupter breaks and makes the
flow of gas, causing the dilatation of the cuff. It is possible to employ a similar apparatus
for the intermittent and isolated compression of single large arteries. A small electric
motor may furnish the power for air pressure, and a pneumatic cushion may be so adjusted
as to compress the femoral artery. jy
THROMBO-ANGIITIS OBLITERANS—TREATMENT 383
Not only theoretic consideration but also practical experience have been
convincing in demonstrating the futility of attempting arteriovenous anasto-
mosis in this disease. Thus we may cite the following instructive instance of:
Functional failure of arteriovenous anastomosis; bone formation in, and
occlusion of anastomosed area.
Case L. W., age 32, Russian Hebrew, June 15, 1913, says that he has been troubled for
two years with pain in the right leg. He had had an arteriovenous anastomosis done at the
Beth Israel Hospital on November 5, 1912, but he did not feel improved by the operation.
On physical examination, June 20, 1913, the right foot was considerably enlarged by
. reason of edema, cyanotic, very painful, showed some atrophy, marked ischemia in the
elevated position.
On June 23 the patient begged for amputation because of the pain. The author
decided to expose the site of the anastomosis both for purposes of discovering what had
occurred and possibly whether another anastomosis was feasible. A considerable amount
of scar tissue was found about the situation of the vessels. The artery and vein were
embedded in a mass of connective tissue. They were liberated with some difficulty and a
piece of artery and vein, three inches in length, was excised. Both the artery and vein fora
distance of five inches were found converted into hard pipe stem-like cords.
Histological examination showed complete obliteration of the vessel by connective tissue
and bone formation.
When this condition was found at operation, it was decided to proceed with PAs
A Gritti-Stokes was done with an excellent result.
In view of the bad outlook in these cases, it is not to be wondered at, that
even peri-arterial sympathectomy of the larger arteries (femoral) should
have been suggested and tried. ‘The author has elsewhere called attention
to the fact that little can be expected from such an operation on @ priori
grounds.
Strauss! reports decortication of the right femoral artery for a distance of 8 cm. in a case
of thrombo-angiitis obliterans. Although the pain is said to have been influenced for a
short time, gangrene soon supervened and pain returned. From the experience in this and
another case, this author concludes that the consequent vasodilatation is only transitory,
and that the beneficial results are only temporary.
Limited Amputation.—Amputation of a toe alone is often unsuccessful
for healing may not take place. In some instances, however, conservative
treatment such as described above, together with ablation of a toe alone, or
several toes if necessary, may be followed by good results. In the majority
of cases amputation at a point higher up will be necessary.
Radical Amputation.—In the majority of cases amputation of at least
a portion of the leg will become necessary. The Gritti-Stokes amputation
is the ideal procedure in these cases, although lower amputations are occasion-
ally successful. The author found that in a series of 65 amputations accord-
ing to the Gritti-Stokes method primary union was obtained in all instances.?
When amputation is performed lower down, healing may take place, but in
many instances sloughing of the flaps occurs, and secondary amputation
becomes necessary. Inasmuch as the disease occurs for the most part in poor
working people, it seems that the Gritti-Stokes amputation is preferable to
those methods which are dubious in their outcome and require many months
for the accomplishment of their purpose. Methods or tests for estimating
the point at which amputation should be done are all unreliable.
Some surgeons would prefer circular amputation through the lower part
of the thigh, if, in their experience a better artificial knee joint can be thus
applied. The author has had eminently satisfactory results with the Gritti-
1 Strauss, Surg., Gynec. & Obst., Feb., 1923, 36, p. 290.
2Tn one case the patient died of pulmonary embolism about eight days after the
operation.
384 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Stokes amputation. Whenever complicating ascending lymphangitis or
severe infection is present, the amputation must be done much higher
through the thigh.
THE SELECTION OF THERAPEUTIC PROCEDURES
Here, as in the arteriosclerotic cases, careful attention to details and
proper clinical inferential reasoning will help us select a combination of
methods that may ward off gangrene or even give considerable comfort to
the patient.
The cases with minimal symptoms, coldness of the toes or foot, possibly
intermittent claudication, with or without spontaneous pain, are those that
should receive special consideration. F or, with intensive prophylaxis, correct
appreciation of the gravity of a seemingly minor affection, the patient’s
limbs may be preserved for many years and their utility prolonged or made
permanent. It is advisable to recommend, in such cases, a preliminary
‘““cure”’ or treatment in which absolute rest in bed is required for at least 4 to
6 weeks. During no part of this time is the patient allowed to walk, although
after the first 2 weeks it is well to permit the shoes to be put on for 14 hour a
day, provided the latter do not constrict or hurt inany way. Smoking is
prohibited. Injections of sodium iodide are given intravenously, and if we
wish, flushing of the alimentary canal with Ringer’s or Locke’s solution
through a duodenal tube may be given a trial. This method has been
recommended (W. Meyer) to decrease the viscosity of the blood.
The greater part of the day is occupied with the manipulations for enhanc-
ing the circulation, namely, the postural and hot air methods. The former
should occupy every other hour of a 16 hour day, excluding an hour’s rest for
lunch and dinner and should alternate with similar periods of hot air treatment
(about 40 minutes each). Restriction of one or the other may be found
necessary by virtue of special reactions of the patient.
After the 4 to 6 weeks, the postural and hot air séances are to be continued
for about 6 hours a day (each 3 hours), the distribution of application being
adjusted so as to suit the patient’s habits. As improvement occurs, reduction
in the daily duration of treatments is in order, a more intensive resumption of
the same being indicated upon the slightest recurrence of symptoms.
When the patient is willing and able to codperate, intermittent com-
pression of the femoral artery for 30 seconds every 5 minutes over hourly
periods, may effect the same reaction as the postural treatment, and enhance
the circulation.
When migrating phlebitis is present, we must distinguish between the mild
and the severe cases. Whilst in the former, the postural and hot air treat-
ments may find no absolute contraindication if carefully carried out and in
reduced measure, absolute rest alone with wet dressings and warmth are the
best means of alleviating the symptoms in the more severe cases.
In the more advanced cases with trophic lesions, we must treat the circu-
lation and the local sequele of disturbed nutrition. Where pain is not
intensified by the changes of position of the limb, the postural method may be
carried out as above described. But careful attention must be given to the
rapidity with which blanching sets in on elevation, lest we unduly prolong the
time of anemia. So, too, the reactionary rubor may be attended with pain,
whose advent may require abridgement of the period of pendency.
Where dry gangrene is present, we combine the postural, hot air, prophy-
lactic measures and intravenous medication. But when ulcers, infection, or
ATHERO- OR ARTERIOSCLEROTIC DISEASE 385
retention of secretions under a nail are observed, the continuous or multiple
baths of hypertonic salt solution may be invaluable. We should not fail to
cut away adead nail that favors retention of secretions in spite of the
patient’s remonstrance. We must then try out whether permanent baths
or intermittent baths alternating with 40-60 minutes of postural exercises
are the best combination in any given case. !
Where there are trophic lesions, the intermittent warm baths are so
valuable as to warrant a trial in every case. The water is kept at go° to
98° F., the temperature being varied according to the patient’s ability to
endure local moist heat. The methods of employing baths that are advo-
cated by the author are the following: The limb is immersed therein during
the dependent phase of the cycles of postural treatment for half hour or
hourly periods. Immersions are arranged so as to alternate with the postural
exercises and banking.
When conservative methods fail, or there is a fulminating type of gang-
rene, when severe infection complicates, or from the very outset larger
areas become mortified, amputation will be indicated.
CHAT BE RPEX VI
ATHERO- OR ARTERIOSCLEROTIC DISEASE—CLINICAL
MANIFESTATIONS
The clinical picture resulting from intense arteriosclerotic disease of
the vessels of the extremities, particularly of the lower extremities, is attribut-
able to the effects of impaired or even arrested circulation in arteries whose
lumina have become narrowed or completely obstructed. By virtue of
proliferative changes that occur in the walls of the vessels, particularly in
the intima, and because of the deposition of atheromatous and calcareous
material, the arterial lumen becomes gradually narrowed, and the normal
elasticity of the vessel walls becomes lost. In addition to the two factors,
obstruction by hyperplastic products and loss of normal elasticity, occlusive
thrombosis may be superadded, these three elements being responsible for the
circulatory changes in the diseased arteries.
Although gangrene is the most striking and most severe termination or
outcome, when the vessels of the lower extremities are afflicted with intense
and extensive arteriosclerosis, the evolution of this final stage is for the most
part gradual, the affected limb passing through a number of prodromal stages,
in which definite evidences of defective circulation can be detected. These
clinical stages should be recognized and properly appreciated, for, then only can
the proper prophylactic measures be instituted to delay or even prevent the develop-
ment of the mortifying process. ‘The most important of these clinical pictures
are briefly the following:
Clinical Forms of Arteriosclerotic Disease of the Lower Extremities.
1. Intermittent Claudication—This symptom may be the only indication of
arterial disease. Intermittent claudication may be the only manifestation
of obstructive disease of the arteries, or, it may be associated with absence or
1 For further details, see Chap. LX XIII, Treatment of Arteriosclerotic Disease of the
Vessels.
25
386 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
pulsation in the dorsalis pedis, or posterior tibial, and poplitealarteries. Later
on, it is overshadowed by othersymptoms. Jt is not to be regarded as a disease
per se, but as one of the manifestations of a number of diseases in which the
arteries of the lower extremities are narrowed or obliterated.
2. Intermittent Claudication with Other Evidences of Arrested or Impaired
Arterial Circulation—Such other phenomena are ischemia on elevation,
possibly also erythromelia or reactionary erythromelia, attended in some
instances with coldness and paresthesie. Vasomotor symptoms are not
uncommon.
3. Cases without Trophic Disorders——Pallor of the foot in the horizontal
position, or increased pallor on elevation, and moderate or fairly marked hyper-
emia, rubor or erythromelia in the dependent position with absence of pulses,
may be associated with coldness or occasional cyanosis, in patients who may
or may not have had symptoms of intermittent claudication.
4. Cases with Trophic Disorders.—In cases with intermittent claudication,
ischemia on elevation, rubor, coldness, paresthesiz, absent pulses in certain
vessels, trophic disturbances in the form of ulcers may develop, slowly or
suddenly after exposure to cold or some other insult.
5. Chronic Cases with Inability to Walk.—These may have been preceded
by intermittent claudication. There gradually develops chronic rubor,
inability to walk, and pain in the foot. The usual signs of impaired circula-
tion can be elicited. In short, the picture is that of a chronic erythromelia,
sometimes with edema, without trophic disturbances, but with moderate
or even intense pain.
6. Cases with Attacks of Thrombosis.—With any of the above pictures or
preceded merely by indefinite history of intermittent claudication, sudden
thrombosis may occur in some of the larger vessels, giving rise to the following
symptom-complex. The patient will be attacked by sudden pain in the calf
or in the foot, with inability to walk, and with pallor and coldness of the fore-
part of the foot. On examination, the blanching is seen to be intense upon
elevation, the dorsalis pedis and posterior tibial arteries may be pulseless,
whilst the vessels of the other leg are pulsating. After a variable period of
time, gangrene may set in, or indolent trophic disorders may develop. In
other cases a condition of chronic rubor may result, with gradual return of
circulation, the usual physical signs of impoverished circulation persisting.
Careful treatment instituted at the very inception of the thrombotic attack,
may ward off threatening gangrene.
In short, the prodromal signs of gangrene, namely, symptoms that may
precede by days, months or years, the development of the mortifying process,
are in the main: intermittent claudication, paraesthesiz, pallor, cold-
ness, pain, chronic rubor (erythromelia) in the horizontal and dependent
positions, attacks of thrombosis, blanching in the elevated position of the
limb or even in the horizontal position, loss of pulsation in the dorsalis pedis
and posterior tibial, sometimes in the popliteal, more rarely in the femoral
arteries, and trophic disturbances such as ulcers, fissures, impaired nail
growth, atrophic skin and edema.
Amongst the more unusual types of clinical course the following (7 and 8)
warrant recording.
7. Cases with Obliteration of All the Pedal Arteries, Popliteals and Femorals.
After a longer or shorter period of intermittent claudication lasting months,
sometimes years, severe almost continuous pain may be localized in one or
both feet, with occasional radiation in the leg or lower thigh. The objective
manifestations in one case were the following.
ATHERO- OR ARTERIOSCLEROTIC DISEASE 387
The left foot was in a condition of very slight erythromelia, some puffiness of the dorsum
of the foot and the toes. The leg was markedly atrophic, particularly the muscles of the
calf, the skin being fairly well preserved. ‘The whole foot seemed to be tender to the touch.
There was no marked coldness of the foot, except the big toe, the temperature of which was
manifestly reduced.
In the dependent position there was fairly marked rubor of the left foot, none of the
right, although pulsations were absent on the right as well as on the left. On elevation
there was distinct ischemia of both feet to a slight degree.
_The striking features of this condition are the inability to walk, continuous
pain in the foot, with atrophy of the corresponding calf, and the absence of
all the pulsations in the lower extremities. The difference in the subjective
|
and objective manifestations in the two legs of the above case can only be
accounted for by differences in the development of the collateral paths.
8. Chronic Gangrene with Atrophy.—Extensive obliteration of the arteries
of the lower extremities may lead to a picture of chronic atrophy associated
with slow development of gangrene that may persist for months or years with-
out infection and without complicating moist gangrene. It is interesting to
contrast the persistence of large gangrenous areas in these cases, with no
tendency to inflammatory process in the neighborhood, with the rapid develop-
y
Fic. 127.—Arteriosclerotic gangrene.
388 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
ment of fulminating putrid gangrene in many of the embolic and thrombotic
cases following infectious diseases and pneumonia. In the latter, possibly
by virtue of the liberation of ferment, be it through the presence of bacteria
or their toxins, secondary bland thrombosis develops rapidly in the deep
veins. In the cases under consideration, however, such venous occlusion is
absent, and a withered condition without infection ensues.
Fic. 128.—Arteriosclerotic gangrene.
It is noteworthy that a senile condition is not necessarily present, and
the atrophic state may appear in patients in their early fifties or even in the
late forties.
An exquisite example of such a process was the following:
L. S., 54 years of age, does not remember having had any trouble with his limbs until
the right leg was injured by a fall from a horse (chronic arterial disease, doubtless with
ATHERO- OR ARTERIOSCLEROTIC DISEASE 389
obliteration without symptoms). A wound over the right shin resulted, which necessitated
a small! operation, the nature of which he does not remember. Since then the wound has
not healed. He has not been able to use the right leg, has been bedridden, and the con-
dition of which he now complains has developed.
The area operated upon showed no tendency to heal, and a slow gangrenous process
developed that spread over the greater part of the shin bone, the latter protruding through
the skin. Until recently almost two-thirds of the length of the bone could be seen through
the self-enlarging wound. For several months he has also had trouble with the left leg, a
change in the appearance of the toes having been noted, and the foot being cold.
Physical Examination, March 1, 1921.—Both feet and legs are markedly atrophic
(Figs. 127 and 128). The anterior aspect of the right leg over the middle two-thirds shows
extensive dry gangrene of the skin, the antero-lateral and antero-internal surfaces of the
tibia presenting through a large aperture or defect, being dry, gangrenous, like dry bone
outside of the body cavity. All the toe nails show hyperkeratosis, discoloration, and there
is marked atrophy of the skin. At the knee there is an area over the outer condyle of the
femur, over which the skin has become mummified (dissecting room type). There is
cyanotic and reddish discoloration of the left foot, and the skin of the whole leg is so
withered that there seems to be little or no circulation in it, but gangrene is threatening.
March 14, 1921, amputation of the right leg through the upper third of the right thigh.
This was followed by sloughing of the flaps.
During his stay at the hospital the left foot became spontaneously gangrenous, mummi-
fication ensuing.
April 11, 1921, the patient left the hospital against advice.
Special Symptoms. Lrythromelia of Upper Extremities in Arteriosclero-
sis.—Just as intermittent claudication may involve the upper extremi-
ties (dysbasia angiosclerotica) so also is a condition of rubor occasionally
observed. Of the author’s atherosclerotic cases with marked rubor of the
hands or hands and feet, the preponderating number seems to have occurred
in diabetics. When such erythromelia is a striking phenomenon, then ische-
mia on elevation can also be elicited. As a rule, blanching of the hands is
relatively more difficult to produce by postural changes than its analogous
condition in the feet and legs, so that an extensive infringement upon the
patency of the vascular channels can be prognosticated, whenever rubor and
pallor are exaggerated in intensity.
A narration of a typical case may not be amiss here, because of the general
trend amongst internists to attribute marked rubor of the hands only to ery-
thromelalgia and other vasomotor neuroses, and because such rubor as an
expression of compensatory efforts attending organic vascular lesions, is so
often ignored.
Atherosclerosis, diabetes, chronic erythromelia of hands and feet.
Case R. B., Austrian, male, aged 57 years, says he has had diabetes for six years. For
the last six months the left hand has been swollen. Both hands get red and painful in the
pendent position. He observed this symptom first in the feet. Six months ago he had
redness of the tips and borders of the hands; three weeks ago the redness passed above the
wrist. Warmth seems to increase the pain whilst cold air makes the hands feel better
There have been no ulcers of the fingers. Eight daysago he had a mild apoplectiform attack
during which he could not speak for one-quarter of an hour.
He complains of sticking pains in the borders of the hands and in the fingers with
neuralgic pains radiating upward. On some days the hands look almost normal and then
there is no pain. There are exacerbations which last days.
Physical Examination: Hands.—Both become pale when elevated to 135°, and become
markedly scarlet when hanging down. The redness extends up three inches above the
wrist on being pendent for a few minutes. There is slight cyanotic discoloration. The
inner borders are most intensely red. ‘The hands look swollen and puffy, especially over
the palmar aspect of the left. Both hands feel fairly warm. There are areas of cyanosis
over the palm, especially over the tips of the fingers. Squeezing the fingers hurts more than
normally. His hands do not feel better when raised, the pulsations being about the same
as when in the horizontal or pendent position. Both radial pulsations are absent.
The brachials and axillaries: Right feels calcareous and pulsation is only felt in the upper
third. Left also calcareous and pulsation felt in the upper two-thirds.
390 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Lower extremities: Have the typical appearance of the atrophic condition usual with
atherosclerotic vessels. Slight erythromelia of the feet in the pendent position; no trophic
disturbances.
Femorals: Both exhibit fair pulsation but are very hard.
Popliteals: Right faint; left absent.
Posterior tibial and dorsalis pulses not palpable on both sides.
In the elevated position, even after ten minutes, there is only very slight ischemia.
Right leg is slightly paler than left. There is only a very slight induced erythromelia, more
on the left than on the right.
Erythromelia of Lower Extremities.—The clinical picture ofa red painful leg,
so characteristic of long standing impairment of the circulation attending
marked atherosclerosis with or without diabetes, is worth mentioning and
illustrating by a clinical case, for differentiation from thrombo-angiitis obli-
terans and erythromelalgia (Weir-Mitchell) will thereby be clarified.
Usually, the clinical symptom-complex comprises a history of long standing
intermittent claudication, with or without previous trophic disorders, possi-
bly an attack of arterial thrombosis without gangrene as a sequela, and
finally a condition of painful red leg, with atrophy. Edema due to renal
disturbances or cardiac insufficiency may complicate:
Erythromelia (red leg) in an arteriosclerotic.
L. S., male, 83 years of age, has had cramps in his left leg for many years, and 1 year
ago an attack of severe pain in the left foot. He has been troubled for about 6 months with
a condition which gives him concern both because of the evident discoloration of the leg,
and because of the attendant frequent pain and discomfort. His wife says that the
pain, the redness and the coldness of the leg to the touch are the chief noticeable changes.
Physical Examination—The whole of the left foot and part of the leg is markedly red,
both in the horizontal and pendent positions, the region of the fifth toe being tender.
Elevation of the limb intensifies the pain in the foot. There is slight edema. The popli-
teal, posterior tibial and dorsalis pedis pulses are absent. There is no gangrene.
Vasomotor Phenomena.—The nervous mechanism with which arteries are
endowed and which modifies their reactions to blood pressure, is a potent
influence wherever local circulatory impairment has taken place. We have
already alluded to the peculiar vasomotor lability and instability attending
obstructive arterial lesions. Allbutt! is not in accord with the oft repeated
impression that the superficial vessels in arteriosclerotic cases are even more
liable to spasm than the healthy. According to this author, plethysmo-
graphic experiments upon the arm in arteriosclerosis, and observations
carried out by more than one skilful investigator,?:* indicate that the response
of the vasomotor mechanism to stimulation is not enhanced but diminished.
Whatever the value of artificial methods for gauging the vasomotor
excitability, the author is convinced from clinical experience that an increased
susceptibility or tendency to vasomotor phenomena on the part of the small-
est arteries is often present in the cases in which obstructive arteriosclerotic
disease of the extremities is present. He is in accord with the view that the
larger arteries do not participate appreciably in effecting the manifestations,
agreeing, therefore, with Albutt in this regard. But in the more peripheral
arteriole and capillary territory, a distinct accentuation of vasomotor
fluctuation occurs that suffices to give noticeable symptoms.
Trophic Disturbances and Gangrene.—It is important to distinguish
between the two large groups of tissue disintegration, which result from
imperfect and arrested circulation, first trophic disturbances, and second,
gangrene.
1 Allbutt, Diseases of the Arteries (Macmillan, 1915).
2 yon Romberg, Deutsch. med. Wchnschr., Oct. 28, 1909.
3 Miiller, O., Deutsch. med. Wchnschr., 1906, 38-39.
ATHERO- OR ARTERIOSCLEROTIC DISEASE 391
1. Trophic Disturbances——Trophic disturbances include all manifesta-
tions of impaired nutrition of the skin and its adnexa, and may develop
months or years before gangrene is established. They occur much less
frequently in arteriosclerosis than in thrombo-angiitis obliterans.
The skin may be atrophic or withered, and the nails may show evidence of
impaired growth. Ulcers at the tips of, or between the toes, the sequelae
of abrasions or small wounds, are occasionally found. More rarely, punched
out indolent ulcers over the dorsum of the foot, or over the lower half of the
leg, may be complications of attacks of extensive thrombosis.
Small bullae, the precursors or prodromal signs of small patches of
gangrene, may lead to ulcers or to the separation of a nail. They may heal,
or may lead to extensive gangrene. Perforating ulcers more often attend the
diabetic cases of arteriosclerosis, and are to be found most frequently over
the plantar aspect of the foot. They are chronic in their course, and often
associated with deep necrosis and suppuration. When they involve the
toes, they lead to necrosis of bone. The toe may become enormously
enlarged. A granulating strawberry-like wound may be formed, which lies
at the orifice of a tract leading down to dead bone.
A bunion at the metatarsophalangeal joint of the great and fifth toes,
not infrequently affords a good nidus for an ulcer which almost always leads
to necrosis of the underlying bones.
Small ulcers, of the perforating variety, near the base of a toe, often
represent the orifice of penetrating abscesses, the necrotic and suppurative
process extending along the tendons and bone, and causing necrosis of bone
for a considerable distance beyond the site of the wound.
In the case of the upper extremities, trophic disorders associated with
arteriosclerosis are very rare, and their presence should, therefore, suggest
either the existence of thrombo-angiitis obliterans, vasomotor disease, or
other neuropathic cause. Gangrene, too, of the upper extremities is exceed-
ingly rare, though a symptom-complex comparable to intermittent claudica-
tion in the lower extremities is occasionally encountered. In rare cases
there may be intense rubor of the hand. The radial artery may fail to
pulsate and can be palpated as a rigid cord. X-ray examination will reveal
intensely calcified arteries, or at least calcareous deposits along the course
of the larger vessels.
2. Gangrene.—Although it is most commonly seen in the aged and,
therefore, has been termed senile gangrene (chronic or Pott’s gangrene), it
may also afflict younger individuals between the ages of 40 or 50, when the
atherosclerosis is precocious in development, or when a secondary thrombosis
occurs early in the disease. In most instances dry gangrene develops. In
some, however, we may see the moist type or combinations of the two.
Dry gangrene usually involves the toes, the big toe being the site of pre-
dilection. Or, there may be multiple areas of gangrene involving the
peripheral parts, and in the more severe cases, extensive dry gangrene of the
greater portion of the foot may be expected. The process may be a slow one,
the toes being spontaneously amputated or removed by operation. The
extent of the gangrene cannot be exactly estimated in the atherosclerotic
and diabetic cases, from the external appearances, nor from the line of demar-
cation when it is present. For, if such an amputated limb be dissected,
extensive, widespread sloughing of the deeper tissues with necrosis of bone
extending for a considerable distance beyond or above the apparent line of
limitation, will often be revealed. It is incumbent upon us, therefore, in
every case to make an X-ray examination of the foot, as this may demon-
392 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
strate that the destruction has implicated tissues beyond the zone of skin
involvement.
Where infection is superadded, the usual signs of phlegmon formation
or lymphangitis will be in evidence. The suppurative inflammation will
spread into the healthy tissues from the site of the gangrene, either in acute
fashion, or subacutely without causing any considerable rise of temperature,
but evoking intense pain.
Moist Gangrene.—Early evidences of threatening gangrene will be intense
cyanosis, coldness of the affected part, usually the toe, and the appearance
of a hemorrhagic bleb or a number of blebs filled with pinkish serum. ‘The
part will have a dark bluish or purplish appearance, or even angry red where
the epidermis becomes lifted off. In the immediate neighborhood, there
will be ecchymoses over smaller or larger areas, and edema with exquisite
tenderness just above the mortifying tissues. Where there is infection, the
typical signs of lymphangitis usually following the course of the internal
saphenous veins will be encountered. In later stages the epidermis becomes
detached, is folded, and hangs loosely in places.
In some cases there will develop spontaneously a number of large bullae
over the toes or dorsum of the foot, and, in these, clear or bloody serum alone
will collect. This is the early stage of moist gangrene. As the gangrenous
process extends, all those changes that have been previously cited and de-
scribed under moist gangrene will make their appearance. Ifinfection occurs,
the phlegmonous process is more rapid and intense than in the case of dry
gangrene, and particularly in diabetic cases will the resistance on the part
of the body be inadequate, and the inflammatory process difficult to check.
Clinical Course in Athero- or Arteriosclerotic Disease.—Although the
variations from the given types are manifold, and it is, therefore, impossible
to recount all the various types of clinical course, the following summaries
include the most common. Many patients have intermittent claudication
and pain on walking for a long time, then develop coldness of the toes or of the
whole foot, paresthesia, but rather rarely are afflicted with ulcers or other
signs of trophic disturbance so characteristic for the disease, thrombo-angiitis
obliterans. They may have attacks of thrombosis, complicated with ulcers or
patches of gangrene, or such attacks may be followed by healing and a state
of chronic erythromelia with discomfort and some disability in the affected
leg; or, practically all symptoms may be absent until after some insult,
traumatism or cold, or without cause a patch of dry or moist gangrene
develops. In a number of cases, particularly in the diabetic, a perforating
ulcer brings the patient to our notice, and this is complicated by necrosis of
bone and the usual signs of deep infection. Many patients complain only of
disability, particularly diffculty in walking. Some develop an, ulcer of the
nail-bed with a patch of dry gangrene that heals.
Others never develop gangrene, but the signs of insufficiency of circulation
are manifest if the limbs be examined as, blanching on elevation, slight
erythromelia, and absence of pulsation are regularly present.
The author has made an observation that these latter patients are prone
to fugitive attacks of erysipeloid infection of the feet and legs, or mild lymph-
angitis with short periods of fever. Perhaps diminished resistance of the
inadequately nourished territories predisposes to such complications.
When gangrene develops—usually of the dry variety—the onset is often
ascribed to some previous injury, the paring of a corn, the wearing of too tight
a shoe, exposure to cold, a bruise or the application of some strong medicament.
The big toe is usually the first to be involved. Its tip or the whole of it
ATHERO- OR ARTERIOSCLEROTIC DISEASE 393
becomes dusky red or purple, gradually becoming purplish-black. These
changes in color and evidences of mortification are attended with intense pain
in the affected region and in the foot. If the gangrene remains dry and no
infection takes place, mummification ensues, the toe becoming dry and
shriveled, into a hard black mass This, however, may be associated, as
referred to above, with necrosis and suppuration in the depth. A line of
demarcation may form, or gangrene may spread, depending upon the presence
or absence of infection, the resistance of the tissues, and the condition of the
arteries.
Clinical Forms of Trophic Disorders and Gangrene.—‘So variegated are the
clinical pictures presented by the various types of nutritive disorders com-
plicating arteriosclerotic closures of the vessels of the extremities with or
without thrombosis, that but a very few types can be mentioned here.
The following review will aid the clinical recognition of this condition.
1. After the removal of a corn by the chiropodist or by the patient himself,
or after the slightest cutting injury a small focus of pus develops, the toe
becomes red and cyanotic either through inflammation or stasis, and gangrene
of this part soon ensues.
2. A blister or larger bulla that is more than usually painful develops over
a toe, or on the dorsum of the foot, the epidermis is cast off leaving a discolored
derma which becomes bluish black, and then gangrenous.
3. Or, the bed of the nail begins to bleed, possibly attended with the
formation or a blister or bleb at the distal margin of the nail, or with more or
less chronic suppuration. And finally, when the nail becomes completely
separated, the gangrenous area or extensive slough is seen to lead down to
bone.
4. After a longer or shorter period of prodromal symptoms, particularly
intermittent claudication, chronic blueness or cyanosis affects some of the
parts, particularly the big toe. Days or weeks pass, then ulceration and
gangrene terminate the picture.
5. Although the big toe seems to be the site of predilection in arterio-
sclerotic cases, gangrenous patches may develop anywhere: over the dorsum
of the foot, over the heel, often in the neighborhood of calluses or fissures.
When these become infected, attacks of lymphangitis or deeper infections are
not infrequent complications.
6. Atypical forms of ulceration of the indolent type are not uncommon.
Multiple ulcers were observed in a case that gave a typical history of inter-
mittent claudication and pain in the feet, there being marked ischemia and
intense erythromelia. There were shallow, punched out, indolent ulcers over
the dorsum of the foot, most of them no larger in diameter than a quarter of an
inch, the result of the separation of the gangrenous patches of skin, their margins
showing no tendency to heal, and no reactive hyperemia. Such ulcers may
persist for a long time until finally, by reason of a fresh accession of thrombo-
sis in the deep vessels, or some mechanical or thermal cause, extensive gangrene
of the foot occurs necessitating amputation.
7. Occasionally there is a history of the existence of previous ulcers that
have healed, with a complete repetition of the clinical course.
8. The big toe may be found in a condition of chronic granulation and
ulceration, being enormously enlarged, almost twice the size of normal,
presenting a large granulating strawberry-like surface at the center of which
a sinus may lead to dead bone.
g. A type is also encountered in which trophic disorders in the form of
ulcers are present, is followed later by dry gangrene involving all the toes.
394 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Hemorrhagic or purple spots appear, are painful, and then may become the
seat of gangrene.
to. The whole foot may be in the state of very intense erythromelia, it
being almost a vermilion red, except over the area of trophic disturbances or
gangrene when such are present. Many of the various forms of trophic dis-
orders may be associated with this intense rubor.
11. Cases with patches of dry gangrene give a history of discoloration and
pain over periods of weeks or more. A _ small purplish or cyanotic spot
develops, particularly over a toe, and then this process after the elapse of
many days, may extend rapidly over to the rest of the toes and foot and
eventuate in a condition of dry gangrene.
12. A type with extensive dry gangrene, shows mummification of all of the
toes, and portion of the dorsum, as well as the sole of the foot. The rest of the
foot, when not involved, is very cold, presenting a cyanotic and hemorrhagic
discoloration. In other cases where the line of demarcation is distinct, there
is no evidences of progressive gangrene above the line. In addition to the
large area of gangrene, corresponding areas of poor circulation arefound. In
other cases there is complete ischemia for a distance above the demarcation,
or hyperemia depending upon the condition of the circulation.
13. Cases with the development of moist gangrene usually develop large
blebs over the dorsum of the foot and toes, the various toes showing different
types of lesions. ‘There may be extensive cyanosis of the toes, coldness, with
blackish discoloration. The epidermis becomes lifted off by a collection of
serum and blood, and certain toes show only cyanosis or black blebs, all of these
being in various stages of the gangrenous process. If inflammation is present,
intense hyperemia of the dorsum must be distinguished from the erythro-
melia. The dorsum of the foot also may show discrete patches of gangrene,
cyanosis and hemorrhagic blebs. Phlebitis and lymphangitis may accompany
this picture, so that when a cross section is made along the course of the in-
ternal saphenous vein after amputation, pus can be expressed out of the
lymphatics.
14. Cases with chronic gangrene and atrophy. Where the limb or limbs
become wasted and almost shrivelled up, a chronic form of gangrene lasting
for a year or more may give aremarkable picture. In such cases the greater
part of the tibia may present in dried form through a large wound that is the
result partly of trauma or the result of whatever cause. The foot or feet
may be almost intact, with, or without gangrene of the toes, but atrophic, cyan-
otic or red, with the patient bedridden for months and years.
CHAPTER LXVII
ARTERIOSCLEROSIS—PATHOLOGY
Pathogenesis.—Arteriosclerosis according to Marchand! is a deteriorative
disease of the vessels. Because of the exquisite fatty changes that occur
in the vascular walls, the affection was termed “‘atherosclerosis”’ in contra-
distinction to the old name “‘arteriosclerosis.” The latter term was first
employed by Lobstein in view of the hardening of the] vessel wall. The
2 Marchand, Verhandl. d. 21 Kong. f. inn. Med.
ARTERIOSCLEROSIS—PATHOLOGY 395
appellation “‘endarteritis’’ was coined by Virchow as descriptive of a reactive
hyperplastic lesion of the intima.
The more recent observations of several authors (Jores, Marchand and
others) interpret arteriosclerosis or atherosclerosis in the light of effects of
deterioration resulting from stresses and wear. Marchand views athero-
sclerosis as a progressive nutritional disturbance of the vessel wall, accom-
panied by thickening and sclerosis of the intima, multiplication and
degeneration of the cellular elements, partial necrosis, and finally disintegration
and calcareous degeneration. In the arteries of the extremities the media is
particularly implicated in the degenerative process.
Recent authorities lean to the view that the peculiar alterations are the
results of nutritive derangement, that is evoked by the excessive functional
stresses. In this sense one would interpret atherosclerosis rather as a
deteriorative disease due to wear and excessive use, rather than as purely a
senile change. The deleterious factors (mechanical factors) do not usually
attain sufficient intensity until a certain age is reached; for, cumulative
action through many years is required to bring about the necessary arterial
responses. From the varied distribution of the process in the vascular
system, it would appear that the individual suffers in those vascular territories
which are most subject to strain in the respective case.
In the light of most recent investigations, the proliferative and degenera-
tive processes in the intima and media are expressions of the same disease, and
the very histologic forms depend upon the particular structure and function
of the vessels involved. |
In the evaluation of such a deteriorative disease, we must not forget that
the end products, we are wont to see, are elaborated over many years. To
investigators, such as Aschoff,' must be given considerable credit, for their
demonstration of the manner in which the characteristic changes are produced
from the normal embryonal arterial types up to the markedly degenerative
senile products. ‘The arteries are in no essential sense different from other
organs in which the process of building up attains a certain climax, and in
which the process becomes stationary for a certain period, only to undergo
regressive subsequent deterioration. Furthermore, it is known that the
structural development of the various organs attains its height at varying
periods and this seems to be true also in the arterial system. Aschoff
through his embryological studies demonstrated clearly that a comparison
of the embryonal arteries with the pictures they offer during early infancy,
afford enough similarity to warrant the assumption that the later changes
are but intensifications of these with secondary regressive degenerative
lesions.
It would seem well, therefore, for a clear understanding to approach the subject with a
description of the arteries of the embryo, those of the child, and those of the adult. For this
the reader is referred to the chapter on Histopathology of Arteriosclerosis.
We need not discuss here the many theories as to the pathogenesis of
athero- or arteriosclerosis. Histologic studies have demonstrated that the
beginnings of arteriosclerosis are recognizable even during youth. These,
however, do not necessarily develop into a diseased process. The alterations
that correspond to the aging process do not constitute a disease per se, but
a manifestation of deterioration. Although all individuals show the well
known evidences of arterial deterioration, only some develop a progressive
1 Aschoff, Ueber Entwick. Wachs. u. Alt. Voginge a. d. Gefiassen, (Fischer—Jena, 1900).
396 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
process of sufficient intensity to be regarded as true arteriosclerotic or athero-
sclerotic disease.
Potent as the mechanical stresses may be in the production of the degen-
erative and hyperplastic changes in the arteries, these moments, as well as
those of deterioration, cannot altogether explain all of the histologic changes
observed. If we extend the term deterioration to include all of the influences
that arteries are exposed to during life, we have a term so comprehensive that
it would naturally include forces of diverse variety. As such, deterioration
would include a complex of influences, in which not only physical, but also
chemical factors, would be engaged. In addition to the generalized wear
and tear that all tissues undergo, the arteries must be affected (Hueck) by
additional factors in order that the lesions known as athero- and arterio-
sclerosis be elaborated. Nor can we accept the view that the causal moments
must necessarily be uniform in all cases. Perhaps the special changes, such
as calcification, depend upon additional toxic factors. Therefore, in this
complicated problem it is impossible to estimate to what extent each of the
many causal moments participates in the production of the end result.
The researches of Jores! because so important, deserve more than mere
passing mention. According to this author, the changes in the intima
although not the only lesions of arteriosclerosis, are the essential alterations;
and an explanation of the intimal thickening will also throw light on the
pathogenesis of the whole process.
Heubner from a comparative study of syphilitic endarteritis of the brain arteries and
arteriosclerotic vessels, had concluded that the latter process suggests true hypertrophy
of the intima with proliferation of existing elements, especially the elastic lamella, so that
the architecture of the intima of small arteries approaches that of the normal larger ones.
All the secondary processes, such as fatty degeneration, calcification, are to be considered
essentially regressive in character, and as unimportant in so far as pathogenesis is concerned.
Jores has laid special emphasis on two types of elastic lamellae in the
intima. The first variety shows reduplication of elastic fibers in a manner
that suggests a cleavage of the membrana interna elastica, with splitting
off of fibers, and is characteristic of the arteriosclerotic process. In the
second type, new formed fibers of more delicate composition appear.
The author in his first publications on the histopathology of thrombo-
angiitis obliterans? had noted and emphasized the difference between the
new formed elastic fibers in the obliterating tissue of thrombo angiitis obliter-
ans, and those so peculiar to the hyperplastic lesion of arteriosclerosis. So
also, Jores had observed a similar discrepancy in the thrombosed arteria
fossae Sylvii of a case, and in the experimentally produced endarterial
lesion following ligation. The aforementioned peculiarities are specific in
his opinion. The hyperplastic intima associated with certain thromboses
and ligation, shows also a multiplication of elastic elements. But this corre-
sponds to the proliferation seen under other circumstances and in other
tissues. The process characteristic of arteriosclerosis is initiated by thicken- .
ing of the internal elastic lamina and consequent cleavage, a lesion that has
no analogy elsewhere in the body.
Elastic Fibers in the Normal Arteries ——For a correct comprehension’ of
the pathology of elastic fibers of the arterial intima, a knowledge of the
normal is a sine qua non, especially since variations in the thickness of this
1 Jores, L., Wesen u. Entwickelung d. Arteriosklerose, Wiesbaden (J. F. Bergmann),
1903.
2 Buerger, Pro. N. Y. Path. Soc., Feb. & Mar., 1908.
ARTERIOSCLEROSIS—PATHOLOGY 397
coat, its elastic fiber content and even reduplication of these lamellae may
occur.
In the newborn and in young infants, the intima is made up merely of
the internal elastic membrane, and the endothelium. A musculo-elastic
layer is only found at the bifurcations of the small arteries. Where vessels
are given off, small protuberances made up of such tissue project into the
vessel lumen. A longitudinally disposed muscle layer is inserted, as it
were, at certain places between two laminae of the internal elastic mem-
brane. Of the two elastic layers, the inner is more prominent than the
outer, and conserves the general course of the vascular fibers. Within
these elastic lamellae are enclosed not only the longitudinal muscle bundles
above noted, but also finer elastic fibers. This complex structure in its
entirety simulates, as can be readily seen, the lesion of intimal thickening
characteristic of the arteriosclerotic process.
Although first limited to the wall near the angles of vascular offshoots,
the duplication of elastic fibers soon extends longitudinally, so that cross
sections will find it at situations independent and far removed from points of
bifurcation. Spreading even in a circular direction, pictures are produced
in which a greater part of the circumference of the vessel wall is occupied by
this process.
Such normal variations of the internal elastic membrane do not appear
to vary in intensity according to age.
In short, a thickening of the intima indistinguishable from that occurring
under certain pathological conditions, is elaborated in the normal, probably
as a reactive response to functional demands.
Both in physiological and pathological hypertrophy of the intima, there
is a concomitant appearance of nuclei between the layers undergoing cleav-
age. It is a mooted question as to whether the longitudinally disposed cells
lying between the elastic lamellae are muscle cells or not. In fact, in longi-
tudinal sections, an intima of considerable thickness is sometimes suggestive
of a muscular media.
We have learned to recognize therefore, two criteria of the normal pro-
ductive variations in the intima, first the elastic tissue alterations, and
secondly the muscular inclusion which manifests a characteristic homo-
geneity. If we contrast here the composition of the intima accompanying
thrombotic processes, we will note the absence of muscular elements.
A third distinctive differential point between the pathological and the
normal is the occurrence of alterations in the media which attend not only
arteriosclerotic processes with thrombosis or calcification, but also are
found in thrombo-angiitis obliterans and arteries after ligation, or the seat
of embolism. These are the infiltration of the media with connective tissue,
and a striking vascularization or invasion with new formed vessels, and are
evidences of the participation of the vessel wall in the reactive processes
incident to morbid changes affecting the intima and arterial patency.
The author! too, has described such morphological alterations in the
media of the arteries in thrombo-angiitis obliterans, calling attention to the
teleological penetration of vessels into and through the muscular coat
through which they can enter or send sprouts into an occluding clot, and
partake in its canalization and connective tissue transformation.
Much discussion has arisen and contentious explanations are many on
the relative réles of the media and intima in the incitement as well as actual
1 Buerger, Proc. N. Y. Path. Soc., Feb. & March, 1908.
398 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
participation of intimal hypertrophy. The weight of evidence, as also
observations of the author, strongly attest to and confirm the importance
of the media and adventitia in the thickening of the intima as well as in
the metamorphosis of occlusive parietal thrombi.
Jores! recognizes firstly an intimal enlargement in which the reduplication of elastic
fibers has its origin in the existing lameliae, and secondly, a form in which proliferation by
virtue of agencies acting from without (media and adventitia) inward are potent. Views
are divergent as to whether the activating factor in the latter is of inflammatory nature or
not.
As for the source of the new formed elastic fibers, contradictory expressions of opinion
are found amongst pathologists. Whilst Jores assumes that new formed elastic fibers
must emanate in the first type (which he calls hyperplastic thickening of the intima) from
the internal elastica, and in the second form (to which he applies the term “regenerative
proliferation”) from prolongation and hyperplasia of existing elastic fibers of the media,
and, whilst he desires to controvert the theory of metaplasia from connective tissue as a
mode of production of such tissue, the author has shown that so restricted a view is un-
tenable. For, newly formed elastic fibers appear around and encircle the new vessels in
the center of the organized occlusive thrombus, at situations widely removed, and in no sense
continuous with similar fibers of the media or intima. Such neoplastic vessels, it is true,
arise from new formed capillaries that may represent prolongations from similar structures
in the media, but the elastic fibers about them could not }have been carried in by the
angioblasts from which the older vessels were born and had matured. This special
perivascular distribution in the author’s opinion, speaks in favor of the following view:
That elastic tissue fibrils are made out of the collagenous connective tissue elements
(metaplasia?) by a stimulus derived from the endothelial cells; and that that impulse bears
a direct relation in intensity, to the intravascular carrying power of the vessel enclosed by
the new formed lamellae; that the endothelial cells themselves do not produce elastic tissue
is fairly certain, but that they predetermine the elaboration and distribution of such tissue
is more than likely. The older and larger the new vessels in the thrombus of thrombo-
anglitis obliterans, the more elastic elements are formed.
Although this view is not in accord with that of Jores, it finds adequate support in the
abundant material elsewhere described (Chaps. LXI and LXII). That this author’s
concept of the varied arterial lesions is limited by lack of experience with that most instruc-
tive form, thrombo-angiitis obliterans, is confirmed by his own words. In the passages on
arterial lesions of ‘‘spontaneous gangrene,” he says: ‘‘Ueber diese Erkrankung stehen
mir eigene Beobachtungen nicht zur Verfiigung”’ (‘‘I have made no personal observations
on this disease”). From his perusal of the literature, which we have elsewhere demon-
strated to! contain fallacious and misleading interpretations, Jores concludes that the
lesions are to be grouped under his form of ‘‘regenerative hyperplasia.”
