THE UNIVERSITY OF ILLINOIS LIBRARY “G\G1s, eae “* a aly =A The person charging this material is re- sponsible for its return on or before the Latest Date stamped below. Theft, mutilation, and underlining of books are reasons for disciplinary action and may result in dismissal from the University. UNIVERSITY OF ILLINOIS LIBRARY AT URBANA-CHAMPAIGN ’ - eC KUL 2 1970 NOV 1/5 1973 MOV NOV 4 ar os L161— 0.1096 THE UNIVERSITY OF ILLINOIS LIBRARY | —6GNG.T,, Eta “* a adiy *s Digitized by the Internet Archive in 2021 with funding from University of Illinois Urbana-Champaign httos://archive.org/details/inflammationinboOOelyl_ 0 THE LIBRARY OF THE UNIVERSITY OF ILLINOIS ‘uINAJSeNbas 9JON ‘ANUII] JO 9daId poazoesad Jo voBjJANS JN, *(q) ‘INUIaJ JO soBVjans yuIOr = *(_) ; ‘BIqt} Jo vdeId payoasar JO soBJANS JN *(D) “BIql} JO aoByINS JUIOF =*(P) “BIQI} PUB INUIJ JO pUd 94} WIOIJ LOJIUITWIO QUO YNOG* Jo [VAOUIAI YIM ‘UOTPVSeY “sey JO SISO;NOIEqN J, INFLAMMATION IN BONES AND JOINTS LEONARD W. ELY, M.D . 3 - . e ASSOCIATE PROFESSOR OF SURGERY, STANFORD UNIVERSITY 144 ILLUSTRATIONS PHILADELPHIA AND LONDON J. B. LIPPINCOTT COMPANY COPYRIGHT, 1923, BY J. B. LIPPINCOTT COMPANY 1) ; ~ PRINTED BY J. B. LIPPINCOTT COMPANY AT THE WASHINGTON SQUARE PRESS, PHILADELPHIA, U. S. A. vv TU» al plat J = ~— 4 oe i z re 7 TO MY WIFE PREFACE To write a book on inflammation in bones and joints requires considerable temerity, and, perhaps, if I disown any undue self-confidence, I shall disarm eriticism in ad- vance. Unlike many subjects in medicine, great difference of opinion exists as to the physiology and pathology of these two organs. We have abundant clinical material on which to draw, but conclusions based on clinical opin- ion are notoriously conflicting. Like a religious argument, and perhaps for the same reason, an argument between the exponents of diverse clinical views is usually character- ized by positive statement and by some acrimony. We have at our disposal also the results of considerable investigative work, but much of this is not as well known as it should be, and the conclusions of the investigators do not always agree. ‘Too often the laboratory worker does not take the trouble to check up his results by clinical evidence, and too often the clinical expert is unwilling to devote the time in the laboratory which is necessary if he would understand the fundamental processes in the tissues with which he deals. Without this knowledge he is simply guessing as to what lies beneath the surface. When all is said, the gap in our knowledge is due to our ignorance of bone pathology, and we shall probably not fill it up until bones and joints are sectioned at necropsy with the same care as are other organs. We may not always agree with an observer’s conclusions, but we all know, when we are searching through a mass of contradic- tory opinions, with what satisfaction we greet the publica- tion of concrete, definite facts discovered in the examination of pathological material. We can draw our own conclu- sions from these facts. | 6 PREFACE Whatever this book lacks must be charged to the limitations of its author. It is based upon personal obser- vation and research, and is not to be regarded as a compilation, though on numerous occasions I have taken pains to set forth the opinions of others where they differ from mine. The chief merit, I think, is its exposition of the results of original research, and of work in the pathological laboratory, and the correlation of this work with clinical findings. The facts unearthed in this way should be of value to others, even when the conclusions drawn from them are not accepted. My colleagues in the Stanford Medical School, by their codperation and encouragement have aided me in many ways, particularly Dr. Frank Blaisdell, Associate Professor of Surgery, in my animal work and in the illus- trations. I am under great obligation to the librarians of the Lane Library, for their unremitting work upon the bibliographies, which should be of the greatest help to the student. The devoted work of my technician, Miss Wallach is beyond all praise. The facilities which Stanford University puts at the dis- posal of its faculty are unique. As toois it furnishes a great library, laboratories, clinics and hospitals, all grouped closely, and grants the leisure to use them. To its president and trustees I make my respectful acknowledgments. I take pleasure in acknowledging my indebtedness to Messrs. William Wood & Company of New York, to the Surgery Publishing Company of New York, and to the editors of The Annals of Surgery, the Archives of Surgery and the Journal of the American Medical Association for permission to reproduce material which has appeared in their publications. San Francisco, California, 1923. The Author. CONTENTS SECTION I. GENERAL CONSIDERATIONS. CHAPTER PACE PRASENERAL CONSIDERATIONS. 0.00200 se eee ccee Re i ee eee 15 SECTION ILI. ACUTE OSTEOMYELITIS AND ARTHRITIS. I. AcuTE SUPPURATIVE H2MATOGENOUS OSTEOMYELITIS................ 79 Il. Acute SUPPURATIVE H#MATOGENOUS ARTHRITIS.................... 94 Ill. SuppurATIvE OsTEOMYELITIS FoLLOWING COMPOUND FRACTURE....... 99 iV) YyPHOID OSTEOMYELITIS AND ARTHRITIS. ......... 0000s 0cceceevenes 100 V. Gonococcic OSTEOMYELITIS AND ARTHRITIS................-0--0005 103 Mrencurn INFLAMMATORY RHEUMATISM...........00csecccccsccccunse 108 MEET TORARTHROSIS INTERMITTENS © ...0: 0. cc coc cc hss cnc ecw cscs ve tarens 110 IIRC T'YC1OOA HTT RITIS Spe ots ke A eres hoe ais seine eieiee ce ee ws 112 Phe SUPPURATIVE ARTHRITIS FROM WOUNDS. ...........0ccc0cccccccens 120 TAPES ELAS) © oS OTIT YG os es se I, 4r och ok bald bce bow wate vue es 123 SECTION III. CHRONIC OSTEOMYELITIS. RECT a ECROSTS tomer em Cr rae ch cic: saci bo bed Ghee ws wh 133 NE REDE Oe Ge Ne oss a1 i)! oie Glas ia Saw wal ele sahilb-dle eve once 4 0 135 III. Cnoronic OSTEOMYELITIS OF UNKNOWN ORIGIN.................20-- 147 eis TCs QR Teo QUEST OSV ion Be OM Tle ar A eed a 147 PaGcet’s DEFORMING OSTEOMYELITIS, OsTITIS DEFORMANS 148 Leontrasis OssEA 155 OsTEOMYELITIS FisprosaA, OstiTis Frsrosa 155 PULMONARY HyPEeRTROPHIC OSTEOARTHROPATHY 156 TOME TS APRIL es re Se iS a icielc se a eG oo owlig cSt y ane ire els OS a Bes 158 SECTION IV. CHRONIC ARTHRITIS. Tue Two Great Types. Jornt TUBERCULOSIS IN GENERAL ........ 173 Tue First Great Tyre or Curonic ARTHRITIS, TUBERCULOUS OTT ns EP Se BR le ee eg 77 fi 8 CONTENTS SECTION V. TUBERCULOSIS OF SPECIAL JOINTS. CHAPTER PAGE I. TUBERCULOSIS OF THE SPINE, PoTT’s DISEASE.........2...csseeeuce 237 IL; Tusercu losis Or TRE HIP.4 ci tec oh eee a ons eee eee 272 Ill. TuseRcuLosis Off THE KNEE Yee. ss aes ee ee eee 295 IV. TuBERCULOSIS Of THH ANKLE AND TARSUS: «,....5 10) oem ene eee 308 V. TUBERCULOSISSOF ‘THE SHOULDER’... 05. se eee 317 VI. TUBERCULOSIS {OF THEY ELBOW? sc). 5% 2 ices eee ee 322 VII.“ TUBERCULOSIS OF THE WRIST... J. 4 eee ee 326 VIII. Tuperct.osis or tam SAckO-In1ac JOINT... ..5+5 55 nee eee 331 IX. TUBERCULOSIS OF THE FINGERS AND. TOES ......6.....i.0--00+++03 ood SECTION VI. OTHER FORMS OF ARTHRITIS OF THE FIRST GREAT TYPE OR GROUP. I, Coccrproman. GRANULOMA } 32 j.550) oc oo ee ee 345 II. Caronic DipLtostREPTococcic ARTHRITIS. ........+6.1.+.05 asses une 349 III. Caronirc ProaresstvE MULTIPLE ARTHRITIS................+.-0:+-- tir IV. Stiti’s-Drsease!. oh sande OO Ae oe ee 360 SECTION VII. THE SECOND GREAT TYPE OF CHRONIC ARTHRITIS. I. Tar Seconp Great Type or Caronic ARTHRITIS:, 42...- voseeses 365 SECTION VIII. ARTHRITIS CAUSED BY DEVELOP- MENTAL ABNORMALITIES. J. Leaa's Drsmasn,.. otf Fo. oan odds he ke in ee 401 II. Looss Bopiss In THE Joint, Joint Mouse, OSTEOCHONDRITIS DissEcANs 409 IIT. Kowauer’s > DISBASHE ss Soo ce ad aces eee eee ee 418 TV. Oseoop-ScuHuaATrer DISEASE. 526 «ic ko oe ee ee 420 INDEX’ OF :- AUTHORS 3,0) iuik el tps dao be kg he Pea 420 INDEX eS Ease ys ee oe ed Re eee ened bose eee 431 ILLUSTRATIONS FIG. PAGE 1. Slice of the distal portion of the normal human femur.............. 16 2. Low-power photomicrograph showing blood vessel entering the bone CES) Gy OS yp ee ear ae en ee i ee ie errr ieee er rere 17 meaumerow DOCcket-on tncioutside.of the Cortex,..:. 2.6 esc e con «wale wera 19 4. Low-power photomicrograph of diffuse tuberculosis in the bone SUN CMT UN ve ta ie ol Se hc ra, = Sie eM a Gitta, nine Ao nls a 0) e/ « cots eng sei vie odnye mid. at'e e 21 5. Low-power photomicrograph of normal human bone, showing peri- BERT MEICL TLE VS OTIS DOUG gris oe Wess PERS a's se ans eae grace Parte ahs 23 6. Photograph of stained slide from a sagittal section of the knee of RNREE TE MANE MCAD re a tere tes When me met aes er a, «ee ae ana Tia aoe Fg sl Lier G ko Taian ale eS 8 ee 25 7. Section of dog’s patella, camera lucida drawing..................... 27 8. Low-power photomicrograph, showing typical appearance of the synovial membrane in an acute inflammation...................... 29 9. Low-power photomicrograph from a case of marrow tuberculosis.... 33 10. High-power photomicrograph of a portion of the preceding slide.... 34 11. Low-power photomicrograph from a case of acute suppurative arthritis 35 12. Low-power photomicrograph from the knee joint of a foetus at term 37 13. Low-power photomicrograph of early stage of intracartilaginous iMpRRE MM COPLEY ERE LOUM re Meta tater Cg A'S yon ace ele a's’) Oona We epudl®