In arteriosclerotic vessels, Jores recognized both varieties of intimal change, the purely
hyperplastic with not only reduplication by cleavage, but also by true proliferation; and
the second type of regenerative connective tissue growth in the intima, or combina-
tions of the two. Often the separated elastic lamellae enclose new formed connective
tissue which may include foci of degeneration.’
Jores emphasizes the importance of the finding of two histologically separable and
diverse types of intimal change, postulating for these different causal agencies. Sucha view
he holds to be contradictory to the accepted* uniformity of explanation for the vascular
lesions in this disease.
The theory that inflammation is responsible he considers untenable, since the typical
hyperplastic manifestations occur in normal arteries, are seen in children and are unaccom-
panied by any of the usual histological structural elements of inflammatory processes.
Since this type of intimal thickening is the predominant one in arteriosclerosis, the inflam-
matory theory is incompatible with the appearances described by the afore-mentioned.
The Hyperplastic Intima.—As for origin of the type with cleavage of
elastic lamellae, two hypotheses may be entertained. Firstly, we may regard
the_overgrowth of the intima as a physiological response, and that this proc-
1 Jores, Loc. cit.
2 That this view is incorrect, the author’s researches on thrombo-angiitis obliterans have
conclusively demonstrated.
’ That is, up to the year 1903 when the monograph of Jores appeared.
ARTERIOSCLEROSIS—P ATHOLOGY 399
ess extends itself in arteriosclerosis, becomes more intense, suffers attendant
fatty degeneration and connective tissue infiltration.
Secondly, a non-physiological basis may be considered. One may
suppose that there are noxious influences that are present to a greater or
less degree in all persons, causing intravascular lesions in certain of them
with the aid of other predisposing factors. The irregularity of the dis-
tribution of the foci of intimal hyperplasia in the very young and the absence
of such a change in the embryo would speak in favor of such a view. Then,
too, the gradual transition into the degree considered pathological is of
moment.
Such an injurious element leading to hypertrophy of the intima is in all
probability an increased functional burden or augmentation of the normal
intravascular pressure. If we consider that there is often a distinct quanti-
tative relationship between the hypertrophy of the longitudinal muscular
fibers and the thickening of the intima, this theory obtains additional
support.
_ According to Fuchs, amongst the developmental irritants for the vascular wall, that
is, of the factors influencing growth, a periodic, physiologic, rhythmic impulse is important.
An increase in pulse tension is to be regarded as such. If we transfer this hypothesis to
the conditions in which the physiological passes over into the pathological, we can assume
that both hyperplasia of the intima, as well as the longitudinal musculature can follow
in proportion to the degree of abnormal physiological irritants.
Genesis of the Regenerative Connective Tissue Proliferation of the Intima——There is no
doubt but that connective tissue growth in the intima may be associated with or without
inflammatory processes. In arteriosclerosis both lesions of intima and media with their
concomitant fibroses would seem to owe their existence to some other than an inflammatory
motivating agent.
The researches led Jores to conclude that hypertrophy of the intima pre-
cedes the arteriosclerotic process, which in the aorta is comparable to the
hyperplasia of the first years of extrauterine life and is attended with hyper-
trophy of the musclo-elastic longitudinal layers.
The hypertrophic intima with the musculo-elastic longitudinal layers,
tends to undergo fatty degeneration. As a result there follows a proliferation
of connective tissue which may be diffuse or circumscribed depending on the
extent of the degenerative foci. Since all diffuse fibroses of the intima are
not of arteriosclerotic nature, and since a diffuse endarteritis fibrosa whose
causation and significance are still unknown, can occur, other characteristics
must be sought to differentiate and stigmatize the arteriosclerotic lesion.
Such are the participation of a hyperplastic intimal layer with fatty metamor-
phosis of the latter, and the development of a connective tissue ground sub-
stance between the elastic lamellae.
An increased functional demand on the arterial wall seems to be the
sine qua non for the origin of the arteriosclerotic process. In respect to the
nature of this change from the normal physiological, intravascular, mechani-
cal and hydrostatic conditions, heightened blood pressure with its concomi-
tant increased tension of the vessel wall would seem to offer the most
satisfactory explanation. Whatever impresses itself upon and especially
influences longitudinal musculo-elastic layers of the vessel wall to an excessive
degree, would be the most probable motivating agent in the calling forth
of structural responses, manifested as “‘arteriosclerotic.”’
Experiments in which the intracanalicular pressure in rubber tubing or
a hose is altered, give valuable information for deduction. Let us inject or
1 Fuchs, R. F., Zur Physiologie u. Wachsturms Mechanik des Blutgefiss-systems.
Habilitationschrift, Jena, 1902.
400 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
force into an elastic tube an increased amount of fluid. We will find that not
only will the tension increase, but a lengthening will take place, showing itself
in a motion of the whole tube. In the arteries the circular muscular coat
whilst in a state of tonicity or contraction, easily limits the expansile increase
of pressure (felt as pulse), whilst the mechanically more restricted action of
the longitudinal fibers permits of considerable elongation of any given
arterial length. This manifestation is clinically observable in the tortuous
temporal arteries. In these an elongation with increasing age and a ser-
pentine motion transmitted by each heart beat are well known phenomena.
Excessive pressure then would seem to make even greater demands in
the longitudinal elements than on the relatively stronger circular ones; and
consequent reactive hypertrophic changes characterized as arteriosclerotic
would be the vascular response.
Experimental Arteriosclerosis.—Because the arteries are under the
influence of so many varied factors, partly hydrostatic, partly pulsatile
forces and constantly changing intravascular stresses, and since they are
subject to the chemical influences of the blood (toxic and bacterial)—the
possible components making for pathologic alterations are indeed many.
Considerable experimental work has been done in animals with a view to
reproducing some of the pathologic alterations seen in the human, particu-
larly the athero- and arteriosclerotic. It may suffice here to recount in
brief some of this work, in order to point out the manner in which possible
etiologic factors should be interpreted.
In the attempt to produce arteriosclerotic changes most experimental
work has failed, in that an exact reproduction of the typical alteration has
not been possible. However, interesting results followed the administra-
tion of adrenalin products in animals. It has been possible to bring about
distinct changes in the arteries. Most of the authors agree with the find-
ings of Josué.! The changes comprise whitish areas and granular changes
in the intima of the aorta; streaks and larger areas of thickening of the same
region, with precocious calcification; discrete or confluent lesions, with partial
umbilication; and aneurysm formation of varying size up to that of a bean.
The lesions vary in size from microscopic up to plaques about o.5 cm. in
diameter.
Microscopically it was found that a primary change occurred in the media, particularly
in its central two-thirds. This is said to be typical, extending in plaque-like fashion
eure the muscular coat, and on cross section appearing as small streaks or segments of
a circle.
The muscle cells show their degeneration in the loss of tinctorial properties, fragmenta-
tion and loss of their nuclei. Most investigators admit that a necrosis of the muscle cells
occurs.
Klotz? mentions that fatty degeneration of the muscles is regularly initiated by adrena-
lin injection. According to his view neutral fat is first formed; this is converted into fatty
acids, and these later produce insoluble soaps with the calcium of the blood and lymph.
Saltykow on the other hand, regards the fatty conversion to be inconsequential, the
essential process being the necrosis.
The elastic elements are said to undergo characteristic changes. The lamellz in the
neighborhood of the foci lose their undulatory course, approach each other and seem to
become somewhat agglutinated. Others (Kiilbs‘) speak of a separation of the elastic
fibers. The lamellae show granules, stain poorly, may tear, become fragmented or split.
Finally they undergo degeneration and may disappear. Klotz refers to such degenera-
1 Josué, Presse méd., 1904, S. 281.
2 Klotz, Jour. Exper. Med., 1906, 8, p. 322; also p. 504.
3 Saltykow, Centralbl. f. allg. Path. u. path. Anat., 1908, XIX, p. 321.
4 Kilbs, Verhandl. d. XXII deutsch. Kong. f. inn. Med., 1905, p. 246.
ARTERIOSCLEROSIS—PATHOLOGY AOL
tion. Calcification is an early process; sometimes the specific foci are visible only
microscopically.
The Intima.—Proliferation of the endothelium is mentioned by Kiilbs and Saltykow;
others speak of degeneration of the endothelium; and still others regard the intima as
thickened with normal endothelial cells covering it (Scheidemandel). The changes in the
intima may precede those in the media (Papadea!). Ziegler interprets the irregularities of
the inner surface of the arteries as due to hypertrophy of the intima.
The Adventitia and Vasa Vasorum.—Changes in the adventitia are either absent or may
be of a reactive nature, with perivascular infiltration. According to Orlowsky? the chief
changes in the arteries are due to an obliterating endarteritis of the vasa vasorum; and
others recognize a similar process with complicating hyalin thrombosis (Trachtenberg?).
Summary.—The essential changes in adrenalin atherosclerosis seem to
be in the media, and the thickening of the intima is secondary. Perhaps
the latter is a compensatory or reparatory process due to the weakness
of the media. Opinions differ as to whether the primary changes occur in
the muscle cells or in the elastic element. The weight of evidence leans
towards the view that the muscle cells are first implicated, although a number
of authors lean to the other contention that the elastic elements are first
damaged.
As cause of the arterial changes a number of different explanations are
given comprising the following: Increased blood pressure due to the action
of the adrenalin extract; a direct elective toxic action upon the muscle
elements of the media and closure of the vasa vasorum, with secondary
trophic derangements of the media; or a combination of both causes.
The Relation of Human and Experimental Atherosclerosis.—Critical and comparative
investigations by a number of authors have led to the conclusion that changes in the arteries
of the rabbit due to adrenalin experiments, show characteristic differences from those lesions
of human atherosclerosis. Distinctive features in the human are the essential localization
in the intima, the degree of fatty degeneration and the subsequent calcification, as the final
stage of the regressive process. In the experimental rabbit, on the other hand, there has
been noted the special localization in the media, a relatively small degree or absent fatty
degeneration, and calcification at the very inception of the disease.
It is still a mooted question as to whether the alterations following adrenalin injection
are attributable to a specific toxic action, or indirectly through the increased pressure
occasioned. That a direct action may play a réle, has not as yet been controverted.
Experiments with nicotin and tobacco have not been convincing; and, although authors
report lesions similar to those produced by adrenalin, the resemblances between the artificial
and the human lesions are not sufficient to permit of positive conclusions.
Experiments have also been made with various chemical substances and bacteria.
The injection of the latter has not resulted in the formation of arteriosclerotic changes.
Saltykow and Klotz, however, report changes not unlike those of human atherosclerosis
after injection of micro-organisms (staphylococci and streptococci). The lesions were
found in the aorta and included fatty degeneration, proliferation and degeneration of the
subendotheliallayers. In Saltykow’s rabbits the degenerative changes were so marked that
he speaks of them as being easily mistaken for the human atherosclerotic processes.
Localization of Arteriosclerosis.—The localized incidence of arterio-
sclerosis as it invades the arterial tree accounts for the frequent clinical
confinement of manifestations to the extremities. The factors productive
of the lesions are variable in that the stresses in the members include a
number of different concomitant agencies. To what extent each of the
determinants, such as static influences, motion, locomotion, the special
affinities of toxins, and others, contribute, cannot be accurately ascertained.
1 Papadea, Riv. di patol. nerv., 1906, Vol. II, fasc. 5. (cit. by Tarantini in Policlinico,
1906, Sez. med., Vol. XIII, p. 311).
2 Orlowsky, Russk. Vrach., 1905, p. 1443; also 1907, p. 364.
8 Trachtenberg, Charkower med. Jour., 1907, III p. 468.
26
402 CIRCULATORY. AFFECTIONS -OF "THE EXTRKREMIT LES
Concerning the sequence and frequency in which this process affects the arteries, there
seems to be little or no unanimity of opinion. The order given by Albutt based upon
statistics of Thoma’s material is: ulnar (94 per cent), anterior tibial (93 per cent), sub-
clavian (88 per cent), cerebral (87 per cent), internal carotid (87 per cent), radial (86 per
cent), splenic (82 per cent), popliteal (79 per cent), axillary (71 per cent), femoral (87 per
cent), common carotid (68 per cent), ascending aorta (67 per cent), abdominal aorta
(64 per cent), external iliac (58 per cent), and brachial (55 per cent).
As far as the arteries of the extremities are concerned, the same partial,
quite unaccountable distribution of hypertrophic and degenerative changes
that are met with throughout the rest of the vascular system, seems to obtain.
In defective metabolism, however, as in diabetes, the degenerative and
calcific varieties tend to be more intensely and diffusely present. The degree
and site of involvement of the several arteries of a limb, too, follow no known
laws. Sometimes we glean the impression that the popliteal, especially at
its bifurcation, and the distal parts of the arteries and posterior tibial are
localities of predilection, only to be surprised at their relative integrity in
other cases.
CHAPTER LXVIII
ARTERIOSCLEROSIS—MINUTE PATHOLOGY
For a comprehension of the organic alterations responsible for the circula-
tory affections and gangrene of arteriosclerotic nature, it will suffice to discuss
merely those arterial lesions that are sufficiently advanced to bring about
nutritional disturbances. And so we give but passing mention to those well-
known early changes in which the intima alone is but slightly involved. In
the chapter on the architecture of the normal arteries, it was pointed out
that limited hypertrophies of the intima begin at a very early age. In Fig.
129 a minute patch of intimal hypertrophy is well depicted in a normal
anterior tibial vein. More pronounced are the lesions in Fig. 130, macro-
scopically apparently ‘‘normal”’ external plantar artery, where thickening of
the intima and hyalin change are easily discernible. The intermediate
alterations from these minimal ones to the exceedingly destructive processes
are so well known as to require no detailed description. We shall confine
ourselves to an exposition of those personal observations on arteries dissected
out from amputated limbs, in which the lesions were responsible for trophic
disorders and gangrene.
The larger arteries in arteriosclerosis are not infrequently narrowed by the
presence of a glassy gelatinous-like tissue of bluish pearly and yellowish
appearance, arising from the inner wall of the vessel.
On section through such arteries this is seen to be made up of altered clot,
or of proliferated intima with secondary degenerative changes. In thrombo-
angiitis obliterans we rarely meet with such regressive phenomena in the
occluding tissue, the latter being better nourished, both by reason of the
number of vascular elements, and also because the nutritional conditions are
far better in vessels of younger people.
Characteristic of the disease of the larger arteries is the production ofa
layer of new-formed tissue (crescentic on cross section), poor in capillaries and
rich in hyalin connective tissue. Two types are met with; one in which the:
ARTERIOSCLEROSIS—MINUTE PATHOLOGY 403.
cells are abundant and in microscopic sections give the tissue an appearance
simulating unaltered young cartilage; and another form, in which the active
tissue shows small compressed spaces containing distorted fixed or endothelial
cells, pigment and degenerate nuclei. In such tissues as these, by reason of a
sort of myxomatous degeneration, a gelatinous macroscopic product is elabor-
Fic. 129.—A*portion of a normal anterior tibial vein showing a small focus of hypertrophy
of the intima (x).
ated. Near the media, vascular spaces are frequently formed, lined with
endothelium, these being the dilated remnants of new-formed vessels that
have penetrated and vascularized the tissues. In addition to the previously
mentioned regressive changes fatty degeneration and atheroma also take place.
Organized clot also may contribute to the formation of the glassy gela-
tinous looking material seen in such arteries. The clot becomes organized
in typical fashion; with this process penetration with new-formed vessels and
404 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
proliferation of capillaries takes place. Later degeneration of myxomatous
and hyalin variety sets in.
The obliterative lesions and the vascular lesions are well shown in Figs. 131
and 132 where the popliteal artery is the seat of typical atherosclerotic lesions
with'some calcification and complete occlusion, atheromatous material and
intimal thickening. A reference to Fig. 131 will make clear the usual type of
reduplication of the internal elastica, and the extent of,the thickening of the
intima, and will also show a recently organized clot whose architecture is
totally different from that of thrombo-angiitis obliterans.
Fic. 136.—‘‘ Normal’”’ external plantar artery with but slight hypertrophy of the intima
(a); early lesions of atherosclerosis.
The paucity of lesions in the adventitia is diagnostic for arteriosclerosis.
There is no cellular infiltration, no thickening and no adhesion between it and
the surrounding structures.
In the media the inflammatory and productive lesions of thrombo-angiitis
obliterans are absent, but characteristic are the lime deposits and the degener-
ation of the musculature. In Fig. 133 elastic tissue stains show clearly that
the normal course of the circular elastic fibres is interrupted by lime deposits,
atheroma, and even bone formation.
The enormous thickening of the intima with the formation of character-
istic plaques is seen in Fig. 132 (6). Here there is a concomitant production
of elastic elements, the tissue having no relation to the clot, but being the
product of a proliferative process. This in places shows the typical degenera-
tive phenomena—cellular and connective tissue degeneration with atheroma.
ARTERIOSCLEROSIS—MINUTE PATHOLOGY 405
Fic. 131.—The difference in healing properties of the hypertrophied intima detached
above (at h) and the organized clot can be appreciated in the greater darkness of the former;
the loss of tinctorial properties of the degenerate intima at c as compared with the portion at
bis well shown. At h the hypertrophic intima between h and the dotted line e-f has been
detached artificially, and fuses in the picture with the organized clot.
406 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
i
detach. ee.
Fic. 132.—High power of the region b and c of the artery previously shown; at b the
markedly hypertrophied intima; at c undergoing myxomatous degeneration, the clot
probably beginning at this point where it is adherent at 7.
ARTERIOSCLEROSIS—MINUTE PATHOLOGY 407
The obturating tissue depicted in the figures will demonstrate the differ-
ences between the occluding tissue characteristic of arteriosclerosis and that of
thrombo-angiitis obliterans, and that the obturating tissue, as here exempli-
fied, is composed of degenerative hyalin or myxomatous fibrillar variety
in which the vascular elements are scarce or absent, plus the fused, partly
organized, partly degenerate thrombus.
FIG. 133.—Cross section of a plantar artery in a case of arteriosclerotic gangrene.
The Larger Arteries in Gangrene. TJhe Obliterating Tissue—It is not
always easy to distinguish microscopically between organized thrombus and
arteriosclerotic proliferating tissue, both of which may partly or completely
occlude the arterial lumen. The pearly, glassy or whitish tissue that com-
pletely fills such a lumen in atherosclerosis is most often the hyperplastic
intima in a state of hyaline degeneration. The production of a peculiar
hyaline tissue in which there is a rather sparse distribution of fusiform or.
stellate compressed cells is a characteristic feature of the obturating tissue
(Figs. 134 and 135). This type of picture offers a noteworthy point of
differentiation between the sclerotic connective tissue of thrombo-angiitis
408 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fic. 134.—Occlusion in arteriosclerosis. The artery in the picture is closed by fibrotic
tissue which is poor in cells and shows hyaline degeneration, as well as two foci of bone
formation. ‘These are seen in the dark areas, which, on magnification, would show bone
cells and lime deposits. Here, too, the characteristic collections of mononuclear cells in
the media without any inflammatory process in the adventitia is pathognomonic and per-
mitting of differentiation from thrombo-angiitis obliterans. The absence of fusion of
artery and vein distinguishes this from the advanced periarteritis of thrombo-angiitis.
ARTERIOSCLEROSIS—MINUTE PATHOLOGY 409
obliterans and that of atherosclerosis. For the most part its lamelle or
pseudo-lamelle (since these are merely separated by cells) are disposed more
or less concentrically, but variations occur. Their course may be longi-
tudinal, and cross sections of bundles are thereby obtained. It is, however,
in the neighborhood of canalizing vessels that a distinct interruption of the
general monotony of this picture is produced, for here the connective tissue
Fic. 135.—Completely obliterated dorsalis pedis artery (part of cross section) in a case
of atherosclerosis with diabetes and gangrene. Lumen completely filled with character-
istic proliferative intima, fibers of which run longitudinally or roughly concentrically;
below, lime deposits and bone formation just under the internal elastic lamina; above, and
elsewhere in the media perivascular and intermuscular collection of round cells; dilated
capillaries, spaces, and sinuses in the media (high power of a part of Fig. 134).
fibers are often disposed in longitudinal fashion about the new-formed vessels,
so that larger and smaller punctuate areas representing fibers transversely
cut distinctly modify the general tone of the picture (Fig. 135).
Often the lumen is filled with connective tissue of less dense structure,
containing pigment, whenever organization of a clot has taken place. Thus
pictures resembling the old obliterative process of thrombo-angiitis may be
410 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fic. 136.—Complete occlusion through organizing connective tissue of an athero-
sclerotic artery; areas of calcification along the internal elastic membrane, thie of the
intima, loose connective tissue occupying the lumen.
ARTERIOSCLEROSIS—MINUTE PATHOLOGY 411
produced (Figs. 136 and 137). The intensive elastic tissue production
sometimes seen in arteriosclerosis is well shown in Fig. 138.
Recent Occlusion of Atherosclerotic Popliteal Artery—The clinical
manifestations of sudden occlusion of the popliteal artery as a complication
sometimes precipitating gangrene are described elsewhere (Chap. LXIX).
Mechanical or stagnation thrombi are not uncommon in arteries that are
more or less stenosed and partly occluded by hypertrophic intima. The
intima usually has undergone considerable hyaline or myxomatous change
Fic. 137.—Low power of the completely occluded dorsalis pedis artery in a case of
arteriosclerosis. The lumen is filled with organized thrombus and large new-formed
vessels. The media above shows infiltration with mononuclears and numerous lime
deposits in places. The intima is thickened in typical fashion.
with secondary atheromatous and lime deposits. Cholesterin and foreign
body giant cells are not infrequently seen. The media also shows regressive
changes, and in addition is characterized in the longitudinal sections of the
arteries by the presence of numerous dilated vessel spaces, that doubtlessly
represent an intramural collateral circulation, if such a term may be employed
in this sense. A reference to Figs. 139 and 140 will show recent thrombosis
in the popliteal artery. In Fig. 139 a cross section shows complete occlu-
sion by clot; and Fig. 140 shows a longitudinal section of the popliteal
artery, with distal termination of the clot.
The Media in the Obliterated Arteries.—For purposes of differentiating
this disease from thrombo-angiitis obliterans, some knowledge as to the
picture presented by the media at various stages of the atherosclerotic and
obliterated process should be well understood. The changes are degenera-
412 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Fic. 138.—Arteriosclerotic lesion in a vein and artery. The typical proliferation of
elastica in arteriosclerosis is shown, as well as the splitting of the internal elastic laminae.
The absence of perivascular inflammation is also seen, and the large vein shows marked
endophlebitis, the intima being markedly thickened so as to occlude about one-third of
the lumen.
ARTERIOSCLEROSIS—MINUTE PATHOLOGY 413
tion of muscle, and at the boundary between the media and intima, atrophy,
disappearance of muscular elements, calcification, bone formation, cellular
infiltration and vascularization.
Media Lesions when the Lumen 1s Filled —When the media itself is free
of lime deposit or larger degenerative processes and fatty deposits, the
reactive responses due to the changes within the lumen find their best expres-
sion. The striking alterations are the areas of cellular infiltrations and the
new-formed vessels.
~
Fic. 139.—Recent thrombotic occlusion of the popliteal artery. The media shows
bone formation, calcification and the usual regressive changes; so also the typical hyper-
trophic and degenerative changes are present in the intima.
Just under the internal elastic lamina, we sometimes see collections of small
round cells that often have a perivascular distribution in that a small capil-
lary or arteriole is found within their midst (Figs. 134 and 135). Such foci
can be traced extending in rows of cells between the more centrally placed
muscle fibers of the media, and separating these considerably. Often such
areas correspond to rather extensive infiltration of similar nature throughout
the central half or more of the muscular layer, where longitudinally or
obliquely penetrating capillaries also invade the media. In general the
appearances here described are those of small foci of lymphoid cells.
In addition there may be an increased number of migrating cells scattered
here and there throughout the middle coat. The vascular changes in the
media are prone to strike the eye as unusual. An abnormally large number
414 CIRCULATORY AFFECTION S7 OP Ta EE XCE REM [1 ies,
of capillaries or even sinuses occupies the central layers of the media, some
traceable for a considerable distance in a circular direction, others found to
connect with vessels traversing obliquely through the media and into the
adventitia; and still others, in direct communication with blood sinuses of
varying size just under the internal elastic coat. The varying sizes of these
capillaries and the sinuses with which they communicate give the impression
that a virtual canalization or collateral circulation through the walls of the
vessels as well as into the obturating tissue can and does occur (Fig. 135).
Fic. 140.—Longitudinal section of the popliteal artery recently occluded (same as
Fig. 139). The media shows numerous dilated vessel spaces (intramural collateral
circulation); the intima is markedly thickened, showing degeneration, atheroma. The
lumen is filled with recent clot terminating distally (below in the picture).
Although an increased vascularity of the media is not pathognomonic for
arteriosclerotic processes and is present also in thrombo-angiitis obliterans,
we have nevertheless, here a distinctive point of differentiation. For, the
larger sinuses and the apparent attempts to form devious vascular surrogates
for the lost lumen are wholly absent in thrombo-angitis obliterans.
Because of the convoluted course of the internal elastic coat and the
marked intrusion of the plicae towards the lumen of the vessel, sclerotic
and obturated vessels often give a picture that is confusing. For, when
foci of special character lie in the peninsular projections of the internal coat,
they may project so far into the obturating mass, as to appear to lie within
the latter. In truth, on closer observation we will notice that the calcific
deposits, the degenerate areas and the bone formation sometimes present,
ARTERIOSCLEROSIS—MINUTE PATHOLOGY 415
are confined to the media or lie in such prolongations. Arteries that show
small areas of lime deposit in the internal coat, in and just outside of the
internal elastic lamina, may often give the appearance of lime plaques within
the occluding mass. However, one sees just at the internal limiting mem-
brane a larger or smaller focus of lime deposition, often partially converted
into bone or osteoid tissue (Fig. 135). It is significant, too, that immediately
adjacent to, or leading up to such areas, we almost always find one or more
minute vessels.
Fic. 141.—Cross section of occluded popliteal artery in atherosclerosis (same as Fig.
131). The greater part of the lumen, were it not for the artificial retraction of the obturat-
ing mass would be filled except for the roughly elliptical area of lumen left at a. The
obturating tissue is composed of hypertrophied intima most marked at b, myxomatous at c,
making a crescentic zone of firm, partly degenerate tissue. The rest of the lumen is filled
by organized clot, also in state of degeneration (hyaline, myxomatous) fusing imper-
ceptibly with degenerate intima, but distinguishable from it by the absence of elastic
tissue. Ataresidual lumen; at b typical intima proliferation; at c hyaline or myxomatous
degeneration of intima; d to e tof to g represents organized somewhat degenerate clot, fusing
intimately with the detached intima along the line ef.
Arteriosclerosis with Mixed Occlusion.—The occlusive process may be
wholly due to the thickened intima and the heaping up of degenerative
products. On the other hand, to the crescentic shaped’ hypertrophy of a
1 On cross section.
416 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
part of the wall of the intima, occlusive thrombosis may be added, and the
end-products after organization, develop into a tissue of varying appearance
and consistency. Sometimes it may be glassy, gelatinous, pale, greyish-white
or yellowish in appearance, or possess an admixture of red areas of recent
clot; or it may contain brownish firm clots that represent earlier stages
of organization. We often find the peculiar gelatinous tissue in the larger
arteries, such as the popliteal.
A study of most of the atherosclerotic lesions and of the occlusive throm-
bosis may be made from Figs. 131 and 141, taken from a popliteal artery
in a case of gangrene.
The media and adventitia show the usual characteristic changes of arterio-
sclerosis. In the adventitia the striking features are the absence of inflamma-
tory lesions and of perivascular fibrosis (the latter so characteristic of
thrombo-angiitis).
Even a gross view of the middle coat reveals a noteworthy disorganization,
in the varying thickness and the degenerative products. While in places it is
very thin, in others the normal girth is well conserved or increased.
In those portions of the-media in which but little attenuation has taken
place, the nature of the process is most easily demonstrated in arteries of this
sort. ‘The degeneration of the muscle fibers, their separation by infiltrating
fatty deposition, and minute granules of lime in streaks or in plaques are the
significant changes. ‘These are so well known as to require but passing men-
tion. However, it should be borne in mind that the infiltration with lime
deposit goes on so insidiously that large areas are already extensively involved
before the calcareous plaques are definitely formed.
The Occluding Tissue.—As above stated this is composed of two distinct
portions which may fuse so imperceptibly as to be microscopically indis-
tinguishable except on close scrutiny, namely, the crescentic and partly annu-
lar intimal hypertrophy in its varying aspects of degeneration and the
organized clot. A reference to Figs. 131 and 132 will make clear how difficult
it may be except with a high power objective to clearly separate the hyalin
(or myxomatous) hypertrophied intima from the organized clot that has
undergone a similar regressive process.
A reference to Fig. 131, which is stained with the elastic tissue stain,
however, clearly shows that even the degenerative intima takes on a suffi-
ciency of this stain (orcein) to demonstrate its greater age, and the concentric
and more or less parallel arrangement of the elastic fibrils therein.
The Intima in the Larger Vessels.—Sufficient emphasis has been laid upon
the nature of these lesions in the text books to make a detailed description
superfluous here. We shall, therefore, dwell only upon those minutiae that
may be important for those who wish to study the relationship of the throm-
botic lesion in these vessels and those in other vascular affections; and those
changes shall receive attention which are at first sight confusing and difficult
of recognition and differentiation from the hyalin degenerative alterations
occurring in bland organizing thrombosis.
Much can be learned from a study of those larger arteries in which the
pulsative and distensive stresses find their most intensively elaborated reac-
tion in hyperplasia, as in the popliteal and femoral arteries.
The typical tissue with its peculiar cell inclusion of a hyalin nature, so
characteristic of intimal thickening forms plaques of varying size, that intrude
into the lumen and bring about a corresponding coarctation. While the
nature of this tissue is easily recognizable under the microscope, certain
portions of it, when undergoing degeneration (Fig. 132), and when the fibers
ARTERIOSCLEROSIS—MINUTE PATHOLOGY 417
are separated by fluid infiltration, may so closely resemble the hyaline
degeneration of organizing blood clots, that confusion may arise.
Elastic tissue stains, however, give the most reliable information and
permit of the best differentiation between a clot and the degenerate intima.
Grossly, such separation is not always possible.
If we refer to the figures, such as Fig. 132, in which the elastic fibers of the
intima are brought into view, three distinctive forms are encountered;
firstly, duplication of the internal elastic lamella; secondly, the old concentric
proliferation of new elastic tissues in the hypertrophied intima; and thirdly,
those sparse and irregularly disposed elastic fibers that are found in the regions
of the intima that have undergone degeneration.
A reference to Figs. 132, 138 and 142 will illustrate clearly the nature of the
reduplication of the internal elastic lamina in typical fashion.
In the second zone (Fig. 132 at 6) clearly brought into view by the stain
the elastic fibers are distinguished by that lack of continuity that has been
previously referred to (Fig. 131). They are detached short fibrils, deposited
in the intercellular substance, and therefore surround and embrace the
characteristic cellular inclusions. From the intensity of the stain, however,
we can adjudge that they are of considerable age, and their general conforma-
tion and interrelationship stamp them at once as a part of a new-formed
intima wholly separate from the organized clot.
The third zone (Fig. 132 at c) may be single or multiple and comprises
that portion of the intima which has undergone degeneration. A lenticular
area of this hypertrophic intima is apparently of different structure, in that it
stains less deeply, and has a greater affinity for the hematoxylin stain,
also in the wide separation of the cells contained therein. In these a sort
of hyaline or myxomatous and in part fatty degeneration takes place, with
a consequent disruption of the few fibers of elastic tissue therein contained.
As a result, the elastic tissue stains are much less deep, since the fibers are
less numerous and broken up. It is these degenerative areas which, when
fused with the organized clot, make a composite mass that might be incor-
rectly interpreted as having the same origin, but which belong on the one
hand to the intima, on the other hand to the blood clot. The absence of
the diffusely deposited elastic fibrils in the organized clot distinguish the
latter (Figs. 131 and 132).
The organized clot in such vessels presents nothing unusual. However
in those obturating masses of thrombotic origin that have undergone degener-
ation, and in which surface vascularization cannot take place by reason of the
poor circulatory conditions in the vessel wall, there is a relative preponderance
of myxomatous or hyaline degenerate connective tissue with rather few
organizing vessels. In places the degeneration may be of a nature similar to
that going on in the contiguous intima, so that the two fuse into a mass whose
identity can only be cleared up through the elastic tissue stain (Figs. 131
and 132).
The peculiar hyaline thrombi give important information regarding the
differences in the response of the more muscular arteries, and of the larger
type of arteries, to the thrombotic processes. ‘The lack of reactionary elastic
activity and hyperplasia in the clots of the larger vessels is in keeping with the
vascular and more elastic nature of the arterial wall. Wherever we are deal-
ing with thromboses in the smaller more muscular vessels, in which easier
penetration with new-formed vessels from the adventitia can take place, we
find more firm connective tissue in the clot,and morerapid organization. The
myxomatous and hyaline clots are characteristic of the larger vessels.
27
418 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
The Pathology of the Smaller Vessels.—By illustrative description of the
varying lesions in the smaller vessels, much of diagnostic value can be learned,
and the interpretation of pictures simulating thrombo-angiitis obliterans can
be facilitated. It is when we are dealing with gangrene and in cases in which
the vessels show but sparse distribution of atherosclerosis, and where the
advent of gangrene seems to be attributable to extensive thrombotic closure
of the popliteal, that the exact nature of obturating lesions in the peripheral
vessels (plantars, dorsalis pedis, posterior tibial, etc.) may require some
analytical skill. In the chapter on the Clinical Course of Arteriosclerosis
Fic. 142.—Cross section of posterior tibial artery in case of atherosclerosis. . The lumen
is completely filled with new-formed tissue; to the left and above, there is a large clear area
with fatty degeneration, with slit-like spaces containing cholesterin crystals, two of which
(needles) can be distinctly seen at about 8 or 9 o’clock as sharp black lines; the character-
istic reduplication of the elastic membrane, and the absence ot periarteritis and the normal
separation of the vein above and to the left in the picture from the artery with no inflam-
matory process intervening, are well shown.
with Thrombosis the manifestations of this combination of lesions have been
discussed. There we have dealt with the differentiation between chronic
atherosclerosis attended with recent popliteal or femoral thrombosis on the
one hand, and thrombo-angiitis obliterans with engrafted thrombotic arterio-
sclerosis on the other. While the recognition of bland thrombosis in the
popliteal is easy when it complicates arteriosclerotic lesions, some of the
older isolated obturating foci in the peripheral vessels may be more difficult
of interpretation.
Although old canalized thrombi in arteriosclerotic vessels occasionally
give pictures almost identical with thrombo-angiitis obliterans, except for
ARTERIOSCLEROSIS—MINUTE PATHOLOGY 419
the associated calcific and degenerate changes in the walls, an investiga-
tion of more material will usually reveal pictures that are distinctive of
arteriosclerosis.
It is the degenerative phenomena of the proliferated intima, the character
of the internal elastic membrane and the regressive and degenerative changes
in the subintimal layers and media that are pathognomonic for arterio-
sclerosis. And so, whenever a large part of the obturating tissue shows these
characteristics, the diagnosis of arteriosclerosis can hardly remain in doubt.
In thrombo- -angiitis obliterans fatty degeneration does not take place in the
obturating tissue.
Fic. 143.—Cross section of artery of the leg in a case of arteriosclerotic and diabetic
gangrene. The lumen is almost closed by onion-like concentrically and eccentrically
placed proliferation of the intima, the larger ovoid space being the narrowed lumen, the
longer narrower spaces being artefacts. The lime deposit in the intima, the nature of the
intimal proliferation, and the absence of vascularization of the media, when thrombosis is
not present, are here well demonstrated.
A reference to Fig. 142 will show a part of the posterior tibial artery in a
case of atherosclerosis associated with popliteal thrombosis. A large part
of the occluding tissue here is made up of tissue in which there are a multitude
of spaces containing cholesterin crystals. The typical retracted spaces along
the margins of which the well known cholesterin giant cells are to be found
in some of the sections are diagnostic of arteriosclerotic intimal degeneration.
The associated regressive foci with lime deposits just under the reduplicated
internal elastic laminae are also striking features. Furthermore, the absence
wee pr 423, Gase o.oo.
420 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
of periarterial fibrosis and the lack of fusion with the practically normal
vein, are features belonging to the same disease.
Arteriosclerosis with Calcification.—A common type is the one illustrated
in Fig. 143, where the distal part of the anterior tibial, at the junction of the
dorsalis pedis depicts the ordinary concentric infringement upon the vessel
lumen. The obturation originating from the walls is usually eccentric in
that the mural thickening is greater at one portion than at another, giving
the characteristic crescentic encroachment of the lumen seen upon section of
Fic. 144.—On the right is a muscular branch of the popliteal artery with extensive
advanced calcification and bone formation (pipe-stem artery). The pale, inner layer is the
zone of intimal thickening with osteoid tissue and calcification on the right. The darker
band encircling the artery represents lime deposit. To the left, an accompanying vein
with marked thickening of the intima, hypertrophy (phlebosclerosis).
the vessel. Such a picture would hardly give any cause for misinterpretation,
since certain distinctive features are represented by it. The new-formed
tissue shows a paucity of cells, the peculiar diffuse degeneration, and the
deposit of lime. ‘The last is more intense near the internal elastic lamina.
The absence of periarterial fibrosis is also well illustrated here.
When the calcareous deposits are extensive—and these may affect the
very smallest branches as well as the large—the well known pipe-stem arteries
are formed. ‘The process is well illustrated in Fig. 144 where the accompany-
ing vein is the seat of marked intimal thickening (phlebosclerosis), and
hypertrophy.
ARTERIOSCLEROSIS WITH THROMBOSIS—CLINICAL COURSE 421
An even more striking picture is that presented by those specimens where
there are large plaques of lime deposit and bone formation (Fig. 133 at 12
o’clock). The lenticular or crescentic hyperplasia of the intima is beautifully
shown.
Bone Formation in Sclerotic Arteries —This process is so well known, that
but a few characteristic pictures need be shown here. These will demonstrate
the cellular activity that accompanies both the resorption of the lime, and
the conversion of connective tissue and lime into osteoid and osseous tissue
(Buerger and Oppenheimer!). The action of cells similar to those known as
osteoblasts and the conversion of lime areas into bone are well shown in
Figs. 133 and 145.
Fic. 145.—A small portion of the media of an atherosclerotic artery in which bone
formation is depicted; above, the fibres of the media infiltrated with small round cells are
seen; in the middle the dark area represents calcified material in which bone formation is
going on; the central portion has been replaced by connective tissue containing small
vessels and numerous round cells; the areas of bone formation are well depicted.
CHAPTER LXIX
ARTERIOSCLEROSIS WITH THROMBOSIS—CLINICAL COURSE
Arteriosclerotic Gangrene with Thrombosis.—Sudden thrombosis or
extension of old thrombotic process in arteriosclerosis must be regarded
as being a complication of extensive arteriosclerotic or atherosclerotic
disease of the vessels of the lower extremities. If we study the pathological
findings in the arteries of legs amputated for gangrene, and compare these
1 Buerger and Oppenheimer, Jour. Exper. Med., April, 1908, Vol. X, 3.
422 CIRCULATORY AFFECTIONS. OF THE EXTREMITIES
with the clinical history, we will note the following causes for gangrene in
athero- and arteriosclerosis: first, that the circulatory inadequacy or insufh-
ciency is partly due to the loss of elasticity in the vessels, partly to concentric
diminution of the lumina of the vessels through atheroma, thickening of the
intima, and calcification; second, that these stages are not sufficient to account
for the sudden advent of gangrene in some cases, nor can other sources, such
as cardiac weakness and trauma alone, be considered sufficient as immediate
causes. But, there is a distinct pathological explanation in the occlusion
produced by sudden thrombus formation. This usually occurs in the popli-
teal artery and extends upward into the femoral, more frequently passing
downward into the posterior tibial artery. Histological examination of the
femoral, popliteal and posterior tibial arteries in such cases, has demonstrated
conclusively the importance of the réle of thrombosis in the causation of the
gangrene, the thrombus being discovered in various stages of organization,
depending upon its age, that is, upon the time that has elapsed between the
onset of its formation and the time of amputation of the limb.
Clinical History.—There is usually a previous history in elderly individuals _
(over forty-five years of age) of intermittent claudication or indefinite pains in
the lower extremities, particularly in one limb. Suddenly, the patient will
develop the following symptoms: trophic disturbances terminating in gan-
grene of small extent (one toe or more); or dry gangrene of a toe or toes, the
foot, or portion of a leg; or, extensive dry or moist gangrene. In other cases
the signs of sudden impairment of circulation due to thrombosis of the pop-
liteal or femoral arteries make themselves manifest without the development of
ulcer or gangrene. ‘These are sudden pain in the calf of the leg or foot, attended
with paresthesiz, coldness, pallor and weakness of the limb. Examination
reveals absence of pulsation in the dorsalis pedis, posterior tibial, possibly also
in the popliteal arteries, pallor of the foot, slight erythromelia on depression
of the limb, at times thrombosed veins, particularly the external saphenous.
Hemorrhagic areas and cyanotic patches suggestive of impending gangrene
may also appear. Improvement in circulation may then take place, so that
the limb gradually becomes warm, the pallor and cyanosis disappear, a
state of chronic erythromelia (rubor) being usually the manifestation of
improved circulatory conditions. Sooner or later, however, even such cases
may have fresh attacks of thrombosis leading to gangrene.
A study of the vessels in such cases has shown either recent organizing
thrombi in the popliteal artery, or, a combination of these clots with old
organized clots, the recent thrombosis extending for a variable distance
downward into the posterior tibial artery. From the observations on the
conditions of the arteries, it seems that extensive obturation due to athero-
sclerosis, atheroma, etc., and old thrombosis in the popliteal artery may be
compatible with fairly good circulation of the imb. But, when an additional
extensive recent thrombosis takes place, or, when extraneous causes (cold, cardiac
weakness, etc.) are added, the limb succumbs to the mortifying process.
Whilst certain patients offer a history that suggests clearly the occurrence
of a fresh accession of thrombus formation, there are others in whom there is
merely the story of a trophic lesion apparently precipitated by cutting a nail
with injury to the nail-bed or surrounding skin, or by an operation for ingrow-
ing nail. When an ulcer thus formed is suddenly complicated by a turn for
the worse, with more deficiency of local circulation, it is usually due to recent
thromboses in the popliteal or posterior tibial arteries.
After pain in a toe (usually the big toe) for a variable time, a period of
intermittent claudication, a trauma, or without cause, an ulcer forms and
ARTERIOSCLEROSIS WITH THROMBOSIS—CLINICAL COURSE 423
refuses toheal. There is gradually deepening cyanosis and coldness about the
affected region. Erythromelia, and ischemia can be elicited and the pulses
up to the femoral are usually absent. Suddenly the toe begins tolook black
and the foot becomes colder, gangrene being imminent (recent thrombosis?).
Even such cases may respond and heal under the postural method.!
Bland thromboses are apt to occur in the popliteal or upper posterior
tibial artery with extensive gangrene of sudden advent asa sequence. The
lesions of thrombo-angiitis obliterans, too, may have preceded with partici-
pation of some of the peripheral vessels, such as the dorsalis pedis and
plantars. When alterations in the latter are of very long standing and second-
ary degenerative changes (calcification) coexist, a clinical differentiation
from arteriosclerosis may be no longer possible. The cases allow of the follow-
ing grouping:
(1) Advanced atherosclerotic diffuse processes, thrombotic occlusion and
organization in the peripheral vessels with superadded recent bland throm-
bosis leading to gangrene of sudden onset.
(2) Advanced atherosclerotic diffuse processes, old thrombo-angiitis
obliterans of limited extent in the peripheral vessels, recent bland thrombosis
and gangrene.
An excellent example with thrombosis of the popliteal artery is the
following:
S. S., male, age 59 years, had intermittent claudication and cramp-like pain in the right
leg on walking, dating back 4 months. Six days before he reported for examination, an
ulcer appeared over the right big toe, which increased gradually in size without much pain.
Two days thereafter the toe became black, and the patient suffered repeated chills. He had
noticed redness, tenderness and swelling of the right leg the following day. He had no other
symptoms.
Physical examination (author’s notes taken January 30, 1915) showed the big toe of
the right foot to be bluish and livid, and evidently the seat of rather extensive gangrene,
the cyanotic color being rather deep, the toe cold. At its root the skin was very deep blue,
blackish and in the early stages of gangrene. The color was apparently altered by reason
of the detachment of the epidermis and a collection of fluid (serum and blood) underneath
it; in short, a large blackish bleb of irregular contour.
remaining more or less circular. Or there is a parietal endarteritis, the lumen
of the vessel being deformed. In certain sections complete obliteration has
been observed, due either to hyperplasia of the walls, or to thrombosis at the
level of a plaque of arteritis. Above the point of stenosis, the caliber of the
artery may be augmented; the narrowings may be few, or multiple over long
stretches of the vessel. In the stenosed areas lesions may be absent or
minimal; or occasionally there may be slight dilatation.
Microscopically the intima is particularly involved, the external and
middle coats being relatively intact. The subendothelial coat is 4 or 5
Fic. 152.—Recent gummatous periarteritis (cerebral); a, intima proliferation; },
inflammatory infiltration in the outer margin of the intima with a giant cell; c, elastic
limiting lamella interrupted by leukocytic infiltration; d, media with small foci of leuko-
cytes; e, adventitia with large gummatous infiltration; at f, necrosis. (Benda)
times the normal size, thickened by virtue of concentric layers of numerous
fixed connective tissue cells. The internal limiting elastic membrane is inter-
rupted in a number of places by new formed tissue of vascular type,
originating in the media. ‘The intima presents protuberances due to rounded
vegetation, which may project into the lumen.
The media shows very little although the muscular tissue may be atrophied.
The adventitia is thickened, and there is distinct periarteritis that may
extend to the accompanying veins.
The lumen of the vessel may be obstructed by clots which show various
stages of organization.
Druelle divides the lesions into 3 types. The first is one in which there
is a panarteritis with all of the arterial coats involved. It may be acute, and
offer a fulminating clinical picture; or chronic, when it constitutes the ana-
tomic substratum for ectasis and syphilitic aneurysm. The second type
shows the lesions of endarteritis. ‘This process is said to lead to sclerosis,
but not to gummata. Asa result, narrowing and even obliteration of vessels
takes place, and hence, an endarteritis obliterans of sclerotic variety. The
SYPHILITIC ARTERITIS AND GANGRENE 459
third is an arteritis and periarteritis with gummatous changes in which the
alterations in the adventitia are more marked than those in the intima, both
as regards intensity and extent. Veritable gummata appear in the arterial
walls, and have been demonstrated in the vessels of gangrenous limbs.
Secondary thrombosis is often an accompanying lesion that leads to the
usual complications. It may be concluded from this exposition that in
the first two types a positive differentiation from other arterial affections
cannot always be made.
Since the larger arteries of the extremities, especially the tibial, femoral
and brachial arteries, when the seat of old luetic lesions may not offer any-
thing absolutely characteristic, the following points have been suggested as
of differential value: the predilection of the disease for certain localities
(central nervous system); the symmetrical distribution; the circumscribed
nature of the lesion in the vessel wall; the predominance of the proliferative
over the regressive degenerative changes; the tendency to form nodules that
resemble gummata; the rather rapid development of the lesions; and the
relative youth of the patient.
In the aorta the adventitia and media seem to be the chief localities for luetic disease.
In the intima there is compensatory proliferation; it is involved only in the most intense
degrees of specific infection and necrosis. In the cases of recent activity true gummata may
be recognized. ‘There are lentil-sized or larger yellowish necrotic foci. They can be differ-
entiated from those of atherosclerosis by the gelatinous thickening of the surrounding
adventitia, and because of the penetration of the necrosis into the adventitia. Small
irregularities of the intima with corresponding depressions and defects of the media are
characteristic in the earlier stages; but later on the macroscopic diagnosis may be impossible.
Cicatricial retraction of the intima with attenuation of the coat has been observed. How-
ever, inasmuch as arteriosclerosis may show a cicatricial form, a differentiation may be well
nigh impossible. Therefore, here again only the finding of gummatous foci, cellular infiltra-
tion with necrosis and giant cells are dependable criteria for diagnosis of luetic disease.
The finding of spirochetz pallida in the non-gummatous form is a recent con-
tribution worthy of note. Benda! reports the presence of numerous spirochetes in the
adventitia (also Strasmann?).
Incidence.—Instances of gangrene of the extremities as a consequence
of syphilitic arteritis are of infrequent occurrence. Of 14 cases (Druelle®)
only 2 were over 50 years of age. The gangrenous process is of the dry
variety, not unlike that of senile gangrene. As to the time that elapses
between the onset of the syphilitic infection and the onset of evidences of
arterial complication and gangrene, weight of opinion leans to the view that
it is a tertiary manifestation. Nevertheless, there is a precocious form that
appears during the secondary phase of the malady (2 years after the chancre
in the case of Fournier). In it, gangrene is described as the sequel of an
acute arteritis; and during this period the chancre may be still present.
These cases belong to a fulminating or malignant precocious form of arterial
affection.
Males are more frequently affected than females, there having been 1
female in the above series of 14. As for the lesions, the late alterations in
the vessels need not be wholly due to syphilis, but may result from a number of
complicating factors, amongst which those leading to atheroma, athero-
sclerosis, alcoholism, and renal disease play a role. This association of
multiple causal moments makes it often difficult to interpret the nature of the
arterial disease. Nevertheless, certain undoubted syphilitic lesions in arteries
have been recognized.
1 Benda, Aschoff, Pathol. Anat., ro1g, p. 86.
2 Strasmann, Beitr. z. path. Anat., 1910, 49.
3 Druelle, Thése de Paris, 1906.
460 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Symptomatology.—We shall discuss here merely the symptoms when
arteries of the extremities are involved, although it must be remembered that
intestinal forms of syphilitic arteritis are described as giving rise to painful
crises, the analogy of intermittent claudication. Intestinal infarction with a
clinical picture resembling that of mesenteric thrombosis has been reported.
There are very few, if any, distinctive features that will differentiate the
symptoms brought on by syphilitic disease of the vessels of the extremities
from occlusive lesions due to other causes, such as atherosclerosis or thrombo-
angiitis obliterans.
The onset may be insidious and progressive, with weakness and heaviness
of the affected extremity. ‘The sensations of cold, formication and vague
pains are described. Or the onset is sudden with severe violent pain in
the lower extremities, causing the patients to stop in their walk. The
affected limb may become livid, and the pulsations feeble. This picture
is comparable with that described elsewhere as due to sudden thrombosis in
arteriosclerosis and thrombo-angiitis obliterans.
At the beginning the dominant symptom is pain which may be lancinating,
prevent sleep, even necessitating injections of morphine. Whilst this
pain may be diffuse at first, it is apt to be localized in the neighborhood of
one of the toes later on, particularly when trophic ulcers or wounds appear.
Discoloration of the skin of the foot or hand has been described as not
unlike the erythromelia of thrombo-angiitis obliterans, or a livid tint may
predominate. The pulsation in the affected vessel or beyond the site of
obstruction disappears. Sensory disturbances have been reported, such
as hyperesthesia, and anaesthesia. Ischemia is not infrequent, and may
possibly be elicited on elevation of the extremity.
Improvement in symptoms may occur spontaneously or after treatment.
Without treatment, however, the condition gradually becomes worse and
gangrene may appear after months or lapse of years. The gangrene is usually
sudden in its appearance and progressive. With it pain becomes excru-
ciating. In most cases a patch of dry gangrene appears in the neighborhood
ofa toe. Usually this gangrene is limited to one or more toes, but may extend
for a variable distance.
Some of the French authors describe a special form with intermittent
claudication, although careful anamnestic data would probably reveal that
this symptom is common to many of the cases. Crises of intermittent claudi-
cation with exceptional pallor of the extremities also occur.
The affected arteries may be tender to touch, their pulsations reduced.
With the more rapid development of lesions, with or without thrombosis,
there may develop sudden pain in the calf of the leg followed by paresthesia
and numbness. ‘The pain is aggravated by motion, often increased at night.
At the same time the extremity becomes colder and pale, and the symptoms
may gradually abate. Or, the symptoms may give way to those of impend-
ing or of well developed gangrene.
Clinical Forms.—A survey of the literature permits of the following
grouping of cases, which, however, must not be accepted as having any further
value than for purposes of clinical orientation.
First, syphilitic arteritis of the lower extremities with clinical picture
of intermittent claudication.
Second, simultaneous clinical involvement of the arteries of the upper
and lower extremities.
Third, associated lesions of the intestinal arteries.
Fourth, lesions of all the vessels of the lower extremities.
SYPHILITIC ARTERITIS AND GANGRENE 461
Fifth, lesions of the digital arteries alone with benign course (gangrene
of digits).
A clinical grouping given by other authors includes a subacute and an
acute variety.
1. The Slow or Progressive Form.—The symptoms may or may not be
accompanied by intermittent claudication (Druelle).
(a) Without Intermittent Claudication.—The first symptom that directs
the attention of the patient to the arterial affection is pain of variable intensity
along the course of one of the known arteries of the limb. This develops
slowly and is aggravated by pressure and movement of the affected extremity.
The artery may be converted into a tender and hard cord. The respective
pulsations are diminished, and the circulation may be impaired in the distal
parts, the skin being pale, cold, or even livid. With treatment, however, and
rest, the circulation may be restored, but recurrences are possible. Of the
other sensory disturbances, there may be formication and other paresthesiae,
or even anaesthesia. Later disturbances in motility and even contractures
may supervene; trophic disturbances are also reported. After administra-
tion of mercury all of these symptoms may diminish and even disappear.
If treatment is not instituted, gangrene may result. This is usually
of the dry type, may be limited to the toes or the fingers, but may involve the
larger part of an extremity.
(6) Cases with Intermittent Claudication.—It is not quite clear why some of
the authors emphasize the occurrence of this as a separate form; for it has
been shown that this complex may obtain in all the varieties of obstructive
arterial affection of the extremities. Possibly its significance has been
emphasized because it may be a prominent feature in young individuals
previously healthy, when attacked with syphilitic lesions of the vessels.
2. Acute Form.—The most characteristic symptom is pain, which is
often intense, indeed, so excruciating that the patient constantly seeks to
alter the position of the limb in the hope of obtaining relief. Some even
pray for amputation because of their suffering.! Other severe symptoms
are associated. The limb may become cold, have a cadaveric appearance,
and even the sensations of certain parts of the limb may become abolished.
In this acute form the French authors speak of painful anesthesia, which
means an association of pain and an anesthesia of the part. With it the
motile functions are in abeyance. The skin may become livid and morti-
fication may set in.
Examination reveals the disappearance of the pedal pulses, posterior
tibial, popliteal and even the femoral. In these types the gangrene may be
more extensive than in the slow forms, and when it begins in the toes, may
rapidly extend so as to invade a large part of the leg.
3. A recurring form of gangrene due to syphilitic arteritis is reported. In
its clinical course this closely resembles that of thrombo-angiitis obliterans.
4. Syphilitic Arteritis in Advanced Age.—Patients, who by reason of their
age, may be expected to present arteriosclerotic changes may, when lues is
present, present a pathological and clinical picture hard to interpret from
the etiologic standpoint.
1 Compare with similar cases of acute thrombo-angiitis (Chap. XLI).
462 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
CHAPTER LXXIX
PERIARTERITIS NODOSA
This is a rather rare disease (about 52 cases reported in the literature),
and was first described by Kussmaul and Maier.! The characteristic lesion
is an exudative inflammation of the periadventitial structures, the adventitia,
the media, and sometimes the intima. By virtue of necrosis of the media,
both true and false aneurysms with thrombosis (sometimes with hemorrhagic
Fic. 153.—Periarteritis nodosa. a, Thrombus containing leucocytes in the lumen;
b, internal elastica interrupted through inflammatory process; c, media; d, fresh process of
degeneration; e, large focus of degeneration; f, inflammatory infiltration of media; g,
external elastic coat with numerous interruptions; h, adventitia with leucocytic infiltration.
(Benda)
extravasation) may develop. These lesions usually effect varying degrees
of injuries to the area supplied by the arteries, such as infarction and coagu-
lation necrosis. Later, proliferative adventitial or intimal changes, reparative
or organization processes may take place. The name was given because
of the presence of so-called nodules formed by multiple thrombosed
aneurysms often arising from vessels of small size.
The important lesions in this disease are the necroses and the hemorrhages of the media,
the inflammatory (leucocytic) infiltrations of all three layers with the associated thromboses
in the lumen (Fig 153), and the aneurysms, which alterations may occur in numerous discrete
foci. The lesions tend to healing with connective tissue cicatrization of the mural changes,
with proliferation of the intima and resulting obliterating endarteritis; or, with organization
of thrombi (Fig 154).
1 Kussmaul and Maier, Deutsch. Arch. f. klin. Med., 1366, I, 484.
PERIARTERITIS NODOSA - 463
Clinical Manifestations.—Depending upon the seat of the arterial
lesion, cardiac, pulmonary, renal, intestinal, cerebral, abdominal, and
manifestations in the extremities, are the chief features of the symptoma-
tology. Detailed accounts will be found in articles by Lamb! and Klotz.’
Here we are concerned only with those data that the literature offers as
referable to involvement of the arteries of the extremities.
Fic. 154.—Periarteritis nodosa in a branch of the superior mesenteric artery with
recent organization of thrombus. a, Adventitia; b, cicatrization of inflammatory focus;
c, external elastic lamina; at d, interruption of the elastica by cicatricial tissue; e, media;
at f, interruption by cicatricial tissue; g, internal elastic lamina; at h, the latter is inter-
rupted; #, granulation tissue in the intima with new vessels (k); /, mass of thrombosis.
(Benda)
Manifestations in Extremities.—Pain and cramp-like sensations have been
described. Where the subcutaneous vessels have shown specific patho-
logical changes, pain and nodule formation in the areas involved have been
demonstrated. When the latter are present, extirpation of a nodule and
pathological examination may lead to correct diagnosis.
Pains in the voluntary muscles and along the peripheral nerves are a
feature and may be so pronounced as to be diagnosticated as neuritis,
poliomyositis or trichinosis.
1Lamb, Arch. Int. Med., 1914, 14, 481.
* Klotz, Jour. Med. Res., 1917, 3'7, No. I, p. 1.
464 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
CHAPTER LXXX
SYPHILITIC DISEASE OF THE VEINS
Only those lesions will be described here that may give a picture of migrat-
ing phlebitis that could be mistaken for similar phenomena in thrombo-
angiitis obliterans.
The lesions of syphilitic phlebitis should be recognized and differentiated
from other forms especially from thrombo-angiitis obliterans. Indeed,
certain histologic similarities may require the following exposition for
clarification.
Clinical Characteristics.—The veins of the extremities, particularly those
of the lower extremities, are usually affected. In rare cases, phlebitis has been
observed in the face. Frieboes! has reported 2 such cases. In 1 of these,
there appeared during the secondary stage, bilateral cord-like indurated areas
114 to 2 cm. in length, and of the thickness of alead pencil. These were situ-
ated in the temporal region just adjacent to the eye, causing some slight promi-
nence of the overlying skin. Under antisyphilitic therapy these disappeared.
In a second case, similar cord-like manifestations appeared along the course
of the vessel, just under the skin in both temporal regions, due to inflamma-
tory processes in the veins.
According to some authors the veins may be involved so gradually that
careful palpation is necessary to elicit pain along the venous cords. However,
the attention of the patient may be drawn to the part by a sensation of dis-
comfort, a tenderness of the affected limb, or, muscular cramps at night, and
formication.
The seat of the phlebitis is usually one of the superficial veins of the
extremities, such as the internal saphenous. On inspection one finds the
affected limb normal in volume, with sometimes a slight rosy discoloration
of the overlying skin, the discolored area has about the width of one finger.
The venous cord is indurated, varying in size from a quill to a lead pencil,
usually not adherent to the skin at first. Three varieties have been described:
first, partial, syphilitic phlebitis; second, segmentary; and third, total. This
grouping depends upon whether the lesion is limited to a portion of the vein,
its course over a segment of the limb, or its total length. Sometimes slight
edema is present in the region of the involved vein.
The clinical course is a rapid onset with inflammatory symptoms, then
a gradual decline, leaving an indurated cord under the skin. All manifesta-
tions disappear within 4-6 weeks. Embolism is very rare in the course of
syphilitic phlebitis. In some cases recurrences have been observed, various
veins being successively involved.
When the deep veins are involved the clinical picture may be that of
milk-leg, but both veins of the upper and lower extremities may be affected.
It is rare for but one vein to be involved, a multiplicity of venous lesions being
the rule.
Pathology.— Descriptions of the histologic changes vary greatly in the
literature. The striking pictures observed by some are produced by the
presence of foci containing giant cells and nodules in the perivascular tissue,
suggestive of miliary tubercles. According to other authors, such lesions
1 Frieboes, Dermat. Ztschr., 1913, 20, 125.
SYPHILITIC DISEASE OF THE VEINS 465
have not been seen, and the alterations are confined to the vessel itself with
the production of a clot without any recognizable, specific, architectural
changes. It would seem, therefore, that for differentiation from thrombo-
angiitis obliterans only those observations in which giant cells are a feature
need special mention.
In most cases red thrombosis was observable, the lumen being more or
less completely filled with a clot. According to Roques the intima is altered,
being replaced by tissue made up of round cells, fusiform cells, and a deposi-
tion of connective tissue. This new formed tissue produces thickening of
varying degrees.
The internal elastica is well preserved, a solution of continuity being
present only in a few places.
The other coats contain a large number of cells of variable shape, some
round, others fusiform or elongated. Giant cells were absent.
Spirochetae pallida have been demonstrated in the vein walls by Ravaut
and Ponselle.!
Fic. 155.—Syphilitic lesions of the vessels and perivascular tissue in phlebitic nodule
removed from veins; obliterating proliferative lesion seen in larger vein on the right; on the
left, a small vein is infiltrated, its elastica conserved; below and above, syphilitic miliary
tubercle-like nodules with giant cells. (Frieboes)
Specimens were extirpated by Frieboes and the lesions found may be
described as (1) of the perivascular tissues, and (2) of the vessels themselves.
A characteristic and distinguishing feature contrasted with thrombo-
angiitis obliterans, is the inflammatory lesion outside of the vascular domain.
These lesions have been variously described, but the presence of giant cells
of the Langhans type associated with endothelioid plasma and mononuclear
cells makes a picture that is not found in the extravascular tissues in thrombo-
angiitis obliterans. Frieboes describes an inflammatory lesion composed
of an infiltrate of epithelioid, mononuclear, and plasma cells, associated
1 Ravaut and Ponselle, Soc. Med. des Hépitaux, Jan. 12, 1906.
30
466 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
with destructive lesions of the connective tissue fibers and degeneration of
capillaries. There are also foci or conglomerates of such cells and occasional
giant cells of the Langhans type. Some of the nodules in the connective
tissue composed of endothelioid, mononuclear and giant cells are suggestive
of tuberculosis.
The smaller vessels in the connective tissue show an arteritis obliterans
with degeneration of the whole vessel by reason of reactive processes. There
is an intense proliferation of the intima of the small vessels, almost occluding
their lumina.
In the larger veins the media is infiltrated with cells, the elastic fibers being displaced
and spread apart and fragmented. With this change, the lumen of the vessel becomes
eccentrically displaced. The process is one of vascular destruction by reason of new formed
inflammatory tissue. The proliferating cells constituting the latter replace the vascular
wall, so that in places nothing but a few elastic fibers remain, as shadows of the inflamed
vessel; or, a few concentrically placed cellular groups within elastic fibers may be the only
remnant of a vessel (destructive lesion).
In another case the infiltrate was found especially confined to the neighborhood of the
vessels, occasional giant cells being interspersed here and there, amongst the new formed
perivascular elements.
Fic. 156.—Destructive inflammatory lesion of syphilitic nature in a vein. The
elastica is destroyed; below, the lumen of the vessel is occupied by new formed vessels,
giant cells, endothelioid and plasma cells. (Frieboes)
The vascular changes in the second case of Frieboes showed all transitions
from early endothelioid proliferation within the vessel, up to complete
destruction.
In Fig. 155 the wall is seen infiltrated with cells causing encroachment
upon the lumen and remarkable enlargement of the total diameter of the
vascular section. ‘The elastic fibers are separated, split, torn and displaced.
On the left in the picture there is a small vein in which the elastic ring is still
conserved, but the lumen is filled with proliferating endothelium. Below
in the picture there are nodules composed of proliferating cells and giant
cells. These are the foci suggestive of miliary tubercles.
SYPHILITIC DISEASE OF THE VEINS 467
Fig. 156 shows clearly the destruction of the elastic ring, and the lumen
contains endothelioid cells, mononuclear and giant cells and new formed
vessels.
In short, the aforementioned lesions differ from those of thrombo-angiitis
obliterans, in that foci of syphilitic inflammatory lesions are present in the
tissues outside of the vessels; secondly, in that they are of exquisitely pro-
ductive nature with a tendency to cause destruction of the vessels. This
is accomplished through the action on the elastic and connective tissue
elements; and finally, complete obliteration of the lumen by new formed
tissue with or without thrombosis may be the significant intravascular lesion.
Fic. 157.—Inflammatory infiltration in the media of a vein in secondary syphilis.
The cells are mostly of the plasma cell type with some endothelioid proliferation and round
cell infiltration. (Hofmann)
The inflammatory changes in the veins vary according to the literature.
Those described by Hofmann! resemble those of thrombo-angiitis obliterans
so closely that the points of differentiation are worthy of note. ‘There are
enough differences in the histologic picture of the two lesions to enable the
microscopist to make a distinction.
A thrombotic and inflammatory lesion is present in the veins (Hofmann).
The presence of giant cells we believe might lead to confusion in differentiation
from lesions of thrombo-angiitis obliterans.
The inflammatory infiltration of the wall of the vessel differs from that of
thrombo-angiitis obliterans in that the predominating cells are plasma cells,
particularly grouped about the vasa vasorum. Besides this, the media is
the seat of marked proliferation of the fixed cells, and of round-cell collections
(Fig. 157). Just under the elastica interna there is an intensive inflamma-
1 Hofmann, Arch. f. Dermat. u. Syph., 1905, 73, p. 245.
468 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
tory lesion represented by proliferation of endothelioid cells, fixed connective
tissue cells, collections of plasma cells, together with occasional giant cells.
This localization (within the vessel wall) together with the presence of
giant cells in this layer (Fig. 158) is characteristic of the syphilitic lesion.
The internal elastic membrane is rarefied, displaced and destroyed in places.
The intima shows extensive proliferation of cells of varying degrees, being
thicker in some places than in others. Parietal thrombi are said to originate
at points where the lesions are most intensive.
Fic. 158.—Syphilitic lesion in vein showing giant cells in clot, and giant cells in foci
under the internal elastic coat. (Hofmann)
The thrombus contains large numbers of giant cells of the Langhans type.
In the periphery of the clot, the connective tissue fibers are developed, but
the greater part of the thrombus is made up of red blood cells and blood
platelets with considerable fibrin.
Tertiary or Late Form.—The studies of Roques have shown that the deep
veins of the upper extremity, the popliteal and posterior tibial may be
involved. In the late stage of syphilis the multiplicity of lesions is not
observed, and the affection seems to be less severe and more diffuse.
The affected limb is painful and heavy, and becomes rapidly useless
from the functional standpoint, by reason of augmentation in volume. With
this there may be a slight elevation of temperature.
The enlargement of the limb is striking due to edema, which may involve
the whole of the extremity. The limb feels hard. When the edema is
distributed about the vein, an elongated area of tumefaction is developed
which corresponds to the course of the vessel.
Sensory and trophic disturbances are not associated. The progress of
the phlebitis is slow and yields to antisyphilitic treatment, the symptoms
SYPHILITIC DISEASE OF THE VEINS 469
disappearing im toto in from 6—8 weeks after treatment has been instituted.
Recurrences have not been observed.
Histo-pathology of Tertiary Phlebitis —The lumen of the popliteal vein in
one case (Roques!) was filled with a clot already in a state of partial organi-
zation. ‘The intima was markedly thickened, containing small rounded cells,
and fusiform cells with new formed connective tissue.
The other coats, the media and adventitia, contained an abundance of
alien cells. These are regarded by this author as representing an infiltration
with young connective tissue.
Diagnosis of Syphilitic Phlebitis.— An indurated cord corresponding to the
anatomical course of a superficial vein in a syphilitic when of recent origin
must be regarded as possibly of luetic origin. The onset, however, is slow and
insidious, and a number of veins may be affected simultaneously or consecu-
tively. This type must be distinguished from a number of others, from
thrombo-angiitis obliterans, phlebitis of rheumatism, erythema nodosum,
nodular lymphangitis, syphilitic myositis and syphilitic gumma in a vein.
Rheumatismal Phlebitis—According to the French authors phlebitis of
rheumatism is accompanied by recrudescence and exaggeration of the
febrile phenomena and of the pain. As a rule polyarthritis is associated, or
cardiac, pericardiac, or pleuritic lesions. ‘The presence of syphilitic stigmata
are of the utmost value in diagnosis.
Erythema nodosum is easily distinguished since in a case of phlebitis the
relation to the vein, the mobility, the absence of adherence to the skin and
the redness of erythema nodosum are characteristic.
Thrombo-angiitis Obliterans —In this disease the nodules are of two types,
the nodules, and the cord-like swellings. In both there is marked tenderness,
adhesion to the skin, and depending upon the situation and extent of the
lesion, the vein is also adherent to the deeper parts. In addition, there are
usually associated the evidences of obliteration of the deep vessels. Biopsy
of exsected veins permits of microscopic differentiation.
Syphilitic Gumma (Tertiary) —Here the skin and deeper parts are also
involved. In the nodular lymphangitides the redness is striking and the
involvement of the regional lymph node is regularly present.
In syphilitic myositis there are also hard nodosities, somewhat elongated,
but these can be demonstrated to lie in muscle, and are much deeper than the
inflammatory lesions in the veins.
In syphilitic gumma of the veins a veritable tumor is developed, that rather
suggests a neoplasm or tuberculoma than thrombo-phlebitis.
LITERATURE
Weljamowitz, Mil. Med. Jour., Oct., 1898; Dermat. Ztschr., 1900, p. 136.
Heuzard, Thése de Paris, 1808.
Proksch, Uber Venensyphilis, Bonn, 1878.
Barbe, Jour. Mal. Cut. et Syph., 1899, p. 183; France Méd., 1898, p. 497.
Fournier et Loeper, Ann. de Dermat., 1899, p. 80.
Bondésio, Thése de Paris, 1899.
Finger, Arch. f. Dermat., 1900, 53, p. 108. Verhandl. der Wien. Dermat. Gesellsch.
Collinot, Thése de Paris, 1gor.
Audry et Constantin, Soc. franc. de Dermat., 12 juin, 1902, p. 321.
Roussy, Gaz. des Hépitaux, 5 sept., 1903, p. 1013.
Hofmann (Eric), Dermat. Ztschr., Oct., 1903, p. 470; Dermat. Ztschr., 1903, p. 546.
Roques, Thése de Toulouse, 1907.
1 Roques, Thése de Toulouse, 1907.
470 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Achard et Demanche, Arch. des Mal. du Coeur, Vaisseaux, Aout 1909, p. 449.
Dieulafoy, Presse Méd., 1909, p. 130.
Etienne et Lucien, Ann. de Dermat., 1909, p. 545.
Strandberg, Verhandl. der dermat. Gesell. zu Stockholm, 22 sept., 1910; Arch. f. Dermat.
Nov., I910, p. 344.
Thibierge et Ravaut, Bull. Soc. Méd. H6pit., 14 avril, 1910, p. 342.
Balzer et Mad. Vaudet-Neveux, Bull. Soc. franc. de Dermat., 12 mai, 1910, p. 141.
Gaillard, Thése de Paris, 1o11.
Torok, Pest. Med. chir. Pres., Budapest, ror2.
CHAPTER LXXXT
MIGRATING PHLEBITIS—MISCELLANEOUS VARIETIES
Whilst the phlebitis of subcutaneous veins is regularly attended with
obturating thrombosis in thrombo-angiitis obliterans and in syphilis, other
non-thrombotic varieties have been described.
Phlebitis Migrans with Pulmonary Tuberculosis.— The following clinical
and pathological picture is given by Schwarz. The affection involves super-
ficial veins acutely with signs of inflammatory swelling, tenderness and
redness of the overlying integument. An inflammatory process takes place
in the vessel wall with edema and leukocytic infiltration of media and adven-
titia. This is followed by the formation of new connective tissue and new
vessels, but 2o thrombosis occurs.
In short, in advanced tuberculous individuals circumscribed painful,
inflammatory foci are found in superficial veins, the latter conserving their
permeability. Fusiform swellings occur implicating the overlying skin. The
acute lesions in the veins gradually give way to chronic fibrotic thickening,
the final product being unknown since no material in this stage has been
studied pathologically.
Other Varieties.—There are a number of different varieties of migrating
phlebitis usually involving the territory of the internal and external saphenous,
the pathogenesis of which is not clear. Microscopic examination, however,
of pieces exsected for histological researches has demonstrated, in the author’s
experience, that the typical lesions of thrombo-angiitis obliterans are absent.
We shall describe some of the cases that have come to our notice, giving
clinical and pathological data.
1. Focal Migrating Phlebitis of Unknown Origin.—In some of these a
history of excessive smoking over many years can be obtained. In others,
however, there are no anamnestic data that throw light upon the etiology.
In one such case the tributaries of the saphenous were excised, and bland
thrombi demonstrated. The media was most involved in the inflammatory
process, the muscular fibers being separated by migrating polynuclear leu-
kocytes. In some sections, foci of migrating polynuclear cells and fibrin
were seen to penetrate the media and enter the lumen through the intima.
The accumulation of leukocytes was most intense in this zone, although also
present throughout the rest of the vein wall.
C. J. R. (April 1, 1922), 33 years of age, American, had trouble in the left foot and leg
for 8 months. This was described by the patient as a pain traveling from one place to
another, since he did not himself detect the local changes in veins that were gradually
taking place.
MIGRATING PHLEBITIS—MISCELLANEOUS VARIETIES A471
On examination of the left leg there were several inflamed and obliterated regions in the
course of the internal saphenous, some along the inner side of the knee and leg, others along
the inner border of the foot, and another inflamed cord over the lower third of the thigh.
A portion of vein about 34 of aninch in length in a situation in which the vein seemed
rather acutely inflamed was excised.
Microscopic Examination.—Lesions of thrombo phlebitis with red thrombus completely
occluding the vein are here found, the early organization being of the bland type. There
is an inflammatory infiltration of the vein. The fibers of the media are separated by round
and migrating cells and edema. The inflammatory exudate does not equally involve the
walls in annular fashion, but seems to be most pronounced over certain portions of the
vessel wall (Fig. 159). In some sections this focal distribution of the inflammatory process
Fic. 159.—Acute phlebitis, a portion of one of the tributaries of the internal saphenous
vein acutely inflamed (migrating phlebitis) in a process of unknown origin (not thrombo-
angiitis obliterans); diffuse leucocytic infiltration of the muscular coat and a focus of
migrating cells located at one point where the black area is seen penetrating the intima.
shows itself not only in the limitation of the inflammatory product to a portion of the wall,
but also in a distinct streak-like invasion of the intima with migrating cells, in direction
perpendicular to the circular fibers, as if a penetration of the intima and clot was thereby
intended. In certain places intensive infiltration of the subintimal layers with inflam-
matory cells can be seen extending in a longitudinal direction for a variable distance (Fig.
160), another evidence of the focal distribution of the lesion. A similar inflammatory
lesion can be traced for a variable distance into the tissues about the vein.
472 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
2. Migrating Phlebitis with Infections (Non-suppurating)—Rheumatic
phlebitis with general manifestations is referred to in Chap. LX XVI.
3. Extensive Recurring Phlebitis—We occasionally encounter slowly
progressive and recurring attacks of migrating thrombophlebitis over the
territory of the internal saphenous vein and many of its tributaries, that may
eventually lead to venous occlusion from the foot up to the cribriform open-
ing in the femoral fascia, and possibly even into the femoral vein. The few
Fic. 160.—Inflammatory focus, wandering cells, leucocytes in the wall or a superficial
vein; above in the region of the intima a focus of intensive migration; througnout the main |
wall infiltration with polynuclear leucocytes. (High power of Fig. 159)
cases observed by the author—in which thrombo-angiitis obliterans and lues
could be excluded—were males, in one of whom a history of excessive smoking
could be elicited. The insidious nature, the lack of exquisite tenderness and
redness so characteristic of thrombo-angiitis obliterans, distinguish this form
as being less intensively inflammatory. The exact etiology is unknown.
4. Migrating phlebitis of unknown cause possibly belonging to group (rz)
has been observed in young men in whom the malady was so limited in extent
and so devoid of marked discomfort that material for exsection and study was
refused by the patient. One case—a physician—interpreted his affection as
of metabolic origin, from the observation that after some recurrences it was
arrested completely by strict dietary régime.
CHAPTER LXXXITI
VASCULAR OCCLUSION OF DOUBTFUL ORIGIN
It is not always possible to fathom the exact nature of the processes that
may obliterate the arteries of the lower extremities. In our experience four
different types of cases have presented themselves in which all of the arteries
VASCULAR OCCLUSION OF DOUBTFUL ORIGIN 473
of this territory are pulseless. In two of these the diagnosis of thrombo-
angiitis obliterans can be made with a fair degree of probability; in the others
no positive conclusions as to the variety of essential lesions can be arrived at.
Succinctly stated, these forms are:
(1) Typical thrombo-angiitis obliterans of one lower extremity with
absence of all the usual pulsations of the other, symptoms in the latter being
almost nil.
(2) Absence of all the usual pulsations of one lower extremity with a
history suggesting an old thrombo-angiitis.
(3) Absence of femoral and popliteal pulsations in cases in which wounds
of the leg fail to heal, eventually necessitating amputation.
(4) Absence of all the pulses of both lower extremities, without trophic
disorders, and of unknown causation.
1. We have referred elsewhere to those rare but interesting cases in which
the diagnosis of the disease as it affects the vessels of one limb is clearly
thrombo-angiitis obliterans, but the patient may be unaware of a similar
process on the other side. ‘This is due to the absence or paucity of subjective
symptoms, but on investigation all the pulses will be found absent.
2. Here enough anamnestic data can be elicited to warrant the belief that
some time in the past evidences of an active or even ‘‘acute”’ thrombo-
angiitis obliterans have been present in the limb under consideration.
3. Not uncommonly will we encounter cases in which there is a history of
a long state of invalidism. ‘This is often attributed to a minor injury, acci-
dental or unwittingly self-inflicted, beginning in a toe or somewhere in the
leg, or even initiated by a minor apparently inconsequential operation done
by a surgeon for a trifling disorder. The wound thus occasioned fails to
heal, chronic ulceration ensues and then the patient is confined to the house
for weeks or months. Eventually a ‘‘conservative’’ amputation is resorted
to somewhere through the leg, and even this wound does not heal. Cases
haye come to the author’s notice where the stump did finally close below the
knee and in others ablation higher up had been eventually found necessary.
In such patients the obliteration of all of the palpable arteries was the
fundamental cause of the local nutritional failure. One could demonstrate
the absence of the external iliac, femoral and popliteal pulsations. Since
all instances of this type so far observed, have had some part of the extrem-
ity removed, the interpretation of the exact nature of the vascular lesions is
difficult. The absence of intermittent claudication, previous trophic dis-
orders, pain, coldness and blueness—in short, all of the usual signs of de-
ranged circulation, and the latency of the affection until the infliction of the
initiating wound—all this puts the affection into a doubtful category, one
admitting of multiple causal interpretation.
Thus, we may assume that any of the following pathological processes
without clinical manifestations may account for the vascular blockage:
(1) Luetic arterial disease; (2) atherosclerosis with insidious thrombosis;
(3) thrombo-angiitis obliterans without symptoms; (4) bland thrombosis of
the small peripheral vessels with ascending accretion clots (mechanical);
(5) embolic closure without symptoms; or finally, (6) an inflammatory
lesion (arteritis) with thrombotic obliteration of unknown variety and origin.
If we analyze these possibilities, only the first, fourth, fifth, and sixth
are at all likely in view of the facts and data elsewhere adduced.
4. We shall give by way of illustration of this variety an instructive
history of a patient in whom inability to walk and pain in both lower extremities
from the hip down were the significant symptoms that led to the discovery
474 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
of the ubiquitous absence of the pulses. Whether we were dealing here with
the result of a succession of latent embolism and thrombosis, or some other
lesion, we are at a loss to decide.
G. G., physician, American, 43 years of age, gave the following history November 16,
1921. The malady commenced suddenly in June, 1919, with symptoms suggesting angina
or pulmonary embolism, the physician in charge stating that there was cyanosis of the neck
and face at the onset, with rapid pulse and threatening collapse. Following this the patient
was very ill for 10 days, with temperature ranging from roo” to 1or°, with a rapid pulse, but
with no symptoms referable to the lower extremities.
In April, 1921, his legs suddenly gave way after a slight exertion because of sudden pain
in both hips radiating down the legs, so that he was unable to walk. He rapidly recovered
from this, but ever since then the pain on exertion and the weakness in both lower extremi-
ties have ‘persisted; leukocyte count 22,000.
November, 1921, complete status (Dr. L. Barker) revealed nothing sufficiently
significant in explanation of the findings of vascular occlusion.
Physical examination made by the author November, 1921, demonstrated absence of
pulsation in both femorals and accessible portions of the external iliacs, the popliteal,
posterior tibial and dorsalis pedis arteries. On elevation of the limbs there is very. slight
ischemia, and there is but a suggestion of rubor on allowing the legs to hang down; trophic
disorders are absent; 17,300 leukocytes.
Ins funemio22, the patient stated that the pain in the lower extremities had diminished in
intensity; that he had had one attack of cardiac pain which left a pericardiac sound and
systolic murmur, and that the leukocytic count had varied from 14,000 to 18,000 since
last November.
In September, 1922, the patient further stated that he had had no pain in the extremities
when at rest, but cramp-like pain on walking. On elevation of both extremities there is a
moderate ischemia, but the color is retained in the dependent position; slight cyanosis of
both feet, more marked in the left; both feet colder than normal; absence of all pulsations
in both extremities from the femoral artery down.
Epicrisis—In the diagnostic interpretation of imperceptible pulses over
so extensive a territory, it must be remembered that absent arterial beat is not
exactly equivalent to occlusion. Perhaps, in cases of this sort, some arteries in
which the pulse is extinct are still patent, and allowa small amount of blood to
permeate, the occlusion being higher up. This assumption is a warrantable
one, for it is based on the pathological findings in other cases in which a re-
turn of pulse in the radial artery occurred after embolic closure (Chap.
LXXXV, p. 495).
If this view is correct, an explanation is at hand for the meager symp-
tomatology in cases of this sort.
CHAPTER LXXXIII
MAL PERFORANT
Our first knowledge of this disease dates back to the year 1852, when
Nélaton! described an affection characterized by an indolent ulcer of the
foot. This complication, although descriptive of a case of lepra, gave impetus
to the study of what since has become known as mal perforant, malum
perforans pedis, or mal plantaire perforant of Vésigné.?
For a correct conception of this symptom-complex—it cannot be correctly
considered as a unity or separate malady—we must accept and comprehend
1 Nélaton, Gaz. d. hép., Jan. 10, 1852.
2 Vésigné, Gaz. d. hép., Feb. 5, 1852.
MAL PERFORANT Als
that not only may the clinical picture vary, but also that the manifestations
may be brought about by wholly and widely varied causes. Here we are
confronted with a situation similar to that described under Intermittent
Claudication (Chap. XXVI) and should more correctly view Perforating
Ulcer of the foot as brought about by widely different causal factors. The
literature, however, is so complete and comprehensive, and so many
authors of note have described the condition under this name (malum
perforans pedis), that it may be well to adhere to the nomenclature, calling
attention to the advisability of investigating every case for the discovery
of the underlying malady.
Although the importance of diseased arteries has been minimized in
this connection by a number of authors, it must be strongly emphasized that
trophic lesions of this type may result from both obstructive arterial and
neurogenic causes.
Etiology.—The condition is most frequently observed in males, par-
ticularly over the age of forty. The laboring and menial classes seem to be
most frequently affected. The site of predilection corresponds with the point
of pressure on standing and walking. Thus, the plantar surface of the foot,
the metatarso-phalangeal joint, especially over the borders of the first and
fifth toes, over the heel, and more rarely in the sole, are the most frequent
sites. It is usually unilateral, but may occur simultaneously in both feet..
The weight of opinion favors the view that a variety of fundamental affec-
tions may produce the same clinical picture.
Several theories regarding etiology have been suggested: first, the mech-
anical theory; second, the vascular; third, the nervous and neurogenic
theories; and fourth the arthropathic and osteopathic theories.
The Mechanical Theory.—Pressure and trauma should be considered
merely as contributory factors in determining the site of development of an
ulcer, and not as the underlying cause. In view of the fact that perforating
ulcers can occur in situations that are not under the influence of mechanical
injury, pressure or trauma, and seem to heal with the patient in bed at
- complete rest, the mechanical theory has justly lost support.
The Vascular Theory.—Although certain authors (Hofmann!) conclude
from a study of the literature that obliteration of the arteries plays but a
subsidiary réle, the author is of the opinion that occluded arteries whether
due to arteriosclerosis, thrombosis, or thrombo-angiitis obliterans may some
time be followed by the development of perforating ulcers, clinically indis-
tinguishable from those of less evident organic cause. Levai? and others are
sponsors for the vascular theory. A careful investigation of the condition of
the vessels of the lower extremities, including the femoral, the popliteal, the
dorsalis pedis and posterior tibial arteries, and a search for the typical objec-
tive manifestations of arterial disease, would often reveal a causal relationship
between the vascular obturation and the trophic symptoms.
The Nervous or Neurogenic Theory.—A number of different diseases of the
nervous system may be attended with sensory or vasomotor paralyses or
palsies in the territory of the lower extremities, and in consequence be asso-
ciated with the appearance of trophic ulcers, of which the so-called mal per-
forant is a prominent and frequent example. Mal perforant may even be a
symptom of either peripheral or central nerve lesion.
Peripheral Nerve Lesions——The nerve lesions may be limited to the
territory in the immediate vicinity of the ulcer, or implicate a larger part of
1 Hofmann, Ergebn. d. Chir. u. Orth., VIII, p. 900.
2 Levai, Deutsch. Ztschr. f. Chir., 1898, 49, 558.
476 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
the nerve distribution of the corresponding lower extremity. Peripheral
neuritis as the result of freezing, burns, wounds, contusions and traumata of
various kinds has been reported; so also lesions of the posterior sacral roots
or injuries to the sciatic nerve, and tumors that involve the larger nerves or
compress them. Other types of neuritis due to leprosy, alcoholism, lues and
arteriosclerosis are also said to lead to the formation of trophic ulcers of the
foot. It would appear that the anesthesia resulting from the observed lesions
is in great part responsible for the formation of ulcers.
Lesions of the Central Nervous System.—These are of greater importance,
particularly tabes dorsalis. Other spinal diseases may play a role in the
x
|
Fic. 161.—Perforating ulcers over the inner margin of the foot, second toe and outer mar-
gin of the foot. (Hofmann)
etiology, such as fractures of the vertebre with injuries to the spinal
cord, tumors of the spinal cord, spina bifida aperta, or occulta, and
syringomyelia. A few cases have been described associated with progressive
paralysis, progressive muscular atrophy, amyotrophic lateral sclerosis, and
spastic paraplegia.
Certain constitutional diseases (diabetes) have been held responsible for
mal perforant, but the pedal ulcer of diabetes does not usually belong in this
category. The painful nature of the ulcer in diabetes is in striking contrast
to the non-painful trophic disturbances associated with nervous disorders.
To what extent the presence of sugar in the blood, the lesions of the
peripheral cutaneous nerves, or the arteriosclerotic changes are participants
in the production of trophic ulcers in diabetes is discussed elsewhere.
MAL PERFORANT AGE
A peripheral localized neuritis, possibly of alcoholic origin is regarded by
Hofmann! as the probable cause of the occurrence of mal perforant amongst
the menial classes of Southern Tyrol. This author observed a large number
of cases (19) in males over 40 years of age, in whom excessive alcoholism seems
to be the most important etiologic factor, and was attended with evidence of
diminished sensibility in the neighborhood of the perforating ulcer. Since
no other cause could be found, the author attempts to explain the development
of the trophic lesion on the basis of alcoholic peripheral neuritis possibly
furthered by arteriosclerotic lesions.
The Bone and Joint Theory—The development of perforating ulcer? has
been attributed to primary bone and joint lesions.
®
Fic. 162.—Extensive destruction of the head of the fifth metatarsal bone corresponding to
a callus in this region. (Hofmann)
Clinical Course and Symptoms.—At one of the sites of predilection, over
the sole, the ball of the big toe (Fig. 161), the outer border of the metatarsal
phalangeal joint of the big toe, or at the heel, we are wont to observe the
formation of a marked callus. Although this of itself is of no diagnostic
import (since it occurs in the healthy individual), the next step in the disin-
tegration of the tissues is significant. In the center of the callus, the horny
layer becomes attenuated and some secretion begins to accumulate, lifting the
overlying skin away and thus producing a superficial defect. The superficial
ulcer thus formed shows little or no tendency to heal, and even though healing
1 Hofmann, Ergebn. d. Chir. u. Orth., 1914, Bd. VIII, pp. 916-917.
’ 2Levy, Ergebn. d. Chir. u. Orth., Berlin, TOLL oO. 56; also Beitr. z. klin. Chir., IQIO,
Toe. 2 and)3.