Selina ¥ bitte ¢ 0'5 2 ahs 315 IEE UB Stole LNG -25 72 eee as ee B74 119. Photograph of stained slide of a section of the head of the femur.... 375 120. Photograph of stained slide from a case of second-type arthritis of the knee. i 25 to0 cose sve 6 oe seen ame Oa 2 eS Site een 376 121.. Eburnated bone; at the articular surface... 05 2... 12. one 377 122. Low-power photomicrograph of articular cartilage.................. 378 123. Typical appearance of cartilage from a second-type arthritis of the | Dip. oi. fsicte Sanches oo eis daub a ere ctieen woe avn! aun ane ata ee ett gta een 379 124. Rather high-power photomicrograph of some of the cartilage tatters. 380 125. Cellular infiltration in thei marrow 205, < 3G spss oo le oe ie 381 126. Low-power photomicrograph of a section of the synovial membrane. 382 127. Articular’ surface of head’ of ‘femurs. 17 sas. 22-2) ee 384 128: Chronic arthritis of the great. second’ type. 2)... 2...5 san te 385 129. Chronic arthritis of the second type involving the thoracic spine..... 387 130. The same patient as shown in the preceding figure.................. 388 131, Légg’s® diseases y.0e. fern aie vn ani oo 20 We ip 404. 132: ‘Lepe’s” disease.|. 5 2. eb ge helt dave tas B film 9 eee ea 406 138. Legp's * diseases 1.5.5 vary an waldes tea: ea peso seesendinl 2 <6 ark Ee ee 407 134. J oint. mice in ‘the. elbow -...205 9 6 605. 6 seis sole 3) de ae ee 410 135. Two joint mice removed, exact size, from elbow shown in Fig. 184... 411 136. Photograph of a section of the larger of the mice shown in the pre- Ceding figure. 225. oie sive ake cute ese ite wierd ele Bie ee eee 412 137. Low-power photograph of the smaller of the joint mice............. 413 138. Loosé. body*removed from ) joint, natural size. 212.222 eee 414 139. Réntgenogram showing defect in surface of condyle of femur....... 415 140. Typical joint mouse from medial condyle of the knee............... 416 141. Low-power photomicrograph of the marked portion of the preceding 416 142.).Osgood-Schlatter disease.) fps. = soa ca wc ie ie 421 143." Oszood-Schlatter ant re PF » : i f or, ol 4 . , Ps, s i , = = © le aD al { ' yt? _-S le ap) ere ear ene ak. eke wr INFLAMMATION IN BONES AND JOINTS CHAPTER I. GENERAL CONSIDERATIONS. _ DiskasE in bone derives its special interest from the fact that it runs its course locked up in a narrow case or shell which influences its manifestations and treatment. Diseases of the sneall bones of the extremities, and of the ends of the long bones, are peculiar also in that they have in their immediate vicinity a closed cavity, the joint, whose involvement often overshadows the disease in the bone, and gives the clinical picture its stamp. In our studies six tissues require examination: (1) Bone tissue proper, (2) Marrow, (3) Periosteum, (4) Cartilage, (5) Synovial membrane, (6) Ligament. In- asmuch as difference of opinion often springs from differ- ence of definition, we shall define these terms as well as describe the tissues they represent. Bone is an animal substance composed of organic ma- terial impregnated with salts of lime and magnesium.’ Bone cells also are an integral constituent. Bone 1s divided into two classes: dense, and spongy or cancellous, but the bone in each is the same, and only differs in its arrangement and in its amount. Dense bone is found at the circumference of the shafts of the long bones, and as a layer on the outside of all spongy * Bone ash consists of calcium phosphate 84 per cent., magnesium phosphate 1 per cent., other calcium salts 7.5 per cent., carbonic acid 5.5 per cent. 15 16 INFLAMMATION IN BONES AND JOINTS bones or portions of bone. Under the articular cartilage it is prolonged as a thin layer in the normal state. On the inside of the cortex of the shaft it may end abruptly or it may be lined by a small amount of spongy bone. ‘The _ second is the more frequent condition. As it approaches the end of a long bone ihe layer of dense bone tapers off, to be prolonged under the cartilage. |S Fig. 1.—Slice of the distal portion of the normal human femur. Note the spongy bone on the inside of the cortex. The inside of the cortex presents no analogue to the periosteum on the outside. ‘There is no such structure as an “endosteum.”” Endosteum is simply marrow. Except under the cartilage the dense bone of the cortex is perforated by canals which transport_ blood vessels. Fibres of the periosteum also pass into it. In other words | the inside of the bone is only relatively a closed cavity. _ Spongy or cancellous bone makes up the bulk of the ends of the long bones, and the bulk of the short and the GENERAL CONSIDERATIONS 17 flat bones, the vertebra, the sternum, the ribs, carpus, tarsus, etc. Bone tissue itself is not subject to inflammation, nor actively to disease, and simply reacts to disease or change in its contained marrow. Usually a mild irritation in the marrow causes an hypertrophy of the bone, a stronger irritation an atrophy. If the irritation in the marrow be Fie. 2.—Low power photomicrograph showing blood vessel entering the bone cortex. Note absence of any such thing as endosteum. very severe, the bone dies. We are accustomed to speak of diseases of bone. It would be more accurate to speak of diseases in bone. Bhs Constant change is going on in the bone, that is, its structure is always changing to adapt itself to the uses to which itis put. Ifa part be put at rest, its bony structure atrophies, if much work is demanded the bone hypertro- phies, but both processes are purely passive and are accom- 2 18 INFLAMMATION IN BONES AND JOINTS plished by the blood vessels in the marrow and in the periosteum. 3 Bone has two great functions. The first is its mechanical function as the framework of the body. ‘This interests us especially in our study of deformities and of fractures. The second is as the container of the marrow. This is important in its relation to infection. Bone can be injured in only two ways. It can be attacked, as we shall see, by disease in its contained marrow, or it can be fractured. It cannot be sprained, strained, or suffer contusion. ‘This seems self-evident, and vet one often hears bone disease ascribed to the late effects of a bone injury, other than fraeture. Such a thing is of course impossible. Marrow is the soft tissue within the bone—all the soft tissue within the bone. Its situation, not its composi- tion, determines its name. Wherever there is bone there is marrow, in the central canal and in the spongy bone, and even, to a small extent, in the dense bone itself. Tissue with all the characteristics of marrow is occasionally seen in the region of the joints, on the outside of the cortex, immediately under the fibrous periosteum. Human marrow is of three kinds; first, red or cellular or lymphoid; second, yellow or fatty; and third, myxoma- tous or fibrous. The structure of marrow is so diverse and changeable that it is often difficult to say what is normal and what is not. Marrow consists of a reticulum of connec- tive tissue, blood vessels, blood spaces or channels, fat, and a greater or smaller number of many kinds of cells. The proportion of fat and of these diverse cells determines the quality of the marrow, whether it is fatty or lymphoid. In myxomatous or fibrous marrow little is present but fibrous tissue. GENERAL CONSIDERATIONS 19 The composition of marrow varies not only in health ‘and disease, but also with age.” In the human infant practically all marrow is lymphoid. In childhood the lymphoid marrow gradually disappears from the shafts, and then slowly with the lapse of years from the ends of the bones also. The adult has little lymphoid marrow 4 Fic. 3.—Marrow pocket on the outside of the cortex. Low power photomicrograph. in his long bones. It persists longer in the bodies of the vertebrae. | In studying diseases in bone, the changes in the bone tissue itself first attract our attention, but give us very little information. Whether we examine the bone with the naked eye, with the microscope or with the Rontgen * Dickson, W. E. Carnecie: “The Bone Marrow.” London, Longmans, Green & Co. 1908. 