478 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
may take place, a recurrence istherule. As the ulcer enlarges, it also increases
in depth, conserving its circular external outline, and being well demarcated
by a wall of thickened epidermis. At first a thin watery or serous secretion
is exuded, and putrid collections form, when secondary infection takes place.
As a rule, this affliction is painless, and in most of the cases sensory distur-
bances with diminished sensibility can be detected in the immediate vicinity.
Where the ulcer and the surrounding parts are tender and painful, certain
authors would rule out true mal perforant. If this view is accepted, the
perforating ulcers associated with thrombo-angiitis obliterans, diabetes,
and arteriosclerosis must be excluded, and only those due to neurogenic
disturbance accepted as belonging to this category.
Joint and Bone Lesions.— Authors are at variance as to the relationship of arthropathies
and bony changes occurring in the immediate vicinity of perforating ulcers. There are
some (Levy) who describe a primary causal relationship between the deep seated and
superficial lesions, whilst there is the opposite school who contend that the bones and joints
are merely secondarily involved. Perhaps the truth would more correctly be placed in a
middle ground, since arthropathies may exist both independently and as a sequence of the
trophic ulcers.
Not infrequently, both in the neurogenic type of mal perforant, as well
as in the deep seated ulcerative lesions associated with vascular disease,
destruction of bones and joints occurs (Fig. 162). This would seem to be
the rule in all the advanced cases. In at least 50 per cent, if not more, of
the earlier cases, the corresponding joint has been found uninvolved in the
X-ray picture. Arthropathies involving a number of articulations of the
foot may simultaneously occur, without necessarily being associated with
correspondingly situated ulcers.
However, the X-ray is of exceedingly great value since the finding of
arthropathies may call attention to the possible existence of spinal lesions.
The X-ray examination will be particularly valuable when it discloses neuro-
pathic joint changes without any definite evidences of nerve disease being
demonstrable, but with distinct signs of local anesthesia.
Prognosis.—This depends greatly upon the underlying nerve disorder.
The possible complications, such as lymphangitis, erysipelas, gangrene and
extensive infection, also the obstinacy of these lesions towards all methods of
treatment, make the prognosis dubious. Even though pain and tenderness
be absent, the gravity of the condition must be brought home to the patient,
and energetic treatment applied early.
Therapy.—This includes the care of the fundamental constitutional
disease and the local condition, the tendency to heal depending upon the
nature of the former. Unfortunately the basic malady is frequently not
amenable to treatment.
Much vaunted as of especial value are remedies such as potassium iodid
and mercury. Of other methods may be mentioned the following: constant
and induced electric currents, X-ray exposures, high frequency diathermy,
and hot air.
Because of the excellent results reported by French and Italian authors
(Chipault,t Fontana? and Tomaselli*) after nerve stretching, it may not be
amiss to record here that the anterior tibial, peroneal, and the larger cutane-
ous nerves have been exposed and forcibly stretched with a view to influen-
cing the trophic condition.
1 Chipault, Presse méd., Sept. 11, 1895.
?Fontana, Riforma med., 1910, 22.
3 Tomaselli, Gazz. d, osp., 199, 106.
EMBOLISM AND THROMBOSIS 479
Local treatment should follow general surgical principles, the value of
permanent baths (Chap. LXV) being particularly noticeable in many cases.
Surgical procedures depend greatly upon whether there is a communication
between the ulcer and the neighboring joint or bone. Excision of ulcers
that do not lead to bones or joints has been found reliable in many cases.
X-ray examination will reveal the extent of osseous involvement. When
the latter or the contiguous joint is affected, the territory must be adequately
cleansed by curettage, or excision of bony fragments on general surgical
lines. When only one toe is involved and excessively so, amputation is the
best procedure; similarly, when the metatarso-phalangeal joint is diseased.
Whenever, by virtue of secondary infection, extensive disease of soft
parts and bone takes place, amputation of larger parts may be advisable.
Perhaps the Leriche operation will be of value here (see p. 525).
CG HAE, UT RXV
EMBOLISM AND THROMBOSIS
Embolism and thrombosis may be considered together, since they are
frequently associated in the pathology of gangrene, and since it is often
difficult to make a differential diagnosis, or to distinguish between the effects
of the pure embolic process and the result of occlusion by thrombosis. In
the veins only extensive thrombosis over large territories is effective in pro-
ducing gangrene of an extremity or portions of an extremity, whereas, in
the arteries, either embolism or thrombosis may lead to gangrene.
Emboli may lodge at the bifurcation of arteries, particularly in the popli-
teal or in the aorta at the division into the iliacs. The source of an embolus
must be sought in a portion of the circulatory system, situated proximally
_ to the obstructed vessel, in the left heart and rarely in the right heart, when
the foramen ovale is patent. Emboli may be dislodged from the ulcerative
lesions of atherosclerosis, from syphilitic arteries, from an aneurysm, or from
arteriosclerotic, injured or infected vessels. A heart that is the seat of
myocarditis and endocarditis or bacterial endocarditis, or that is altered in
consequence of previous infectious diseases, such as typhus, variola, scarlet
fever and bacteriemia (so-called pyogenic infection) may be the source of
emboli. When the emboli contain organisms, they are called infectious
emboli, and may give rise to metastatic abscesses.
The cases may be divided into: (1) embolic obturation with insidious
course; (2) thrombosis and embolism after infectious diseases, including
pneumonia; (3) cases secondary to cardiac diseases; (4) cases following
abdominal operations, and complicating pregnancy, in both of which the
exact mechanism is not well understood; (5) peripheral thrombotic gangrene, !
or thrombotic gangrene in healthy or but slightly diseased vessels; (6) embo-
lism and thrombosis complicating arteriosclerosis; (7) embolism and thrombo-
sis complicating acute aortitis; and (8) embolism with aortic aneurysm.
1 First described by the author, no reference to this type having been found in the litera-
ture. However, clinical and pathological investigations have demonstrated the existence
of this form.
480 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
It must be remembered, however, that a discussion of these forms of
gangrene under arbitrary categories must result in overlapping and possibly
repetition of classes. For example, acute arteritis of infectious diseases
may be complicated by thrombotic gangrene; and on the other hand, throm-
boses occur in large arteries during acute infections where no evidence of
arterial inflammation is discoverable. For purposes of orientation and as
clinical aids, however, this classification is wilfully permitted.
J. ARTERIAL OBTURATION WITHOUT IMMEDIATE SYMPTOMS
There are cases in which embolic closure of a large artery of the lower
limbs may occur apparently without symptoms, for the patient will not
remember having experienced anything abnormal in the affected part.
Collateral circulation may then become so well established, that there may
either be no subsequent symptoms at all, or such as are vaguely described
as rheumatic or as local weakness of the affected part. Ensuing secondary
signs may be intermittent claudication, tendency to coldness, or weakness
of the limb, and a history of poor healing powers. Such pictures have
developed under our own observation where one leg had been recently
amputated for embolic gangrene. Suddenly, on careful examination, it
is noted that the other foot becomes cold, and that the dorsalis pedis and
posterior tibial (or even the popliteal) arteries are pulseless; and yet
the patient seems unaware of any local change. Gradually, the circulation
improves, but a certain degree of functional vascular impairment persists.
It is in such instances that the future observer may be in doubt as to the
nature of the cause of the vascular obliteration. Vascular spasm is not
present here, for evidences of lost pulsation persist.
For a further discussion of gangrene complicating infectious diseases, the
reader is.referred to Chap. LX XVI on Acute Arteritis.
The following instance of sudden arterial blockage is one that may occur
unbeknown to the patient in the apparently healthy limb. Here adequate
collateral circulation compensates for the circulatory deficiency, and subse-
quently effaces the symptomatology.
I. L., male, 48 years of age (November 8, 1918) suddenly developed the typical picture of
post- pneumonic, embolic gangrene of the right foot during his period of convalescence.
Amputation (November 13, 1918) through the mid-thigh by the author for dry gangrene
of the foot, the proximal adjacent portion of the leg almost to the knee presenting the picture
of moist gangrene.
Dissection of the vessels of the ablated extremity shows that the popliteal artery was
filled with red clots, and all of the larger veins of the leg were distended with red blood
clots. The walls of the popliteal artery were very slightly thickened, and microscopic
section showed some degeneration of the media.
The initial occlusion probably occurred above the point of ablation judging from the
nature of the clot at the point of section. This had the appearance of a “tail” clot (Aschoff)
or stagnation thrombosis distal to the original point of blockage.
Immediately after leaving the operating room and when he was brought to his bed, the
left foot was found to be cold and cyanotic, so much so that a diagnosis of blockage of the
proximal part of the posterior tibial artery was made. The symptoms gradually abated,
and except for the loss of the pulses in the dorsalis pedis and posterior tibial arteries, all gross
evidences of circulatory impairment completely disappeared.
Embolism Without Gangrene-—Sudden blockage of the popliteal or lower
femoral artery is not necessarily followed by gangrene. In cases with
cardiac disease, during or after an acute infectious malady, the usual signs
of arrested circulation in the territory supplied by the affected artery may
1See Chap. LX XXII.
EMBOLISM AND THROMBOSIS 481
make their appearance; to wit: sudden pain in the calf of the leg or foot,
blanching and coldness of the foot, with disappearance of the dorsalis pedis,
posterior tibial and popliteal pulses. Through elaboration of adequate
collateral circulation, both trophic disorders and gangrene may be averted.
2. EMBOLIC AND THROMBOTIC GANGRENE AFTER INFECTIOUS DISEASES
Gangrene complicating pneumonia may be described as a good example of
this type. Sudden thrombosis of the femoral or popliteal artery may
occur within a few days (four to eight) or much later (three to four weeks)
after the onset of pneumonia. The character of the symptoms, and the
extent of the gangrene will depend upon the site of the embolus or limits
of the thrombosis; and the general symptoms will be determined rather by
the general condition and disease which gave rise to the thrombotic process,
than by the gangrene itself, subsequent emboli often causing sudden death.
As early as six to eight days after the onset of pneumonia, or at a much
later period, the patient will experience numbness of the foot, coldness,
cyanosis, weakness, followed by loss of active motion, and then cyanosis of
the distal part. On examination the dorsalis pedis, posterior tibial and
popliteal may be found pulseless. Gangrene rapidly ensues, and, if amputa-
tion is done, the femoral artery and vein are usually found filled with red clot.
It is often difficult in these cases to determine just where the thrombus
began, or just where the embolus became lodged. If amputation is done
after the lapse of a week or more, beginning organization of the clot can be
demonstrated.
In other cases, thrombosis may occur as late as three to six weeks after the
onset of pneumonia, beginning with sudden onset of pain in one limb, coldness
and blanching followed by cyanosis, the peripheral arteries being pulseless.
Clinical Course.—Either during the course of the pneumonia, or as a
sequel, embolism or thrombosis of the iliacs, femorals, popliteals or brachial
may occur. Symptoms of thrombosis or embolism may begin with sudden
pain or numbness and coldness in one foot, which rapidly becomes blanched,
later cyanotic, the dorsalis pedis, posterior tibial and popliteal pulseless.
The typical signs of gangrene then develop, associated with distinct aggrava-
tion of the general condition. Where the condition of the patient has
allowed it, amputation was done in many of the reported cases. The mor-
tality, however, has been exceedingly high, the patient often becoming deliri-
ous then stuporous shortly after operation, or even before amputation was
done. ‘The prognosis is grave, either because of the extent of the thrombotic
process, and the development of other emboli, or because of the menace of
pulmonary edema and heart failure. In some instances, where amputa-
tion was postponed for weeks or more, the amputated limbs revealed exten-
sive organizing thrombosis of all the larger arteries and veins.
An excellent example of gangrene of the lower extremities complicating
pneumonia is the following.
A. W., 30 years of age, with a history of pneumonia, and with consolidation at the right
base, was treated at the hospital in April and May, 1914, having been discharged on thej11th
of May. He was again admitted on the 13th day of July because of shortness of breath,
palpitation, hacking cough with sputum. On July 25, there was sudden pain in the left leg,
the leg being found cold and cyanotic, with pulses in the femoral, and distal to this artery
being absent. ‘Tenderness along the vessels could be elicited. About this time the
patient’s mental condition changed being frequently irrational.
July 28, the entire left foot was markedly discolored, having a purplish mottled appear-
ance, the whole leg being cold.
31
482 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
August 5, the foot was edematous, swollen. The tip of the big toe was deeply cyanotic,
the skin of the rest of the big toe was vermilion red. This discoloration appeared to be due
to the fact that the epidermis was lifted off. Over one half of the dorsum there was a large
bleb 4 by 3 inches probably filled with bloody serum. All the toes were intensely red, also
due to the separation of epidermis. Over the inner aspect of the ankle there was a mild
degree of lividity, and behind the Achilles tendon there was an enormous bleb. The red
condition extended up to a point 4 inches above the ankle.
In short, the early stage of moist gangrene. The leg was brawny, hard, and very tender
to the touch, and especially hard over the calf. This did not appear to be due to superficial
edema.
Diagnosis —Thrombosis of the femoral artery and vein.
August 7, the patient was mentally confused, but rational. From now on the left leg
passed through the various stages of gangrene. August 10, 1914, the bluish discoloration
and patches of red and blue color seemed to be progressing upward towards the knee and
over the outer side of the leg, the temperature of the limb being very low as far as the knee.
The redness was still intense over the anterior half of the foot where the skin had been
separated, and the foot had increased considerably in size. The femoral artery did not
pulsate.
August 12, the whole foot was cyanotic, and in an advanced stage of moist gangrene.
August 15, the limb was much smaller, although the calf was still brawny. The whole
leg was exceedingly cold. It presented a variegated appearance due to various changes in
different parts of the limb. The foot had a greyish livid appearance, partly purplish and
cyanotic. At the ankle there were patches of purple and deep red where the skin had been
separated. The discoloration extended to the upper fourth of the leg, and was limited from
the normal skin by a zone of purplish discoloration. The fluid having filtered out of the
blood, the epidermis being too large, was now wrinkled over all the toes, leaving the tips of
the toes bluish black. Evidently the whole foot is in a condition of wet gangrene. The
external popliteal vein could be felt as a hard cord. The right foot was edematous, prob-
ably due to the impaired cardiac and renal function.
August 24, amputation at junction of the upper and middle third of left thigh.
August 27, very irrational, having marked hallucinations.
September 1, some sloughing of the skin flaps. The patient was removed to another
hospital because of his mental condition.
The Gangrenous Leg.—Just before amputation the appearance of the limb was character-
istic of the late stages of moist gangrene. Over the foot, the epidermis was completely
loosened, lying in folds, torn in shreds in places, the purplish or reddish weeping cutis
vera shining through. Higher up over the calf in the anterolateral aspect of the leg,
there was a large patch of dry gangrene. The periphery of the gangrenous process, where
the demarcation was taking place, showed areas of hemorrhage. (These are undoubtedly
very similar to those which we find in early stages of gangrene.) In this process, the blood
evidently passed through the capillaries and produced subepidermal or intra-epidermal
ecchymoses.
The hardness of the calf was still present, but altogether the size of the foot and the leg
was diminished as compared with the early stages of the gangrenous process.
At the time of operation, it was noted that the popliteal and posterior aspects of the
thigh were very edematous, and the vessels, arteries and veins, at the point of section, were
filled with clots, a red clot occupying the vein, a thicker clot in the periphery, with a whitish
center in the popliteal artery.
Dissection of the vessels showed these bound or matted together and filled with red
clots. In places the artery was filled with a decolorized clot. Nowhere was there any well
organized firm thrombus, such as we see in the later stages of thrombo-angiitis obliterans.
The arteries showed a moderate amount of atherosclerosis.
Conclusion—A case of thrombotic gangrene or embolic gangrene probably beginning
higher up in the femoral or in the iliac, extending rapidly down into the popliteal and poster-
ior tibial.
Microscopical Description—The femoral artery is completely closed by a mixed clot,
and shows no evidences of organization. The adventitia and the other layers of the
muscularis show slight evidences of a reactive process, there being an extensive infiltration
with small mononuclear cells, but only slight migration of polynuclear leucocytes through
the muscularis. Here and there wandering cells have reached the internal elastic coat.
The popliteal vein is filled with a bland clot whose periphery is being organized in the
typical fashion. The inflammatory reaction here is less marked than in the artery, the only
evidences being polynuclear leucocytes in the wall. Some of the small tributaries of the
popliteal show more advanced stages of organization.
EMBOLISM AND THROMBOSIS 483
Types of Gangrene.—When the edema is absent and the veins remain
patent sufficiently long, then the characteristic picture of dry gangrene results.
The initial coldness and pallor are also followed by blueness or bluish purple
discoloration. Gradually the peripheral parts are depleted of their water
content, and the tips of the toes and outer border of the foot dry up rapidly,
gaining the characteristic appearance of the desiccated dissecting room corpse.
The color soon changes from the dried beef appearance to a blackish brown,
as the process extends up for a variable distance, usually almost to the ankle,
rarely much above.
_ When the condition of mozst gangrene develops, because of more extensive
thrombosis in the femoral vein, and possibly earlier thrombosis in the veins
than in the arteries, the following picture of the local condition is typical,
but may also be characteristic of embolic and thrombotic gangrene due to
other causes.
First Stage-—After a preliminary blanching which rapidly follows the
onset of the embolism or thrombosis, the limb becomes intensely cold and
soon develops bluish patches that give the limb a mottled appearance
(ischemia and cyanosis). The cyanosis becomes intense, spreads rapidly;
replacing the areas of pallor; the limb becomes livid and dusky, save for
patches of vermilion red scattered here and there.
Second Stage of Subepidermal Exudation.—The foot sometimes becomes
edematous, the calf brawny and hard, and extremely tender; the soles are
livid or they show a striking vermilion red. Over the dorsum of the foot,
large blebs or bullae form, which contain bloody serum, and some of the
toes may become intensely red, because of the separation of the epidermis,
the weeping cutis vera shining through. The red condition of the foot extends
up for a variable distance to the ankle, or even higher, giving the limb an
angry red appearance, characteristic of the second stage of moist gangrene.
When edema precedes the gangrene, the brawny and swollen condition of the
limb may be intense.
Third Stage of Intense Lividity—As the gangrenous process becomes
more advanced, the bullae become larger; the epidermis hangs in folds,
breaks and allows the serum to escape. The color of the skin changes to a
deep purple, except for places where the weeping cutis vera still shines
through. ‘The general color is often a grayish purple, because of the combina-
tion of the dead epidermis and the bluish red cutis vera. Associated with
these typical signs of moist gangrene there may be patches of dry gangrene.
Higher up, at the periphery of the gangrenous process, where demarcation
begins to take place, there are’ usually areas of hemorrhage, or ecchymosis.
The limb above this line is indurated, tender, and usually much enlarged.
Sometimes the external popliteal vein can be felt as a hard cord. The
popliteal and the femoral are frequently pulseless.
The jinal stage of disintegration has been previously described.
Pathology.—Although it has not been possible in the author’s experience
to demonstrate the relationship between arteritis and the thrombotic
processes in the larger arteries (femoral, popliteal) leading to gangrene in
pneumonia, a number of authors describe such acute arteritis as a complica-
tion of this malady. Head! mentions three cases in which gangrene followed
after resolution in pneumonia, and according to the literature, an arteritis
was supposed to have existed. In one of these, where a clot was found
lodged in the femoral artery, the pathological report described multiple
round cell infiltration in the adventitia of the femoral artery.
1 Head, Am. Jour. Med. Sc., 1921, 162, p. 157.
484 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
On dissection of limbs (of pneumonic cases) the vessels are found matted
together by intense edema and infiltration. The posterior tibial and femoral
arteries are filled with red clot, decolorized in places, but nowhere show-
ing advanced organization, even when the limb is removed eighteen to
twenty days after the onset of the thrombosis. Histological examina-
tion of such vessels shows a bland clot undergoing early stages of organi-
zation. ‘The peripheral layers of the muscle, of the media and the adventitia
show extensive infiltration with mononuclear cells. No definite data as
to the cause of the thrombosis can be learned from the study of the vessels
unless they can be obtained within a few hours after embolism or throm-
bosis has occurred. In the later stages, the usual signs of organization
are present, the organizing process being often older in the veins in the cases
of moist gangrene.
In one of the cases of post-pneumonic gangrene described, where dissection
was made by the author, vessels of the amputated leg revealed the following:
The large vessels (femoral and popliteal) were matted in their sheaths
surrounded by considerable edema everywhere filled with red clots. Some of
these were found decolorized in places, but nowhere were they firm, nor did
they suggest the picture of thrombo-angiitis. The femoral, popliteal and
posterior tibial showed these changes. Recent thrombosis was found in
other vessels situated distally. Macroscopically one could have concluded
that here was a case of either thrombotic or embolic gangrene with the
vascular occlusive lesion probably beginning in the femoral or possibly in the
external iliac artery, with thrombosis extending rapidly downward.
Histological examination of the femoral and popliteal arteries showed the
following lesions: The lumina of the arteries were filled with clots. The
adventitia and media were infiltrated with mononuclear cells interspersed here
and there by a moderate invasion with migrated leucocytes. ‘The veins,
too, revealed similar changes with some organization of the clots.
All these changes could be regarded as being secondary to, rather than as responsible for,
the occlusive thrombosis, for the cite of the initial lesion cannot be determined in the limited
vascular territory obtained by amputation.
Gangrene with Other Infections.—Rolleston reported a case in which a
lower extremity was thus affected in a case of diphtheria. He could find
but one reported in which an upper limb was involved.
Thrombosis in veins (with phlebitis) has been described as an important
and relatively frequent sequela of znfluenza.' It is peculiar that both veins of
the lower and upper extremities are frequently affected (brachial and axillary).
The onset may be very acute and rapidly progressive. ‘The process may be
bilateral in large venous channels and may lead to gangrene.
Occasionally venous thromboses of the arm and leg veins may be associ-
ated and complicated with gangrene of the foot.2. Almost all the veins of the
limb may become thrombosed. Closure of one popliteal artery, or of both
iliac, femoral, or popliteal arteries with symmetrical gangrene has been
described.* Orth‘ has reported a case of symmetrical gangrene due to throm-
bosis of both popliteal arteries; also a case of gangrene of the distal phalanges
1 Leichtenstern, Deutsch. med. Wchnschr., 1890, Nos. 11, 15 and 18; also Spez. Path. u
Therap. (v. Nothnagel, 4, Wien).
2 Johannsen, St. Petersb. med. Wchnschr., 1890, No. 46.
3 Friederich, Die Influenza Epidemie, etc., Arbeit. a. d. k. Gsndhtsamte, 1894, 9, Berlin.
4 Orth, Deutsch. med. Wchnschr., 1918, No. 47, p. 1208.
EMBOLIC GANGRENE 485
of all the fingers of one hand. A more detailed account of this subject will
be found under Acute Arteritis (Chap. LX XVI).
Embolic gangrene complicating chorea was observed by Chodak.!
V. H., aged 12 years, was admitted into the Royal Free Hospital on December 7, 1918,
suffering from chorea of a week’s duration. This was a first attack, and there was no pre-
vious history of rheumatism; no history of shock or overwork. ‘Two years previously she
had had diphtheria, with a bad attack of tonsillitis during convalescence. The mother
had had rheumatism and one sister has had chorea. On admission the patient, a thin slip
of a girl, was found to be suffering from a moderately severe attack of chorea, all parts of the
body being affected. There was very little loss of strength on the left side, but the right
hand grip was poor and feebly sustained. All reflexes were exaggerated.
Ten days after admission the right hand began to go white, the finger-nails blue, though
the hand did not actually feel cold to the touch. The onset may be described as rapid
rather than sudden, and it was fully a week before gangrene of the finger-tips and ball of the
thumb had definitely set in. During this time the pallor spread up the forearm. There
was no pulse at the wrist, but the brachial could be felt pulsating about half way down the
upper arm, and after a time there was distinct pulsation of the superior profunda artery.
The temperature throughout never rose above 99° F. and was rarely as high as that.
Later still, the brachial pulse slowly disappeared, and the brachial artery could be felt like a
thick cord along the arm.
The little finger recovered, and lines of demarcation gradually formed on the remaining
fingers. The ball of the thumb appeared at first to have escaped as the discolored skin
peeled away from it, but there must have been considerable damage to the muscle, followed
by contraction of the scar tissue, which has led to considerable deformity of the thumb.
It was the consensus of opinion of those to whom this case was presented
that it was due to embolic gangrene.
Puerperal Gangrene.— Under this appellation quite a number of authors
have described gangrene of the extremities complicating pregnancy. Of
76 cases,? 53 involved the lower extremities, 10 the upper. Arterial obstruc-
tion through embolism or thrombosis is given as the cause in 29 cases.
CHAPTER LXXXV
EMBOLIC GANGRENE—CONTINUED
3. EMBOLIC GANGRENE WITH CARDIAC DISEASE
When this occurs in young and middle-aged individuals, the source of
the embolus is usually the left heart. Autopsy not infrequently reveals
thrombi in the left auricle as the probable source, or chronic endocarditis
with valvular lesions, particularly mitral stenosis. In the older individuals,
particularly the senile cases, with intense athero- and arteriosclerosis and
ulcerations of the aorta, a lesion proximal to the site of the embolism, may
furnish one causative factor of the embolic process.
The clinical history in cardiac cases is typical and striking. There may be
a fulminating course, terminating in death within a few hours or a few days
(less than a week) after the onset, or a more protracted course in which case,
the mortifying process in one or both lower extremities or even upper extremi-
ties may have progressed so far that demarcation has set in, allowing amputa-
tion to be done. Even here, the mortality is exceedingly high, death usually
following within a short time after operation.
1 Chodak, Royal Soc. Med., 1918-1919, Vol. XII (Sect. Dis. Children, p. 87).
2 Stein, Surg., Gynec. and Obst., 1916, 23, p. 442.
486 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
A typical course of a fulminating case is the following: With a distinct
antecedent history of cardiac disease, the patient suddenly experiences pain
in one or both lower extremities, or pain in the abdomen or back, followed
by coldness of one foot or leg, loss of sensation, paresthesiz and loss of
active motion. Onexamination the affected limb will be found to be blanched,
soon after the onset, cold, flaccid, and somewhat tender above the zone of
frigidity. The toes soon become livid, purplish or cyanotic, or the ischemic
condition of the foot gives way to a mottling, patches of bluish purple appear-
ing over the foot and lower part of the leg. The muscles of the calf of the
leg, or the thigh frequently manifest fibrillary twitching. After 48 hours,
this mottling gives way to a diffusely livid color, here and there scarlet patches
shining through. The zone of coldness and of discoloration corresponds
fairly well in extent, the upper portion of the discolored area showing exten-
sive ecchymoses. Death may occur within 24 hours, or within a week, the
patient becoming delirious, then stuporous, cardiac failure or cerebral
emboli leading to sudden exitus.
In protracted cases dry gangrene often develops; rapid evaporation takes
place and the distal parts are the first to become mummified. A type of
gangrene which in its objective manifestations can be compared to the desiccat-
ing process seen in the drying parts in the dissecting room, is not uncommon.
This form of gangrene, when it involves a considerable portion of the foot,
or the whole foot, is almost always due to embolism.
Where there is a more chronic course over a period of weeks or more than
a month, the history may be as follows: With the story of an old cardiac
complaint, there suddenly develop shortness of breath, precordial distress,
possibly palpitation with or without vertigo and fainting. This is followed
by pain in one or both lower extremities, loss of motion and loss of sensation.
One or both limbs becomes rapidly cyanotic, the extent of the discoloration
depending upon the situation of the thrombus. On physical examination,
the dorsalis pedis, posterior tibial and popliteal arteries are regularly found
pulseless. The femoral may or may not pulsate. ‘Then the typical changes
incident upon the development of dry gangrene ensue. ‘The general condition
of the patient will depend particularly upon the cardiac condition, and
upon the presence or absence of infection. Usually there is more or less
cyanosis due to the impaired cardiac action and evidences of a cardiac
murmur.
Such cases may last for a variable time (6 weeks or more) before amputa-
tion is done. Although the operation of amputation through the thigh
may be temporarily well borne, the mortality is exceedingly high. The
patients may suddenly become stuporous. Evidences of cerebral embolus
may appear, death occurring within a few hours or several days after
amputation.
Embolism at Bifurcation of Aorta.—The following cases taken from the
author’s files, will illustrate the clinical and pathological findings.
Case I.—Saddle embolism at bifurcation of aorta with complete occlusion
of right, and partial of left iliac artery, gangrene of right lower extremity, ampu-
tation, lethal outcome.
A young woman (M. K.), 32 years of age, Mar. 28, 1912, reports that 5 years ago, soon
after childbirth, she had had palpitation of the heart. She was free from symptoms until
8 days ago when she fainted, had shortness of breath and precordial distress. On attempt-
ing to leave her bed, she began to have burning pain in both feet and legs, and found that she
could not stand. These symptoms were more marked on the right side. Both feet and
legs, and to a lesser extent, the thighs, became blue and the patient lost all sensation up
to the knee. The weakness in her right leg and foot became so marked that she could not
EMBOLIC GANGRENE 487
raise her leg nor move the toes. The same symptoms developed to lesser degree in the left
extremity. The right leg and foot have become more and more blue with marked tender-
ness on pressure over the right popliteal space. The excitement attending her, leaving home,
and the transportation caused palpitation, shortness of breath and cyanosis of face and limbs.
Physical Examination.—The general condition was very poor, there being marked
cyanosis, dyspnea, some exophthalmos, and dilated pupils.
Heart.—Pulsation seen over mid-sternum; apex felt in 5th space, sounds of very poor
quality; irregular action; occasional extra systole with compensating pause. First sound
accompanied by systolic murmur, transmitted to left. Pulses equal, small, irregular,
of low tension.
Lower Extremities: Right—Complete loss of muscular power, cyanotic with loss of
surface warmth up to a hand’s breadth above the knee; big toe colorless. There are ecchy-
motic patches of varying sizes up to 5 inches in diameter over the extremity.
Left.—Cyanosis up to the ankle joint, and active motion in ankle joint absent.
Vessels —The femoral pulsation is absent on the right, present on the left. In the popli-
teal, absent on the right, faint on the left. Both dorsalis pedes pulseless. The lower third
of the right thigh hypersensitive, below which part there is complete anesthesia. Knee
jerks absent.
April 4.—This A. M. there is marked purplish discoloration up to the junction of the
upper third with the lower two-thirds of the right thigh. In the left femoral and the popli-
teal, there is a faint pulse. The left foot is cyanotic and edematous. The lips of the face
are cyanotic, cardiac action being very irregular, a systolic murmur now heard.
Liver palpable, general condition very poor.
April 16.—Line of demarcation just below the right knee, the toes and leg mummified
with loss of tactile sensation up to the knee.
May 2.—Circular amputation of right thigh through the middle third well above the
line of denfarcation. Fat and muscle at the point of amputation looked gelatinous and
glassy.
May 5.—Patient is semi-stuporous, occasionally reacts and becomes very noisy,
occasionally twitching of extremities, nystagmus, eyes deviating to left. Condition
apparently due to cerebral embolus.
May 6.—Patient became stuporous and ceased.
Diagnosis: Chronic endocarditis (vegetations), embolism at the bifurcation of the aorta
with partial occlusion of the left iliac; gangrene of right leg and impending gangrene of the
left, and cerebral emboli.
Pathologic Study of Arteries in Amputated Limb.—The popliteal and femoral arteries
especially were sectioned and the complete dissection of the limb made.
Extending from the junction of the upper and middle thirds of the leg and involving
the rest of the extremity, there is dry gangrene. This area is sharply marked off from the
healthy tissue by a definite line of demarcation. The vessels, arteries and veins, as traced in
the healthy tissue show thrombi. The muscle tissues seem normal. The fat has a more or
less gelatinous appearance. The femoral and popliteal arteries and veins are closed by
thrombi.
Microscopically, the walls of the femoral and popliteal arteries show a slight reactive
inflammation, due to the beginning of organization of very small portions of the periphery
of the clot.
Conclusions.—The vascular lesions do not account for the occlusive thrombosis, and are
slight and secondary so that the lesion responsible for the peripheral thrombosis and
gangrene must be sought above the point of amputation.
The embolic involvement at the bifurcation of the aorta may be transitory
or momentary as the symptoms would indicate, the clot becoming broken up
into two parts each, suddenly and violently dislodged and thrown into the
corresponding peripheral vessels, usually either the lower femoral or popliteal.
When this is the case, we will expect to find both common femoral arteries
pulsating (or absent but for a brief period) but both popliteal arteries pulse-
less. Where there is a saddle shaped aortic thrombus at the bifurcation,
all vessels of the lower extremities may be pulseless, or, if there be partial
occlusion of one iliac, a faint or moderate pulse can be detected on the corre-
sponding side.
The history of transitory aortic emoblism with subsequent lodgment of
fragments in the peripheral arteries of both lower extremities may be the
following: Sudden onset of severe bearing-down pain in abdomen and lower
488 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
back (oft likened to labor pains) with immediate coldness, pallor and weakness
of both lower extremities and inability to use these limbs. Following this
comes the advent of gangrene of both legs with absence of pulses in all the
vessels from the popliteal downward, the femoral pulses being palpable.
Case II.—Mitral stenosis, onset with symptoms of embolism at aortic
bifurcation, subsequently only signs of bilateral embolic gangrene, autopsy
revealing absence of clot either at aortic bifurcation or in the iliac artertes.
E. R., age 48 reports that she has had signs of cardiac trouble for some 20 years
(prior to Nov. 24, 1915).
Patient has known that she has a cardiac condition for 20 years. She coughs after
severe exertion and has cardiac palpitation. During the past 2 weeks she has had severe
attacks of cardiac palpitation necessitating her remaining in bed. She arose this morning
(Nov. 24) at 6.30 and about one hour later she experienced severe pains in her lower lumbar
spine and lower abdomen. The pains in the spine seem to have passed forwards. The
abdominal pain resembled “‘labor pains”? and continued for one half an hour. Then a
sensation of coldness with the feeling of prickling spread over both legs, these becoming
weak and then powerless.
Physical Examination.—Marked cyanosis of lips with red flush of cheeks. A diffuse
weak cardiac impulse is palpable, action is irregular and slightly accelerated. At the
apex there is a presystolic murmur ending ina sharp short first sound. Pulses are equal and
of fair volume, perpetually irregular.
Lower Extremities—A faint pulsation is felt in both femoral arteries, and no pulsation in
both popliteal and dorsalis pedis arteries. The entire right lower extremity feels cold and
the foot and leg are blanched. The left foot and leg are cold, the thigh is warm, color of toes
is fair, nails are pink. Motion is normal in left lower extremity, whilst there is inability to
move the toes and ankle joints of the right leg with preservation of motion in knee joint.
Summary.—Embolism at bifurcation dislodged into both lower femorals or popliteals with
more advanced occlusion of arteries of right than of left leg in a case of cardiac disease.
Clinical Course.—After the initial pallor of the right foot, a puplish mottling set in,
covering the foot and the distal half of the leg, over which region the parts were intensely
cold to the touch. After 48 hours this color deepened, the foot and leg became
livid and very cold to the touch. Here and there were peculiar scarlet red patches. The
small veins of the skin separated the bluish and purplish mottling into irregular areas, and
the uppermost portion of the discolored region was somewhat redder. ‘The skin was the
seat of diffuse hemorrhages, the bluish green veins being distinctly seen in the ecchymotic
skin. Portions of the ecchymotic skin then became dry, whilst others were moist. Above
the skin at the middle of the leg the parts were slightly swollen and intensely tender.
The left Jeg was also cold at first. Evidences of gangrene, however, did not set in until 24
hours later, when the leg was cold up tothe knee. The foot was then blanched, later mottled,
the venous markings being even more distinct than normally, although not prominent, giving
the leg the general appearance of a dissection specimen, the numerous veins and venules
with their greenish blue blood standing out prominently against the white background,
giving the whole surface the appearance of a geographic drawing. Here and there was a
pale livid hue extending almost to the knee. Both femorals at this time were pulsating
faintly, the popliteals, dorsalis pedes, posterior tibials pulses being absent.
On Nov. 28 gangrene of both legs was well established: exitus on this day.
Autopsy Findings.—Mitral stenosis, dilated left auricle with antemortem clot in auricu-
lar appendix; no embolism at bifurcation of aorta, nor in iliac arteries.
Case III.—An exquisite example of initial blockage of the aorta at the
bifurcation with subsequent liberation of one iliac due to detachment of the clot,
will be cated.
M.M., female, 77 years, had been suffering with recurrent pains in the lower extremities
for some four years. When seen by the author (May 5, 1914) she had had a sudden
attack of abdominal cramps and pain in both lower extremities with weakness and cold-
ness of the legs nine days before. Some four days later, having been confined to bed
since the onset, the legs showed considerable purplish discoloration, and had become quite
we ane lifeless. According to her physician, pulsation in neither femoral artery could be
etected.
Examination on May 5, 1914.—The right foot is gangrenous, dry, resembling a dried
dissecting room specimen; the leg above and up to the mid-thigh is cold and bluish; the right
femoral artery can be felt as a hard cord.
EM BOLIC GANGRENE 489
There is gangrene of the left leg in the early cyanotic and bluish stage up to the knee.
There 1s good pulsation in the left femoral artery although none of the distal arteries can be
felt.
_ In view of the bilateral absence of the general pulses at the onset, and the
subsequent establishment of good pulsation on the left side, the diagnosis of
detachment and peripheral lodgment of clot was warranted.
Diagnosis.—The recognition of embolic or thrombotic gangrene must be
based upon the following facts: The existence of the proper etiologic factor
(cardiac disease, aneurysm, etc.), the suddenness of the onset with the distri-
bution of the gangrene, the affected territory corresponding to sudden oblitera-
tion of one of the larger arterial trunks, popliteal, femoral, and iliacs. The
differential diagnosis between embolism and thrombosis cannot always be
made, for the gangrene may be due to extensive secondary thrombosis, rather
than to the primary lodgment of an embolus in a larger vessel. The mere
closure of an artery alone does not account altogether for the extent of the
gangrenous process in many instances. Furthermore, the pathological
examination of the amputated limb, too, may corroborate the view that
secondary thrombosis is responsible for the extent of the lesion. Nor, is it
always possible to locate exactly the site of the embolism or thrombosis.
Although simultaneous involvement of both lower extremities with feeble pulse
in the femorals speaks for saddle-shaped thrombus in the iliac, a similar pic-
ture may be due to simultaneous lodgment of emboli in both popliteals with
secondary thrombosis extending up to the femoral artery. The study of
clinical cases, however, together with pathological findings have demonstrated
that even where we strongly suspect saddle-shaped embolism at the bifurcation
of the aorta, this portion of the vessel may be found free at autopsy. In
such cases it may be assumed with some justification, that the saddle-shaped
embolus was broken up and dislodged, and thrown into both femorals or
popliteals.
When the femoral pulse is lost in both legs, the presence of a saddle-
shaped thrombus is almost certain. When there are symptoms in both
extremities, and the femoral pulse absent in one, present in the other, a saddle-
shaped embolus may or may not be present. If it is, it occludes one iliac
more thoroughly than the other. ‘The femoral artery may be felt as a hard
cord usually due to secondary thrombosis. The clinical picture may be
complicated by sudden exacerbation in the limb which was at first but
slightly affected, an argument in favor of the view that another embolus
had been cast off in the corresponding vessel. Occasionally embolism or
thrombosis of the external iliacs will give the symptoms of ischemia, which
will be soon followed by improvement due to the establishment of collateral
circulation through the internal iliac arteries.
4. POST-OPERATIVE EMBOLIC OR THROMBOTIC GANGRENE
We are concerned here not with the pulmonary emboli and thrombosis,
but merely with the lodgment of emboli in the peripheral arteries, where
they may produce gangrene. Surgical operations seem to be a very com-
mon cause, or at least seem to provoke, in some way or other, the detach-
ment of emboli in the formation of thrombi in veins and in arteries. Schenk!
found that of the cases of thrombosis and embolism following operations, 58
per cent occurred after the removal of large pelvic tumors. In 3204 myoma
1 Schenk, New York Med. Jour., Sept. 6, 1902; also Am. Gynec. Soc., 1913.
490 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
operations, 96 or 3 per cent were followed by thrombosis. McLean! in his
studies of a series of 1310 laparotomies found 26 or about 1.9 per cent com-
plicated by thrombosis or embolism.
The production of gangrene of this type is not thoroughly understood.
Doubtless traumatism to the iliac vessels or pressure on the popliteal in the
Trendelenburg posture may explain some of the cases; or a complicating
cardiac lesion may be the source of an embolus in others. There still remains
a fairly large number in which no satisfactory interpretation of the patho-
genesis has as yet been offered.
Similarly in the cases of gangrene complicating pregnancy (so-called
puerperal gangrene), the causal factors have not been adequately clarified.
Most of the reported cases have occurred after confinement, a very few during
pregnancy and after abortion.
5. THROMBOTIC GANGRENE IN HEALTHY OR BUT SLIGHTLY DISEASED VESSELS
There is still another class of cases in which the etiology of the thrombus
formation is not clear, and in which pathological studies have revealed a
bland thrombosis of the peripheral vessels, in the territory of the dorsalis pedis
and plantar arteries, that is undoubtedly the cause of the gangrene. It may
occur in elderly individuals, who have slightly or moderately atherosclerotic
vessels, or may occur in vessels that are practically normal save for plaques ©
of thickened intima. ‘These must be distinguished from the cases of thrombo-
angiitis obliterans. The specific and characteristic lesions of the latter are
absent, and the thrombotic process is less extensive, coming on suddenly,
without the long history so characteristic in thrombo-angiitis obliterans.
The author has been unable to find a description of this type of gangrene
in the literature.
Clinically there is the history of exposure to cold or other insult or trauma.
Or, without a cause, one of the toes, usually the big toe, becomes cyanotic;
the distal portion of the foot shows areas of blanching. The big toe, or the
other toes, may show marked blanching on elevation, or the cyanosis may be
so marked that blanching is masked. Sometimes pain 1s altogether absent,
another distinguishing feature from thrombo-angiitis obliterans, as well as
from the cases of acro-asphyxia. There may or may not be slight erythro-
melia or reactionary erythromelia. Both lower extremities may be affected,
although not simultaneously as in Raynaud’s disease. There may be a
history of gangrene of one limb, presumably following a mechanical or
thermal trauma. Or, no such history may be obtainable. Thus, the first
symptom to be noticed may be the appearance of bluish or cyanotic spots
or areas at the tips of one or more toes, usually the big toe or the big and
adjoining toe. Rather significant, too, is the absence of pain in some of the
cases.
Low amputation may not suffice and re-amputation may have to be
resorted to in some cases, at the knee or higher.
Pathological studies have revealed that the larger vessels are practically
negative, and the small peripheral arteries only are closed. Bland organizing
thrombi are found in the territory of the dorsalis pedis and plantar vessels
(Figs. 163 and 164). In such cases it is almost impossible to differentiate
clinically between chronic acro-asphyxia to which thrombosis has been super-
added, slight arteriosclerosis with thrombosis in the distal vessels, or delayed
thrombosis following a so-called paralytic functional condition. The last
1 Jour. Am. Med. Assn., Aug. 29, 1914.
EMBOLIC GANGRENE 49]
has been described by certain authors (Ménckeberg) as responsible for those
late cases of gangrene developing weeks and months after exposure to severe
cold (angioparesis).
From the diagnostic standpoint, the cases are interesting because they may
be confounded not only with chronic acro-asphyxia, but with thrombo-
angiitis obliterans and arteriosclerosis. The suddenness of the onset, the
sudden disappearance of the pulses, and the rapid development of symptoms,
Fic. 163.—Bland thrombosis in slightly diseased vessel.
the absence of pain in some instances, the absence of evidences of marked
arteriosclerosis in spite of the age of the patient, are rather characteristic;
in thrombo-angiitis obliterans there is a long prodromal period in much more
youthful individuals.
Illustrative Case.—A survey of the clinical and pathological findings in a
case observed by the author in 1914 will be instructive.
In a man, L. S., 52 years of age (April 1, 1914), who had had none of the premonitory
symptoms of arterial disease of the lower extremities, there was a history of exposure to cold
with “‘frost bite’ 7 weeks previously. Subsequently, though not immediately there-
after, the big toe of the left foot became cyanotic, pain being absent. After some 6 weeks,
during which gangrene slowly developed and spread from the big toe across the foot involv-
ing all of the toes, amputation was deemed advisable. This was carried out just above the
knee. The material for pathological studies thus afforded revealed the following:
The specimen is in two parts, one portion consisting of the knee and upper third of the
leg, the other of the remainder of the leg and foot. All the toes and about one inch of the
foot above show the terminal stage of dry gangrene. A line of demarcation is well marked.