20 INFLAMMATION IN BONES AND JOINTS rays we observe that the changes in it are of the simplest kind, and are only three in number,—absorption or atrophy, production or hypertrophy, and death or necrosis. ‘The farther we investigate, the stronger grows our conviction that all changes of bone tissue are purely passive,’ and are simply the result of changes in the contained marrow. The marrow is one of the most complex, changeable, active and interesting tissues of the body, and reacts quite promptly to most infections. Fraenkel? found typhoid bacilli in the bone marrow of every one of 110 patients dying of typhoid. Areas of necrosis in the marrow are frequently observed in autopsies of patients who have died of infectious diseases. In laboratory animals dying of an infection, I have often noticed a marked engorgement of. the marrow; so often that I have come to regard it as a pathognomonic sign of an infection. Probably the “aching bones” at the be- ginning of an infectious disease are due to this congestion. As we shall see later, the marrow in tuberculosis shows typical tubercles, in suppurative osteomyelitis, engorge- ment, pus cells, colonies of bacteria, etc., in chronic bone disease the fibrous changes later to be described. The theory of the purely passive role of the bone tis- sue itself is not by any means generally accepted. In fact, it must be said that by far the weight of opinion les on the other side. Most writers believe that the bone tissue itself is capable of active inflammation, and attempt to differentiate ostitis from osteomyelitis. In the same way the differentiation is made between periostitis and inflam- mation of the marrow (or bone) immediately below the * Kiemm, P.: “ Die Osteomyelitis des Kindesalters.” Berlin, 1914. S. Karger. 4 FRAENKEL, Eve.: “‘ Ueber Knochenmark und_ Infektionskrankheiten,” Miinchener medicinische Wochenschrift, 1920, xlix, 561. GENERAL CONSIDERATIONS 91 periosteum. Klemm, in his book on osteomyelitis, discards completely the terms ostitis and periostitis. Probably the periosteum, like any other fibrous tissue is subject to inflammation, but I think that the term periostitis as ordi- narily employed is a misnomer, and that what we know as periostitis is really an inflammation of the subjacent bone Fig. 4.—Low power photomicrograph of diffuse tuberculosis in the bone marrow. marrow. The terms rarefying ostitis and productive ostitis are used synonymous with bone absorption and bone production, but seem to possess no particular merit. The marrow, especially the lymphoid marrow, is to be regarded as a chemical laboratory, the bone simply as the building which houses it. A knowledge of the composition of the marrow gives us a ready comprehension of its vul- nerability to infections and to their location as well. 22 INFLAMMATION IN BONES AND JOINTS The marrow of spongy bone, at least well into adult life, and in children the marrow of the shafts also, is essentially a lymphoid tissue. If pus germs of sufficient virulence are carried in the blood stream to a lymph node, the lymph node suppurates and breaks down; if they are carried to the bone marrow, the bone marrow does the same. ‘The difference in the course of the disease in the two cases is, in the first place a question of the amount of tissue involved, and in the second place one of environment. In osteomye- litis the products of suppuration are shut up in an almost impermeable shell and this fact makes the process much more severe, and increases the danger immeasurably. This explanation of the frequency of the occurrence of infections of the bone marrow in the young is not the standard one. Most authorities emphasize the etiological importance of trauma. Some affirm that rapid growth pre- disposes to infection. Lexer’ ascribes to the arrangement of the blood vessels about the epiphyseal line, the causal role in the frequency of infections near the end of the bone. His view might be said to be at present the accepted one. The matter will be taken from the realm of speculation when the bones are sectioned at necropsy with the same thoroughness as the other organs of the body. Tuer PERiIostEUM is the tissue which covers the bone in all places except those covered by the joint cartilage. Its structure and function have been the subject of much discussion, into which we shall not enter at any length here. The difference of opinion is due partly to a lack of exact definition, and partly to faulty reasoning. A knowledge of the subject is advisable if one would understand the subject of bone formation. °Lexer, E.: “ Weitere Untersuchungen iiber Knochenarterien und ihre Bedeutung fiir krankhafte Vorgaenge,” Arch. f. klin. Chir., 1904, lxxiii, 481. GENERAL CONSIDERATIONS 23 If one looks at the periosteum of the shaft of a growing bone, that is, of a bone of a child, one will often distinguish two layers, an outer or fibrous, and an inner or cellular layer. ‘The cells in the latter are probably osteoblasts or bone-forming cells, such as are seen on the margin of all growing bone; such as are seen on the margin of bone 5 Fia. 5.—Low power photomicrograph of normal human bone, showing periosteum and fairly dense bone. The section was taken of the so-called metaphysis, that is in the region where the dense bone is changing to spongy. In this stained slide the bune cells appear as small dots. trabecule in the interior, when they are growing in thick- ness. ‘These cells are described as part of the periosteum, but they really are part of the bone, and have nothing whatever to do with the periosteum proper. In the speci- men from an adult this cellular layer may be present or absent. The periosteum consists of a rather loose-meshed fibrous tissue. Here and there this fibrous tissue may be 24 INFLAMMATION IN BONES AND JOINTS replaced by cartilage, or by fibrocartilage. ‘This is perios- teum none the less, no matter what its structure. Fibres of the periosteum run down into the bone, but, of course, as soon as they enter the bone they cease to be periosteum, and become marrow. With both marrow and periosteum the situation, not the structure, determines the name. The blood vessels of the periosteum send branches into the bone. ‘These run in small canals, and anastomose with the vessels of the marrow. LIGAMEN'ts are composed of dense white fibrous tissue, and serve to bind the bones of an articulation together. Their fibres pass into the articulating bones, but some of the more superficial are continuous with the periosteum. A JoIntT is usually a closed cavity between two or more bones, and is bounded by two tissues, the synovial membrane and the cartilage. CARTILAGE consists of cells and basement substance. The cells have a definite capsule and a characteristic ap- pearance which often helps to identify the tissue under the microscope. ‘The basement substance consists of col- lagen fibrils impregnated with chondromucin. Cartilage contains according to age 3 to 6 per cent. of mineral sub- stances, of which calcium sulphate forms from 48 to 92 per cent. The articular cartilage is of the hyalme type. Its basement substance appears homogeneous in the normal subject, but in certain joint diseases it loses this homogen- eous appearance and takes on a distinct fibrous structure. The fibres run parallel to the surface superficially, but deeper in, at right angles to it. This fibrillar appearance GENERAL CONSIDERATIONS 25 it ‘said to be present also in Joints which have been immobil- ized for any length of time. The joint cartilage in the foetus is covered by a perichon- drium, but in infancy, after function has been established in the joint, the perichon- drium disappears. In certain diseases thereafter the superficial portion of the cartilage may take on the appearance of a peri- chondrium, especially about the margin where it shades into the synovial membrane, but the normal joint cartilagein the adult a : is without perichondrium. g. iis The dense, smooth i ay) VAS nature of the joint carti- lage adapts it admirably for its functions of motion and of weight bearing, and these functions are subserved by the absence from it of blood vessels and of nerves, It is well to remember that in childhood the joint cartilage is simply a portion of the cartilaginous epiphysis. As time goes on the growth of the bone nucleus separates it from the epiphyseal cartilage, until, with the disappear- ance of this, the articular cartilage becomes the sole remnant of the mass of hyaline cartilage of which the whole bone was originally composed. Cartilage may really be viewed as essentially an embryonal tissue doomed eventually to Fic. 6.