492 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
The branches leading to the internal saphenous vein are all free. The external saphenous
vein is filled with postmortem clot. The popliteal vessels are not thrombosed. ‘The wall
of the artery is much thickened at the level of the head of the tibia. The anterior and
posterior tibial vessels and the peroneal vessels are all free, and show no macroscopic lesion.
The dorsalis pedis artery contains a fresh clot which is somewhat adherent to the vessel wall
and is dark red in color. In the terminal portion of the dorsalis pedis artery, the clot has a
light color and where the metatarsal branch and the digital branch of the vessel come off
from the main stem, the clot is lighter in color, and in the digital branch has a yellowish
appearance and seems firmly united in the vessel wall. The digital branch referred to arises
Fic. 164.—Organized bland thrombus in thrombotic gangrene, arteries being seat of
moderate degree of arteriosclerosis.
from the main trunk of the dorsalis pedis artery itself. ‘Those branches for the other toes
and the terminal portion of the metatarsal artery are all hidden in the gangrenous portion
of the foot and toes.
Microscopically the affected vessels showed none of the lesions of thrombo-angiitis
obliterans, but the vessel walls were slightly atheromatous, enclosing the “bland type”
of occlusive thrombus in various stages of typical organization.
Clinical Course-—About the beginning of July, the big and second toes of the right foot
became bluish, being unattended by pain. ‘The cyanosis was followed by formication in
this region, and the discoloration persisted for about a month when he was again examined
by the author (August 3).
Physical Examination.—August 3, 1914.—The foot was very cold to the touch almost up to
the ankle, the tips of all the toes being cyanotic. The sole as well as a portion of the dorsum
showed distinct blanching without edema or tenderness. There was a slight increase of
ischemia on elevation of the limb without eliciting any pain. A very moderate reactionary
rubor was also demonstrable, and differed from that seen in thrombo-angiitis in that it
appeared first only and above the ankle from which it extended gradually downward towards
the toes. No chronic or constant rubor was present.
EMBOLIC GANGRENE 493
The dorsalis pedis and posterior tibial arteries were not palpable whilst the popliteal
and femoral were found pulsating.
The symptoms, objective manifestations and diagnostic methods of examination gave
data strongly in favor of a repetition of a lesion identical with that of the other already
amputated limb.
_ The chronic cyanosis, the absence of chronic rubor and intermittent
claudication, the short duration of the disease before the advent of gangrene,
make a characteristic symptom-complex. Occurring in an_ individual
beyond middle age with vessels already slightly atheromatous, the scope of
diagnostic possibilities naturally is widened by virtue of the necessity for
considering arteriosclerosis as a factor.
From the pathological standpoint, the patent popliteal, peroneal, anterior
tibial and posterior tibial arteries with bland thrombosis in various stages of
organization in the peripheral arteries (plantar and dorsalis pedis) differen-
tiate this type of case from thrombo-angiitis, and warrant its recognition as
a separate entity until further researches will have been made.
Theoretically, lesions of thrombo-angiitis but confined to small parts of the plantar
arteries with superadded bland accretion thrombosis, would constitute a pathologic picture
beyond the pale of even microscopic recognition. For, the detection of such minimal
foci would require a complete study of every bit of the arterial course.
6. EMBOLISM AND THROMBOSIS COMPLICATING ARTERIOSCLEROSIS
Embolism may occur when the larger arteries (particularly the aorta)
are markedly diseased. Small thrombi attached to ulceration may become
detached and lodged in the more peripheral parts of the circulatory system.
In such cases, the symptoms are similar to those described as secondary to
cardiac disease. ‘This type may coincide with post-operative embolic gan-
grene after operation on individuals with the arterial lesions referred to.
Thrombosis of the peripheral vessels complicating arteriosclerosis has been
described under the section on arteriosclerotic gangrene. The most character-
istic cases are those in which the symptoms of threatening gangrene occur.
7. EMBOLISM AND THROMBOSIS IN ACUTE AORTITIS
Inflammation of the aorta complicating gonorrheal infection is said (Guil-
lain and Rendu!) to have resulted in gangrene of the upper extremity from
‘“‘obliteration”’ of the subclavian artery; and in gangrene of a lower extremity
through embolism of the femoral artery.
8 AORTIC ANEURYSM AND EMBOLISM
Gangrene of the leg and feet have been observed as a complication of
aortic aneurysm, usually as a sequence of embolism.
The Treatment of Embolic and Thrombotic Gangrene.—The modern
approach in the therapy of embolic closure of the vessels of the extremities
should be one of operative prophylaxis. By this we mean that every effort
should be made to diagnosticate the initial blockage of the main or large
artery of the affected limb, and to make accurate localization thereof, so
that the thrombus or embolism can be removed in due time, the artery sutured,
and the circulation restored. While this is not difficult either from the
clinical or operative standpoint, in the case of embolic closure of the axillary
or brachial artery, somewhat more acumen and experience are required for
the timely and correct interpretation of symptoms due to similar occlusion
of the femoral or popliteal artery. An awakened interest and a few germane
hints may suffice, however, to stimulate the practitioner to the acceptance
of this more advanced and fruitful attitude. |
1 Cit. by Roger and Gouget, Maladies des Artéres, 1915, p. 370.
494 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
The methods recommended for such diagnosis are discussed elsewhere.
The following operative methods have been proposed for dealing with
thrombosis and embolism of arteries: First, igation; second, arteriovenous
anastomosis; third, arteriotomy; fourth, arterial resection; fifth, arterial
catheterization.
1. Ligation has been suggested with a view to avoiding the dangers of
embolism. However, Stewart! contends that when the diagnosis is certain,
thrombosis is usually occlusive, the danger of embolism past; and there-
fore does not recommend ligation. We are concerned here with the role of
thrombosis and embolism in the production of gangrene, and certainly liga-
tion can in no way improve the circulatory condition.
2. Arteriovenous anastomosis at the present stage of our knowledge
seems to be theoretical rather than practical. Stewart believes that in most
of the cases reported favorable, even if the arterio-venous fistula remains
patent, the blood deflected from the artery into the vein does no more than
hinder the return of blood in those veins, producing a sort of passive hypere-
mia. Stetten,? from his experimental studies, concludes that the operation
is dangerous, and the results have been most unsatisfactory, except in a very
small percentage of cases, and that even if the anastomosis functionates, which
it rarely does, there is no possibility of circulatory improvement, and that the
usefulness of the operation is restricted to an unappreciable minimum.
3. Arteriotomy (embolectomy) is an operation which must be seriously
considered if the diagnosis be made sufficiently early, and if operation be
permitted before the effects of occlusion of the vessels have set in, namely,
advanced gangrene. Success can only be obtained if the arterial wall is still
undamaged at the site of the embolism, and before the secondary extensive
thrombosis has occurred. ‘The operation was first proposed by Sabanajew in
1896. Stewart reported a successful case in May, 1907, in a man aged 61, in
whom 36 hours after the onset of pain, the femoral was opened, and an embo-
lus extracted and the artery sutured. Pulsation immediately appeared in the
femoral below the point of suture, and also in the popliteal, but not in the
tibial. Forty-two days later, the leg was amputated below the tubercle of the
tibia, and evidences of good circulation were obtained at operation.
Mosny and Dumont? were able to save a limb by the removal of an embolus 6 hours
after its lodgment in the femoral artery. Murphy‘ removed a clot from the iliac and
femoral in a case after gangrene had already set in, making an incision in the superficial
femoral. By means of a spoon or scoop and catheter, the clot was dislodged, the catheter
passed up into the aorta, a good flow of blood obtained and the artery sutured. He believes
that in cases of aseptic embolism, immediate removal by division of the artery in the line of
embolism or below should be resorted to. Although in his case he used a spoon and catheter
for probing and dislodging the clot, he believes that aspiration through a catheter is a better
means of removing the plug. If the catheter be divided on the slant, its open end can
be easily introduced into the artery, and, unless the embolism is hard, it can be sucked or
drawn into the catheter. He does not advise incision into the artery at the site of the
embolism, because this region is already roughened, and the tendency to subsequent
thrombosis is favored.
Bauer® has reported a successful case of removal of embolism from the aorta just above
the bifurcation through an incision into the artery made by the trans-peritoneal route.
The embolus was about 3 cm: long, had the form of a molar tooth with two short roots, these
lying in the iliac arteries. The symptoms referable to the lower extremities promptly
disappeared, except for some pains in the left foot and calf. This operation, performed 3
hours after the onset, was followed by recovery, the patient leaving his bed on the 25th day.
WANN SOurge saL015; Pe 520:
2 Surg., Gynec. and Obst., April, 1915, p. 381.
3 Bull. de l’Acad. de med., LX XV, No. 43.
4 Jour. Am. Med. Assn., 1909, LII, p. 1661.
6 Zentralbl. f. Chir., Dec. 20, 1913; also Zentralbl. f. d. ges. Chir. u. Grenzgeb., 1914, 4.
EM BOLIC GANGRENE 495
The early removal of an occlusive clot from the larger arteries of the
extremities—such as the brachial, femoral or popliteal—gives promise of
being an effectual mode of coping with impending gangrene of embolic
nature. Unfortunately, the practitioner is not aware of the value of imme-
diate surgical intervention in such cases, and the re-establishment of the
circulation is hoped for through the mere institution of conservative methods.
The condition should be recognized at the very onset of the arterial block-
age, and arteriotomy with removal of the clot should be advised.
As soon as the following symptoms are in evidence, arteriotomy should
be advised: pain in the affected extremity, coldness of the hand or foot,
sensation of the parts falling asleep and formication, interference with
motility, loss of sensation, increasing pallor and coldness with or without
cyanosis; in short, the usual signs of abolishment of circulation. Coldness,
pallor, and absence of pulses may be the only signs.
A typical cardiac case with multiple detachment of emboli demonstrating
the value of arteriotomy is the following.
R. S., girl 11 years of age was suddenly attacked with coldness, formication, and pain in
the right leg and foot. The dorsalis pedis, posterior tibial and popliteal pulses became
imperceptible, but gangrene did not set in because of the rapid development of the collateral
circulation (May 25, 1923).
June 8, 1923 it was noticed that the fingers of the right hand suddenly became cold. At
8.30 A. M., when seen by the author, the hand and arm up to the upper fifth were found
blanched and cold. The brachial, ulnar, and radial pulses were absent, but the axillary
and beginning of the brachial artery were pulsating.
At 10 A. M. arteriotomy under novocain anesthesia was performed. On exposure,
after dissection of the axillary and upper brachial arteries, the former was found pulsating;
the brachial found bluish, and distended with a clot. Careful liberation of these vessels
from the surrounding tissues disclosed the fact that the clot extended to the origin of the
superior profunda. The brachial and superior profunda were temporarily clamped with a
serrefine, and a Crile compressor applied proximally to the pulsating axillary artery. On
longitudinal incision into the anterior wall of the artery the clot, dark reddish in color,
was spontaneously extruded. To ascertain whether no further minute clots were present,
the axillary was allowed to bleed through the incision and then again controlled. Running
suture completed the operation.
The circulation in the hand and forearm was immediately restored but the radial pulse
remained absent for a few hours, gradually returning to normal. Two weeks later the
radial pulse was still normal as well as the circulation of the hand.
It is neither difficult from the diagnostic nor from the therapeutic stand-
point to accomplish the localization of the embolus in the case of the upper
extremities. Because of the accessibility of the brachial and axillary arteries
to the touch and the deductions that perceptible or imperceptible radial
and ulnar pulsations can afford us, the recognition of the site of the lesion is
easy.
In the case of the lower extremities exact localization may offer a some-
what more intricate problem; but the extent of the coldness of the extremities,
its upper limit, and the condition of the dorsalis pedis, posterior tibial,
popliteal, femoral and external iliac pulsations may permit us to restrict
the possible territory in which the clot may lie to within a very short distance.
The following case is instructive even though the patency of the arterial
channels beyond the site of the removed embolus could not be completely
restored.
In a young man operated upon for gangrenous appendicitis by a colleague! (Feb. 14,
1920), the right forearm suddenly became cold, cyanotic and motionless early in the morn-
ing of the third day after the operation. The brachial artery did not pulsate below its
upper fifth.
1 Dr; P. Aschner,
496 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Feb. 17, some 3}% hours after the onset of symptoms, the author exposed the upper
portion of the brachial artery at the site of the thrombus, under novocain anesthesia, and
by arteriotomy removed the clot, about 2 cm. in length, closing the artery by suture
according to Carrel technique. ‘There was excellent pulsation in the brachial below the
site of the clot and no leakage after completion of the suture. In spite of this demonstrable
patency of the brachial artery below the site of the embolism and thrombosis, no pulsation
could be detected in the radial artery. It was, therefore, believed that secondary clots
had previously become detached and lodged in the peripheral vessels, or had grown upon
the embolism (stagnation clots).
Clinical Course.—Feb. 18, in spite of the reestablishment of the circulation in the lower
brachial artery, the right hand was somewhat cold, but there was definite evidence of
marked improvement in its circulation. On Feb. 109, the color of the thumb looked doubtful,
being somewhat cyanotic and cold. Furthermore, there were signs of muscular palsy and
some tendency to contracture of the fingers in the flexed position. Extension of the hand
seemed impossible, although motion of the fingers was excellent.
On Feb. 20, after the application of dry heat in an electric baking apparatus in which
a contact burn could have taken place, trophic disturbances became manifest over the
posterior surface of the forearm. A long whitish area, suggesting dead skin, with loss of
sensation over at least 3 inches X 11% inches appeared. ‘There was another similar smaller
area over the posterior aspect of the wrist and the skin just above. Later in the day, the
central portions of these areas showed blebs.
Feb. 25, the fact that a certain amount of gangrene would develop was well established
since the following lesions could be demonstrated: First—The trophic lesions. Second—
Evidences of gangrene. Third—Circulatory disturbances.
The trophic lesions: The areas of circulatory insufficiency were well demarcated on
Feb. 25,there being an elongated area some 3 inches < 1)4 inches surrounded by a well-
defined narrow line of deep red, as if a red chalk mark had been drawn around it. Within
this there was a distinctly white zone less than 1 cm. in diameter enclosing a central purplish
space, in which the typical blebs of gangrene were to be seen.
Evidences of gangrene: The thumb showed a deep purplish color; was somewhat
withered, evidently in the early stage of a dry gangrene.
Circulatory changes: Although the postero-external aspect of the forearm was fairly
warm, the internal aspect changed color suggesting a possible future necrosis. Between the
thumb and the dorsal trophic disturbance, over the thenar eminence and thereabout on the
posterior surface, there was a peculiar ham colored red with diminished temperature due
to marked circulatory disturbances. ‘The four fingers, however, were in fairly good con-
dition, of good color and the motility good.
Feb. 23—6 days after thrombectomy—slight wrist drop developed, and there were
definite sensory and motor phenomena, said by the neurologists to have been due to implica-
tion of the ulnar and musculospiral nerves. In the region of the brachial wound there was
some induration, possibly due to deep infection.
March 8, chill and rise of temperature to 105.4° with a negative blood culture, the fever
disappearing in 24 hours. March 12, again chill and temperature to 106°, and the blood
culture showed hemolytic streptococci. March 16, some pus was evacuated from the
brachial wound. An abscess of the right thenar space was evacuated on March 18, and
on March 20, the temperature gradually attained the normal by lysis.
April 7, the gangrenous area of the thumb had become well demarcated, and the
terminal phalanx was disarticulated. A few days later the patient was discharged from
the hospital.
In May of the same year the condition of the hand and forearm was as follows: It was
atrophic, weak, of a dusky red color, and the fingers purplish. There were trophic dis-
turbances of the nails, which were discolored and poorly nourished. Hyperhidrosis was
also present. In the dependent position, paresthesia and pain were very severe. Neuro-
logic examination demonstrated marked impairment of the motor and sensory functions of
the median and ulnar nerves. There were still small sequestra at the site of amputation,
and these were spontaneously extruded in the course of the next 4 weeks.
Postular exercises and electrical stimulation were given. Improvement rapidly took
place, so that in a month the fingers could be semiflexed. Three months later a normal
range of motion was reestablished, the atrophy of the muscles was almost abolished, and
the color and texture of the skin approached the normal.
It was reported that on Sept. 7:—7 months after the vascular occlusion—the radial pulse
had returned (through collaterals?); one month later the patient was able to resume his
work as a chauffeur.
1 Personal communication from Dr. Aschner.
EMBOLIC GANGRENE 497
Although successful from the purely technical standpoint, the radial
pulsation was not restored until late, due to the presence of thrombi distal
to the site of the embolism. Nevertheless, the operative procedure served a
purpose in that an additional part of the brachial became patent, and the
source of collaterals thereby widened.
In view of the presence of a bacteremia, there obtained here an additional
factor (probably toxic) predisposing to the extension of thrombi. It has
been often observed by the author that stagnation thrombosis may spread
rapidly from emboli in the larger arteries in cases of pneumonia and influenza,
while the field of obturation is more apt to remain restricted and anastomotic
paths conserved in pure cardiac disease and atherosclerosis.
The question of removal of the embolus, therefore, should be entertained
very early wherever an additional toxic element may vitiate the result. In
the above case, although the first clinical manifestations of embolism were
noted about 3!4 hours before the operation, the occlusion was doubtless of at
least 10 hours’ duration, judging from the appearance of the clot. This
may be too late; for, on the one hand, time is given for the detachment of
clot through the action of reflux currents and motion of the limb into more
remote territories, and, on the other hand, rapid growth of the clot by
stagnation, abnormal currents and vortices, and through the forces of ferment
liberation, may be expected.
That these factors need not be reckoned with to the same extent in afebrile
and atoxic cases, and that the results are more favorable, the citation of an
additional case will illustrate.
It is a good example of successful removal of an embolus from the brachial
artery and demonstrates that the removal of an embolus about 5 to 6 hours
after its lodgment in the brachial artery may be followed by complete restora-
tion of the circulation through the normal vascular paths.
L. G., aged 57, was said to have chronic endocarditis with mitral murmur, there having
been a previous history of a number of attacks of erysipelas. About September 14, 1922,
he was suddenly seized with a cramp in the right leg, lost consciousness temporarily, but
recovered without medical assistance. The right leg became cold, blanched, and gradually
darker and darker, developing dry gangrene.
The patient was seen by the author on September 20, at which time dry gangrene involv-
ing the greater part of the foot, and moist gangrene over the upper part of the leg had
already developed; the lower third of the thigh also being cold to the touch. None of the
pulses from the femoral downwards was palpable.
Diagnosis.—Embolic gangrene.
September 21 (8:35 A. M.) a typical circular amputation (without tourniquet) was done
by the author through the upper fourth of the right thigh, the femoral artery being found
filled with recent clot.
2.45 P. M. of the same day the nurse was unable to obtain a pulse in the right arm; she
noticed that the fingers were very cold, the hand pale, and that the patient complained of
numbness and weakness in the corresponding hand and forearm. This condition was also
observed several hours later by physicians, who recognized the embolic nature of the arrest
of circulation in the right upper extremity; but the matter was not reported to the author.
The patient was seen by the author at 7.15 P. M. of the same day, and the following
status noted: The general condition of the patient was fairly good; the hand and forearm
were cold and pale; neither the right radial nor the ulnar pulsation was perceptible. On
palpation along the course of the brachial and axillary arteries, the pulse was found absent
below the lower margin of the teres major muscle. The diagnosis of embolism in the upper
brachial artery was made, and the operation of arteriotomy was immediately advised.
After consent was obtained, operation was performed at 9.06 P. M. of the same day.
Operation.—The skin over the lower axillary and the upper part of the brachial artery
was infiltrated with 1 per cent novocain solution, and about 2}4 inches of the course of the
brachial artery exposed in the typical fashion, and the point of obstruction located. At
about the level of the origin of the superior profunda artery a clot could be distinctly felt in
32
498 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
the artery, pulsation below this point being absent, and the arterial girth considerably less
than that of the vessel above or at the site of the occlusion.
A Crile artery compressor and one serrefine were applied above and below, and a small
incision about 14 inch in length made longitudinally, immediately over the clot. Just asa
compressing and milking movement was attempted in order to force the clot out of the
opening, and as a portion of it protruded through the gap, the whole embolus was suddenly
projected outward, evidently by virtue of a circulatory force within the artery itself. In
spite of the presence of the clamps, bleeding was continuous, copious and non-pulsatile, so
that more intensive compression both above and below was applied. As the slit was opened
with two delicate forceps, the bleeding which continued in spite of change to the above
measures, caused the sudden evacuation of a small shred-like clot, evidently a tail-piece or
accretion clot, that had blocked either the superior profunda or was riding upon the embolus
in the brachial.
In view of the uncontrollable bleeding through the artificial orifice, it seemed evident
that the artery had been opened just opposite to the point of origin of the superior profunda
artery, through which a collateral reflux was going on.
It was decided, in view of the importance of the superior profunda as an anastomotic
channel, to attempt closure and suture of the artery without tying off this vessel. After
thoroughly lubricating the vessel with sterile albolene, the longitudinal aperture was com-
pressed and closed with the thumb and index finger of the left hand. Then arterial suture
was begun from above downwards, with the finest silk (doubled) and the finest and smallest
Kirby needles (Carrel pattern). Running suture was easily applied, the assistant pulling
taut, tying the first knot, the last knot being tied by the operator. After the removal of
the clamp not a drop of blood oozed out of the suture line, and it was not deemed wise to
reinforce this.
Pulsation and dilatation of the brachial artery below were immediately restored, and the
pulsations were confirmed to exist in the corresponding radial and ulnar arteries by an
assistant.
Inspection of the fingers and hand immediately after the wound was closed demon-
strated a return of color and warmth to the hand and forearm, and restored motility. The
patient also noticed a prickling sensation throughout the fingers and hand.
Although the incision in the arm healed by primary union and the pulses were restored
and remained so, the patient succumbed subsequently to the lodgment of multiple emboli,
one in the left external or common iliac artery, and another possibly in a vessel of the right
half of the cerebrum.
On September 28, 8 A. M., the left leg suddenly became cold and blanched, the femoral
and the popliteal pulses being imperceptible. From then on the usual manifestations of
early gangrene developed, the cyanotic discoloration of the foot and leg, and the coldness
which extended up to the groin.
Although the patient was seen about one hour after the lodgment of the embolus in the
iliac artery and operation for it was advised, consent was withheld.
September 29, the patient was distinctly weaker, pulse more irregular, and he was at
times irrational.
September 30, sudden left-sided palsy, cerebral disturbances, exitus. Up to the time
of death, the right radial pulse remained as strong as the left and the circulation of both
arms equally good. ‘
In short, a case in which embolectomy with removal of a large clot from
the right brachial artery was successfully performed, with restoration of the
circulation until death which occurred 9 days after the operation.
Technique.—When the embolism is located in the brachial artery, the
following technique will be found useful.
Under novocain anesthesia and sharp dissection, the artery both at the
site of the thrombus as well as for some 2 cm. above and below is exposed,
kept moistened with saline and lubricated with liquid vaseline. The extent
of the thrombus can then be easily determined both visually and by palpa-
tion. After the application of a serrefine or arterial compressor above and
below the clot, a site for arteriotomy is selected either at the very upper
end of the clot or over it. A longitudinal incision is made either just above
or over the clot with a spear pointed or triangular knife. The clot may
be spontaneously extruded, if through collateral branches (or the superior
profunda artery) the circulation in the segment within the compressing
VASOMOTOR AND TROPHIC NEUROSES—GENERAL CONSIDERATIONS 499
forceps is not completely arrested. If necessary, however, and to avoid
injury of the intima, the thrombus is milked outward by digital compression
above and below. Washing of the artery with saline and longitudinal suture
of the artery in Carrel fashion completes the operation.
CHAPTER LXXXVI
THE VASOMOTOR AND TROPHIC NEUROSES—GENERAL
CONSIDERATIONS!
Vasomotor and trophic phenomena may accompany a number of different
diseases, such as other neuroses, or organic arterial and nerve affections.
But there remains a large group of diseases divisible into distinctly differ-
entiable clinical entities, some of which will be here described under the
appellation vasomotor and trophic neuroses. A thorough comprehension of
all of their manifestations is essential for a diganosis of the organic vascular
morbid processes that they so closely imitate.
The well-known clinical types include the following: (1) vasomotor; (2)
sensory; (3) secretory; and (4) trophic disturbances.
The vasomotor symptoms may be subdivided into local syncope, local
asphyxia and local hyperemia.
The sensory include paresthesia and pain, and in certain cases thermo-
paresthesia and thermalgia are especially notable.
Amongst the secretory we group anhidrosis and hyperhidrosis and anoma-
lies of sudoriferous secretion.
The trophic lesions are represented by gangrene or necrosis of lesser degree
as well as atrophies, hypertrophies, and that unique type of nutritional
phenomenon known as sclerodermal change.
, Distinctive Criteria.—There are sufficiently striking qualities that charac-
terize these groups, and concern (1) the character of the pain, (2) the localiza-
tion of symptoms, (3) the peculiarities of the clinical course, (4) the etiologic
and predisposing factor, and finally, (5) the other signs of involvement of
the sympathetic.
1. The pain is never confined to the distribution of a single peripheral
nerve or nerve root.
2. The localization is signalized by a remarkable affinity for the peripheral
distal parts, as fingers, toes, nose, ear, chin and tip of the tongue.
3. An intermittent chronic course which is not progressive. This feature
is in striking contrast with the progressive course of organic vascular affec-
tions such as thrombo-angiitis obliterans.
4. The influence of previous infectious diseases, cold, or other functional
neuroses and a neuropathic heredity.
5. The coexistence of instability of the vegetative (autonomic and
sympathetic) system, a sort of vasomotor lability, and often vagotonic
phenomena.
Not all of these maladies are complicated by gangrene and marked trophic
disturbances. Those which can be mistaken for the organic vascular diseases
will receive special consideration.
1 For the latest views on capillary microscopy in these affections see Chaps. CVI, CVII
and CVIII.
500 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
The following will be discussed:
(1) Atypical forms of vasomotor and trophoneuroses that are intermediary
between the well known clinical entities.
(2) Raynaud’s disease.
(3) Erythromelalgia.
(4) Acroparesthesia.
(5) Chronic acroasphyxia.
(6) Multiple neurotic gangrene.
(7) Scleroderma.
Although it is most useful, for purposes of clinical segregation, therapeutic
indications and prognosis, to follow a grouping of the vasomotor neuroses in
some such manner as Cassirer has indicated, we must keep in mind that, as
yet, students and investigators of this subject are far from being unanimous;
nor are they altogether in accord with the above categorical subdivisions of
these disorders. Curschmann! will not even admit that erythromelalgia
merits the distinction of being a discrete malady, and interprets the mani-
festations as but a single ‘‘phase” in the course of vasomotor neuroses.
Common to a number of these conditions, according to this author’s experi-
mental work, is an abnormal type of vascular reaction or an absence of the
normal arterial reaction in the affected extremities, when these are exposed
to sudden temperature changes.
Employing the plethysmograph, as applied by von Romberg and O. Miiller, this author
investigated the problem of estimating the arterial response to thermal influences, in 5 cases
of Raynaud’s disease, 1 case of scleroderma, 3 typical instances of acroparesthesia with
erythromelalgic phenomena, 2 cases of angioneurotic edema, and 2 patients with ‘‘inter-
mittent claudication.”
Miiller’s researches on the vascular reaction in arteriosclerotic arteries led also to an
amplification of our comprehension of what a normal response to cold and warmth should
be. Subjecting the proximal portion of the healthy extremity—that which was not in the
plethysmographic compartment—to cold, he recorded a sudden diminution in the volume of
the distal parts. A similar result followed bodily pain. In arteriosclerotics, this reaction
was less marked or absent, in consonance with the intensity of the lesion. Warmth would
produce a contrary but slower and inconstant increase in volume.
Adopting this procedure for investigation of the vasomotor neuroses, Curschmann
approached this problem, as to whether a continuous or intermittent abnormal vascular
tonus exists.
In Raynaud’s disease and scleroderma, the normal reaction was absent. Warmth, at
times, evoked a paradoxical arterial constriction. ‘The conclusion was drawn that a primary
disturbance of vascular innervation, therefore, must be a factor in this malady. So also,
in his experiments in the acroparesthesi@ the normal experimental responses were missing.
We refer the symptomatology in Raynaud’s and the allied maladies to the
vasomotor system, and to disturbances in the whole vegetative apparatus,
and perhaps correctly to the central portions of this system. Organic changes,
however, have not as yet been discovered, and doubtless such are not present
in the case of most of these affections. The free intervals and the intermittent
course speak strongly against the existence of pathologic anatomic alterations,
except in the case of chronic asphyxia and scleroderma.
Some authors, stressing the close interdependence of the vegetative system
and the internal secretions, would attribute the manifestations to endocrine
dyscrasias. Others consider it more likely that a disorder of the vegetative
system is responsible both for the derangement of the vasomotor innervation,
as well as for abnormalities of internal secretions.
As mere attendant symptoms (symptomatic form) the manifestations may
accompany organic nerve and arterial disease, and hence the confusion and
1 Curschmann, Miinchen. med. Wchnschr., 1907, No. 51, p. 2510.
VASOMOTOR AND TROPHIC NEUROSES—GENERAL CONSIDERATIONS 501
mistakes in diagnosis that are often made by experienced practitioners even
up to this day. Zhe recognition of the existence of coincidental organic nerve
or arterial disease will do much towards classifying the manifestations as
merely symptomatic, as opposed to the idiopathic or intrinsic complexes that
we designate as vasomotor and trophic neuroses and subdivide in the forms
indicated above.
Theoretical Concept of the Neuroses of the Vegetative Nervous System.
The clinical manifestations and their mode of origin have been variously
interpreted by physiologists and clinical observers. Perhaps the most accep-
table views are those according to which disturbances of the function of the
vegetative centers are brought into causal relationship with the well-known
clinical phenomena. It has been pointed out previously that the center in the
corpus striatum may influence the centers in the midbrain in such a
manner that the latter (with its subordinate parasympathetic and sympa-
thetic centers) can maintain a certain threshold or state of equilibrium
between the parasympathetic and sympathetic functions. Whilst Eppinger
and Hess consider the so-called vagotonic complex as an expression of
increased excitability of the parasympathetic paths and refer such alterations
in irritability to an imbalance between the internal secretions—adrenalin—
and an hypothetical ‘‘autonomin”’ (excitant of the parasympathetic), more
recent observers would explain the variabilities in the responses of the
vegetative system to changes in the higher nerve centers themselves. Dresel
refers the para- and sympatheticotonic disposition or predisposition to
functional alterations in the state of excitability of the corpus striatum, the
latter, as previously stated, containing the regulatory mechanism.
So that increased or diminished adrenalin secretion per se, and alone,
could not be the cause of a sympatheticotonic or vagotonic disposition, as
many authors believe. For an increased production of adrenalin should
stimulate the midbrain regulatory mechanism in such a manner as to call
forth an antagonistic response in other glands, with a view to restoring the
old equilibrium. ‘Therefore, it has been concluded that only disturbances in
the central nervous mechanism can altogether explain the deficiency symp-
toms. In short, a true central neurosis, or a functional dislocation of the
excitability of the corpus striatum would be the more modern explanation
of the clinical manifestations referred to derangements in the two large
groups of the vegetative paths.
When we attempt to explain the vascular neuroses, it is well to remember
that these, just as the other vegetative neuroses (vagotonic and sympathetico-
tonic), may be either of a chronic or paroxysmal type. In the former, would
belong the cases of chronic vasomotor lability or instability; in the latter,
‘those in which paroxysms or crises are in evidence, as in Raynaud’s disease.
It is well known that there are evidences of functional disturbances of
the vegetative system that appear suddenly in predisposed individuals,
and then disappear. They may arise by reason of various causes. Both
psychic and reflex irritants may play a réle; and pharmacologic excitation
may modify the centers and the peripheral parts of the nervous system. And
so, in individuals with certain predispositions (¢.g., parasympathetic dis-
position) minimal excitement, psychic or sensory, may bring about an attack
of asthma. In the healthy, such slight irritants may not evoke responses in
excess of the physiological. In the vagotonic and sympatheticotonic
dispositions, with central functional disturbances, paroxysmal symptoms
may be brought about through irritants that attack the corresponding
nervous system at any point, evoking manifestations in consonance with
002 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
the existing hyperexcitability. Perhaps also in the special forms of vaso-
motor neurosis the well-known crises or paroxysmal appearance of symptoms
may be activated by irritants, the nature of which is unknown (toxic, reflex),
on a predisposed central nervous system.
Internal Secretions and the Vegetative Functions.—Many data seem to
favor the view that internal glandular secretions (hormones) may not only
act in a direct fashion, but indirectly through the nervous system. ‘Thus, it
was demonstrated that adrenalin exerts the same effect as when the sympathe-
tic nervous system is stimulated. Clinically, too, nervous factors seem to be
the exciting causes of many of the diseases of internal secretion, as well as
being their most important manifestations. The close relationship, therefore,
between the vegetative nervous system and internal secretions seems proven
beyond peradventure. Not only does adrenalin selectively influence the
sympathetic nervous system, but pilocarpin or physostigmin acts upon the
nerve endings of the parasympathetic system in the same manner as electric
irritation.
Arterial hypotension has been regarded as a resultant of endocrine disease
by a number of authorities since Addison first described epinephrin insufh-
ciency in 1855. A number of different blood pressure states also have been
brought into relationship with abnormal activities of the endocrine glands.
Numerous publications attest the general proclivity of modern authors to
bring into causal relationship certain arterial diseases and those of the internal
secretions that markedly affect the non-striated muscle of the vessels with
consequent vasoconstriction.
Antagonistic hormones, too, have been recognized as counteracting
epinephrin in vasoconstricting effect. Thus the secretion of the thyroid .
is believed to neutralize or counterbalance the influence of epinephrin, so
that certain authorities (such as Weber, Rolleston, and Williams!) have
suggested insufficiency of the thyroid secretion as a cause for the so-called
senile, involuntary or decrescent type (Allbutt) of arteriosclerosis. Others
take exception to this view.
The importance of thyroid hormones in arterial affections receives further
confirmation in the observation that arteriosclerosis is rather a common
concomitant of cretinism. Wilson? regards the increased blood pressure
frequently following the climacteric as due to the absence of the vasodilating
influence of ovarian secretion. Engelbach# believes that the hypertension in
these cases must be due to causes other than the disturbed secretion of the
ovaries, or else it would occur in a larger percentage of cases. He offers
clinical evidence in support of the theory that a certain selected group of
cases of arterial hypertension is associated with endocrine dyscrasias.
Krogh states that a hormone in the blood, probably derived from the
activity of the pituitary gland, maintains the ‘ ‘normal” state of contractility |
of the capillaries.
Mosenthin‘ expresses the view that in scleroderma we are dealing with
deranged internal secretions with increased tonus of the sympathetic, basing
his opinion on a study of the vegetative system in one of his cases, and on an
analysis of the literature. What glands are responsible, however, he does
not make clear. Cases are reported in which scleroderma is attended with
disturbances in the thyroid, parathyroid, adrenal, sexual glands and hypo-
1 Allbutt’s Diseases of the Arteries, 1915, I, 230.
2 Wilson, S. A. K., Brit. Med. Jour., I, 1261.
s Engelbach, Wm., Jour. Am. Med. Assn., June 12, 1920; 74, p. 1610.
4 Mosenthin, H.., Arch. f. Dermat. u. Syph., 1913, Bd. TIS; S0r<-
VASOMOTOR AND TROPHIC NEUROSES—GENERAL CONSIDERATIONS 503
physis. Of late years, there has been a distinct trend to associate thyroid
disorders with scleroderma, though it is evident that the glandular malfunc-
tion could be secondarily produced, reasoning by analogy, and recognizing
that other glands, skin, bones and musculature suffer in this disease. That
erroneous conclusions may be arrived at in attributing clinical complexes to
certain endocrine disturbances, is illustrated by the case of Rasch,! who
described a case of scleroderma supposedly influenced or caused by a hypo-
physis lesion. At autopsy a normal hypophysis but with complete destruc-
tion of one of the suprarenal glands was found.
The role of the endocrine states in scleroderma is still a mooted question.
Josefson? reports that certain cases of acrocyanosis were cured under
thyroid therapy, believing the symptoms attributable to hypothyroidism. In
a girl 13 years of age, he also saw improvement after organotherapy. The
so-called acrocyanosis associated with tuberculosis is attributed by Rasch? to
endocrine dyscrasia.
Of recent years the pendulum has swung towards the theory of endocrine
influences in explanation of the vegetative functions. And perhaps too much
importance has been attributed to lesions and derangements of the glands of
internal secretion. Conversely, too little weight has been given the rdle of
the vegetative nervous system per se, which in itself exerts a regulatory
control of the activity of these very glands.
As an example may be mentioned the influence relegated to the pancreas in the produc-
tion of diabetes, and to the thyroid in evoking the Basedow complex. In reference to the
former it may be said that Claude Bernard’s puncture was proof of the relation of the nerv-
ous system and diabetes, and that the sugar metabolism is also influenced through the action
of the nervous system upon the adrenal, liver, and muscle cells.
So, too, in the case of essential hypertonia much importance has been attached to the
adrenal gland. The rdéle of the nervous system has been neglected.
In diabetes Dresel and Lewy succeeded in showing important degenerative changes in
the corpus striatum. Experimental work on rabbits developed that the exclusion of the cor-
pus striatum was followed by a permanent hyperglycemia and glycosuria. From this the
conclusion was warranted that at least in a percentage of cases of diabetes, localized changes
in the brain stem are responsible. Just how these views can be harmonized with the more
recent therapeutic results with insulin is a matter for conjecture.
Dresel emphasizes the parallelism between essential hypertonia and the hyperglycemia
of diabetes. In the one instance it is the blood sugar, in the other the blood pressure which
suffers a rise in threshold. Because of these facts and the observation that even intensive
alterations in the vessels themselves may produce no increase in blood pressure in the
presence of properly attuned regulatory mechanism, have convinced this author that
another explanation must be sought. He offers, therefore, the hypothesis that essential
hypertonia is due to a derangement of the central regulatory mechanism, in the sense of an
excessively high threshold for blood pressure; and that the arterial changes may be but
secondary organic manifestations.
In addition to these generalized expressions of central nerve derangements,
more localized vasoconstrictor effects in circumscribed territories may be
referable to central influences. When general, central, or peripheral (para-
sympathetic or sympathetic) irritation exists, local attacks (of vagotonic
and sympatheticotonic nature), such as asthma may result. In the latter
affection, psychic, sensory and toxic irritants may be the motivating factors.
In the case of angiospastic forms of intermittent claudication a local hyper-
tonic condition of the vessels of the lower extremities may be the response
of a functional excitant. (For the theory of the reversal of the normal
vasodilating reflex or response to a vasoconstrictor action, through altered
1 Rasch, C., Dermatologen Kongress, Christiana, 1916.
2 Josefson, A., Svenska la kare sallskapels handlungar, rors, Bd. 41, p. 1.
3 Rasch, Loc. cit.
504 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
chemistry in the tissues in the obstructive arterial types of intermittent
claudication, the reader is referred to Chap. XX VI.)
Internal Secretions and Trophic Disturbances.—With the recent impetus
given endocrinology, and the trend to explain numerous skin affections,
scleroderma, Raynaud’s disease, and the other vasomotor and _ trophic
neuroses on the basis of endocrine dyscrasias, opinions on the relationship
of the internal secretions to skin lesions are worthy of mention.
Thus Strandberg! in his summary concludes that: (1) the endocrine organs and their
secretions have a distinct influence on the integument; (2) that endocrine disturbances can
predispose to, and ‘‘produce”’ skin affections; (3) that some of the dermatoses whose patho-
genesis is doubtful seem to have a common endogenous cause. Cases of family dermatoses
show, not infrequently, a combination of various anomalies of cornification, hair develop-
ment, nail growth, sclerodermal and vasomotor manifestations.
The Hypersensitiveness of the Vegetative Nervous System.—Clinical observa-
tions are being accumulated that point to the possibility of a condition
of increased suspectibility or hyperirritability of the vegetative nervous
system. It has been pointed out that climatic influences on the organism
affect both the function of the endocrine glands, and the vegetative nervous
system. Most of the deductions are pure hypotheses, but enough observa-
tions are at hand to warrant entertaining some of these. In the case of
tetany, the intimate relationship between the endocrine functions and the
nervous system seems to have been proven beyond peradventure.
In certain animals, it has been shown that the autonomic nervous system varies in its
sensibilities with the seasons. In rabbits irritation of the heat center by acupuncture has
proven the varying and seasonal susceptibility of this center. Further data that concern
the vacillating irritability of the vegetative nervous system are derived from the clinical
observations, that so-called eczema death? and disturbances of the heat center occur ina
seasonal way. In the former, a hyperexcitability seems to occur in the spring time, while
in the latter, crises or periodic variations in the susceptibility of the vegetative nervous
system would seem to take place.
The unusual and interesting disease known as “idiopathic cutaneous
atrophy, Erythromelie,”’ has been regarded by some as due to endocrine dys-
crasias. A short description of this malady will be found in the chapter on
Scleroderma (Chap. C).
CHAPTER LXXXVII
THE SKIN AND THE VEGETATIVE NERVOUS SYSTEM
So important is the control of many of the functions of the skin by the
vegetative nervous system, that a general discussion of its influence, and a
summary of the nerve paths and of the vasomotor manifestations in the
skin may afford an apt explanatory prelude to the clinical description of the
vasomotor and trophic affections.
1 Strandberg, J., Beitr. z. Frage d. Bedeutung d. inneren Sekretion.
2 Eczema death is mentioned here as a manifestation of the varying susceptibility of the
vegetative nervous system, for it is believed that the cases of sudden, inexplicable death
occurring in infants suffering from so-called constitutional eczema, may be due to status
lymphaticus, or sudden cardiac paralysis occasioned by vagus malfunction.
THE SKIN AND THE VEGETATIVE NERVOUS SYSTEM 905
The integument in its vascular and other component parts, including the
hair follicles, the sweat glands, and the pigment cells, is under the control
of the vegetative nervous system. The contractile elements of the skin,
the vessels, the hair follicles, and the smooth muscle are affected through
direct stimuli, namely, by substances that course in the blood and in the tissue
fluids; or, zzdirectly through the nervous system. Centers lying in the spinal
cord, and governing these functions are in their turn modified and influenced
through the quality and warmth of the blood, through psychic impulses,
or impulses emanating from the periphery. In this way, vegetative skin
reflexes are brought about.
One of the most commonly observed examples of the vegetating functions
is the reaction to heat and cold. Whenever, by virtue of external cold, the
temperature of the body would tend to drop, a regulatory function is set
into action. The vessels of the skin contract, and the blood cannot find
its way into the superficial layers of the skin; thus, radiation of heat is pre-
vented. Conversely, with the body overheated, dilatation of the skin vessels
takes place, and increased radiation. If this function is inadequate, the
action of the sweat glands is brought into play.
In this mechanism, two separate forces or impulses are set into activity:
firstly, a direct action upon the vessels and muscles of the hair follicles which
contract through cold (reacting contrarily to heat); and secondly, a reflex
is set into motion, whose impulses pass through the sensory skin nerves to
the vegetative centers in the cord, and thence centrifugally, bringing about
contraction or relaxation of the muscular elements of the skin and increased
perspiration.
The Vegetative Reflexes in the Skin.—These include the responses that
take place exclusively through the route formed by the nerve paths and
nervecenters. Twogroupshavebeenrecognized. Inthe first group the result
of irritation is limited to a territory that closely approximates the region
of stimulation. ‘The reflex arc is probably confined here to the spinal cord
without participation of the higher centers. As examples may be mentioned
the contraction of the smooth muscle of the nipple areola; and the so-called
reflex dermatographia. |
Whenever larger areas react, we speak of reflexes of higher order (second
group). We may mention, to illustrate, the remote action of vasoconstrictor
types after cold foot baths, and also the pilomotor reaction that may extend
so as to involve a whole extremity or part of the body.
Whenever the reflex becomes still more extensive so as to implicate a
large part or the whole of the body surface with chilly sensations and goose
flesh, the higher centers (cerebral) are probably at work. Whereas such
extensive responses usually require rather severe and intensive irritants, in
certain conditions susceptibility may be so heightened that very slight
excitation suffices. It has, therefore, been assumed by a number of authors
that generalized reflexes are dependent upon certain internal conditions.
Given a certain threshold of excitability of the corresponding centers and
possibly a certain predisposition of the peripheral vegetative organs, we have
the possibilities for reaction to but limited or minimal external influences.
With a certain degree of receptivity that is tantamount to a full nerve load,
very slight impulses may lead to a discharge; and this explosion, as it were,
follows certain existing nerve paths. Secondarily thereto, changes in the
innervation of the vegetative organs of the skin may follow. 3
Alterations in the vegetative innervation of the skin of psychic course
(blushing, goose flesh) may expose emotional states no longer under control
of the will.
506 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Certain general concepts regarding the lability of the vegetative nerve
innervation must be kept clearly in mind for a comprehension of the diseases,
such as Raynaud’s and erythromelalgia. The skin reactions are subordinate
to so many conditions, that we are often unable to draw conclusions regard-
ing the condition of the vegetative nervous system, or, indeed, of the nervous
system in general. What may be regarded as a morbid reaction both as
regards intensity and feebleness in one case, may still be within the physio-
logical in another case. Many of the conditions that determine the reaction
may vary at different times in the same individual; others may be con-
genital, hereditary or acquired. Of the various coefficients, the following
may be mentioned; the condition of the skin, the nervous status, the momen-
tary psychic state, chemical influences (metabolism, internal secretions, auto-
intoxication), and so forth.
The Nerve Paths —The fibers for vasoconstriction controlling the hair
follicle muscles over the whole body surface are traceable to the dorsal and
three upper lumbar roots, the sympathetic centers lying at corresponding levels
in the spinal cord.
The cervical sympathetic contains the preganglionic vasoconstrictor,
pilomotor and secretory sweat paths for the face. The vasodilator and sweat
inhibiting paths for the face emanate from the cranial autonomic system; for
the trunk and the extremities, fibers emanate also from the dorsal and upper
lumbar segments that leave the spinal cord through the posterior and not
through the anterior roots. In the peripheral sensory nerves of the skin
there are fibers for all the constituent functions of the vegetative skin
innervation.
It is believed that sensory paths and centers exist for the various skin
functions (vasoconstriction and dilatation, pilo-erection and blood secretion),
for, these activities are independent.
The vegetative skin reflexes take place through the following reflex arc—
the sensory paths constitute the afferent limb of the arc, being traceable from
the skin through the skin nerves into the spinal ganglion and posterior root
into the spinal cord, then communicating with the vegetative center of the
lateral horns. For the vasoconstrictor, pilomotor, and secretory fibers the
efferent limb passes through the anterior root, the ramus communicans albus,
and the sympathetic ganglion through the spinal nerve. The self-inhibiting
and vasodilator fibers pass through the posterior nerve to the peripheral
nerve. For vegetative skin reflexes of the higher order the interpolation of
the center in the mid-brain may be assumed.
The Vasomotor Phenomena of the Skin'.—Although the mechanism of
all the varied pictures presented by or due to.active constriction or dilatation
of the smaller vessels of the integument is not altogether understood, it may
be well to briefly discuss the nature of some of these for a better comprehension
of the clinical affections. In the chapter on Capillary Circulation we have
alluded to the response on the part of arterioles, capillaries and venules,
both to direct influences, as well as to nerve stimuli. The total capillary loop
may be affected through the nervous system even by emotion, or externally
through cold or other impulse (even mechanical as in dermatographia),
active constriction of the loop may result. Thus, narrowing or dilatation of
the vascular loops may occur. ‘The greatest fluctuations are noticed in the
arterial limbs. Some authors believe that there is a special innervation for the
arterial limb in view of the clinical manifestations.
The skin presents either a normal color or deviations therefrom: These
are increased redness, transitory rubor, chronic rubor, induced rubor or
1 For data to be gained from Capillary Microscopy, see Chaps. CVI et seq.
THE SKIN AND THE VEGETATIVE NERVOUS SYSTEM 507
reactive hyperemia, reddish blue cyanosis or asphyxia, complete pallor
(syncope), and the so-called marmorated appearance.
The blood content accounts to a great degree for the normal color of the
skin, and under ordinary circumstances only a part of the capillary territory
is filled. The arterial blood tends to flow rather through the deeper and
shorter communicating paths into the venules. When there is hyperemia,
rubor or redness, we assume an increased filling of the superficial vascular
strata with red arterial blood, with adequate patency of both afferent and
efferent channels. At the same time the blood stream is more rapid than
normal, and the skin feels warm under such conditions.
The various forms of rubor, transitory rubor of neurogenic origin, or
permanent rubor following chronic obstructive arterial disease, and reactive
hyperemia (induced or reactionary rubor, or erythromelia) are described in
detail elsewhere. Here we need merely mention that a reactive hyperemia
may take place in a normal individual after a temporary impediment to the
circulation has been withdrawn. And so it is visible as a reactive ischemia
due to the application of an Esmarch or Martin bandage, after Bier’s method
of producing stasis, and after cold or pressure anemias. Opinions vary as to
the explanation of this phenomenon, some believing that an exhaustive or
paralytic state in the capillaries occurs, others, that there is an active dila-
tation of the cutaneous vessels. Bier had already suggested the theory that
by virtue of metabolic derangement, and absence of oxygen, an active
dilatation of the capillaries ensued. This theory is somewhat in accord
with the recent views of Hooker who had demonstrated that metabo-
lites or tissue products are capable of inducing an active dilatation of the
capillaries.
On the other hand, reflex vasoconstriction in the arterioles and smaller
vessels has been laterally interpreted (Zak) as a neurogenic response to
accumulating waste products (CO.), and more properly lactic acid in the
muscles; and is assumed to occur in territories poorly supplied with blood
after exertion.
Reflex action may also account for the capillary response, as is seen after
irritants, such as cold. A livid or cyanotic discoloration of the skin presup-
poses dilated vessels and stasis. In view of the arrest or sluggishness of the
circulation, the temperature of the part also becomes lower, and the skin
may become cold to the touch. Neurogenic spasm in the smallest arteries
with stagnation in the capillaries and venules (as in Raynaud’s disease)
may cause asphyxia, or, a combination of circulatory weakness (in obstructed
arteries) and the effects of gravity (as in the pendent position), may bring
about the same color. Not infrequently can the chronic dilatation of the
venules and their immediate channels of higher order be demonstrated in a
condition of chronic dilatation, when the cyanotic or livid toes in thrombo-
angiitis obliterans are depleted of their blood by elevating the extremities.
Then we note that ischemia sets in because the capillaries cannot be filled
in this position, and that the venous paths, either by virtue of dilatation of
the venules or vasoconstriction of the larger veins, fail to empty themselves,
and remain as livid markings.
Active contraction (vasoconstriction) of the vessels of both skin layers
produces complete pallor or syncope.
A reticular patchy lividity or reddish and purplish discoloration of the
skin produces the so-called marmorated appearance. We distinguish the
livid and the hyperemic form of cutis marmorata. The former occurs
usually after exposure to cold. It is not known to what extent a reflex
508 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
nervous mechanism, or in how far direct action of thermic influences are
responsible.
It is often impossible to segregate the effects of purely vegetative nerve
function from the other forces liberated, or already existent in the various
morbid entities affecting the vascular system of the extremities. In inter-
preting the vasomotor manifestations of the organic obstructive diseases, we
have to take into account (1) the hydrostatic, mechanical and gravity factors;
(2) the central and peripheral reflexes; (3) the reflexes evoked through changes
in local circulation (ischemia on elevation); and (4) the local influence of
metabolites on the capillary and venule territories.
1. The first of these is discussed in detail in the chapters on Obstructive
Arterial Affections. We need merely admonish the clinician, here, that
whenever organic interference with vascular patency impedes the flow and
diminishes the force of the stream, the state of fulness of the peripheral
capillaries and venules is influenced thereby. Indeed, changing position of
the limb may alter the circulatory conditions so as to give manifestations
of incongruous nature, easily mistaken for those of nerve origin. They may
be summed up as being of the nature of rubor, cyanosis or asphyxia, ischemia
or syncope, or simultaneous combinations of any of these.
2. The reflexes capable of calling forth alterations of the state of con-
tractility in the vessels of the integument are also referred to elsewhere.
For clarity, we may note here that even emotional states and the nervous
habitus are not without influence through the higher centers; and peripheral
afferent impulses such as cold, motion and trauma are clinically known to
produce striking effects.
3. If a limb in which the circulation is impaired through arterial obtura-
tion be raised, depletion of the distal surface vessels is produced, and thereby
localized ischemia or anemia.' Per contra in the hanging position of the
limb a condition of rubor, cyanosis or intense cyanosis alone may develop.
To what extent are these appearances of purely hydrostatic origin; how far
are vasomotor influences at work; and what are the direct effects of local
tissue changes or products responsible for the responses in the arterioles,
capillaries and venules? ‘These are questions that cannot be categorically
answered, but the mere placing of the queries should arouse food for thought,
and a correct attitude of interpretative analysis.
Let us analyze but one phase, that of artificially induced ischemia on
elevation of such a limb. What are the forces besides the hydrostatic, the
gravity, the impaired force of the stream that are then brought into play,
and that could modify or cause reaction in the peripheral vascular territory ?
4. As a result of the depletion, automatic constriction of the arterioles
and venules could be predicted in conformance with known laws. But, is
there not a simultaneous elaboration of metabolites in such an ischemic terri-
tory that would make for dilatation of these paths?? Clinical observation
recognizes that dilatation of the capillaries and even of the venules does
actually occur. Have the vessels already dilated in the elevated position,
and is the pallor merely due to mechanical forces and inadequate circulatory
power? Or, does vasodilatation begin only when the limb begins to hang
down, and does it require the filling of the vessels to evoke the intensified
response?
To answer these questions studies on the morphology of capillaries, and
on the capillary pressure in the toes held in such positions, should be made.
1 See application of these terms by extension, in Chap. X on Local Circulation.
2 See work of Krogh, Dale and Hooker, Chap. VII.
DIAGNOSIS AND LOCALIZATION OF VEGETATIVE NERVE LESIONS — 509
And only then will we know which of the forces, mechanical, neurotic or
chemical, plays a dominant role.
The Cutaneous Responses to Thermic and Actinic Irritants—It has been
observed that rays of long wave length develop warmth energy and act as
heat irritants, whilst rays of short wave length, when absorbed, bring about
chemical changes. The action of sun rays is well known, the primary hypere-
mia, the consequent painful reddening, swelling and sunburn. Protracted
exposure to light may cause a permanent dilatation of the capillaries.
A moderate degree of heat brings about dilatation of the capillaries of
the skin by direct action upon the contractile substance of the capillary
endothelium and the musculature of the smallest vessels. It has been shown
that the limbs or the neck of an experimental animal when deprived of
nerve continuity still respond by a hyperemic reaction to hot air. Very
intense heat causes an effect similar to that of cold in the constriction of the
cutaneous vessels, particularly in the small arteries. Later, however, with
continued exposure a hyperemia of the congestive variety, similar to that
produced by cold, is noticed. In this the arteries are constricted, the capil-
laries and veins dilated.
When severe cold is of but short duration, arteries and capillaries are
contracted, and when the external temperature rises again a hyperemic
reaction occurs. Continued cold produces a paralysis of the vasoconstrictor
action with a livid hyperemia, in which the venous portion of the capillary
loop is engorged. In the case of cold, however, reflex action is more apt to
take place as is borne out by the observations that a distant part of the body
may respond synchronously. As an example, we may quote the contraction
of the cutaneous vessels of the other limb when one is plunged into cold water.
The immediate effect of cold comprises the action of both a reflex and direct
mechanism. So, too, does this obtain in the case of heat (Rehberg and
Krogh).
COARTER 2 Oox Vill
DIAGNOSIS AND LOCALIZATION OF VEGETATIVE NERVE
LESIONS
The multiplicity of vasomotor centers makes possible the substitution of
subordinate centers to compensate for lesions that bring about vasomotor
disturbances. ‘This can be all the more effectively brought about, in that the
minor centers have a greater independence of action than the superior. On
the other hand, this far-seeing provision of Nature has its draw-backs. For
the recognition of the seat of lesions of the vasomotor system is consequently
made difficult, and oft impossible. The existence of two systems of contrary
powers and their susceptibility to varied reflexes from all over the body
still further complicates diagnostic work. One may conclude, therefore,
that it is quite impossible to make deductions regarding the pathogenesis of
vasomotor disturbances from their character and distribution. Perhaps
only where the vasomotor derangements are closely limited to the course and
distribution of certain peripheral nerves, can we diagnosticate the seat of
the lesion.
510 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
Deficiency symptoms in the vasomotor system show great tendency to
recovery, a fact that is easily explained by the substituting action of numerous
other centers. On the other hand, however, when we are dealing with the
results of irritation of such centers or paths, other centers cannot act as
surrogates, and no compensatory action takes place. With continued irri-
tation we do not expect any abatement of clinical manifestations until the
excitability of the corresponding nerve segment ceases and is followed by
paralysis. For an understanding of the clinical cases of vasomotor disturb-
ance, we must remember that through reflex paths irritation of the vaso-
motors can persist for a long time. So, too, it is observed that irritation
within the vasomotor system has a more potent action than the paralytic
causes. ‘Therefore, whenever we see vasomotor symptoms of long duration,
we should look to reflex irritation as possible causes rather than to paralytic
conditions.
Although no final knowledge regarding the localization of lesions in this
domain is at hand, some of the salient facts that clinical observations and
pathological conditions have furnished may be worthy of recapitulation.
Cerebral Lesions and Localization.—Vegetative disturbances following
lesions of the cerebrum with motor and sensory symptoms regularly occur on
the contralateral side. This would indicate that vegetative fibers, as well
as motor and sensory fibers undergo complete crossing on their way to the
periphery.
It is well known that in those cases of Brown-Séquard palsy, where the
lesions reside in the cervical cord, the vasomotor paralyses take place on the
side of the lesion. And so it is assumed (Depisch) that the crossing of the
vegetative paths occurs somewhere between the thalamus and the cervical
cord.
Vasomotor disturbances on the opposite side are reported as resulting from operations
on the brain (Schlesinger!). Nothnagel also describes such derangements complicating
cerebral lesions.
Rossolino? reports a case with attacks of Jacksonian epilepsy attended with edema and a
livid discoloration of the affected upper and lower extremities. The temperature of the
hand was 2-3° C. lower and the temperature on this side of the body was also 1° lower.
At operation a cyst was found in the anterior frontal gyrus of the opposite side, and after
evacuation of the cyst the motor power of the extremity, which had been diminished, and
the circulatory phenomena returned to normal.
In a study of the vasomotor disturbances in hemiplegia, Goldstein and Parhon? found in
13 out of 18 cases diminished temperature on the paralyzed side; in 4 no differences.
Mager! describes a bluish discoloration of the skin below the middle of the paralyzed leg
with lowering of the skin temperature in a case of right-sided hemiparesis. Autopsy showed
a small apple sized-tumor involving the lower part of the central convolutions.
Deficiency symptoms in cases of disease of the cerebrum, where large
ganglia are implicated but not wholly destroyed, are associated with distur-
bances in the vegetative processes of the contralateral side in the form of
paralytic or irritative phenomena.
Amongst the paralytic symptoms may be mentioned palsies of the
ocular sympathetic and palsy of the vasomotors; of the irritative symptoms,
occasionally mydriasis, increased constriction of the cutaneous vessels, in-
creased secretion of sweat, the salivary glands, and mucous membrane.
The vegetative paths crossing in the medulla oblongata for the eye, the
vasomotor and sweat glands of the face are believed on the other hand to
1 Schlesinger, Arch. f. Dermat. u. Syph., Festschrft. Kaposi, 1900.
2 Rossolino, Deutsch. Ztschr. f. Nervenh., 1895, 6, p. 76.
’ Goldstein and Parhon, La Roumaine med., Apr., 1890.
* Mager, Vide Obersteiner, Arbeit. a. d. neurol. Inst., 1907, XVI.
DIAGNOSIS AND LOCALIZATION OF VEGETATIVE NERVE LESIONS O11
connect directly with the same side of the body. ‘The crossing point of these
fibers, therefore (Breuer and Marburg!), would have to take place between
the pons and the internal capsule.
The Vasomotor Paths for the Trunk and Extremities.—The cases of apoplec-
tiform bulbar paralysis would seem to indicate that the crossing point of these
fibers lies somewhat lower than that of the vegetative paths for the face.
\\
\\.
PK
/ St+k
Loman ee
je
WV mak
AM a E ae
te
Fic. 165.—Decussation of vegetative nerve paths. (After Depisch)
P = pyramidal paths K = vegetative paths for the head
St + E = vegetative path for the trunk and extremities
YV—4
eel
—
For, the clinical cases demonstrate that the vasomotor lesions occur on the
contralateral side (Fig. 165).
For elucidation of diagnostic interpretations the following recent views
concerning the cerebrospinal vegetative paths may be of some value. They
1 Breuer and Marburg, Quoted by Depisch. Wien. Archiv. f. inn. Med., 1920, I, p. ror.
912 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
may serve as an aid to localization when additional data will have been
forthcoming.
t. The vegetative paths from the cerebrum and the large ganglia of the
brain-stem undergo a crossing on their way to the periphery.
2. The decussation is complete at a level of the lowermost portion of
the cervical cord; and below this the fibers undergo no further crossing.
3. The decussation of the paths of the ocular sympathetic and of the
vasomotor and secretory (sweat) impulses is accomplished in the region of
the pons.
4. The crossing point of the vasomotor and secretory paths for the trunk
and extremities would appear to take place somewhere in the neighborhood
of the pyramidal decussation.
In short, these vegetative paths cross lower than those of the head,
though higher than the motor fibers.
These facts are in consonance with the clinical observation that either
crossed or homolateral disturbances of the vegetative function can occur in
lesions of the superior cerebrospinal tract.
There would, therefore, be a region in which lesions would implicate
vegetative paths before any decussation takes place and with homolateral
derangements as a sequence.
Pharmacologic Tests of the Vegetative Functions.—The three poisons,
adrenalin, pilocarpin and atropin, are mainly used. Of these adrenalin
acts on the whole sympathetic system; pilocarpin only on part of the para-
sympathetic. The latter may be regarded as a substitute for that hypo-
thetical substance—autonomin—which, according to Eppinger and Hess,
normally keeps the parasympathetic nerve endings in a constant state of
excitability.
Adrenalin is a poison that acts as an excitant on the points of junction
between the sympathetic nerve endings and the end organs (myoneural
junctions). Tests for the production of general or local symptoms have been
evolved, with a view to estimating the irritability of the sympathetic system.
Injection of adrenalin (1 cc. of 1:1000) subcutaneously causes normally
the following reaction: after a few minutes palpitation, feeling of distress
and tremor of the extremities, and local pallor and blanching of the face ensue.
In individuals whose sympathetic system is hyperexcitable, the reaction is
excessive; the whole body may shake, there being precordial distress, cardiac
pain, perspiration and even transitory collapse.
Persons whose parasympathetic system is over excitable suffer little or
no reaction after adrenalin injection. However, by reason of the inordinate
vagus response, these individuals show numerous extra systoles.
A reaction of excessive glycosuria is also regarded as a sign of hyper-
sensitiveness of the sympathetic; absence of such, a vagus susceptibility.
Responses on the part of the blood pressure, too, have been interpreted
as of value in this connection. A rapid reaction with an abnormally high
adrenalin blood pressure curve is said to be characteristic for a hypersensitive
sympathetic system.
Loewi believes that mydriasis following the instillation of 1-3 drops of a
I: 1000 adrenalin solution in the conjunctival sac indicates defective tonus
of the vagus or hypersensitiveness of the sympathetic.
Pilocarpin, since it excites the parasympathetic system, is employed to
estimate the responsiveness of the latter. The reaction after subcutaneous
injection of 1 cc. of a r per cent solution is observed. ‘The normal effect
is a feeling of heat, perspiration, redness of the face and increased salivary
VASOMOTOR AND TROPHIC DISTURBANCES 913
secretion. When the reaction is excessive, it indicates an increase of the
irritability of the parasympathetic system, or generalized hypersensitiveness
of the whole vegetative nervous system.
Atropin has been used to detect the influence of the vagus on arhythmia.
If symptoms supposedly due to over excitability of the vagus disappear
after atropin injection, then confirmation of their vagus or parasympathetic
nerve origin is at hand.
CHAPTER LXXXIX
VASOMOTOR AND TROPHIC DISTURBANCES IN LESIONS OF
THE CENTRAL NERVOUS SYSTEM
Intensive emotions may in susceptible individuals be followed by the
appearance of pruritus or urticarial types of eruption. It is well known that
severe shocks or psychic insults may cause the hair to turn grey, and a partial
or total alopecia may result. Paroxysmal or long continued swelling of the
skin may occur upon the paralyzed side after cerebral injuries—expressions
of vasomotor disturbances—and even ungual dystrophies and anomalies of
hair growth may complicate. Almost all the forms of trophic disturbances
may be associated with spinal cord diseases.
In myelitis we occasionally find bullous eruptions and herpes zoster.
During paroxysms of tabetic origin, crises of herpetic eruption or urticaria
or purpura have been observed.
Herpes zoster is regarded as a reflection of disease of the spinal ganglia;
an expression of abnormal increased excitability of the peripheral sensory
neuron, or more probably of the peripheral vasosensory motor neuron. It
may also attend lesions of the sympathetic gangliated cord.
Tabes Dorsalis.—Trophic disorders here will hardly be confounded with
_the vasomotor and trophoneuroses, except in the case of associated malum
perforans. Spontaneous gangrene has also been reported as complicating
this disease. As a rule muscular atrophy involving large muscle groups,
trophic affections of the joints and bones, and the so-called tabetic arthro-
pathies are the well-known evidences of trophic derangement.
Syringomyelia and Gliosis Spinalis——The manifestations of disturbed
nutrition are exceedingly varied, very often in the form of small vesicles or
larger blebs over the hands. After rupture of the blebs, indolent ulcers
develop. Wounds and cicatrices so often encountered over the hands of these
cases are usually due to an inability to perceive pain and thermic impulses,
and hence burns readily occur without the knowledge of the patient. Remak,
Schlesinger and Oppenheim describe reddish blue discoloration of the hand
and forearm (vasomotor phenomena). More extensive trophic disorders
may take the form of bone necrosis, destruction of the terminal portions of
the digits; or, if infection supervenes, phlegmonous processes may be expected.
A peculiar appearance of the hands with enlargement simulating that of
acromegaly has been observed (Schlesinger, Oppenheim). Even a myxce-
dematous change in the skin may be associated. Marinesco is responsible
for the term ‘‘main succulent” as descriptive of a striking alteration in the
consistency and texture of the soft parts of the hands. A diffuse swelling
especially of the dorsal aspect sufficient to mask the underlying bony and other
33
5014 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
landmarks, often attended with vasomotor phenomena, is regarded as
characteristic. By virtue of muscular atrophy, a narrowing of the hand
may take place. Arthropathies are frequently associated.
A consideration of these manifestations will facilitate differentiation from
the other forms of vasomotor and trophic neusosis (Chap. XCIX ).
Injuries of the Spinal Cord.—The relationship between the nature of the
vasomotor disturbances and the character and extent of the spinal cord lesions
has not been definitely established. After total transverse lesions extensive
vasomotor palsy of regions below the level of injury are often seen. They
may, however, occur after incomplete interruption in continuity of the cord,
and may be present in spastic conditions. Even so-called “‘ vasomotor _
disturbance of the lymph system” has been described by Marburg and
Ranzi, reflected in the condition of pasty swelling of the leg, following spinal
cord lesions. With the vasomotor disturbances there may be trophic dis-
orders, decubitus, vesicle formation and ulcers.
These authors describe the following picture: The legs are swollen, the skin tense and
stretched, glistening, of a waxy white color, occasionally bluish, the skin devoid of the usual
characteristics of edema; or occasionally, too, edema, cyanosis, and coldness of varying
degrees are observed.
Vascular dilatation may appear over the paralyzed region; later coldness
and cyanosis, signifying chronic vascular relaxation. Vasomotor disturb-
ances are also responsible for the engorgement of the corpora cavernosa in
such cases.
In Brown-Séquard’s symptom-complex (unilateral transverse lesion) the
skin may be reddened and warmer on the same side; later on, this may give
way to a chronic condition of coldness and cyanosis. An interruption of
the vasoconstrictor fibers of the lateral column of the same side is given as
the explanation therefor.
Decubitus may occur rapidly after traumatic lesions of the spinal cord.
Kroh saw it develop 18 hours after injury; Henneberg on the morning follow-
ing the trauma; and Krause emphasizes the unfavorable significance of its
rapidadvent. Decubitus may occur in places that are not subject to pressure.
Total transverse lesions of the cord are not necessary for the development of
such lesions.
Two factors deserve recognition as of etiologic importance in the neuro-
genic type of decubitus; namely, alterations in the circulatory function of the
affected parts, and the direct influence of pressure, which, in most instances
at least, is a factor. Nevertheless, the occurrence of acute decubitus with
central nerve lesions has been so frequently described by competent observers,
that a mechanical, traumatic or pressure effect has been proven to be not
essential.
GHAP LE RES
NEUROTROPHIC DISORDERS IN SPINA BIFIDA
Syringomyelia and spina bifida occulta may be complicated by trophic
lesions that should not be confounded with those due to impaired circulation.
Those associated with spina bifida occulta may occasion doubts as to diag-
nosis. ‘These, however, should be easily dispelled if we remember that in
the latter, the arterial pulsations are normal, that sensory derangements of
NEUROTROPHIC DISORDERS IN SPINA BIFIDA 515
the lower lumbar and sacral nerve roots or segments are usually present,
and that true gangrene is absent.
We are interested here merely with those vasomotor and trophic mani-
festations that may lead to difficulties in differential diagnosis. A short
resumé of the salient features of the affection, however, may clarify
doubtful points.
Spina bifida occulta is said (Recklinghausen) to be attributable to an intrauterine healed
myelomeningocele. According to this theory there should be a defect in the dura, but this
is not always present. Hair growth and tumors are frequently found at the site of the
defect in the spinal column. This manifestation is explained by the fact that in intrauterine
-life tissue elements are displaced. According to other authors (Marchand) cystic dilatation
with spina bifida exists in intrauterine life with healing and spina bifida occulta as the end
product. The existence of mixed tumors, fibromyomata, myofibromyomata is explained
on the assumption that an intrauterine myelomeningocele, the product of the healing
process in spina bifida occulta arises; and that through the traction of the scar, the skin,
musculature and connective tissue become transferred or displaced into the depth and even
into the spinal canal; from such, elements of neoplasms may arise.
Symptoms of Spina Bifida Occulta.—These may be divided into: (1)
those at the site of the sacral cleft; (2) those resulting by reason of involve-
ment or lesions of the spinal canal contents, namely, the cauda equina, and
the nerve roots and peripheral nerves.
We are concerned only in this connection with the sensory, vasomotor
and trophic disturbances. The latter will receive detailed consideration.
whereas the other symptoms will be given merely passing mention.
1. The Local Symptoms.—Of these the abnormal hypertrichosis is the
most important, being noticeable in the region of the cleft. Cicatricial
changes in the skin, with elephantiasis deformation, dimples, telangiectases,
localized hyperhidrosis, funnel-like retraction of the skin.or pseudo fistula
formation, or abnormal depressions on this region—all these should arouse
the suspicions of spina bifida occulta. But in many cases a sacral deficiency
may exist even under normal skin.
Occasionally a small tumor may be felt under the skin, which in itself is
suggestive of spina bifida occulta. Any tumefaction in this region should
arouse suspicion of the existence either of a spina bifida vera, or cystica,
or one of the occult or concealed variety without protrusion of the contents
of the spinal column. A tense elastic consistency would point to the former,
a lobulated more solid nature to a lipoma over an occult variety. Local
subjective symptoms include, vague pain, particularly on changing the
position of the body or on exertion, probably due to traction of the cauda
equina or nerve roots.
2. Nerve Lesions of the Cord or Cauda Equina.—From the diagnostic
standpoint it is valuable to know (Miller) that sensory irritative symptoms
are absent when the lower part of the spinal cord is diseased, but paralytic
symptoms are present, the latter in part as disassociated sensory phenomena.
When alteration occurs in the cauda equina from compression due to a tumor
or from traction, sensory, irritative manifestations are intense, and paralytic
symptoms for all sensory qualities,appear simultaneously.
From the therapeutic and operative standpoint, it is important to deter-
mine whether the cauda equina is mostly involved. For in the latter case,
more is to be expected from therapy. Indeed, the cauda is capable of under-
going some regeneration after operative work. Miiller believes that when
the trophic centers for the motor fibers in the spinal cord and the trophic
centers for the sensory fibers in the spinal ganglia are conserved, regenera-
O16 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
tion of axis cylinders and medullated sheaths may occur after the deleterious
forces in spina bifida have been put into abeyance.
Disturbances Due to Lesions of the Nerve Apparatus.—These comprise
neuralgia, pain in the region of the cleft, irritative or paralytic symptoms
in the perineal region, genito-urinary apparatus and the lower extremities.
It may not be necessary to give a detailed account of these here, since they
are well known, resulting from congenital degenerative processes. Club-
foot, pes cavus, trophic disorders of the lower extremities, particularly of
the feet, and bladder symptoms, particularly enuresis, are amongst the most
common manifestations.
Fic. 166.—Trophic ulcer in the plantar aspect of clubfoot in a case of
spina bifida. (Beck)
Vasomotor and Trophic Disturbances.—Sensory disturbances of varying
intensity, not always confined to the territory of certain nerves, usually
coexist with other deficiency symptoms. There may be either irritative or
paralytic symptoms. Sensibility may be either diminished, or tactile anes-
thesia, especially for pain and temperature, may occur. Usually the hypes-
thesia or anesthesia is limited to the foot-or a part of the foot, or to a small
territory over the leg or thigh. The various sensory disturbances may not
be equal, inasmuch as tactile sensation may be conserved coincidentally
with diminution or absence of temperature and pain sense. Or, the usual
symptoms of cauda equina lesions may be present, with the typical saddle
shaped area of anesthesia, sometimes attended with paroxysmal pain.
Diminished pain and temperature sensation is rather characteristic for spina
NEUROTROPHIC DISORDERS IN SPINA BIFIDA 517
bifida occulta. In the mild cases sensory disturbances may be slight or
absent. Irritative phenomena and neuralgias indicate participation of
the cauda.
As for the vasomotor and trophic derangements, these are usually limited
to one lower extremity comprising bluish red discoloration of one or both
lower extremities or parts of the extremities, involving the foot or leg, and
atrophy of an extremity with poor development of muscles of the whole leg.
Mal perforant is considered one of the characteristic manifestations (Fig.
166). Complicating this condition osteomyelitis, sequestra, necrotic bone
particles, loss of toes, with consequent deformity of the foot and phlegmonous
processes, have all been described. Amputation is required in a number of
cases, after which healing may be poor. Secondary ulcers may necessitate
reamputation. Ulcers may appear even in more central parts.
Motor disturbances not infrequently accompany the above, with slight
paresis or weakness of the single muscles, and even extensive paralytic
complexes; more rarely irritative motor phenomena, such as fibrillary
twitchings and spasms.
An instructive case reported by Brickner! is worthy of brief citation, for the type of
trophic lesion is well exemplified.
S. H., female aged 18, presented herself for examination December, 1907, because of an
extensive ulceration of the inner and flexor aspects of the great toe of the left foot, indolent
in appearance and with foul discharge.
She was a native of Jenkoping, Sweden, where at the age of 7 the second left toe was
ulcerated from what was presumed to be frost-bite. This ulceration recurred each winter,
and at the age of 12, partial amputation of the toe was required.
Three years later (aged 15) the stump of the toe ulcerated and the phalanges necrosed.
Six months later the fifth toe ulcerated, refused to heal, and was amputated. The first
phalanx was necrotic. The wound was laid open and this bone was removed. Slowly
the wound healed, without granulating, after the head of the first metatarsal spontaneously
discharged. Specific medication seemed to exercise no influence. The dorsalis pedis,
popliteal and posterior tibial vessels pulsated normally.
In April, 1908, the two remaining toes (third and fourth) ulcerated and the two last
phalanges of these were removed, leaving stumps. The foot was then quite edematous,
but not painful, although there developed at this time a plantar ulcer near the base of the
third toe.
Over the lower lumbar and upper sacral regions, extending down from the third lumbar
vertebra is a circular tumor about 434 inches in diameter, symmetrically situated over the
midline. This tumor was present since birth and has grown with the patient. In the
spine no cleft can be felt. Tests show sensory paralyses of the left lower extremity.
Roentgenogram shows a cleft in the Jeff lamina of the fourth lumbararch. The fifth lumbar
arch is not of normal shape.
Clinical diagnosis: Spina bifida occulta associated with congenital lipoma over the lower
end of the spine; cleft in the fourth lumbar arch with a lesion involving the posterior fourth
and fifth lumbar, and first, second and third sacral roots or cord segments.
Operation, July 3, 1908: The sac was removed, the nerve roots were reduced into the
spinal canal, and the dura was sutured over them. ©The lumbar aponeurosis was closed over
the hiatus by a plastic operation.
The ulceration in the third toe had progressed and the plantar ulcer had also increased
in size, exposing the head of the second metatarsal bone.
By September 28, these ulcers were healed without any bone necrosis, and the patient
was again discharged with a raised sole on her right shoe and crutches. In November the
plantar ulcer reopened. During the next few months the ulcers improved and relapsed, and
others developed. The patient was readmitted to the hospital.
July 26.; Typical Pirogoff amputation. All the blood vessels appeared quite normal.
Primary union.
Pathological report (amputated foot): The vessels were practically normal, but there
was marked bone atrophy. This atrophy was found in portions of the bone remote from
the inflammatory process. The nerves of the foot showed no degenerative changes. In
the immediate vicinity of the ulcers there were moderate inflammatory changes in the
nerves.
1 Brickner, Am. Jour. Med. Sc., April, 1918, p. 473.
O18 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
CHAPTERS CL
VASOMOTOR AND TROPHIC DISORDERS IN PERIPHERAL
NERVE LESIONS
Some of the symptoms, particularly the trophic disorders associated with
peripheral nerve lesions may simulate manifestations attending organic
obstruction of the arteries.
The characteristic changes of the integument after nerve lesions are not
altogether the sequence of altered circulatory conditions. The effects of
exclusion of trophic nerve influences have already been given consideration.
Regarding the circulatory derangements some authors describe these as
anemia and venous hyperemia. In the former the skin may be pale, dry, and
brittle; in the latter, tense, glistening, bluish red or almost cyanotic. These
alterations do not seem to depend upon the seat of the nerve injury, but
rather are related to fortuitous mechanical factors. Inactivity and atrophy
of the musculature play a réle in influencing the influx of blood. Perhaps
the impaired venous return due to deficient muscular action is also an impor-
tant factor; indeed, this mechanism seems to suffer more than the arterial
influx. Although the bearing of direct trophic nerve influences upon the
nutritive condition of the peripheral tissues is an important one, many
commentators emphasize the preponderating influence of altered or defective
circulation as a cause of the trophic lesions.!
Breslauer, in experimental work on the circulation in extremities whose main nerves had
been injured, comes to the following conclusions: That after interruption in continuity
of large peripheral nerves or posterior roots the local powers of reaction of the vessels may
remain undisturbed in the anesthetic territory for a short period (about 1 week). Subse-
quently, however, the vascular responses are partly lost. Whilst active vasoconstriction
may be conserved, active vasodilatation upon peripheral nerve irritation becomes lost.
Superficial anesthesia of the skin and the mucous membrane_Jis associated with diminished
vasodilating responses due to inflammatory and other irritants, whilst the vasoconstricting
power remains unimpaired.
According to these findings the absence of normal reactive hyperemia
would be of great significance as a factor in the causation of trophic disturb-
ances.2. The normal integument must adjust itself constantly to the exigen-
cles of external conditions and respond to numerous deleterious influences.
As long as the normal physiological vascular reaction is present, active local
hyperemia can readily set in, and healing may take place. This means of
defense is lost when the vessels in a tissue no longer respond; infection is
inadequately combatted, and degeneration of tissues ensues.
The rubor and erythromelia of thrombo-angiitis obliterans and arterio-
sclerosis may be interpreted as one of Nature’s modes of supplementing or
counterbalancing local circulatory deficiencies.
After peripheral nerve injury, particularly those injuries due to bullet
wounds, two types of manifestations may develop and mimic the symptoms
of arterial disease. In the first there are the effects of complete loss of
continuity of the peripheral nerves; and in the second irritative phenomena
due to partial nerve injury.
1 Breslauer, Deutsch. Ztschr. f. Chir., 150, p. 51.
2 The important réle of direct nerve influences on the nutritive integrity of the tissues is
described elsewhere.
VASOMOTOR AND TROPHIC DISORDERS o19
I. Symptoms with Complete Nerve Destruction.—Anesthesia, cyanosis,
and pallor may occur and are due to the exclusion of the fibers inhibiting
the vascular mechanism. ‘These fibers cross or travel in the peripheral nerves.
In addition there may be absence of the excretion of sweat, wrinkling of the
skin, hyperkeratosis, loss of hair and stunted growth of the nails. The
cyanosis and pallor may give a confusing clinical picture. The anesthesia
and trophic disturbances, however, may speak strongly in favor of nerve
lesions.
Sciatic Nerve Injury.—When trophic ulcers develop after injury to the
sciatic nerve, they do not usually appear until several months have elapsed.
Besides the nerve trauma, repeated mechanical excitation of the affected
peripheral part is required (rubbing and pressure). Hence the same localiza-
tion of the ulcerations is observable as in mal perforant. Without trans-
verse section of the nerve, the peripheral lesions do not usually follow. The
ulcers have little or no tendency to heal spontaneously; they are rebellious
to local treatment and persist for months or years without improvement,
being complicated from time to time by attacks of local infection. Amputa-
tion may eventually become indicated.
Leriche! claims that perifemoral sympathectomy (decortication of the
artery) in its course through the upper part of Hunter’s canal may bring
about healing; and that an equally good result may follow resection of a
neuroma of the proximal end of the cut sciatic nerve, if such be a complica-
tion. Indeed, this author attributes the trophic ulcers of this type to the
reflexes engendered in such neuromata. Only temporary healing of the
ulcers may follow removal of the neuroma, whilst permanent cures have
been observed when nerve resection and repair are done.
2. Irritative Phenomena Attending Partial Nerve Lesions.—The symp-
tom of pain so often noted with the irritative nerve lesions is one that may
cause confusion with the intense pain of thrombo-angiitis obliterans. Other
associated symptoms, however, would permit of the differential diagnosis.
Neuralgia with or without vasomotor accompanying symptoms is
frequently observed after bullet wounds implicating the larger nerves of the
extremities.
The pain that follows injuries to both sensory and mixed nerves may be
intense if the median nerve and the tibial nerve are involved (Mauss-Kriiger?).
It may be of great severity and obstinacy with hyperesthesiz and paraesthe-
sie; and usually attended with somewhat less marked vasomotor and trophic
disorders. Rubor and swelling are coincidental phenomena, and roughly
correspond to the territory of the pain and the paraesthesie. The distal
parts of the extremities are sites of predilection. The balls of the toes are
usually affected in the injuries of the tibial nerve, and also the terminal
phalanges of the first three fingers in median nerve lesions. The hyper-
sensitiveness of these parts makes even the slightest tactile impressions
unbearable, and renders function impossible.
As the result of the traumatic lesions of nerves, extensive cicatricial
strangulation and penetration with connective tissue result, with some
endoneural involvement, so that a partial disorganization of the nerve on
cross section can be demonstrated. Sometimes the nerve is completely
torn, and after cicatrization, although in apparent organic continuity, may
be regarded as having suffered complete interruption of functional impulses.
1Leriche, Lyon Chirurg., 18, 1921, p. 33.
2 Mauss-Kriiger, Bruns’ Beitr. z. klin. Chir., 1917, 108, p. 163.
020 CIRCULATORY AFFECTIONS OF THE EXTREMITIES
The fact that some cases are attended with severe pain, that others with
similar lesions do not suffer at all, would arouse the suspicion that causes
outside of the cicatricial tissue are responsible. Some authors suggest that
there is a general neurotic predisposition, a sort of neurotic component that
has to be reckoned with. Given a preformed nervous potentiality, an
accentuation of the sensory threshold is brought about through the injury.
This suffices, in predisposed individuals, to keep these in a condition of con-
stant hyperexcitability. In this latter state centrifugal impulses that ordi-
narily do not cause irradiation into sensory territories are intensive enough
to arouse the sensation of pain.
Vasomotor and Trophic Symptoms.—Some authors describe the skin
as moist, edematous, livid, thinned out and as easily injured. ‘The transverse
furrows are obliterated, the integument reddened, parchment like and shiny.
Trophic ulcers are to be expected whenever slight traumata, such as burning
with cigarrettes, pressure of tight shoes or other insults, unwittingly take
place. Hypertrichiasis is a striking and important symptom. ‘The nails
grow abnormally fast, become friable and distorted, and show transverse
ridges. Hyperhidrosis occurs because of the irritation of the sympathetic
fibers. Since the secretion of sweat is dependent upon sympathetic and
not upon vascular influences, we accept this phenomenon as a symptom
characteristic of nerve lesions. It occurs when the nerve lesion is incomplete.
In the descriptions elsewhere given, sensations of cold are mentioned, as
also edema, marked cyanosis, blotchy skin and differences in temperature.
Even mal perforant has been observed. A severe degree of trophic disturb-
ance is usually only present in those cases where considerable interruption
in the nerve paths has occurred. Marked trophic disturbances of the foot
and leg may attend lesions of the sciatic nerve. Both the intense pain and
the neurotrophic manifestations may disappear after successful nerve
suture.
Vasomotor Trophic Symptoms Following Bullet Wounds.—Our know]-
edge of these manifestations has been considerably broadened and clarified by
observations made during the Great War on results of bullet wounds involv-
ing the pheripheral nerves. In a discussion of vasomotor and trophic dis-
orders, the secretory and sensory must also be mentioned, since these may
play a part in the symptom-complex.