—Photograph of stained slide from asagittal section of the knee of a normal dog. 26 INFLAMMATION IN BONES AND JOINTS _ ossification. Some of it ossifies early, some of it late. The individual constitution influences the time of ossification, as does the manner of life, and possibly, the occupation. Viewed in this light the stiffening of the joints as age advances, is easily understood. On the other hand some persons have supple joints which work smoothly even at an advanced age. Fibrocartilage is found.in the joints in the shape of interarticular discs or menisci. ‘They serve to lessen shock or to add security. In structure they partake of the nature of the ligament and of hyaline cartilage. In the vertebral joints they add motion and stability. The joints of the vertebral bodies possess no hyaline cartilage, no joint cavity and no synovial membrane. The articular cartilage possesses no blood vessels. No lymph vessels have ever been found in it, though their ex- istence has been assumed by some authorities. Exactly how the cartilage is nourished is not known. It is supposed to draw its nourishment from the marrow beneath, and possibly from the synovial membrane at its margin. Cer- tainly its whole reaction to disease seems to depend upon the condition of these tissues. It is not subject to inflam- mation, nor directly to disease. It simply suffers second- arily from involvement of the synovial membrane and of the marrow. Probably there is no such thing as a primary disease of the articular cartilage nor invasion of it from the joint side; authorities differ on this last point, the majority holding the contrary opinion. The articular cartilage, and the epiphyseal cartilage while it is present, form a barrier to the spread of infection, practically an absolute one. The broad general rule may GENERAL CONSIDERATIONS 27 be laid down that an infectious process can not make its way through a cartilage whose nutrition is intact. Hence infectious processes in the bone marrow, in order to reach the joint, must either travel around the margin of the cartilage, or else first shut off its nutrition from beneath, and then perforate it. If the view is correct, as I believe it is, that the cartilage is immune from invasion from the Fig. 7.—Section of dog’s patella, camera lucida drawing. Joint cartilage below. Note the little pouch at either end of the cartilage, lined with synovial membrane, to allow for motion. Note also the buttress of bone beneath the cartilage, and the absence of any perichondrium. joint side, then any infection, to pass from the joint to the bone marrow must travel around the margin of the cartilage. THE SynoviAL MEMBRANE is a connective tissue structure which bounds the joint in all places except those bounded by the articular cartilage. It covers intra- articular ligaments, and, in certain joints, notably the knee, is prolonged inward in the form of fringes or curtains. It secretes a viscid fluid which lubricates the joint, and normally is just sufficient to serve this purpose and no 28 INFLAMMATION IN BONES AND JOINTS more. ‘The membrane is continuous with that lining cer- tain of the burse in the immediate neighborhood of some joints, so that disease in one readily spreads to the other. There is, of course, no such thing as a hernia of a joint. The normal synovial membrane is smooth and shining, but in the region of its Junction with the cartilage, it is thrown into folds, to accommodate it to the movement of the bones. Here its cells have much the appearance of epithelium. The junction of the cartilage and the synovial mem- brane is not abrupt, but the two tissues shade gradually into each other, so that it is not possible to say exactly where one stops and the other begins. When a joint is immobilized for any reason, the synovial membrane encroaches upon the cartilage at its periphery, replaces it, so to speak, and extends especially over its surface. When motion is restored, provided the joint has not been damaged by disease, the cartilage extends again at its periphery, and regains its former limits.* This is probably the cause of the stiffness of joints after immobilization. It is doubtful if any adhesions, properly speaking, are ever caused in a normal joint by mmobilization. The reaction of the synovial membrane to injury or to disease is very interesting. If it be irritated it pours out a °Narnan, P. W.: “ The joint cartilage in its relation to joint pathology.” Am. J. of Orth. Surg. 1909-10, vii, 85. Brann, Hernricu: “ Untersuchungen iieber Binder Synovialmembranen und Gelenkknorpel.” Deut Zeit. f. Chir., 1894, xxxix, 35. Revser, Cart: “On the cartilages and synovial membranes of the joints,” Jour. Anat. and Physiol. 1874, viii, 261. Hammar, J. Aua.: “ Ueber den feineren Bau der Gelenke.” Archiv. f. Mik. Anat., 1894, xliii, 266, 813. GENERAL CONSIDERATIONS 29 secretion whose nature depends, of course, upon the irri- tant. ‘The mere presence of this fluid probably causes thickening and inflammation of the membrane. It is thrown into folds, and takes on a villous structure. These villi may attain great size and number, giving to the inner sur- face of the joint a marked shaggy appearance. No stomata ever have been demonstrated in the mem- Deane, and the method of the subse- quent exit of the fluid from the joint is not known. Strange to say, fluid does not accumulate in the joints in cases of edema of the extremities. Any infection of the synovial mem- brane causes the thickening and villous condition, and #'*.,8-—Low, power photomicrograph, showing typical appearance of the synovial membrane in an acute inflam- mation. This is from a case of probable syphilitic arthritis the characteristics of wrongly diagnosed as tuberculosis and infected at oper- Sr, : ation. Synovial membrane above. Ligament below. certain infections are beautifully shown in the membrane, as they are in the bone marrow. The opinion formerly prevailed that the synovial mem- brane was a closed sac extending out over the cartilage, but this is not a fact. It is a section of a tube, ending at the border of the joint cartilage, with which, as has been said, it is continuous. In the embryo, however, and for a 30 INFLAMMATION IN BONES AND JOINTS while after birth, the synovial membrane is continuous with the perichondrium. In all joint inflammations the synovial membrane is to be regarded as the active tissue, the cartilage as the passive. It follows that the terms synovitis and arthritis are synonymous. With an arthritis, the adjacent bone marrow may or may not be involved; that is,-an osteomyelitis may or may not be associated with the arthritis. We recognize, then, in inflammations of bones and joints, only two active tissues; the bone marrow and the synovial membrane. ‘The ligament, the cartilage, the bone tissue itself, and probably the fibrous periosteum all play a purely passive role. We are wont to use the term “ periostitis ” quite frequently, but the real inflammation in such a case is usually in the bone marrow in the imme- diate vicinity. Broadly speaking the marrow and the synovial mem- brane are vulnerable to the same infectious agents. Any bacteria which invade one can invade the other. However, certain infections show a preference for the marrow, cer- tain for the synovial membrane, while certain others affect both tissues without preference. A knowledge of this fact helps us in our diagnosis... Thus treponema_ pallidwm belongs in the first class, the gonococcus in the second, and the tubercle bacillus in the third. We note also that while some infections always start in the lymphoid marrow, and practically always remain there, others start in either the lymphoid or the fatty marrow, with about equal frequency. The lymphoid marrow in the ends of the long bones seems to be the great chemical lab- oratory in which most infections germinate; that in the GENERAL CONSIDERATIONS 31 short bones to a lesser degree. We shall see how they may never travel beyond the limits of this tissue in certain instances. Indeed, as in the lungs, only the necropsy may reveal that they have ever been present at all. In most cases, however, they show a tendency to spread. The direction in which the various infections spread is also a matter of interest, and often an aid in diagnosis. Tuberculosis always travels toward the joint if it travels at all. Pus infections usually travel toward the shaft, less often towards the joint, but streptococcic infections show the contrary tendency, and travel toward the joint. Fundamentally the pathological characteristics of all bacterial bone and joint infections are the same, as are the characteristics of flowers or of trees. We distinguish among them by their minor traits. One great difference exists between the botanist’s task and ours. He has his object exposed to his-senses, while ours is covered by the skin and subcutaneous tissues. Not until we have a culture of the offending organism are we sure of its identity, but the more carefully we study its habits, its life history, so to speak, and its effects. the more often shall we be able to recognize it well enough for all practical purposes, and to institute our measures of cure, without waiting for a posi- tive identification. On the other hand, remembering the impossibility of reaching a positive conclusion without the aid of the microscope, we do not overestimate our diagnos- tic ability, and consequently do not so often make humili- ating mistakes. 32 INFLAMMATION IN BONES AND JOINTS THE FORMATION OF BONE, * ®: 9, 10, 11, 12, 18 The phenomena of bone production have been known for a long time, but the identity of the active agents of the process, and their exact role, are still a subject of discussion. Until comparatively recently the “ metablastic ” theory of bone formation prevailed. According to this the various members of the connective tissue group possessed the power in certain circumstances of changing to one another. This theory is at present not widely held. It has generally been displaced by the “ neoblastic ” theory, which predi- cates the existence of a definite bone-forming cell, r, “* osteoblast.” ‘The exact identity of the osteoblast is not known. It is described as a small, round or polyhedral cell, with sharply staining nucleus, usually seen on the borders of the trabecule or on the outside of the cortex, but without characteristics clearly enough defined to permit its identi- fication away from its accustomed habitat. We see these cells in great numbers on the outside of young growing bone, and on the edge of the trabecule when we believe that bone is being built up, and we are wont to conclude, there- 7 Arey, L.: “The Origin, Growth and Fate of Osteoblasts,” Amer. J. of Anatomy, 1920, xxvi, 315. * Topp, T. W.: “ Development and Growth of Bone,” Journal of Anatomy and Physiology, 1912-1918, xlvii, 177. * Buscn: “ Die Osteoblastheorie auf normalen und pathologischen Gebiete,” Deutsche Zeitschrift fiir Chirurgie, 1878, x, 59. ” BirrotH: “Anatomische Beobachtungungen iiber das normale Knochen- wachsthum,” Archiv fiir klinische Chirurgie, 1864, vi, 712; ‘“ Ueber Knochen- resorption,” Archiv fiir klinische Chirurgie, 1862, ii, 118. ™ Meyer, Arruur: “Side Lights on Multiple Myeloma.” American Journal of Medical Sciences, 1918, clvi, 329. 2 Eiy, Leonarp W.: “The Formation of Bone,’ Ann. of Surg., 1919, Ixix, 225. * Leser, Epmunp: “ Ueber die histologischen Vorgaenge auf der Ossifi- cations Grenze,” Archiv f. klinische Chir., 188, xxxvii, 511. be. GENERAL CONSIDERATIONS 33 fore, when we see these small cells in this situation that bone formation is going forward. This is not always true. The borders of the trabecule often present the same appear- ance when we know quite well that the bone is being torn down. This has led some observers to the conclusion that #. Fig. 9.—Low power photomicrograph from a case of marrow tuberculosis. The bone is being torn down, not built up, but the edges of the trabecule are covered with cells corresponding to the ordinary description of osteoblasts, Note the interval between these cells and the trabecula. the same cell which builds bone up, can also tear it down, that is, that the osteoblast is the same as the osteoclast. In this view I am inclined to concur. I have in my possession stained slides of marrow of tuberculosis and of acute osteomyelitis, m which all the evidence points to bone absorption, but in which cells with the typical appearance 3 34 INFLAMMATION IN BONES AND JOINTS _of osteoblasts are seen in great numbers on the borders of the trabecule. | The prevailing view is that the osteoclast is a large cell —a giant cell—seen usually in an excavation on the border of the trabecula (Howship’s lacuna) or at a short distance. from it. Some observers believe that this giant cell is the eT ee Fic, 10.—High power photomicrograph of a portion of the preceding slide. result of the bone absorption, and not its cause. Bone probably can be absorbed without the agency of any special cell, by simple absorption of its lime salts—* halisteresis.” Whence comes the osteoclast, if there be such a cell, is not known. The origin of the osteoblast is still unsettled. Geddes ** says it wanders in from the epiblast, but it is generally considered a mesoblastic cell. Some say that it * Geppes, A. C.: “Origin of the Osteoblast and Osteoclast,” Journal of Anatomy and Physiology, 1912, xlvii, 159. GENERAL CONSIDERATIONS 35 is brought by the blood stream, but Moschcowitz '° says that it is simply a mesothelial cell arising in the process of angiogenesis. He says that the endothelial cell in the vessel wall, the osteoblast, the osteoclast and the bone cell are all fundamentally the same, with the same potentialities. Fie. 11.—Low power photomicrograph from a case of acute suppurative arthritis. T, tra- becula, M, marrow. Most of the trabecula is dead, but its upper left, and its lower right hand border show signs of a deposit of new bone. The bone cells here stain. The marrow is the seat of an intense inflammation. At R appears what is known as rarefying osteitis. What function they eventually possess simply depends upon their surroundings. Stained slides from specimens of fractures or resec- tions, or from the inside of the cortex of growing bone, where nature is rearranging the architecture of the bone, show the classical giant cell osteoclast in great numbers. When, *® Moscucowitz, Eri: “The Relation of Angiogenesis to Ossification,” Johns Hopkins Hospital Bulletin, 1916, xxvii, 71. 36 INFLAMMATION IN BONES AND JOINTS however, the bone is being absorbed as the result of an infectious process in the marrow, or after being buried experimentally in the soft tissues, these giant cell osteo- clasts are few in number or are absent altogether. If the neoblastic theory is correct, as we shall assume » that it is, then three things are necessary for bone forma- tion, and these are: first, the active agent, the builder; second, the building material; and third, the stimulus. Ollier,"® in 1867, first described a “ cambium ” layer of the periosteum and ascribed to it a bone forming function. The question was debated for years, until finally the periosteum came to be regarded as the great active agent in bone formation. In 1912 MacKwen ™ denied this func- tion, and affirmed that the periosteum was simply a limiting membrane and that the marrow formed bone. The question is still being debated, and much experimental and clinical evidence has been adduced on both sides.** Without gong into the details of the controversy, let us assemble the known facts concerning bone formation, and see if we can- not reach a satisfactory conclusion and one that will be of practical service. Manifestly we cannot throw out the evidence submitted by reliable observers, and yet we cannot accept conclusions diametrically opposed. The chief diffi- culty disappears when we remember that neither the periosteum nor the marrow forms bone, but the osteoblast. * Ortrer: “Le Régénération des Os,” 1867, v, Masson et fils, Paris. ™ Mac Ewen, Wirxuiam: “ Growth of Bone, The,” 1912, Maclehose and Sons, Glasgow. The Macmillian Co., New York. 1912. * Hass, S. L.: “ Regeneration of bone from periosteum,” Surg. Gyn. and Obst., 1918, xvii, 174. Joxor: “ Experimentelle Beitrag zur Knochenneubildung durch Injections bez. Implantation von Periostemulsion,” Deutsche Zeitschrift fiir Chirurgie, 1912, exviii, 433. GENERAL CONSIDERATIONS 37 The following statements will hardly meet with opposition: 1. Intracartilaginous bone formation begins with the pushing of blood vessels into the cylinder of cartilage in a long bone. Around these blood vessels calcification and ossification take place. A similar process takes place later Fic. 12.—The blood vessel has pushed _ its. way into the epiphyseal cartilage, and has initiate bone formation in the centre of ossification. Low power photomicrograph from the knee joint of a foetus at term. New bonein upper left hand corner. in the epiphysis. This is bone formation without marrow or periosteum. 2. Bone is formed in the walls of the aorta, and in the kidneys of laboratory animals whose renal vessels have been tied off." Again bone formation without marrow or periosteum. 3. Bone is formed from cartilage or from fibrous Tex: “Zur Frage der heteroplastischen Knochenbildung,”’ Archiv fiir klinische Chirurgie, 1906, Ixxx, 278. 38 INFLAMMATION IN BONES AND JOINTS tissue, in the marrow of adult bones, without the aid of the periosteum. 4. Bone is formed in fibrous tissue—intramembranous bone formation—before any marrow is present. Fie. 13.—Low power photomicrograph of early stage of intracartilaginous bone formation. Blood vessels pushing their way into the cartilage. 5. Bone is formed on the outside of the cortex, beneath the periosteum, again bone formation without marrow. 6. New bone is sometimes formed in necrotic or hyaline tissue, ¢.g., lymph nodes, tuberculous foci, corpora albi- cantia, thickened pleure, etc., etc. 7. Buried bone contacted with other bone and enjoying a functional use, persists and is renewed. Bone buried in the soft tissues, without function, slowly disappears. GENERAL CONSIDERATIONS 39 8. Bone is never formed except in the presence of blood vessels. ‘he entrance of blood vessels into a tissue to be ossified is the first step in the process. If we sum up our facts we find that three things are necessary for bone formation: 1. Blood vessels—the builder. 