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BIBLIOGRAPHIC INDEX
ABADIE, 524
Achard and Demanche, 470
Achard and Lévi, 536
Addison, 502
Adrian, 567
Allbutt, 63, 390, 402, 502
Allan and Matas, 167
Aschner, 495, 496
Aschoff, 15, 19, 101, 105, 106, 107, 108,
Fa0,trt 4.8810, 120, 100, 102;. 201, 305
Aschoff and Welch, 124
Askanazy, 123
Audry and Constantin, 469
BABES, 188
Balzer and Vaudet-Neveux, 470
Banting, 443
Barbe, 469
Bardy, 61
Barker, 474
Barker and Sladen, 528, 554
Baruch and Kiittner, 524, 525
Bauer, 494
Baumel and Lardennois, 199
Baumgarten, 108, 189
Baumler, 456
Bayliss, 25, 34, 37, 38, 40, 55
Bayliss and Gaskell, 34 |
Belk, 452 |
Benda, 121, 459
Beneke, 103, 111,
Bernard, 503
Bernheim and Popsischill, 189
Bessau and Pfeiffer, rox
Bieling and Conradi, 192
Bier, 54, 165, 195, 206, 507
Bier and Specht, 198
Bikeles, 533
Bing, 46, 148, 152, 154
Binkler, 564
Bjerre and Cronequist, 567
Boas, 63, 65, 67, 68
Bolognesi, 83
Bonardi and Chvostek, 529
Bondésio, 469
Bonnet and Gayet, 94
Bordet, 103
Borscher, 201
Borst, 205
Bother, 139
Boullay, 139
Bourgeois, 142, 157
Boutelier and Thibierge, 566 |
Braun, 212 |
I22
“Hy
He ee 4:
| Breslauer, 518
_ Breuer and Marburg, 511
| Brickner, 517
Briggs, 184
Briscoe, 40, 59, 60, 75, 76, 254
_ Bronson, 567
Bruce, 61
Bruce and Meyer, 37
Brugsch, 30
Brugsch and Dresel, 56
_ Brugsch, Dresel, and Lewy, 30
Brugsch, Kraus, and Dresel, 30, 38
| Buchwald, 566
Buday, 189
_ Buerger, 147, 149, 293, 308, 396, 397, 552,
$55
_ Buerger and Heimann, 194
| Buerger and Kaliski, 277
_ Buerger and Oppenheimer, 421
- Bundschuh, 180, 181
| CANNON, 61, 527
| Cannon and Dale, 62
| Cardi and Castellino, 552, 553
Cassirer, 46, 47, 94, 95, 97, 98, 99, 136,
DATES As 1555057 fy OO) 275d 203 5305
6308533395900 550s 542505455 5475549;
352s 5395545155071 1g 502 50531507;
509
Cassirer and Oppenheim, 140
Castellino and Cardi, 552, 555
Gatianos 177
(Chareot, 170 ,.1408.5 52.5057
| Charcot and Hallion, 157
Chiari, ror
| Chiari and Froéhlich, 581
Chipault, 478
Chodak, 485
Chvostek and Bonardi, 529
Cilimbaris, Coenen, and Thorn, 174
Coenen, Lexer, Henle, and von Frisch, 168
Coenen, Thorn and Cilimbaris, 174
Collinot, 469
Colmers, 170
Comte and Hallion, 41
Conradi and Bieling, 192
Constantin and Audry, 469
| Continental School of investigators, 38
Cotton, Slade and Lewis, 60
Cramer, 545
Crocq, 554
Cronequist and Bjerre, 567
Curschmann, 144, 500
Cushing, 558
604 BIBLIOGRAPHIC INDEX
DALE, 61
Dale and Cannon, 62
Dale and Richards, 63
Dale, Krogh, and Hooker, 508
Danielsen, 213
Danzer and Hooker, 61, 63, 66, 67, 68
Dectjen, 106
Dehio, 552
Déjerine, 129, 146, 147
de la Vergne and Sacquepee, 201
Delbet, 524
Demanche and Achard, 470
Depisch, 510, 511
de Rothschild and Levi, 545, 546
Determann, 139, 146, 148, 153
Dienst, 120, 124, 125
Dieter and Weiss, 64, 65, 588
Dietrich, 119
Dieulafoy, 470
Dinkler, 567
Dogiel, 35, 46
Donath, 574
Dostre and Mathews, 105
Doutrelepont, 567, 560
Dresel, 30, 38, 43, 44, 501, 503, 581
Dresel and Brugsch, 56
Dresel and Lewy, 503
Dresel, Brugsch and Lewy, 30
Dresel, Kraus, and Brugsch, 30, 38
Dreyer, 174
Druelle, 458, 459, 461
Dumont and Mosny, 494
Dutil and Lamy, 152
EBERTH-SCHIMMELBUSCH, I14
Edinger, 41
Eichorst and Mornet, 450
Elsberg, 379
Engelbach, 502
Eppinger and Hess, 43, 501, 512
Erben, 598
Erichsen, 187
Etienne and Lucien, 470
FAHR, 70
Farner and Klinger, 580
Fessler, 200
Ficker, 191, 196
Finger, 469
Fiolle, 524
Fleisch, 52, 156
Flércken, 173
Flottes, Prat, and Violle, 185
Foérster,.537
Fontaine and Voivenel, 545
Fontana, 478
Foulerton, 561
Fournier, 459
Fournier and Loeper, 469
Frankel, 192
Franz, 194
Frieboes, 464, 465
Friederich, 484
Friedlander, 152
Friedmann, 538
Frohlich and Chiari, 581
Friind, 200
Fuchs, 399
GAILLARD, 470
Gartner and Stricker, 40
Gaskell, 55
Gaskell and Bayliss, 34
Gayet and Bonnet, 94
Ghon and Sachs, 192
Ginsberg, 381
Girgolaf and Oppel, 545
Girou, 523
Glaser, 29, 35, 43
Glaser and Miiller, 35
Goldflam, 141, 151, 152, 153
Goldscheider, 46
Goldstein and Parhon, 510
Goubaux, 139
Gouget and Roger, 449, 450, 405
Grasset, 147
Gross, 199
Grossman, 139, 140
Griinfeld, 186
Guilera, 185
Guillain and Rendu, 493
| HALPERT, 67, 69, 599
Hallion and Charcot, 157
Hallion and Comte, 41
Hamann, 51
Hamilton, 535
Hancken, 194
Hardy, 147, 561
Harrop, Krogh, and Rehberg, 60
Hartman, 56
_ Hasebroek, 51
Haskovec, 538
Hayem, 117
Head, 97, 483
| Heidrick, 210
Heitz; 52
- Heimann and Buerger, 194
Heller and Lewin, 560, 562, 564, 565, 566
Henius and Pribram, 67, 69
Henle, 210
Henle, Lexer, von Frisch, and Coenen, 168
Henneberg, 514
Hercher, 199
Hering, 79, 156
| Herxheimer, 566
is Hess) 25
Hess and Eppinger, 43, 501, 512
Heubner, 61, 396
Heuzard, 469
| Heveroch, 574
Hewlett, 76
Higier, 139, 140, 144, 146, 149, 150, 152,
_ 153, 154, 155
Hinter, 567
Hintner, 5609
| Hodara and Riehl, 173
Hodesmann, 194
Hoesslin, 547, 558
| Hofmann, 70, 121, 467, 469, 475, 477
_ Hoffmann and Kiister, 189
| Holmgren, 125
BIBLIOGRAPHIC INDEX
Hooker, 52, 58, 59, 60, 61, 62, 507, 590
Hooker and Danzer, 61, 63, 66, 67, 68
Hooker, Krogh and Dale, 508
Hopkins, 82, 156
Horrax, 525
Hoskins, 56
Hotz, 85
Hueck, 396
IDELSOHN, 152, 153, 154
Isensch and Krehl, 28
Ivens, 199
JACOBSOHN, 25
Jacoby, 186
Jaffe, 203
Jansen, 123
Johannessen, 212
Johannsen, 484
Jores, 15, 19, 20, 95, 395, 396, 398
Josefson, 503
Joseph, 567
Joslin, 443
Josué, 400
Jungmann, 185
KAHN, 154
Kaliski and Buerger, 277
Kamen, 196
Kaposi, 569
Karplus and Kreidl, 28, 44
Klein, 521
Klinger and Farner, 580
Klose, 190, 203
Klotz, 400, 463
Klotz and Saltykow, 4or
Kobert, 186
Kocher, 30
Koga, 381
Kohler, 154
Kohlschiitter and Meyer, 174, 180
Kollants, 554
Kopp, 567
KG6rte, 205
Koyano, 277
Kramer, 452, 454
Kramer and Krumbhaar, 453
Kraus, 30, 592
Kraus, Brugsch, and Dresel, 30, 38
Krause, 514
Kravkof, 274
Krehl and Isensch, 28
Kreibich, 98, 567, 560
Kreidl and Karplus, 28, 44
Kretz, 127
Krogh, 11, 38, 49, 54, 57; 59, 60, 61, 63, 75,
502, 595, Oor
Krogh and Rehberg, 57, 500
Krogh and Vimtrup, 58
Krogh, Dale and Hooker, 508
Krogh, Harrop, and Rehberg, 60
Kroh, 180, 206, 514
Krumbhaar and Kramer, 453
Kiilbs, 400, 401
Kussmaul and Maier, 462
Kiister, 104
605
Kiister and Hoffmann, 189
Kiittner, 171, 194
Kiittner and Baruch, 524, 525
LAEWEN, 588
Lamb, 463
Lamy and Dutil, 152
Landois, 39
Langley, 30, 35, 38, 39, 579
Lapinsky, 95
Lardennois, 199
Lardennois and Baumel, 199
Laveran, 152
Lawson, 200
Leclerc, 183
Legros, 193
Legroux, 560
Lehman, 583
Lehmann, 521
Leichtenstern, 484
Leloir, 567, 568
Lenhossek, 93
Lenmartz, 589
Leriche;$ 36/05, 90,0510, 522). 52375524
525, 559, 580, 581, 582, 583
Leriche and Lyon, 98, 519
Leriche and Pollicard, 69, 207
Levai, 475
Lévi and Achard, 536
Lév: and de Rothschild, 545, 546
Levy, 477, 478
Lewandowsky, 40, 536
Lewaschew, 39, 54
Lewin and Heller, 560, 562, 564, 565, 566
Lewis, Cotton and Slade, 60
Lewy, 30
Lewy and Dresel, 503
Lewy, Brugsch, and Dresel, 30
Lexer, Henle, von Frisch and Coenen, 168
Libman, 369
Libman and Strauss, 450
Liepmann, 185
Lilienthal, 382
Linser, 550
Lobstein, 394
Loeb, 120
Loeper and Fournier, 469
Loewl, 512
Lombard, 63
Long, 147
Lovén, 41
Léwi, 580
Dubarschyy 11, 221,11 20,1127
Lucien and Etienne, 470
Lyon and Leriche, 98, 519
MacCativm and Végtlein, 580
Mackenzie, 46
Mager, 510
Magnus, 588
Maier and Kussmaul, 462
Mallory, 445, 446, 447
Mandlebaum, 369
Marburg and Breuer, 511
Marburg and Ranzi, 514
Marchand, 17, 177, 179, 394, 395) 515
606
Marchand, Orth and Weigert, 455
Marinesco, 93, 513
Marwedel, 194
Matas, 51, 165, 166, 167
Matas and Allan, 167
Mathews and Dostre, 105
Matzenauer, 187
Mauss-Kriiger, 519
Mayer, 11
Mayesima, 537
Mayesima-Koga, 277
McCartney, Sladden, and McNee, 527
McLean, 490
McLeod, 443
McNee, Sladden and McCartney, 527
Melchior, 194
Mendel, 126
Ménétrier, 456
Mercier and Sieur, 199
Mertz, 60
Meyer, 278, 381, 384
Meyer and Bruce, 37
Meyer and Kohlschiitter, 174, 180
Mitchell, Weir, 97, 390, 531, 532, 533
MoObius, 545
Moleen, 536
Monakow, 92, 94
Monckeberg, 21, 491
Monro, 545, 546, 548, 558
Morat and Stricker, 37
Moreau and Souques, 550
Morgan, 533, 544
Mornet and Eichorst, 450
Mosenthin, 502
Moskowicz, 165, 166, 167
Mosny and Dumont, 4094
Miller, 235938, 40,742;545,7155) 300,500,
515, 567, 580, 584, 586, 589, 590, 593,
594, 595, 598, 599
Miiller and Glaser, 35
Miiller and Parrisius, 590
Miiller and Spalteholz, 585
Miiller and von Romberg, 500
Miiller and Weiss, 64, 584
Murphy, 214, 494
NAGELSBACH, 53, 179
Nasse, 187
Nélaton, 474
Neuberger, 568
Neumann, 567
Niekau, 584, 599
Noesske, 181
Nothnagel, 142, 148, 510, 537, 538, 539,
542, 553; 554
Novy, 192
Nuttall and Welch, 193
OECONOMAKIS, 520, 530
Oppel, 274
Oppel and Girgolaf, 545
Oppenheim, 29, 138, 139, 140, 142, 143, 144,
145, 140, 153, 256, 529, 533, 534
Oppenheim and Cassirer, 140
Oppenheim, Schlesinger and Remak, 513
Oppenheimer and Buerger, 421
BIBLIOGRAPHIC INDEX
Orlowsky, 401
Orth, 171, 484
Orth, Marchand and Weigert, 455
Ortner, 146
Osborne, 545
Oslerser 17
PAL, 70, 558
Panas, 152
Papadea 4o1
Parhon and Goldstein, 510
_ Parrisius, 69, 571, 584, 590, 592, 504, 598
_ Parrisius and Miiller, 590
Passini, 190
| Paul and Walton, 139
Payr, 195
| Pearlman and Vincent, 70
Pehu, 554
| Pelnar, 150
Perthes, 188, 189
Pfeiffer and Bessau, 191
Pibram, 565
Pick §263349" 500
Pollicard and Leriche, 69, 207
Ponselle and Ravaut, 465
Popsischill and Bernheim, 189
Porta, 83
Potts, 35
Prat, Flottes and Violle, 185
Pribram, 196, 559
Pribram and Henius, 67, 69
Proksch, 469
RADEMACHER, 139
Ranzi and Marburg, 514
Rasch, 503
Ravaut and Ponselle, 465
Ravaut and Thibierge, 470
Rehberg and Krogh, 57, 509
Rehberg, Krogh and Harrop, 60
Rekord, 147
Remak, Schlesinger and Oppenheim, 513
Renaut, 567
Rendu and Guillain, 493
| Renshaw, 567
Ribbert, 110, 111
Rich, 61
Richards and Dale, 63
Riedel, 184
Riehl and Hodara, 173
Rischtler, 173
Roger and Gouget, 449, 450, 493
Rolleston, 484
Rolleston, Weber, and Williams, 502
Roques, 465, 468, 469
Rosset, 457
Rossolino, 29, 510
Rouget, 11, 58, 60
Roussy, 469
Riilf, 144
Rumpel, 194, 201
SABANAJEW, 494
Sabinset iss
Sachs, 535
Sachs and Ghon, 192
BIBLIOGRAPHIC INDEX
Sacquepee, 201
Sacquepee and de la Vergne, 201
Saltykow, 400, 401
Saltykow and Klotz, 4o1
Salzer, 205
Samuel, o1
Sartorius, 178
Schade, 176
Schaeffer, 94
Schaffer, 56
Schaumleber, 195
Scheidemandel, 401
Schenk, 489
Schimmelbusch, 114, 188
Schlesinger, 143, 256, 510, 513
Schlesinger, Remak and Oppenheim, 513
Schmidt, 452
Schvene, 213
Schultze, 553, 554
Denuize, 537, S42
Schum, 209
Schwarz, 121, 470
Seguin and Weinberg, 201
Seiffert, 189
Sencert, 210
Seydel, 526
Shaw, 535
Sherrington, 44
Sick, 203
Sieur and Mercier, 199
Silberstein, 191
Silbert, 379
Simon, 41, 142
Singer, 507
Sinkler, 567, 560
Sippmann, 173
Sladden, McNee, and McCartney, 527
Slade, Cotton and Lewis, 60
Sladen and Barker, 528, 554
Solis-Cohen, 452, 545
Sollier, 147
Sommer, 139
Sonnenburg and Tschmarke, 180
Souques and Moreau, 550
Sowles, 184
Spalteholz and Miiller, 585
Specht and Bier, 198
Starling, 29, 34, 36, 37; 52, 55
Stauuing, 200
piteel, 381
Stein, 485
Stetten, 382, 494
Stewart, 50, 54, 56, 76, 80, 494
Stich, 204, 210, 213
Sticker, 175
Stiefler and Volk, 174
Strandberg, 470, 504
Strasmann, 459
Strauss, 383
Strauss and Libman, 450
Stricker and Gartner, 40
Stricker and Morat, 37
Strohmeyer, 181
Strumpell, 570
Sudeck, 95
Sutter, 185
607
ip DALEE, 116
| Thandavaroyan, 184
Thibierge, 561
Thibierge and Boutelier, 566
Thibierge and Ravaut, 470
Thoma, 402
| Thomas, 279
Thorn, Coenen and Cilimbaris, 174
Tinel, 522
| Tobias, 148
Tomaselli, 478
Torok, 470
Trachtenberg, 401
Treves, 210
Truff, 568, 5609
Tschmarke and Sonnenburg, 180
Tuffier, 524
USCHINSKI, 179
| VAN BEUREN, 199
| Vaudet-Neveux and Balzer, 470
| Vésigné, 474
Vimtrup, I1
Vimtrup and Krogh, 58
Vincent, 56
Vincent and Pearlman, 70
| Violle, Prat, and Flottes, 185
| Virchow, 395
| Virchow, von Recklinghausen and Zahn,
117
Voégtlein and MacCallum, 580
Voivenel and Fontaine, 545
Volk and Stiefler, 174
von Bardeleben, 119
von Frisch, Lexer, Henle, and Coenen, 168
vonsliaberer;.21c, 213
von Hibler, ror
von Kries, 63
von Manteuffel and Weiss, 307
von Mosettig, 526
von Recklinghausen, 179, 187, 515
von Recklinghausen, Virchow and Zahn, 117
von Romberg, 390
von Romberg and Miiller, 500
von Stapelmohr, 184
von Winiwater, 174, 179, 307
Votsch, 139
WALTON, 140
Walton and Paul, 139
Wassermann, 196
Wachtel, 181
Weber, Rolleston and Williams, 502
Wedensky, 148
Weigert, Orth, and Marchand, 455
Weinberg and Seguin, 201
Weir Mitchell, 97, 390, 531, 532, 533
Weiss, 53, 68, 547, 550, 584, 588
Weiss and Dieter, 64, 65, 588
Weiss and Miiller, 64, 584
Weiss and von Manteuffel, 307
Welch, 192, 193
Welch and Aschoff, 124
Welch and Nuttall, 193
Weljamowitz, 4609
Welsh, 125
608 BIBLIOGRAPHIC INDEX
Westphal, 143, 256, 550 AABN SLL tytl), 125 oe
Wiesel, 454 Zahn, von Recklinghausen and Zahn, 117
Wieting, 177, 179, 181, 194, 382, 526 Zak, 45, 155, 507
Williams, Weber and Rolleston, 502 Zenker, 104
Wilonski, 307 Zeiss, 586
Wilson, 502 Ziegler, 401
Wolf, 381 Zieler, 567, 570
Wolff, 210, 212 Zuckerkandl, 174
Wormeer, 449 Zurhelle, 278
INDEX OF SUBJECTS
ABSCHEIDUNG’S thrombus, ror
Absence of pulsation distal to occlusive
thrombi, 134
in gangrene, 129
Accretion thrombus, 110
Acid, lactic, effect of, on blood vessels,
Acroasphyxia, acromegaly and, 529
chronic, 527
diagnosis, 530
Raynaud’s disease and, differentiation,
554
hypertrophica
changes, 528
54
with marked trophic
in cardiac irritability, capillary pressure |
in, 76
Acrocyanosis, 75
capillary microscopy in, 598
capillaries in, 66, 68
chronica anaesthetica, 528
diagnosis, 530
in Raynaud’s disease, 71, 72
thyroid therapy in, 503
Acromegaly, acroasphyxia and, 529
gigantism and, 530
Acromicria, 563
Acroparesthesiz, 537, 592
pralyets of symptoms, 538
clinical course, 538
objective sensations, 538
Alcohol as causal factor in atherosclerosis,
22
Amputation, spontaneous, in gangrene, 159
Anaerobic bacilli, 192
sepsis, 196
Anastomosis, arteriovenous, in treatment
of thrombo-angiltis obliterans, 382
circumpatellar, 86
normal, ro
Anatomical considerations, 3
Anatomy, recent views on, 30
Anemia, local, 71
causes, 71
diminished arterial influx in, 72
mechanical diminution of patency of
arteries in, 72
neuro-irritative, 72
obstructive, vasoconstriction and vaso-
dilatation as sequences, 74
spastic, 72
Anemic territory, role of chemicals in, 156
Aneurysm, aortic, and embolism, 493
false, 208
circumscribed, 209
diffuse, 209
_ Aneurysms, 208
of Schultze, Raynaud? s disease and, lion. |
entiation, 553
pathogenesis, 539
prognosis, 539
treatment, 539
vasomotor symptoms, 538
Actinic influences, thrombosis due to,
irritants, cutaneous responses to, 509
Acute arteritis, 448; see also Arteritis, acute.
Addison’s disease, adrenalin in, 70
Adrenalin as vasoconstrictor, 72
effect of, on sympathetic nervous sys-
tem, 580
on vegetative functions, 512
nervous system, 55
in Addison’s disease, 70
injections in experimental arteriosclero-
sis, 400
with glucose solution,
gangrene following, 185
Adrenin, effect of, on blood vessel tonus, 55
Agglutination in thrombus formation, 102
process of, 102
Air embolus, 205
hot, treatment, in arteriosclerosis, 437
Akinesia algera, intermittent claudication
and, differential diagnosis, 157
123
injection of,
39
circulatory symptoms, 209
complications, 209
false, 208
gangrene complicating, 209
ligation and treatment of, 211
pseudo-, 208
symptoms, 209
traumatic, 208
treatment of, 211
true, 208
_ Angina cruris, 140
| Angioneurotic intermittent claudication
with Raynaud’s disease of finger, 144
| Angiosklerotische intermittierende Muskel-
parese, 140
paroxysmal myasthenia, 140
Angiospasm, cause of, theories of, 156
relation of, to organic type of intermittent
claudication, 144
Angiospastic gangrene, 544
Angle of circulatory sufficiency, 163
Antagonistic innervation of vessels, 34, 40
Antidromic impulses, 37
| Antithrombin, 104
Antitoxin and toxin formation in gas gan-
grene, 190
Aorta, bifurcation of, embolism at, 486
Aortic aneurysm and embolism, 493
Aortitis, acute, embolism and thrombosis
in, 493
609
610 INDEX OF SUBJECTS
Apokamnosis, 151
Apparatus for visualization of capillaries,
586
Arocyanosis, cyanosis resembling, 577
Arsenic as cause of gangrene, 183
Arsphenamin, injection of, gangrene of
fingers due to, 185
Arterial diseases, organic, Raynaud’s dis-
ease and, differentiation, 557
vasoneurosis and, 578
hyperemia, 73
hypotension, endocrine disease in, 502
obturation without immediate symptoms,
480
pulsation as diagnostic symptom, 132
in Raynaud’s disease, 550
in thrombo-angiitis obliterans, 263; |
see also Thrombo-angiitis obliterans, |
arterial pulsation in.
spasm, 77
thrombosis with traumatic gangrene, 170
Arteries, anatomy, 13
blood delivered by, and pressure in,
factors influencing, 48
development of, and subsequent path-
ological changes, 21
hypertrophy of, 447
in embryonal development, elastic type,
13
muscular type, 14
structure of, 13
in extrauterine development, 15
elastic type, 15
muscular type, 15
large, neurovascular syndromes after |
ligation of, 212 |
larger, relation of, to nutrition of part, |
210
lesions due to disturbances of growth |
and development, 445 |
to disturbed nutrition, 445 |
to infectious lesions, 446 |
to special infectious agents, 447
to toxic effects, 446
miscellaneous affections of, 445
pathology, 445
sclerotic, bone formation in, 421
senile changes in, 19
shortly before birth, 15
tuberculosis of, 455
Arterioles, anatomy, 12
Arteriorrhaphy, 212 |
Arteriosclerosis associated with thrombo-
angiitis obliterans, 306
chemical action in, 82
clinical course, 392
manifestations, 385
diagnosis, 431
embolism and thrombosis complicating,
493 |
erythromelia of upper extremities in, 389 |
experimental, 400
human and, relation of, 401 |
localization of, 401
minute pathology, 402
in calcification, 420 |
ui
Arteriosclerosis, minute pathology, intima
in larger vessels, 416
larger arteries in gangrene, 407
media in obliterated arteries, 411
lesions when lumen is filled, 413
mixed occlusion, 415
occlusive process in, 415
of smaller vessels, 418
recent occlusion of atherosclerotic
popliteal artery, 411
of lower extremities, clinical forms of, 385
of trophic disturbances and
gangrene in, 393
special symptoms, 389
trophic disturbances and gangrene
In, 390
pathogenesis, 394
pathology, elastic fibers in normal arteries,
396
hyperplastic intima in, 398
Jores’s theories of, 398
peripheral, 71
precocious development of, 22
prognosis, 434
simulating thrombo-angiitis obliterans,
431
treatment, 435
according to case types, 438
amputation, 440
Buerger’s postural, 436
diathermic, 438
hot air, 437
methods of improving circulation, 436
of gangrene with hyperglycemia, 442
without hyperglycemia, 442
of trophic disorders and gangrene, 438
postural, Buerger’s method, 436 |
surgical, 443
cases with hyperglycemia, 444
without hyperglycemia, 444
vascular insufficiency in, 71
vasomotor phenomena in, 390
with calcification, minute pathology, 420
with mixed occlusion, minute pathology,
420
with thrombosis, atrophy as sequel, 425
clinical course, 421
diagnosticated as acute intermittent
claudication, 150
of larger more central paths, 424'
gangrene with diabetes, 427
complicating infection, 428
pathology, 427
with thrombosis, 421
clinical history, 422
_ Arteriovenous anastomosis in treatment
of thrombo-angiitis obliterans, 382
Arteritis, acute, 448
etiology, 4409
of unknown origin, 452
pathogenesis, 454
pathology, 449
symptomatology, 450
elastica, 307
migrating, 305
parietal, 451
INDEX OF SUBJECTS
Arteritis, rheumatic, 451
syphilitic, and gangrene, 456
clinical forms, 460
incidence, 459
pathology, 456
symptomatology, 460
with thrombosis simulating thrombo-
angiitis obliterans, 454
Artery, axillary, anatomy, 3
brachial, anatomy, 5
dorsalis pedis, anatomy, 10
femoral, anatomy, 6
common, nerve distribution about, 36
popliteal, anatomy, 7
palpation of, Buerger’s method, 133
radial, anatomy, 5, 6
tibial, anterior, anatomy, 10
posterior, anatomy, 9
and vein, normal, characteristics, 18
ulnar, anatomy, 5, 6
Artificial intermittent claudication, 151
pallor, 151
Aschoff gas edema bacillus, 191
Asphyxia, localized, with arteries pulsating, |
572
of fingers, hands, and feet, 75
of irritable hearts, 75
Asphyxie locale et gangrene symmétrique
des extrémités, 544
Asthma, 503
Atheroma, thrombus formation in, 121
Atherosclerosis; see Arteriosclerosis.
Atony and spasm of capillaries, 592
Atrophy as sequel to arteriosclerosis with
thrombosis, 425
of skin, idiopathic, 566
secondary, of nervous system, 94
Atropin, effect of, on vegetative functions,
513
Atypical vasomotor neuroses, 572
Autonomic action of capillaries, 58
and vasomotor responses, 53
nervous system, 23
Axillary artery, anatomy, 3
pulse, 5
vein, 5
Axon reflexes, 37
BABINSKI-FROMENT type of reflex con-
tractures, réle of sympathetic in, 582, 583
Bacillus aerogenes capsulatus, 190
anaerobic, 192
Frankel, gas, 190
gas, 190
Ghon-Sachs, 192
of malignant edema, ror
paratyphus, 203
paredema, Pfeiffer-Bessau, 191
Pfeiffer-Bessau, 191
phlegmones emphysematosz, 190
von Hibler, ror
Welch, gas, 190
Bacteria and thrombus formation, 120
pyogenic, gangrene due to, 202
Baths, hot, action of, on vascular tonus,
70
611
Bees and wasps, poison of, gangrene from,
183
Bifurcation of aorta, embolism at, 486
Birth, arteries shortly before, 15
Blanched condition of extremity in gan-
grene, 129
Blanching, 73
_ Blood, color of, in acrocyanosis, 75
flow in capillaries, 66
in extremities, measure of, 49
measuring, Stewart’s method, 50
normal, in capillaries, 586
movement, bloodvessels and, 51
capillary circulation and, 52
pressure, capillary, estimation of, 67
Blood vessel tonus, effect of adrenin on, 56
Blood vessels, blood movement and, 51
chemical regulation of, 54
effect of metabolites on, 54'
in gas gangrene, 193
injuries to, and gangrene, 204
arteriorrhaphy in, 212
complications, 206
control of hemorrhage, 209
permanent, 210
due to treatment, 204
ligation and treatment of aneurysms
in, 211
nerve injury complicating, 206
of main artery or vein, 207
pathology, 204
recent, 204
results of, 205
relation of larger arteries to nutrition
of part, 210
surgical treatment, principles under-
lying, 211
treatment, 209 7
control of hemorrhage, 209
permanent, 210
role of, in thermic gangrene, 177
trophic influences of nerves on, 95
Bluish discoloration in gangrene, 129
Blushing, 73, 505
Bodies, solid, thrombosis due to, 122
Boiterie intermittente des chevaux, 140
Bone formation in sclerotic arteries, 421
Borderline cases, 575
cyanosis resembling arocyanosis, 577
developing ischemia, probably
thrombo-anglitis, 577
early thrombo-angiitis obliterans, 576
incipient thrombo-angiitis obliterans
with apparent vasomotor symptoms,
- 576.
varieties, 575
vasoneurosis and organic arterial dis-
ease, 578
with cyanosis of toes as chief symp-
tom, 577
with limited asphyxia and with pain,
578
_ Brachial artery, anatomy, 5
pulse, 5
_ Bronze erysipelas, 190 lees
| Brown-Séquard theory of tropic disorders, gt
612
Buerger’s method of palpating popliteal
artery; 133
postural treatment, 77
Bullet wounds of peripheral nerves, vaso-
motor and trophic symptoms fol-
lowing, 520
spasm of vasoconstrictors following,
206
Burns, thrombosis after, 119
Catcium chloride in circumscribed edemas,
78
effect of, on sympathetic system, 581
metabolism, altered, in spasmophilic
conditions, 580
salts, réle of, in spasmophilic tendency, 79
Cancer aquaticus, 188
Cancrum oris, 188
Capillaries, abnormalities of permeability
of, 507
anatomy, II
autonomic action of, 58
blood flow in, 66
contractile cells of, 12
dilatation of, following action of cold, 53
direct response of, to chemical stimuli, 60
to mechanical stimuli, 60
endothelial layer of, 11
fullness of, in vasoneurotic diathesis, 594
function of, summary of, 61
granular streaming in, 586
in acrocyanosis, 66, 68
in vasoneuroses, morphology of, 595
minute structure of, 11
morphology of, 65
muscular coat. of, 11
nerves of, 11
normal flow in, 586
papillary, contractile
588, 589
paralytic action of poisons on, 61
physiology of, 57
spasm and atony of, 592
spasms of, in Raynaud’s disease, 67
vascular, intermittent spasm of, 144
visualization of, apparatus, 586
Capillary activity and capillary stream, 588
blood pressure, estimation of, 67
circulation and blood movement, 52
derangement of, 76
general considerations, 57
in closed vascular territory, Weiss
and Dieter’s studies, 64
Lombard’s method of studying, 63
methods of investigating, 63
results of tests, 68
nerve control of, 59
spasm in, 589
stases in, 589
variations in, 64
Weiss-Mitiller method of studying, 64
microscopy, 584
anatomical considerations in, 584
in acrocyanosis, 598
in erythromelalgia, 598
in erythromelia, 601
phenomena in,
INDEX OF SUBJECTS
Capillary microscopy in Raynaud’s disease,
599
in special forms of vasomotor dis-
ease, 598
microscopy in vasomotor neuroses, 590
abnormalities of permeability in,
597
morphology of capillaries in, 595
nature of vasoneuroses in, 501
spasm and atony of capillaries
In, 592
stream and pressure conditions
in vasoneurotic diathesis, 592
Miiller’s Zeiss apparatus for, 587
motility, nerve influences in, 38
stream and capillary activity, 588
Carbolic acid gangrene, 183
Carbon dioxid, effect of, on blood vessels,
54
monoxid gangrene from, 184
Cardiac disease, embolic gangrene with, 485
weakness as factor in thrombosis, 123
Causalgia, sympathetic nerves in relation
LO, 522
nervous system and, 583
Cellifugal degeneration of nervous sys-
tem, 92
Centers, cerebral vasomotor, 28
subcortical vasomotor, 30
vascular nerve, 44
vasomotor, physiology of, 41
spinal, 31
Central nervous system, vasomotor and
trophic disturbances in lesions of, 513
' Cerebral lesions of vegetative nervous
system, localization of, 510
vasomotor centers, 28
~ Charcot-Erb type of intermittent claudica-
tion, 140
Chemical regulation of blood vessels, 54
stimuli, direct response of capillaries to, 60
Chemicals, gangrene due to, 181; see also
Gangrene due to chemicals and drugs.
réle of, in an anemic territory, 156
Chilblain, 173
Chorea, embolic gangrene complicating, 485
Chromic acid as cause of gangrene, 182
Circulation, capillary, and blood move-
ment, 52
general considerations, 57
in closed vascular territory, Weiss and
Dieter’s studies, 64
Lombard’s method of studying, 63
methods of investigating, 63
results of tests, 68
nerve control of, 59
spasm in, 589
stasis In, 589
variations in, 64
Weiss-Mtiller method of studying, 64
collateral, 82
course of new channels in, 84
demonstration of collaterals in obstruc-
tive vascular disease, 84
Mosckowicz test for investigation of, 210
when peripheral arteries are patent, 85
INDEX OF SUBJECTS
Circulation, effect of adrenalin on, 56
of histamin on, 61
of hypophysis cerebri on, 56
of pituitrin on, 56
general, under pathological conditions, 69 |
Henle-Coenen test for, 168
impaired, symptoms of, in gangrene, 128 ©
in extremities under pathological con- |
ditions, clinical manifestations, 87
internal secretions and, 55
ischemia an index of, 242
local, pathological, 71
Matas test for, 166
methods of improving, in arteriosclero- |
sis, 436
Moskowicz test for, 166
peripheral, elementary principles, 48
functional disturbances of, 76
derangement of capillary flow
in, 76
due to impaired exchange of
fluids, 78
functional derangement of lym- |
phatic system in, 79
physiology of, 48
superficial, in obstructive vascular dis-
eases, 80
changes in vasomotor mech-
anism in, 81
chemical action on tissues in, 81
diminished force of stream in, 80
exhaustion in, 81
hydrostatic and gravity forces |
in, 80
tests for, 165
value of, in thrombo-angiitis oblit-
erans, 167
vasomotor function and, 52
Circulatory disturbances in blood vessel
injuries, 206
neuroses, vasomotor, Raynaud’s disease |
and, differentiation, 554
sufficiency, angle of, 163
Circumpatellar anastomosis, 86
Circumscribed edema, 96
calcium chloride in, 78)
false aneurysm, 209
Claudication, intermittent, acute forms, 148 |
age incidence, 152
angioneurotic,
ease of finger, 144
angiospasm in, theories as to cause, 156 |
artificial, 151
as diagnostic symptom, 137
Charcot-Erb type, 140
circulatory and vasomotor phenomena
in, 141
clinical course, 142
clinical types, 140
critical summary, 154
differential diagnosis, 157
Erb type, characteristics, 137
examination of pedal and crural ar- |
teries, 142
explanation of phenomena in, 155
functional vasomotor type, 142
with Raynaud’s dis- —
613
| Claudication, intermittent, historical, 139
in gangrene, 129
in other territories, 146
of inactivity, 136
of spinal column, 146
of upper extremities, 147
of vasomotor type, 138
organic type, relation of angiospasm
to, 144
par obliteration artérielle, 140
pathology, 151
Raynaud’s syndrome and, differentia-
tion, 138
sex and race incidence, 153
tobacco as etiologic factor in, 153
type accompanying organic vascular
disease, 139
with healthy arteries, 155
Clinically borderline cases, 575
varieties, 575
Closed circuit and nerve impulses, 91
Coagulation, extravascular, 102
fibrin, 103
in process of thrombosis, 108
in thrombus formation, 102
thrombosis, ror
primary, 108
Cold as vasoconstrictor, 72
dry, effect of, on human tissues, 172
effect of, on human tissues, 172
local changes due to, first degree, 173
second degree, 173
third degree, 174
neuralgia due to, 174
reflex response to, 72, 76
wet, effect of, on human tissues, 173
Coldness in thrombo-angiitis obliterans, 261
of extremity in gangrene, 129
Collateral avenues, 83
circulation, 82
course of new channels, 84
demonstration of collaterals in obstruc-
tive vascular disease, 84
Mosckowicz test for investigation of,
210
when peripheral arteries are patent, 85
hyperemia, 82
Collaterals in obstructive vascular disease,
demonstration of, 84
therapeutic development of, 87
when peripheral arteries are patent, 85
Colliquation necrosis, 183
Communicating hematoma, 208
Compression test, 77
Congelation, 100
in thrombus formation, 105
Conglutination, too
thrombosis, ror
Constitution, vasoneurotic, 572
Contracture, ischemic, of muscles, without
gangrene, in blood vessel injury, 206
Contractures at elbow, sympathetic in its
relation to, 582
Coreri27
Corpus striatum, nuclei in, 31
Crises, vascular, 70
614
Cutaneous responses to thermic and
actinic irritants, 509
Cyanosis and rubor, 573
in gangrene, 129
in thrombo-angiitis obliterans, 250; see
also Thrombo-angtitis obliterans, cyano-
sis In, 250
of fingers, hands, and feet, 75
resembling arocyanosis, 577
Cytozym, 103
DANZER and Hooker’s method for capillary
blood pressure estimation, 67
Death, eczema, 504
molecular, 127
tissue, signs of, 128
Décollement, 169
Decubitus, 160
acute, 97
acute traumatic, 170
after spinal cord lesions, 514
Défense musculaire, 45
Degeneration, indirect, of nervous system,
94
Lenhossek cellifugal, of nervous system,
Q2
nerve, interdependence of portions of
nervous system in, 92
retrograde, of nervous system, 93
Wallerian, of nervous system, 92
Demarcation, line of, in gangrene, 159
Dermatographia, 60, 247
rubra, 247
Dermatoscleroses, 559
Diabetes, endocrine glands in, 503
with arteriosclerotic gangrene, 427
Diabetic gangrene, 427
Diagnostic symptoms, 132
arterial pulsation, 132
intermittent claudication, 137
pain, 135
Diapedesis, 77
causes, 79
endothelial symptom in, 80
individual susceptibility to, 80
postanemic, 77
Diathesis, vasoneurotic, 590
fullness of capillaries in, 594
stream and pressure conditions in, 592
Dieter and Weiss’s}! method of studying
capillary circulation, 64
Diffuse false aneurysm, 209
Dilatation of capillaries following action
of ‘cold;-52
Diphtheria, gangrene with, 484
Diphtheritic form of hospital gangrene,
188
Direct response of capillaries to chemical
stimuli, 60
to mechanical stimuli, 60
Discoloration, bluish, in gangrene, 129
Diseases, general, thrombosis and, 123
Distant thrombosis, 109
Doigt mort, 72
Dorsalis pedis artery, anatomy, Io
pulse, ro
INDEX OF SUBJECTS
Drugs, action of, on sympathetic nervous
system, 580
gangrene due to, 181; see also Gangren
due to chemicals and drugs.
Dry gangrene, 157, 158, 391
of one or more phalanges, 202
Dysbasia angiosclerotica, 145, 389
intermittens, 140
neurasthenica, intermittent claudication
and, differential diagnosis, 157
Dysergia, 591
Dyskinesia intermittens angiosclerotica, 148
Dyspragia intermittens angiosclerotica in-
testinalis, 146
EcLAmpsIA, tendency to thrombosis in, rrg
Eczema death, 504
Edema, 79
circumscribed, 96
calcium chloride in, 78
evanescent, 78
fugax, 79
gas, 190, 197
bacillus, Aschoff, ror
inflammatory, 79
malignant, bacillus of, 191
war, 70
Elbow, contractures at, sympathetic in its
relation to, 583
Emboli, infectious, 479
Embolic and thrombotic gangrene after
infectious diseases, 481
clinical course, 481
pathology, 483
types of gangrene, 483
arteriotomy in, 494
technic, 498
arteriovenous anastomosis in, 494
diagnosis, 489
embolectomy in, 494
technic, 498
ligation in, 494
post-operative, 489
treatment of, 493
gangrene complicating chorea, 485
with cardiac disease, 485
Embolism and thrombosis, 479
arterial obturation without immediate
symptoms, 480
classification, 479
complicating arteriosclerosis, 493
in acute aortitis, 493
at bifurcation of aorta, 486
in gangrene, 161
without gangrene, 480
Embolus, air, 205
Embryonal development,
arteries in, 13
Emotions, intensive, effects of, 513
Emphysematous gangrene, 190
Endarteritis obliterans, 214, 307
tuberculous, 456
Endocrine glands and functions of vegeta-
tive nervous system, 502
relation of, to vegetative nervous
system, 55
structure of
INDEX OF SUBJECTS
Endogenous poisons in thrombosis, 119
Endothelial symptom, 80
Epidermolysis bullosa hereditaria, 550
Epilepsy, Jacksonian, vasomotor, 29
Erb-Charcot type of intermittent claudica-
tion, 140
characteristics, 137
Erb’s syndrome, 129
Ergot as cause of gangrene, 181, 186
Ergotism, 72, 186
Ergotoxin as vasoconstrictor, 72
effect of, on sympathetic nervous system,
580
gangrene from, 186
Erkaltungsneuralgie, 174
Erysipelas, bronze, 190
Erythema, 523
nodosum, differential diagnosis, 460
Erythemata of nervous origin, 74
Erythromelalgia, 216, 531
associated symptoms, 532
capillary microscopy in, 598
clinical course, 534
coexisting maladies, 533
diagnosis, 534
extent of rubor in, 532
Foerster operation in, 537
hyperesthesia in, 532
local motor disorders in, 533
pain in, 135, 531
pathogenesis, 533
prognosis, 534
Raynaud’s disease and, differential diag- |
nosis, 553
redness and swelling in, 532
secretory disturbances in, 532
sensory disturbances in, 533
syndrome of, 534
thrombo-angiitis obliterans and, differ-
ential diagnosis, 534
treatment, 536
trophic lesions in, 533
Erythromelia, 74, 89, 129, 163
capillary microscopy in, 601
chronic, 163
in thrombo-angiitis obliterans, 242; see
also Thrombo-angiilis obliterans, ery-
thromelia in.
of lower extremities, 390
of upper extremities in arteriosclerosis,
389
Erythromelie, 242, 566
Evanescent edema, 78
Exercise of neurotrophic influences, 91
Exogenous poisons and infectious agents,
action of, in thrombus formation,
120
in thrombosis, 120
Expression test, 163
Extrauterine development, arteries in, 15
Extravascular coagulation, 102
Extremities and trunk, vasomotor paths of,
511
blood flow in, measure of, 49
circulation in, under pathological condi-
tions, clinical manifestations, 87
| Fissures
| Focal
615
Extremities, lower, arteriosclerotic disease
of, clinical forms of, 385
erythromelia of, 390
in arteriosclerosis, 389
intermittent claudication of, 147
involvement of, in thrombo-angiitis
obliterans, 294
Extremity, coldness of, in gangrene, 129
Factat blush, 73
hemi-atrophy, progressive, 91
False aneurysm, 208
circumscribed, 209
diffuse, 209
Feet, asphyxia of, 75
cyanosis of, 75
Females, thrombo-angiitis obliterans in, 226
Femoral artery, anatomy, 6
common, nerve distribution about, 36
pulse, 7
vein, ligation of, in treatment of thrombo-
angilitis obliterans, 382
Fibrin coagulation, 103
Fibrinogen, source and quantity of, 105
Fibrinolysis, 104
Fingers, asphyxia of, 75
cyanosis of, 75
gangrene of, due to injection of arsphen-
amin, 185
Dinewicet:
obliterans, 236
migrating phlebitis
origin, 470, 472
Foerster operation in erythromelalgia, 537
Formalin as cause of gangrene, 182
Frankel gas bacillus, 190
Freezing, effect of, in thermic gangrene, 176
local, first degree, 173
second degree, 173
symptomatology of, 173
third degree, 174
thrombosis as cause of gangrene after,
179
treatment, 180
Fugitive edema, 79
Functional vasomotor type of intermittent
claudication, 142
in thrombo-angiitis
of unknown
GANGRENE, absence of pulsation in, 129
and syphilitic arteritis, 456
clinical forms, 460
incidence, 459
pathology, 456
symptomatology, 460
and trophic disturbances in arterio-
sclerotic disease, 39
clinical forms of, 393
angiospastic, 544
arteriosclerotic, with diabetes, 427
with thrombosis, 421
clinical history, 422
lanched condition of extremity in, 129
bluish discoloration in, 129
carbolic acid, 183
chemical] causes, 160
classification, 160
616
Gangrene, clinical examination in, 162
coldness of extremity in, 129
complicating aneurysms, 209
infectious diseases, 203
pneumonia, 481
scleroderma, 561
course and termination of, 159
cyanosis in, 129
definition, 127
diabetic, 427
diseases of blood vessels in, 161
dry, 157, 158
of one or more phalanges, 202
due to chemicals and drugs, 181
to ergot, 186
to external or direct causes, 160
to internal or indirect causes, 160
to microbic agents, 160
to neurogenic causes, 161
to thermic causes, 160
to poisonous gases, 184
to pyogenic bacteria, 202
embolic and thrombotic, after infectious
diseases, 481
clinical course, 481
pathology, 483
types of gangrene, 483
arteriotomy in, 494
technic, 408
arteriovenous anastomosis in, 494
diagnosis, 489
embolectomy in, 494
technic, 498
ligation in, 494
post-operative, 489
treatment, 493
complicating chorea, 485
with cardiac disease, 485
embolism in, 161
embolism without, 480
emphysematous, 190
examination in, absence of pulsation as
indication of arterial occlusion, 164
angle of circulatory sufficiency in, 163
appearance of limb, 162
blanching in, 163
color in, 163
erythromelia in, 162
in prodromal stages, 162
ischemia in, 163
reactionary hyperemia, rubor, or reac-
tionary erythromelia in, 16 5
rubor in, 162
tests for circulation i in, 165
for patency of veins in, 168
following injection of medicaments, 185
of quinin, 185
forms of, 157
foudroyante, 190
frequency of, after ligation of arteries
at certain levels in lower extremities, 85
gas, 190
bacteriologic etiology, 190
blood transfusion in, 201
blood vessels in, 193
diagnosis, 198
INDEX OF SUBJECTS
Gangrene, gas, edema in, 197
gangrene in, 198
gas formation 1 IN GIO7
histogenic poisons of, 196
incidence of, 194
infection, epifascial form, 195
superficial form, 195
types of, 195
latent infection with anaerobes, 194
local medication in, 201
symptoms, 197
localization of, 195
morbidity and mortality in, 199
non-putrefactive type of bacteria i in, 190
obstructive hyperemia i mn, 201
oxygen insufflation in, 201
pathogenesis of, 194
pathological anatomy, 192
period of incubation, 193
putrefactive type of bacteria in,
serum therapy, 201
skin in, 197
stages in development of, 193
surgical treatment, 200
symptoms, general, 196
local, 197
the wound in, 197
toxins and antitoxin formation in, 190
toxins of, 196
treatment, 199
with hyperemia, 200, 201
vessel injury and, 198
general considerations, 127
hospital, 187
diphtheritic form, 186
pulpy form, 188
treatment, 188
in recurrent fever, 203
in typhoid fever, 203
injuries to blood vessels and, 204
injury of main nutrient vessels in,
intermittent claudication in, 129
ischemia in, 129
line of demarcation in, 1 59
mechanical causes, 160
methods of investigation of, 130
microbic, 157, 159, 160, 190
moist, 157, 158, 392
characteristic clinical stages, 158
multiple incisions for prevention of, 180
neurotic, 567
clinical course, 569
etiology, 567
hysteria in, 568
of skin, 97, 98
pathogenesis, 569
prognosis, 569
symptomatology, 568
treatment, 570
neurogenic, pathogenesis of, 98
of fingers due to injection of arsphen-
amin, 185
Pott’s, 391
premonitory symptoms, 128
prodromal stages, examination in, 162
puerperal, 485, 490
IQI
160
INDEX OF
Gangrene, putrid, 158
redness of toes in, 129
senile, 158, 391
spontaneous amputation in, 159
symptoms of impaired circulation in, 128
thermic, 172
causes of, 160
clinical course, 174
direct tissue injury in, 175
effect of freezing in this type of gan-
grene, 176
effect of stasis in, 178
etiology, 175
freezing in, symptomatology, 173
general consideration, 172
internal causes, 175
operative treatment, 181
pathogenesis, 175
predisposing factors in, 175
prognosis, 180
role of blood vessels in, 177
thrombosis as cause of, 179
treatment, 180
vessel palsy in, importance of, 179
tests for circulation in, 165
thrombosis in, 129, 161
thrombotic, in healthy or but slightly |
diseased vessels, 490
peripheral, 572
traumatic, 168
causes, 168
from accidental entombment, 170
of an extremity, 170
of deep tissues, with main arteries
Intacteryt la
of limited extent, 170
superficial, with main vessels intact,
171
symptoms, 169
treatment, 172
with arterial thrombosis, 170
without involvement of main arteries,
171
SUBJECTS 617
Gliosis spinalis and syringomyelia, 513
Glossy skin, 97
origin of, 96
Glucose solution with adrenalin, injection
of, gangrene following, 185
Goldflam’s type of intermittent claudica-
tion, I51
Goose flesh, 505
Granular streaming, 66
in capillaries, 586
diagnosis, 469
Gumma, syphilitic tertiary, differential
diagnosis, 469
| Hanns, asphyxia of, 75
cyanosis of, 75
| Heart, irritable, 59, 60
trophic disorders in, 129
with diphtheria, 484
with other infections, 484
without organic vascular disease, 539
Gangrenous slough, 127
stomatitis, 188
Gas bacillus, 190
infection, Van Beuren’s treatment, 199
edema, 190, IgI
bacillus, Aschoff’s, ror
formation in internal organs, 193
gangrene, 190; see also Gangrene, gas.