2. Kither (a) a loose meshed fibrous tissue, or (b) a homogeneous (cartilaginous matrix), or a granular or a necrotic material—the building material. 3. A stimulus, physiological or pathological as the case may be. It is this stimulus which causes the blood vessels to push into the cylinder of cartilage in the first place, and which causes the bone production in the aorta, for instance. We recognize function as a stimulus, and the mere presence of bone as another. It is therefore seen that neither periosteum nor marrow is essential for bone production, and that neither of them forms bone, in the proper meaning of the word. In each tissue we simply conclude that the conditions are suitable for bone production. The materials are there, and given the stimulus, physiological or pathological, bone will be manufactured out of the fibrous or cartilaginous tissue in the periosteum or marrow. ‘The true marrow cells, the characteristic marrow cells, the cells which give the marrow its stamp and its function, probably have no role whatever in bone building. We observe other phenomena in the formation of bone, which are of use to us in our clinical work: Cavities in bone are filled up to the old level, in the absence of infection. Normally the new bone will not go beyond the old level. The shape of the cavity does not materially influence this process. In the presence of a pus infection the shape of the cavity does influence it. 40 INFLAMMATION IN BONES AND JOINTS In such a case steep walled cavities will not fill in. The walls must be beveled off before healing will take place. It is doubtful if nature ever fills up with new bone the cavities in bone caused by certain old closed chronic infec- tions. Old cheesy tuberculous foci may persist for years. They may show calcification but not ossification. They do — not become vascularized. Old bone cysts may persist indefinitely. On the other hand, bone destroyed by a syph- ilitic process, can probably be restored by nature without artificial aid. The examination of old specimens of buried bone teaches us that sterile dead bone, under the stimulus of function, is replaced by nature. She employs the old bone asa seaffold. The details of this will be set forth under the head of bone transplantation. Bone cannot grow out any distance from its own level, unless it have a bridge or scaffold on which to grow. If the head of the femur be cut off, a new head will not grow on the neck. If the shaft of the tibia be removed for the cure of a suppurative osteomyelitis, new bone grows out for a very short distance from the pieces of bone left behind, and then stops. Nature perhaps uses the perios- teum as a scaffold and builds bone along it to connect up the fragments. It may be laid down as a general rule that in bone, as in other tissues, a mild irritation, especially an intermittent one, causes an hypertrophy, a severe one, an atrophy. If the irritation be very severe, the bone dies—necrosis. Whatever the ultimate cause of the process may be, the immediate cause of the hypertrophy, the atrophy or the necrosis 1s to be sought, in the interior of the bone in the vessels of the bone marrow, at the surface in the vessels of the periosteum, and of the superficial cortical marrow. GENERAL CONSIDERATIONS 41 HA. IsterEsis.—Iormerly the view was widely held that bone could be removed by the action of some ferment which first dissolved the lime salts without the medium of any special bone destroying cell, any osteoclast. One sees this view seldom now-a-days in American text-books, but there is much evidence to support it, and J believe it is true, in many instances, possibly in all.”? In sections from malig- nant growths in bone, this halisteresis is often evident. The dense bone of the shaft has less marrow and fewer blood vessels than has the spongy bone, and therefore we should expect to see it in less activity both in destruction and repair, than in the spongy bone or in the central marrow canal. In point of fact all the activity in the process of repair after a fracture, is observed at the surface of the cortex, as will appear hereafter. THE HEALING OF FRACTURES If a hole be bored through the cortex, new bone is not built straight across the gap, but bone trabecule, springing from the inner aspect of the cortex, form in the marrow of the central canal. These slowly increase in number and in thickness until they plug up the hole and extend up into it. This is the so-called “ internal callus.” 'To a lesser extent the same process takes place on the outside of the cortex. Bone trabecule spring from the exterior surface of the cortex, bridge the gap on the outside, extend down into the gap, and meet those coming up from the marrow. The resulting callus is beautifully lkened by Nichols,*’ of 2” KAUFMANN, Epwarp: “Lehrbuch der speziellen pathologischen Anatomie,” Berlin, G. Reimer, 1917. 1'The late Docror Epwarp Hatt Nicuotrs had a most remarkable series of slides showing this process, and to him I am indebted for my knowledge of it. In his death the medical profession suffered an irreparable loss. 42 INFLAMMATION IN BONES AND JOINTS Boston, to a collar button, which it strongly resembles in its shape. It is probable that, after a fracture, if the fragments could be brought into accurate apposition and could be held in absolute immobility, this same collar button would form, with a small head and base, and with an infinitely slender | shank. In practice, however, this is not what we find. The continuity of the marrow is broken as well as that of the cortex. Nature seems to find great difficulty in building bone across the smallest gap, unless she have a scaffold or bridge on which to build it. She builds this bridge in the following manner: — Immediately after a fracture hemorrhage takes place into the marrow canal and on the outside of the cortex beneath the periosteum, which has already been stripped from the cortex by the fracture to a greater or less extent. The hemorrhagic exudate on the outside of the cortex is replaced by granulation tissue, and this in turn by fibrous tissue and cartilage. As time goes on then the cartilage is ossified by penetration of blood vessels. The greatest activ- ity in this process is seen to be manifested on the external aspect of the cortex, and especially in the angle between the cortex and the periosteum. I have watched this process taking place in three series of experimental fractures on cats, and in no instance have I been able to detect any evi- dence that the periosteum takes an active part in it. The sole function of the periosteum is to hold the soft callus firmly against the bone until cartilage has formed in it. This external callus is the chief means of joining the two bones together and may be compared to the “ wiped joint ” with which the plumber solders together two pipes. It holds the bone ends absolutely immobile until the union is complete, and until the external surface of the cortex of GENERAL CONSIDERATIONS 43 one fragment is firmly united to that of the other. It prob- ably takes about a year for the fractured fragments to be united directly, and for the normal bone architecture to be restored. ‘Then, if the apposition have been absolutely exact, the callus presumably is removed entirely. The apposition probably never is absolutely exact; hence some Fic. 14.—Low power photomicrograph from a stained slide taken from a section of the out- side of the cortex of the tibia of a dog. The knee joint in the immediate vicinity had been resected fourteen days previously. Note the new trabecule, T, T, T, T, forming on the outside of the cortex under the periosteum, of the callus always remains, and betrays the site of the fracture. The formation of this external callus may be seen in laboratory animals, and its development may be watched also with the Rontgen rays. The bone fragments are seen to be united by a firm bony bridge long before there is any evidence of union between the ends of the cortices. This 44 INFLAMMATION IN BONES AND JOINTS direct cortical union probably does not take place for about a year. The so-called internal callus, so prominent when a hole is bored in the cortex of a laboratory animal, plays an insig- nificant role in the healing of an actual fracture. In my | experimental fractures it was usually rudimentary, and never bridged any gap be- tween the two fragments. It certainly does not show in the X-ray plate. The bridge of bone from the external sur- face of the cortex of one fragment to that of the other seems to be the essential feat- ure of the union. Where for any reason it does not form non-union is wont to result. Nature seems to inaugu- rate two distinct and opposite processes after a fracture. Fic. 15.——Photograph of a stained slide from With one hand she starts to a sagittal section of the knee of a dog. Knead been erected seventeen devs pre: build a bony bridge under the panes periosteum and in the mar- row, as described, with the other she tries to construct a joint. If one looks through the microscope at the ends of the bones of a laboratory animal some days after the production of a simple fracture, one sees that they are separated rather than joined by fibrous tissue which streams out from the marrow canal to the periosteum. The same thing is seen after experimental resection of GENERAL CONSIDERATIONS 45 the dog’s knee joint.*? If non-union result, this fibrous tissue becomes greatly thickened, and increases in amount. Some of it runs across from side to side, some of it between the marrow and the periosteum. Cartilage cells often appear in it, and almost invariably clefts, which may or may not be lined with a syno- vial membrane. Eventually a new joint is established at | the site of the resection, a new joint which bears a striking resemblance to that seen at the site of an old un- united fracture. In the great majority of these experimental resec- tions a new joint is formed. Bony ankylosis is extremely hard to secure. The exact | reverse prevails after sim- ple fractures in laboratory animals. Bony ankylosis is > almost invariable, but bony : : 5 Fic. 16.—Photograph of stained slide from mio is very rare if the sagittal section of knee of dog, resected 374 days previously. Small pieces of bone had periosteum be divided circu- penser. erofibig: Rosas usion with larly. If the periosteum be ™*¥ *™#l! clefts in the fibrous tissue, simply slit before the bone is fractured, union may or may not take place. | Non-union is very rarely seen in the child, in whom new bone formation under the periosteum is very active. It is said to occur often in certain constitutional diseases, notably syphilis. A favorite site of bone syphilis is immediately under the periosteum. Impacted fractures almost invari- Se a Rene j cnet & re . vik ¥ 6 , eee *“Exy, Leonarn W.: “Experimental resection of the dog’s knee joint,” Annals of Surgery, 1919, Ixx, 586. 46 INFLAMMATION IN BONES AND JOINTS ably unite firmly if they are left alone. Non-union is notoriously frequent in portions of bone not provided with periosteum, such as the carpal bones and the head of the femur and the head of the radius. Lack of contact between the fragments tends to prevent union, as does the inter- . position of soft tissue. Weighing all the evidence, clinical and experimental, we reach the following conclusions: If the two fragments of a fractured bone not cov- ered by periosteum can be brought into exact apposi-. tion, and can be held firmly together without motion, they will unite directly after a long time. If they be not held close together, or if any motion take place, a new joint probably will be formed. The role of the perios- | _, teum in the healing of frac- Fig. 17.—Photograph of stained slide of sagittal Lures as to hold@sthemeurg section of knee of dog, resected twenty-seven d ly. Small fb h beén removed ‘The end of te femur had been sawn callus against the outside inbepeemnetninanerveietadarancrmeryOlk Tie (eemnens, MN ie ee are tightly united by fibrous tissue, . . periosteum is absent or divided, non-union is wont to occur. Various other reasons have been advanced for the occurrence of non-union, notably deficient blood supply and alcoholism. The opinion is quite widespread that fractures fail to GENERAL CONSIDERATIONS 47 unite much more frequently than formerly, and for this the Rontgen rays have been held responsible. ‘The work of Albee and Morrison ** tends to disprove this. They found that exposure to the Rontgen rays did not retard the process of union after experimental fracture of rabbit’s Fic. 18.—Photograph of a stained slide from a sagittal section of the knee of a dog, resected 150 days previously. Note the absence of bony union. The union is fibrous and in the fibrous union are large clefts. bones. On the other hand, non-union is extremely rare in animals under any conditions. I have seen it only once in a simple fracture, but have produced it in two out of four open operations on cats, in which I divided the periosteum completely, and fractured the humerus. In another series of simple fractures, union was almost invariable, if the *® ALBEE AND Morrison: “ Studies in bone growth: an experimental attempt to produce pseudarthrosis,” Amer. Jour. Med. Sciences, 1920, clix, 40. 48 INFLAMMATION IN BONES AND JOINTS animals were permitted to live long enough for the ordi- nary fracture to unite.” Besides the changes at the site of a false joint set forth above, there are others even more important from a clinical standpoint. If the bone ends are exposed to pressure, as in the tibia after a simple fracture, new bone often is Jaid down at their periphery, so that they become broad- ened, like the ordinary ept- physis of a long bone. All the elements of a permanent joint are then present, in- cluding fibrocartilage over the bone ends, and a synovial membrane. ‘The fibrous tis- sue between the two bones 1s dense and is incapable of conversion into bone. It sep- arates the two marrow . canals. It replaces the peri- Fra. 19.—Photograph of a stained slide froma OSteum. Frequently also one saggittal section of the knee of a dog. The knee had been resected 790 days previously. oy both marrow canals are Moderately large pieces had been removed eee ortise feekina” ‘Note thet the herac ee Shut Off by alayvetea aeons separated by a band of fibrous tissue, in which . . iia lar cerclens from this fibrous tissue. Without artificial assistance no union is possible. In other instances, especially after compound fracture, more or less absorption of the bone ends takes place. They become conical, very dense and hard, “ eburnated,” and “Three series of operations were done. In the first the fracture was a simple one, by direct violence: In the second, the periosteum was slit long- itudinally, and the bone was divided with Liston forceps: In the third, every effort was made to sever the periosteum in continuity, before the bone was divided. Archives of Surgery, 1922, v. 527. GENERAL CONSIDERATIONS AQ contain little soft tissue except a few blood vessels. Their ends are bound together with dense fibrous tissue. ‘Two bones whose ends are eburnated will never unite, as wit- ness the great second type of chronic arthritis. For the treatment of non-union, or pseudarthrosis, many expedients have been recommended. Among these may be mentioned massage, tapping the fragments with a hammer, setons, counter-irri- tation, weight bearing, rub- bing the ends of the bones together, perforating them with a drill, wiring, plating and doweling. The last four | expedients are still employed. The bone dowel has many advocates, and doubtless will continue to be employed in special cases, but otherwise the inlay bone graft bids fair to displace other means of treatment in the ordinary case of ununited fracture. It Fig. 20.—Photograph, of stained slide from possesses the one great ad- Gi previously, Large pieces of bone had vantage that it is a nor- been removed. Bony union, mal tissue in its physiological place. The dowel is inserted into the marrow canal, where it does not belong, displaces its volume of marrow tissue, and probably must be eventually absorbed. BONE TRANSPLANTATION The subject of bone transplantation is an interesting one, and has attracted much attention. The discussion, 4 50 INFLAMMATION IN BONES AND JOINTS at first more or less academic, recently with the develop- ment of the operative treatment of fresh fractures and of ununited fractures, has attained a very real and practical importance. Difference of opinion. as to details still exists, and if one would employ the treatment intelli- gently, one would do well to possess oneself of a knowledge of the general principles governing its use. Two things are well settled and we shall mention them before proceeding with the discussion: 1, Live bone from another animal, or from another person, should never be used. It will practically always result in fail- ure; 2, in) thesnres. ence of suppuration, the transplant will al- most always, if not in- variably, be cast out. Fic. 21.—Stained slide of section of piece of condyle of femur buried fresh in the thigh muscles of the animal from If f whom it had just been removed; 922 days after burying. a p 1e€ce oO The fragment had not decreased greatly in size. Most of the bone is alive, some of it is dead. The trabecule are b one be removed, spear ine geat and be immediately buried again, in the same animal with aseptic precautions the bone dies.?> Whether it dies immediately after removal, *>Cowan anv Exy: “A Study of Buried Bone,” Journal of Orthopaedic Surgery, 1919, i, 109. Exy, Leonarp W.: “Experimental study of Buried Bone,” Annals of Surgery, 1919, Ixx, 747. ered after 1103 days. GENERAL CONSIDERATIONS Fig. 22.