inflammation, 190
phlegmon, 190
local, 195
progressive, 196
Gases, poisonous, gangrene due to, 184
Ghon-Sachs bacillus, 192
Gigantism, acromegaly and, 530
Glands, endocrine, functions of vegetative
nervous system and, 502
relation of, to vegetative nervous
system, 55
acroasphyxia of, capillary pressure in,
76
asphyxia of, 75
| Hematoma, communicating, 208
pulsating, 208
_ Hemi-atrophy, progressive facial, or
| Hemorrhages of vicarious menstruation, 79
Henle-Coenen test for circulation, 168
Herpes zoster, 96, 97, 513
Heterologous stimulation, theory of, in
trophic functions of nervous system, 94
Histamin, effect of, on circulation, 61
Hooker and Danzer’s method for capillary
blood pressure estimation, 67
Hormones, thyroid, importance of, in arte-
rial affections, 502
Hospital gangrene, 187
diphtheritic form, 188
pulpy form, 188
treatment, 188
Hot air treatment, in arteriosclerosis, 437
Hyalin thrombi, ror
Hydrochloric acid as cause of gangrene, 182
Hyperemia, 73
collateral, 82
neuroparalytic, 73
theory of, in trophic disorders, gt
postanemic, 74
reactionary, 156
rubor, 75
venous, 7
consequences of, 75
Hyperhidrosis in erythromelalgia, 532
Hypersensitiveness of vegetative nervous
system, 504
Hypertrophy of arteries, 447
Hyphemia, local, 71
Hypophysis cerebri, effect of, on circula-
tion, 56
Hypoplasia of vascular system, congenital,
as predisposing to vascular affections, 83
Hypotension, arterial endocrine disease in,
502
Hypotonia, chronic, 70
Hysterical pseudotetanus, 143
IDIOPATHIC atrophy of skin, 566
cutaneous atrophy, 504
Illuminating gas, gangrene from, 184
618
Impulses, antidromic, 37
Incipient thrombo-angiitis obliterans with
apparent vasomotor symptoms, 576
Incisions, multiple, for prevention of
gangrene, 180
Indirect degeneration of nervous system, 94
Induced rubor, 163
Inflammation, gas, 190
Inflammatory edema, 79
Infection, gas bacillus, Van Beuren’s treat-
ment, 199
gangrene, types of, 195
role of, in thrombosis, 126
Infections, vasomotor and trophoneuroses
following, 574
Infectious agents, action of, in thrombus
formation, 120, 121
diseases, gangrene complicating, 203
emboli, 479
polyneuritis, vasomotor symptoms in, 521
type of thrombosis, 108
Influenza as cause of acute arteritis, 449
Tniuries to blood vessels, and gangrene, 204
Innervation, antagonistic, of vessels, 34, 40 |
vascular, double, recent views on, 38
Instability, vasomotor, 570
Insufficiency, vascular, 70
in arteriosclerosis, 71
Insulin in diabetic gangrene, 435
in treatment of gangrene with hyper-
glycemia, 442
Intensive emotions, effects of, 513
Interdependence of nerve paths with par-
ticular reference to trophic function, 92
Intermittent claudication, acute forms, 148
age incidence, 152
angioneurotic, with Raynaud’s disease
of finger, 144
angiospasm in, theories as to cause, 156
artificial, 151
as diagnostic symptom, 137
Charcot-Erb type, 140
circulatory and vasomotor phenomena
in, I41
clinical course, 142
clinical types, 140
critical summary, 154
differential diagnosis, 157
Erb type, characteristics, 137
examination of pedal and
arteries In, 142
explanation of phenomena in, 155
functional vasomotor type, 142
historical, 139
in gangrene, 120
in other territories, 146
in thrombo-angiitis obliterans, 255
see also Thrombo-angittis obliterans,
intermittent claudication in.
of inactivity, 136
of spinal column, 146
of upper extremities, 147
of vasomotor type, 138
organic type, relation of angiospasm to,
144
pathology, 151
crural
INDEX OF SUBJECTS
Intermittent claudication, Raynaud’s syn-
drome and, differentiation, 138
sex and race incidence, 153
tobacco as etiologic factor in, 153
type accompanying organic vascular
disease, 139
with healthy arteries, 155
limping of horses, 140
spasm of vascular capillaries, 144
Internal organs, gas formation in, 193
secretions and vegetative functions, 502
circulation and, 55
trophic disturbances and, 504
Irritable heart, 59, 60
acroasphyxia of, capillary pressure in,
76
asphyxia of, 75
Irritants, thermic and actinic, cutaneous
responses to, 509
Ischemia, 71
an index of circulation, 242
causes, 71
diminished arterial influx in, 72
in gangrene, 129
in thrombo-angiitis obliterans, 237; see
also Thrombo-angittis obliterans.
local, consequences of, 73
mechanical diminution of patency of
arteries in, 72
neuro-irritative, in trophic disorders, 91
paradoxical, 84
Ischemic contracture of muscles, without
gangrene in blood vessel injury, 206
degeneration, lesions of, following liga-
tion of large or main arteries, 207
JACKSONIAN epilepsy, vasomotor, 29
KALTE-GANGRAN, 177
Lactic acid, effect of, on blood vessels, 54
Lenhossek cellifugal degeneration of ner-
vous system, 92
Leukodiapedesis, 77
Leukocyte thrombus, ror
Ligation of aneurysms, 211
of femoral vein in treatment of thrombo-
angiitis obliterans, 382
Line of demarcation in gangrene, 159
Linsenkernschlinge, 30
Local anemia, 71
circulation, pathological, 71
freezing, symptomatology of, 173
gas phlegmon, 195
hypemia, 71
shock, 526
Localized asphyxia with arteries pulsating,
572
derangements of vascular tone, 70
Lombard’s method of studying capillary
circulation, 63
Lymphatic system, disturbance in con-
tinuity of vessel constituents, 79
of capillary origin, 79
functional derangement of, 79
Lysol, gangrene from, 184
INDEX OF SUBJECTS
Main succulent, 513
Mal perforant, 97, 474
alcohol in etiology, 477
bone and joint theory, 477
clinical course and symptoms, 477
etiology, 475
lesions of central
in, 476
local treatment, 479
mechanical theory, 475
nervous neurogenic theory, 475
peripheral nerve lesions in, 475
prognosis, 478
treatment, 478
vascular theory, 475
plantaire perforant of Vésigné, 474
Malfunction, nerve, causes, 81
Malignant edema, bacillus of, ror
Malum perforans pedis, 474
Mask, sclerodermal, 562
Matas test for circulation, 166
Measure of blood flow in extremities, 49
Mechanical stimuli, direct response of
capillaries to; 60
Medicaments, gangrene following injection
of, 185
Menstruation, vicarious, hemorrhages of, 79
Mental symptoms in thrombo-angilttis
obliterans, 270
Mercurial poisons as cause of gangrene, 183
Mercury as cause of gangrene, 183
nervous system
Metabolites, effect of, on blood vessels,
54
Metastatic thrombosis, 109
Metatarsalgia, intermittent claudication
and, differential diagnosis, 157
Microbic gangrene, 157, 159, 160, 187, 190;
see also Gangrene, microbic.
poisons, gangrene from, 183
Microcapillary tonometer, 67, 68
Microscopy, capillary, 584; see also Capil- |
lary microscopy.
Migrating arteritis, 305
phlebitis, 214
focal, of unknown origin, 470, 472
in thrombo- -angiitis obliterans, 270
miscellaneous varieties, 470
with infections, 472
with pulmonary tuberculosis, 470
Moist gangrene, 157, 158, 392
Molecular death, 127
Monoplegia, vasomotor, 29
Morphea, 559
Morphology of capillaries, 65
in vasoneuroses, 595
Mortification, 127
Mosckowicz test for investigation of
collateral circulation, 210
for circulation, 166
Motility, capillary, nerve influences in, 38
Motor paralyses following arterial lesions,
584
Miiller’s Zeiss apparatus
microscopy, 587
Miiller-Weiss method of studying capillary
circulation, 64
for capillary
619
Multiple neurotic gangrene, 567
of skin, 97, 98
Mummification, 127
Muscular contracture,
relation of, 583
Myasthenia gravis pseudo-paralytica, inter-
mittent claudication and, differential
diagnosis, 157
paroxysmal, 155
Myelitis, bullous eruptions in, 513
Myositis, syphilitic, differential diagnosis,
469
sympathetic and,
NAILs, alterations in, in thrombo-angiitis
obliterans, 236
trophic disorders of, 97
Necrosis, 127
colliquation, 183
signs of, in a limited part, 128
Nerve cells, role of, in production of trophic
disturbances, g2
control of capillary circulation, 50
degeneration, interdependence of por-
tions of nervous system in, 92
disease, organic, Raynaud’s ‘disease and,
differentiation, 554
distribution about
artery, 36
fibers, vegetative, course of, 23
impulses and closed circuit, 91
influences in capillary motility, 38
on blood vessels, 95
on osseous tissues, 94
injury, complicating injuries to blood
vessels, 206
malfunction, causes, 81
paths in skin, 506
interdependence of, with particular
reference to trophic function, 92
sciatic, injury, 519
Nerves of capillaries, 11
peripheral, lesions of, irritative phe-
nomena attending partial lesions,
519
symptoms with
destruction, 519
vasomotor and trophic symptoms,
520
following bullet wounds, 520
vasomotor and trophic disorders in
lesions of, 518
sympathetic, causalgias of,
_ 523 3
in relation to causalgia, 522
painful lesions of, 522
periarterial, neuroses and, 521
vascular, centers, 44
peripheral course of, 34
vasoconstrictor, 36
vasodilator, 37
Nervous system, autonomic, 23
central, vasomotor and trophic dis-
turbances in lesions of, 513
indirect degeneration of, 04
interdependence of portions of, in
nerve degeneration, 92
common femoral
complete nerve
treatment,
620
Nervous’ system, Lenhossek
degeneration of, 92
parasympathetic, 23, 28
retrograde degeneration of, 93
secondary atrophy of, 94
sympathetic, 23, 25
effect of adrenalin on, 580
of calcium on, 581
of ergotoxin on, 580
pain and, 46
réle of, in certain pathologic condi- |
tions, 583
in reflex contractures of Babinski- |
_ Nitric acid as cause of gangrene, 182
| Noma, 188
Froment type, 583
spinal system and, relation of, 32
trophic functions of, 90
reflex theory of, 93
theory of heterologous stimulation
in, 94
vasomotor, 22
course of vegetative nerve fibers, 2
effect of nicotin on, 579
functions of, 36
summary of, 46
vegetative, cerebral lesions of, localiza-
tion of, 510
diagnosis and localization of lesions
of, 509
effect of adrenalin on, 55
hypersensitiveness of, 504
internal secretions and, 502
neuroses of, theoretical concept of,
501
pharmacologic tests of functions of, |
12
relation of endocrine glands to, 55
skin and, 504
Wallerian degeneration of, 92
Neuralgia due to cold, 174
Neuritis complicating injury to blood-
vessels, 206
intermittent claudication and, differen-
tial diagnosis, 157
Neurogenic gangrene, pathogenesis of, 98
Neuro-irritative anemia, 72
ischemia in trophic disturbances, 91
Neuroparalytic hyperemia, 73
theory of, in trophic disorders, 91
Neuroses of vegetative nervous system,
theoretical concept of, 501
periarterial, sympathetic nerves and, 521
traumatic, with vasomotor disturbances
of hands and feet, 574
vasomotor and trophic, general consider-
ations, 499 Ry
as prodromal stage of thrombo-angiitis
obliterans, 574
atypical, 572 ;
capillary microscopy 1n, 590
circulatory, Raynaud’s disease and,
differentiation, 554
surgical treatment, 581
operation, 582
thrombo-angiitis and, differential diag-
nosis, 375
treatment, 578
cellifugal |
INDEX OF SUBJECTS
Neurotic gangrene, multiple, 567
of skin, 97, 98
_ Neurotrophic disorders in spina bifida, 514
of skin, 96
influences, exercise of, 91
skin changes in syringomyelia, 97
Neurovascular syndromes after ligation of
large arteries, 212
| Newborn, sclerema of, 559
Nicotin,.action of, upon ganglion cells, 23
as causal factor in atherosclerosis, 22
effect of, on vasomotor nervous system,
579
treatment, 189
Normal anastomoses, 10
Nuclei in corpus striatum, 31
Nucleus sympatheticus lateralis inferior, 25
superior, 25
medialis inferior, 25
OBSTRUCTIVE vascular disease, demonstra-
tion of collaterals in, 84
Obturation, arterial, without immediate
symptoms, 480
| Occlusion, vascular, of doubtful origin, 472
_ Occlusive thrombi, absence of pulsation
distal to, 134
| Oppenheim’s type of intermittent claudica-
tion, 142 .
Organic arterial disease, Raynaud’s disease
and, differentiation, 557
vasoneurosis and, 578
nerve disease, Raynaud’s disease and,
differentiation, 554
obstructive arterial diseases, pain in, 136
vascular disease, gangrene without, 539
Organs, internal, gas formation in, 193
Orthoform as cause of gangrene, 183
Osseous changes in thrombo-angiitis
obliterans, 275
tissues, nerve influences on, 94
Oxalic acid as cause of gangrene, 182
PAIN as diagnostic symptom, 135
in erythromelalgia, 135, 531
in organic obstructive arterial diseases,
136
in Raynaud’s disease, 135, 549
in thrombo-angiitis obliterans, 135, 258;
see also Thrombo-angiitis obliterans,
pain in.
in trophic disorders, 137
induced by prolonged pendency of limb,
136
paroxysmal, of diffuse variety, 136
referred,135
sympathetic nervous system and, 46
Painful lesions of sympathetic nerves, 522
Pallor, 73
artificial, 151
Palpation of anterior tibial artery, 10
of axillary artery, 5
of brachial artery, 5
of dorsalis pedis artery, ro
INDEX OF SUBJECTS
Palpation of femoral artery, 6
of popliteal artery, 7, 9
of radial and ulnar arteries, 5, 6
Papillary pressure, variations in, in capil-
laries, 594
Paradoxical ischemia, 84
Paralyses, motor, following arterial lesions,
584
Paralysis douleureuse ischémique, 140
Paralytic action of poisons on capillaries, 61
Parasympathetic nervous system, 23, 28
Paratyphus bacillus, 203
Paredema bacillus, Pfeiffer-Bessau, r91
Parietal arteritis, 451
Paroxysmal myasthenia, 155
pain of diffuse variety, 136
Patency of veins, tests for, 168
Periarterial sympathetic nerves, cutting of,
characteristic signs following, 582
neuroses and, 521
Periarteritis, 455
nodosa, 462
clinical manifestations, 463
manifestations in extremities, 463
thrombus formation in, 122
Peripheral arteriosclerosis, 71
circulation, elementary principles, 48
functional disturbances of, 76
due to derangement of capillary
flow, 76
to impaired exchange of fluids, 78
physiology of, 48
course of vascular nerves, 34
nerve lesions, irritative phenomena at-
tending partial nerve lesions, 519
symptoms with complete nerve
destruction, 519
vasomotor and trophic disorders in,
518
symptoms, 528
following bullet wounds, 520
parasympathetic and sympathetic fibers,
antagonistic influence of, on single
vegetative organs, 43
thrombotic gangrene, 572
venopressor mechanism, 59
Pfeiffer-Bessau bacillus, ror
paredema bacillus, ror
Phalanges, dry gangrene of one or more, 202
Pharmacologic tests of vegetative functions,
512
Phlebitis, extensive recurring, 472
migrating, 214
focal, of unknown origin, 470, 472
in thrombo-angiitis obliterans, 279
miscellaneous varieties, 470
with infections, 472
with pulmonary tuberculosis, 470
rheumatic, 452
rheumatismal, differential diagnosis, 469
syphilitic, diagnosis of, 469
tertiary, histopathology of, 469
Phlebosclerosis, 420
Phlegmon, gas, 190
local, 195
progressive, 196
621
Phosphorus as cause of gangrene, 183
Physiology of capillaries, 57
of peripheral circulation, 48
of vasomotor centers, 41
recent views on, 43
Pigmentation in scleroderma, 560
Pilocarpin, effect of, on vegetative func-
tions, 512
Pituitrin, effect of, on circulation, 56
Platelet thrombus, 106
cause of development of, 107
Pneumonia, gangrene complicating, 481
Poison of bees and wasps, gangrene from,
183
Poisonous gases, gangrene due to, 184
Poisons, endogenous, in thrombosis, 119
exogenous, and infectious agents, action
of, in thrombus formation, 120
in thrombosis, 120
microbic, gangrene from, 183
paralytic action of, on capillaries, 61
selective action of, on sympathetic and
parasympathetic systems, 580
Polyneuritis, infectious, vasomotor symp-
toms in, 521
Raynaud’s disease and, differentiation,
554
Popliteal artery, anatomy, 7
palpation of, Buerger’s method, 133
pulse, 8
manner of detecting, 132
Postanemic diapedesis, 77
hyperemia, 74
Postural treatment, Buerger’s, 77
Pott’s gangrene, 391
Precipitation thrombosis, 108, 110
Primary coagulation thrombosis, 108
Progressive facial hemi-atrophy, o1
gas phlegmon, 196
Proserozym, 103
Pseudo-aneurysms, 208
Pseudophthisis, 425
Pseudotetanus, hysterical, 143
Psychoneurosis, vasomotor, 574
Puerperal gangrene, 485, 490
thrombosis, 108
Pulmonary tuberculosis
migrans, 470
Pulpy form of hospital gangrene, 188
Pulsating hematoma, 208
Pulsation, absence of, distal to occlusive
thrombi, 134
in gangrene, 129
arterial, as diagnostic symptom, 132
in Raynaud’s disease, 550
in thrombo-angiitis obliterans, 263;
see also Thrombo-angiitis obliterans,
arterial pulsation in.
Pulse, axillary, 5
brachial, 5
dorsalis pedis, 10
femoral, 7
popliteal, 8
manner of detecting, 132
radial, 6
tibial, ro
with phlebitis
622 INDEX OF
Pulse, ulnar, 5
vagus, 44
Pulsion thrombosis, 111, 117
Putrid gangrene, 158
Pyogenic bacteria, gangrene due to, 202
QUININ, injection of, gangrene following,
185
RADIAL artery, anatomy, 5, 6
pulse, 6
Raynaud’s disease, 542
acroasphyxia chronica and, differentia-
tion, 554 ;
acrocyanosis in, 71, 72
acroparesthesiz of Schultze and, differ-
entiation, 553
arterial pulsation in, 550
capillary microscopy in, 599
clinical picture, 543
demonstrable phenomena in, 550
diagnosis, 553
differentiation from vasomotor and
trophic neuroses, 553
erythromelalgia and, differential diag-
nosis, 553
etiology, 545
evidences of vasomotor instability in,
_ 550
incidence, 544
local asphyxia in, 546
local syncope in, 546
nomenclature, 544
of finger, with angioneurotic inter-
mittent claudication, 144
organic arterial diseases and, differ-
entiation, 557
osseous changes in, 548
pain in, 135, 540
pathology, 552
polyneuritis and, differentiation, 544
remote clinical phenomena in, 550
sclerodactyly and, differential diagno-
sis, 552
scleroderma, and sclerodactyly, 551
sensory symptoms in, 549
simple vasomotor circulatory neuroses
and, differentiation, 554
spasms of capillaries in, 67
stage of vasomotor phenomena in,
540
symptomatology, 546
syringomyelia and, differentiation, 555
thrombo-angiitis obliterans and, differ-
entiation, 555
treatment, 558
trophic disorders and gangrene in, 547
vascular disease and, differentiation,
555
Reactionary hyperemia, 156
rubor, 163
Recurrent fever, gangrene in, 203
Redness of toes in gangrene, 129
Referred pain, 135
Reflex theory of trophic functions of
nervous system, 93
SUBJECTS
Reflexes, axon, 37
vaso-vasomotor, 45
vegetative, in skin, 505
viscero-vasomotor, 45
Refrigeration, local, effects of, in thrombus
formation, 123 !
Responses, vasomotor and autonomic, 53
Rete patelle, 86
Retrograde degeneration of nervous system,
93
Rheumatic arteritis, 451
phlebitis, 452
Rheumatismal phlebitis, differential diag-
nosis, 469
Rubor, 89
and cyanosis, 573
chronic, 163
hyperemia, 74
induced, 163
involving toes in gangrene, 129
reactionary, 163
SCHIENBEIN Schmerz, 173
Schultze, acroparesthesize of, Raynaud’s
disease and, differentiation, 553
Sciatic nerve injury, 519
Sciatica, intermittent claudication and,
differential diagnosis, 157
Sclerema neonatorum, 559
Sclerodactyly, 378, 559, 563
Raynaud’s disease and, differential diag-
nosis, 552
scleroderma and Raynaud’s disease, 551
Scleroderma, 559
clinical course, 564
deranged internal secretions in, 502, 503
diagnosis, 565
disturbed motility in, 562
gangrene complicating, 561
general symptoms, 563
joint lesions complicating, 563
mucous membranes in, 563
neurogenic theory in, 565
osseous changes complicating, 562
pathogenesis, 564
pigmentation in, 560
prognosis, 566
secretory changes in, 560
sensory disturbances in, 562
sclerodactyly, and Raynaud’s disease, 551
symptomatology, 560
symptoms of erythromelalgia associated
with, 563
theory of malfunction of endocrine glands
in, 564
thyroid imbalance theory in, 564
treatment, 566
trophic disturbances in, 561
true, thrombosis-angiitis obliterans and,
differential diagnosis, 378
vascular theory in, 565
vasomotor disturbances in, 561
symptoms in, 563
Sclerodermal mask, 562
Sclerotic arteries, bone formation in, 421
Secondary atrophy of nervous system, 94
INDEX OF SUBJECTS
Secretions, internal, and vegetative func-
tions, 502
circulation and, 55
trophic disturbances and, 504
Senile changes in arteries, 19
gangrene, 158, 391
Sepsis, anaerobic, 196
Serozym, 103
Serpent venom, gangrene from, 183
Serum therapy in gas gangrene, 2o1
Shock, 62
local, 526
Silver nitrate as cause of gangrene, 183
Skin changes, neurotrophic, in syringo-
myelia, 97
composition of, 584
glossy, 97
origin of, 96
histology of, 584
idiopathic atrophy of, 566
lesions due to trophoneurotic causes, 97
multiple neurotic gangrene of, 97, 98
nerve paths in, 506
trophic disorders of, 96
summary, y9
vascularization of, 585
vasomotor phenomena of, 506
vegetative nervous system and, 504
reflexes in, 505
Slough, gangrenous, 127
Sloughing, 127
Sloughs, 127
Sodium chlorid
following, 185
Spasm and atony of capillaries, 592
arterial, 77
intermittent, of vascular capillaries, 144
of vasconstrictors following bullet
wounds, 206
of venules, 77
traumatic vasomotor, 523
treatment, 525
Spasmophilic conditions, altered calcium
metabolism in, 580
Spasm of capillaries in Raynaud’ s dis-
ease, 67
Spastic anemia, 72
Sphacelation, 127
Sphacelinic acid, gangrene from, 186
Sphacelus, 127
Spina bifida occulta, disturbances due to
lesions of nerve apparatus, 516
local symptoms, 515
nerve lesions of cord or cauda
equina in, 515
neurotrophic disorders in, 514
symptoms, 515
vasomotor and trophic disturbances
injection of, gangrene
in, 516
Spinal column, intermittent claudication
of, 146
cord injuries, vasomotor disturbances
in, 514
vasomotor paths in, 32
nerves, sympathetic nervous system and,
relation of, 32
!
623
Spinal vasomotor centers, 31
Spodogenic thrombi, ror, 118
thrombosis, 110
Spontan-Gangrin, 307
Spontaneous amputation in gangrene, 159
Stagnation thrombosis, 111, 116
thrombus, r10
Stases in capillary circulation, 589
Stewart’s method of measuring blood flow,
50
Stimuli, chemical, direct response of capil-
laries to, 60
mechanical, direct response of capillaries
to, 60
Stomatitis, gangrenous, 188
Stream and pressure conditions in vaso-
neurotic diathesis, 592
Streaming, granular, 66
in capillaries, 586
Subcortical vasomotor centers, 30
Sulphuric acid as cause of gangrene, 182
Superficial circulation, in obstructive vas-
cular diseases, 80
changes in vasomotor mech-
anism in, 81
chemical action on tissues in, 81
diminished force of stream in, 80
exhaustion in, 81
hydrostatic and gravity forces
in, 80
Sympathectomy, periarterial, characteristic
signs following, 582
Sympathetic and peripheral parasympa-
thetic fibers, antagonistic influence of,
on single vegetative organs, 43
nerve, periarterial, cutting of, charac-
teristic signs following, 582
nerves, causalgias of, treatment, 523
in relation to causalgia, 522
painful lesions of, 522
periarterial, neuroses and, 521
nervous system, 23, 25
effect of adrenalin on, 580
of calcium on, 581
of ergotoxin on, 580
pain and, 46
role of, in certain pathologic con-
ditions, 583
in reflex contractures of Babinski-
Froment type, 583
spinal system and, relations of, 32
Symptoms, diagnostic; see Diagnostic symp-
toms.
Syndrome, Erb’s, 129
Synesthesalgia, 523
Syphilis, thrombus formation in, 121
Syphilitic arteritis and gangrene, 456
clinical forms, 460
incidence, 459
pathology, 456
symptomatology, 460
disease of veins, 464
clinical characteristics, 464
histopathology of tertiary phlebitis,
469
pathology, 464
624
Syphilitic disease of veins, tertiary or late
form, 468
thrombus in, 468
gumma of veins, differential diagnosis,
469
tertiary, differential diagnosis, 469
myositis, differential diagnosis, 469
phlebitis, diagnosis of, 469
Syringomyelia and gliosis spinalis, 513
neurotrophic skin changes in, 97
Raynaud’s disease and, differentiation,
SES)
TaBES dorsalis, trophic disturbances in, 513
Taches cerebrales, 74
Tarsalgia and intermittent claudication,
differential diagnosis, 157
Tertiary phlebitis, histopathology of, 469
Test, compression, 77
expression, 163
Henle-Coenen, for circulation, 168
Matas, for circulation, 166
Moskowicz, for circulation, 166
Tests for circulation, 165
value of, in thrombo-angiitis oblit-
erans, 167
for patency of veins, 168
pharmacologic, of vegetative functions,
512
Tetany, altered calcium metabolism in, 580
Theoretical concept of neuroses of vege-
tative nervous system, 501
Therapeutic development of collaterals, 87
Thermic gangrene, 172; see also Gangrene, |
thermic.
Thermic causes of gangrene, 160
influences, thrombosis due to, 122
irritants, cutaneous responses to, 509
Thrombi, appearance of, 105
cause of formation, 1or
forms of, 100
hyalin, ror
leukocyte, ror
mixed, ror
occlusive, absence of pulsation distal to,
134
red, 101
spodogenic, ror, 118
types of, 1or
white, ror
Thrombo-angiitis obliterans, 81, 213
acute stage, 149, 218
acute symptoms, 218
alterations in nails in, 236
appearance of limb in, 235
arterial pulsation in, 263
absent pulses, 263
cases with insignificant symptoms,
265
one or both limbs compro- |
mised early and lost, 266
disappearance of pulses com-
patible with arrested symptoms,
267
importance of popliteal pulse, 267
in certain early cases, 263
INDEX OF SUBJECTS
Thrombo-angiitis obliterans, arterial pulsa-
tion absent in all arteries of a
limb, 264
and angle of circulatory suffi-
ciency in, 269
pulsations disappearing under ob-
servation, 266
pulses of upper extremities, 269
present, 266
relation of pulsation and clinical
duration, 269
return of pulsation, 269
sequence of loss of pulsation in, 268
severity of symptoms correspond-
ing to arterial occlusion, 267
arteriosclerosis associated with, 306
simulating, 431
arteritis with thrombosis simulating,
454
as borderline case, 576
chemical action in, 82
chronic stage, 219
arrested stage or temporary heal-
ing in, 229
cases in elderly individuals, 228
in females, 226
in young with grave prognosis,
224
losing the limb last affected, 222
of exquisite chronic rubor, 219
of long duration without trophic
lesions, 224
of short duration, acute and
subacute, 220
with all extremities involved,
225
with all vessels pulsating, 226
with apparent healing or cure,
228
with chronic course in one limb,
acute course in other, 223
with intermittent claudication
and migrating phlebitis only,
221
with intermittent claudication
only, 221
with lethal outcome, 224
with pain only, 225
without symptoms, 220 —
without tropic disorder or gan-
grene requiring amputation,
225
without trophic lesions or gan-
grene, 210
doubtful cases, 231
relapsing cases, 223
sudden gangrene simulating em-
bolic type, 220
trophic lesions first symptom, 220
classification, 231
clinical concept, 214
picture, 231
coldness in, 261
directly attributable to vascular
occlusion, 262
neurotic types, 261
Thrombo-angiitis obliterans, coldness in,
INDEX OF SUBJECTS | 625
|
prolonged vasomotor and hydro-
static coldness with ischemia, 261
transitory vasomotor, 261 |
cyanosis in, 250
local chronic, 251
pathogenesis of, 253
temperature conditions in, 252
diagnosis, 374
clinical, 375 |
differential, from true scleroderma,
378
from vasomotor neuroses, 375
symptoms characteristic of, 374
early, 576
edema in, 254
persistent, harbinger of gangrene,
255
erythromelalgia and, differential diag- |
nosis, 534
erythromelia in, 215, 242
action of specific toxins in, 249, 250
chronic, 243
duration of, 245
exhaustion of
mechanism in, 249
explanation of, 247
inflammatory, 242 |
intrinsic, 243
local action of metabolites or katab- |
olic agents in, 249, 250 |
reactionary or induced, 243
significance of, 245
types of, 242
vasomotor, 245
etiology, 277
fissures of soles in, 236
gross pathology, 311
histopathology, 314, 321
acute lesion in deep vessels, 334
elastic tissue in, 358
healed or old stage, 338
in acute or specific lesions, 317
stage of disease, 321
in healed or organized stage, 316
intermediate stage of healing, 337
pathology of the relapsing lesion,
354
specific lesions in deep vessels, 334
terminations of occluding tissue, 350 |
incipient, with apparent vasomotor
symptoms, 576
intermittent claudication in, 214, 255
vasomotor symptoms with, 256
with pulsating arteries, 256
introduction, 213
involvement of upper extremities, 294
early symptoms of, 294
simulating scleroderma and
sclerodactyly, 305
with acute arteritis of portions |
radial and ulnar arteries, 305
with atrophy and gangrene, 303
with extensive gangrene, 302
with gangrene of slight extent,
300
vasoconstrictor |
40
| Thrombo-angiitis obliterans, involvement
of upper extremities with
lesions simulating neurogenic
disturbances, 297
with trophic and vasomotor
phenomena, 299
with trophic disorders only, 299
with vasomotor symptoms pre-
dominating, 295
without subjective symptoms,
295
ischemia in, 215, 237
an index of circulation, 242
mechanical or hydrostatic type, 237
angle of elevation that pro-
duces it, 238
arc or angle in which it per-
sists, 248
extent of, 239
obstinate areas of pallor in,
240
situation of its appearance, 238
time interval of its establish-
ment, 239
vasomotor type, 240
mental symptoms in, 270
migrating phlebitis in, 279
both playing equally important
réles in symptom-complex, 284
cases in which absolute evidences
of deep arterial involvement
are lacking, 291
with symptoms of limited vein
involvement, 280
without symptoms, 280
causing patient to seek treatment,
281
conclusions from vein lesions, 292
extensive fulminating, 291
involving both upper and lower
extremities, 286
mottling of skin in, 236
neurotic types, 261
of lower extremities, 232
forms of onset, 232
unusual clinical pictures in, 234
osseous changes in, 275
pain in, 135, 258
continuous, in toes, 260
sequence of various types, 260
varieties of, 258
pathological concept, 214
pathology, 307
in accidental exitus, 369
in cases with slow termination, Gye!
in lethal cases, 368
predisposition to thrombosis in etiology
of, 278
Raynaud’s disease and, differentiation,
555;
rubor in, 215
scleroderma and, differential diagno-
sis, 378
statistical data, 276
syphilitic phlebitis and, differential
diagnosis, 469
626
Thrombo-angiitis obliterans, tenderness in,
260
thrombosis in, 109
treatment, 378
conservative, 380
diathermic, for enhancing circula- |
tion, 380
heat for enhancing circulation, 381
intermittent compression of main
arteries for enhancing circula-
tion, 382
internal medication, 382
local, 382
methods of enhancing circula-
tion, 380
postural method for enhancing
circulation, 380
subcutaneous or intravenous in-
jection of solutions for enhanc-
ing circulation, 381
of pain, 379
operative, 382
arteriovenous anastomosis, 382
ligation of femoral vein, 382
limited amputation, 383
radical amputation, 383
prophylactic, 379
selection of therapeutic procedures,
384
value of tests for circulation in, 167
vasomotor neuroses and, differential
diagnosis, 375
as prodromal stage of, 574
vasomotor symptoms in, 271
evidences of altered function
in, 274
in early stages only, 273
syncope or ischemia after exertion,
; 273
without pain, 258
Thrombophilia, 126
Thrombophlebitis, 214
associated with thrombo angiitis oblit-
erans causing patient to seek treat-
ment, 282
cases in which absolute evidences of deep
arterial involvement are lacking, 291
extensive fulminating type, in thrombo-
angilitis obliterans, 291
involving both upper and lower extremi-
ties, in thrombo-angiitis obliterans, 286 |
thrombo-angiitis obliterans and, both
playing equally important rdles in
symptom-complex, 284
with symptoms of limited vein involve- |
ment in thrombo-angiitis obliterans, 280
without symptoms in thrombo-angiitis
obliterans, 280
Thrombosis and embolism, 479
arterial obturation without immediate
symptoms, 480
classification, 479
complicating arteriosclerosis, 493
in acute aortitis, 493
and general diseases, 123
arterial, with traumatic gangrene, 170
INDEX OF SUBJECTS
Thrombosis, arteriosclerotic gangrene with,
clinical history, 422
as cause of gangrene after freezing, 170
chemical alterations of total blood
in, 124 :
varieties, 119
coagulation, 1or
conglutination, rot
distant, 109
due to actinic causes, 123
to solid bodies, 122
to thermic influences, 122
effects of local refrigeration, 123
endogenous poisons in, 119
exogenous poisons in, 120
general causes, 123
general considerations of, 100
in gangrene, 129, 161
in thrombo-angiitis obliterans, 109
increased viscosity of blood in, 125
mechanical types of, 111
metastatic, 100
of cachectic conditions, 125
of chemical origin, 118
inflammatory processes in, 119
of larger more central paths with arterio-
sclerosis, 424
physical explanations of, 105
precipitation, 108, 110
primary coagulation, 108
process of, classification of, r10
process of, coagulation in, 108
puerperal, 108
pulsiong 101; a7
relation of, to age, 125
role of infection in, 126
special conditions in, 125
spodogenic, 110
stagnation, 111, 116
types of, 100
with arteriosclerosis atrophy as sehen
425
clinical course, 421
diagnosticated as acute intermittent
claudication, 150
with arteritis simulating thrombo-angiitis
obliterans, 454
Thrombotic and embolic gangrene after
infectious diseases, 481
clinical course, 481
pathology, 483
types of gangrene, 483
arteriotomy in, 494
technic, 498
arteriovenous anastomosis in, 404
diagnosis, 489
embolectomy in, 494
technic, 498
ligation in, 494
post-operative, 489
treatment, 493
gangrene in healthy or but slightly
diseased vessels, 490
peripheral gangrene, 572
| Thrombus, accretion, 110
formation, 106
INDEX OF SUBJECTS
Thrombus formation, bacteria in, 120
coagulation and agglutination in, 102
congelation in, 105
determining factor in, 100
forces engaged in, 102
in peri-arteritis nodosa, 122
in syphilis, 121
in tuberculosis, 121, 122
in vessels implicated in war wounds,
205
platelet, 106
cause of development of, 107
stagnation, 110
Thyroid hormones, importance of, in
arterial affections, 502
Tibial artery, anterior, anatomy, 10
posterior, anatomy, 9
and vein, normal, characteristics, 18
pulse, 10
Tissues, osseous, nerve influences on, 94
Tobacco as etiologic factor in intermittent
claudication, 153
as predisposing factor in
angiitis obliterans, 278, 279
Toes, bluish discoloration of, in gangrene,
129
redness of, in gangrene, 129
Tonometer, micro¢apillary, 67, 68
Tonus, vascular, localized derangements
of, 70
vasomotor, 42
Toxins and antitoxin formation in gas
gangrene, 190
of gas gangrene, 196
Traumatic aneurysms, 208
decubitus, acute, 170
‘gangrene, 168; see also Gangrene, trau-
matic.
neuroses with vasomotor disturbances
of hands and feet, 574
vasomotor spasm, 523
treatment, 525
Trophedema, 98
Trophic and vasomotor disorders in lesions
of central nervous system, 513
in peripheral nerve lesions, 518
neuroses, general considerations, 499
disorders and gangrene in arteriosclerotic
disease, 390
clinical forms of, 393
in gangrene, 129
internal secretions and, 504
of nails, 97
of skin, 96
summary, 99
pain in, 137
slight, with vasomotor symptoms, 573
function, independence of nerve paths,
with reference to, 92
of nervous system, 90
reflex theory of, 93
theory of heterologous stimulation
in, 94
influences of nerves on blood vessels, 95
nerves, special, theory of, in trophic
disorders, 91
thrombo-
627
Trophoneuroses and vasomotor neuroses
following infections, 574
Trophoneurotic causes, skin lesions due to,
97
True aneurysms, 208
Trunk and extremities, vasomotor paths of,
511
Tuberculosis of arteries, 455
pulmonary, with phlebitis migrans, 470
thrombus formation in, 121, 122
Tuberculous endarteritis, 456
Typhoid fever, gangrene in, 203
UHRZEIGERBAZILLUS, I9I
Ulceration, 127
Ulnar artery, anatomy, 5
pulse, 5
Urticaria, 96
gangrenosa, 570
VAGUS pulse, 44
Van Beuren’s treatment of gas bacillus
infection, 199
Vascular affections, congenital hypoplasia
of vascular system predisposing to, 83
capillaries, intermittent spasm of, 144
crises, 70
disease, obstructive, demonstration of
collaterals in, 84
organic, chronic acroasphyxia ‘and,
differential diagnosis, 531
gangrene without, 539
Raynaud’s disease and, differentiation,
555
innervation, double, recent views on, 38
insufficiency, 70
in arteriosclerosis, 71
nerve centers, 44
nerves, peripheral course of, 34
occlusion of doubtful origin, 472
system, congenital hypoplasia of, as
predisposing to vascular affections, 83
tone, localized derangements of, 70
Vascularization of skin, 585
Vasoconstriction as sequence to obstructive
anemia, 74
Vasoconstrictor nerves, 36
Vasoconstrictors, spasm of, following bullet
wounds, 206
Vasodilatation, 53
as sequence to obstructive anemia, 74
Vasodilator function, 40
nerves, 37
Vasomotor and autonomic responses, 53
and trophic disorders in lesions of central
nervous system, 513
in peripheral nerve lesions, 518
neuroses, following infections, 574
general considerations, 499
centers, cerebral, 28
physiology of, 41
spinal, 31
subcortical, 30
circulatory neuroses, Raynaud’s disease
and, differentiation, 554
628
Vasomotor disturbances of hands and feet,
traumatic neuroses with, 574
function and circulation, 52
instability, 570
Jacksonian epilepsy, 29
monoplegia, 29
nervous system, 22
course of vegetative nerve fibers, 23
effect of nicotin on, 579
functions of, 36
summary of, 46
neuroses and organic arterial disease,
578
as prodromal stage of thrombo-angiitis
obliterans, 574
atypical, 572
capillary microscopy in, 590
morphology of capillaries in, 595
nature of, 591
surgical treatment, 581
operation, 582
thrombo-angiitis obliterans and, differ-
ential diagnosis, 375
treatment, 579
paths for trunk and extremities, 511
in spinal cord, 32
phenomena in arteriosclerotic disease,
390
of skin, 506
psychoneurosis, 574
spasm, traumatic, 523
treatment, 525
symptoms in infectious polyneuritis, 521
in thrombo-angiitis obliterans, 271
with slight trophic disorders, 573
tonus, 42
type of intermittent claudication, 142
Vasoneuroses; see Vasomotor neuroses.
Vasoneurotic constitution, 571, 590
diathesis, 590
fullness of capillaries in, 594
stream and pressure conditions in, 592
Vaso-vasomotor reflexes, 45
Vegetative functions,
and, 502
pharmacologic tests of, 512
nervous system, cerebral lesions of,
localization of, 510
diagnosis and localization of lesions
of, 509
effect of adrenalin on, 55
hypersensitiveness of, 504
INDEX OF SUBJECTS
Vegetative nervous system, internal ‘secre-
tions and, 502
neuroses of, theoretical concept of,
501
pharmacologic tests of functions of,
512
relation of endocrine glands to, 55
skin and, 504
reflexes in skin, 505
| Vein, axillary, 5
femoral, ligation of, in treatment of
thrombo-angiitis obliterans, 382
Veins, patency of, tests for, 168
syphilitic disease of, 464
clinical characteristics, 464 .
histopathology of tertiary phlebitis,
469
pathology, 464
tertiary or late form, 468
thrombus in, 468
gumma of, differential diagnosis, 469
Venom, serpent, gangrene from, 183
Venopressor mechanism, peripheral, 59
Venous hyperemia, 75
consequences of, 75
_ Venules, anatomy, 12
spasm of, 77
Vessel injury and gas gangrene, 198
Vessels, antagonistic innervation of, 34
Vicarious menstruation, hemorrhages of, 79
_ Viscero-vasomotor reflexes, 45
_ Visualization of capillaries, apparatus for,
586
_ von Hibler bacillus, 191
WALLERIAN degeneration in nervous sys-
tem, 92
| War edema, 70
internal secretions |
Wasps and bees, poisons of, gangrene from,
183
Weiss and Dieter’s method of studying
capillary circulation, 64
Weiss-Miiller method of studying capillary
circulation, 64
_ Welch gas bacillus, 190
Wounds, bullet, of peripheral nerves, vaso-
motor and trophic symptoms follow-
ing, 520
spasm of vasoconstrictors following,
206 ‘
war, thrombus formation in vessels
implicated in, 205
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