—Stained slide of section of piece of head of tibia buried fresh in the thigh muscles of the animal from whom it was taken, and recovered 473 days later. The fragment had decreased decidedly in size, and is well incap- sulated. The bone tissue is small in amount, the trabecule are scant, the cortex is thin and in places is wanting. Most of the bone is dead, but many of the trabecule show live bone cells, especially near their margin— ‘border appo- sition.’ The marrow is about one-half fibrous and one-half fatty, 51 Fig. 23.—Photograph of stained slide of sec- tion of a piece of the condyle buried im- mediately in the thigh muscles of the animal — from which it had just been removed, and recovered after 374 days. It had decreased in size. Most of the bone is dead, but many of the trabecule show life at their edges and there are a few trabecule under the cartilage, lying in the midst of dead bone, whose base- ment substance stains sharply in contrast to that of the dead bone, and whose cells also stain. Fie. 24.—Photograph of a stained slide of a cross section of a fragment of the femoral condyle, buried fresh in the thigh muscles of the animal from which it had just been removed, and recov- The fragment had decreased markedly in size. It was a mere shell and cut easily with the knife. Even the shell had been partially replaced by fibrous tissue. The bone trabecule are very few and small—mere fragments—but they are all alive. 52 INFLAMMATION IN BONES AND JOINTS or whether it lives for a short time is not settled, but that it can live long enough for the blood vessels which are necessary for its nourishment to push their way into it, is so improbable, that we are justified in concluding the death of the graft to be invariable, until positive proof to the contrary shall be adduced. All the experimental evidence points in this direction. ‘Those who have examined _ buried bone are practically unani- mous on this point. The evi- dence on the other side is clinical. From the moment of im- bedding of such a piece of bone two distinct processes arise, one of absorption and one of rebuilding, and, accord- ing to circumstances, one of these processes will exceed the other. If the bone have been Fic. 25.—Cross section of piece of condyle of femur, boiled before being buried in the thigh muscles of the animal from which it was taken and recovered after 1&0 days. The fragment had decreased greatly in size and is incapsulated by fibrous tissue. No bone cortex is present except for a_ short distance. The marrow spaces are bounded by the connective tissue capsule. The tra- becule are about the normal number and size, but most of them are dead. A few placed in the soft tissues, where it has no function, although at all times evidences of new bone formation may be however show live bone at their margins. seen on the edges of the trabeculae, it will slowly decrease in size and become rarefied, and finally will disappear. It may even last for several years, but its fate is always the same. On the other hand, if the bone be buried in bone, where it will have function, it will persist indefinitely. The same processes are set up in this as in the other, but the process of repair outweighs that of absorption. Even after GENERAL CONSIDERATIONS 53 years, areas of dead bone are still visible in it.*° Nicety of technique will influence the outcome. ‘The bone must be held firmly in contact with the receiving bone, and immovy- able, or it will share the fate of the graft in the soft tissues. If boiled bone be employed for the transplant the same thing occurs except that its absorption will be more rapid, and hence, when employed as a graft between two bones, it is not quite so likely to be replaced and rebuilt as is live bone. Barth®* years ago, basing his opinion on experimental research, declared that, as all transplanted bone died and served only as a scaffold for new bone, the employment of live or of boiled bone was a matter of indifference. Clini- cal experience caused him to modify his opinion, and it has caused others to modify theirs. Whether a bone grafted in contact with another bone persists, seems to depend upon the rapidity with which it is vascularized. If a piece of bone with periosteum be examined seven- teen days after it has been buried alive, its bone and marrow are seen to be dead. The marrow is without blood vessels. At the periphery, however, where the fragment is coucred by periosteum, blood vessels are seen pushing their way into the bone, and evidences of bone production are secn on the edge of the trabeculae. 'This explains the superiority of the living graft to the boiled one; the soft tissues at the surface probably live, are quickly vascular- ized, and thus hasten the vascularization of the graft. The above question has a double interest, as bearing on the employment of a graft covered with periosteum. The periosteum acts not only as soft tissue for vasculariza- * Exy, Leonarp W.: “ Ankylosing operations on the Tuberculous Spine; An Examination of two Specimens in the Laboratory, “Journal of the American Medical Assn., 1917, Ixviii, 183. * Bartru: Archiv. fiir klinische Chirurgie, 1893, xlvi, 409: 1894, xlviii, 466. 54 INFLAMMATION IN BONES AND JOINTS tion, but possibly also as a matrix for the production of new bone. Albee, who has done much to popularize the use of the inlay bone graft and to perfect the technique of its insertion, insists that it should be composed of spongy and | i j . ates | Fig. 26.—Section of condyle of femur of dog, removed at knee-joint resection, and buried immediately in his muscle; removed seventeen days later. Photograph of stained slide, about ten diameters. The bone and marrow are dead, the bone lacune are empty. Over the inked square the bone is provided with periosteum. Joint cartilage on the right. dense bone, and should be covered by periosteum, and that like tissue should be applied to like. Other rules also should be observed. In old ununited fractures the conditions should be made as much like those of a fresh fracture as possible. If the ends of the two frag- ments are sclerosed—eburnated—they must be removed, wF GENERAL CONSIDERATIONS 55 and the marrow canals beyond must be opened. Healthy bone should be employed for the graft. Its new bed should be prepared before it is removed, and after its removal it should be inserted as quickly as possible, without unneces- sary handling, and under strict aseptic precautions. The motor saw should be kept cool to prevent killing the graft ind bor Rk Fic. 27.—This low power photomicrograph, taken of the bone in the inked square in the preceding illustration shows well how all activity in bone formation in the dead buried frag- ment is carried on through the medium of the imbedding tissues. A blood vessel, B, is push- ing its way from the periosteum into the dead bone, and is starting up the formation of new bone. New bone trabecule, T, T, are forming on the surface of the fragment where it is covered by periosteum, and right close tea surface, where blood can reach them, the bone cells stain. by heat. A motor saw makes the operation much easier, but the graft may be removed with hammer and chisel. The graft must be fitted accurately in place and must be firmly secured there. Subsequent immobilization must be furnished by a splint. In old ununited fractures we shall have no assist- 56 INFLAMMATION IN BONES AND JOINTS ance from a splint laid down under the periosteum; hence, until enough new bone has been laid down across the gap to stand all ordinary strain, external splints must be provided to prevent refracture. In fresh grafted fractures, splints will be found necessary for a longer time than in simple fractures which have not been operated upon, but in old ~ ununited fractures the time is much longer, running up to three or four monthsmape more, and depending upon the expected strain. For example, after operation for ununited fracture of the neck of the femur, appara- tus should be worn for at ; | least eight or ten months. A piece of the antero- A medial cortex of the tibia, less often its crest, or a piece of split rib, is usually chosen for the graft. Sometimes, Fra. 28.—This shows how the large trag- Specially with fracture of reuntval of the pall one, and how theaman the tibia, a sliding sore tare one is used to fill in the gap left proximal to ; the large one. used. A small piece of bone is removed on one side of the fracture, and a large piece on the other. The large piece is then simply slid across the gap and the small piece is employed to fill the space left at its far end. This procedure obviates the necessity of two wounds and is quite feasible, provided that the bone tissue of the graft in the vicinity of the fracture is normal in structure. , To avoid the possibility of fracture of the bone from which the graft was taken, this bone also must be splinted for some time after the operation. Removal of the crest GENERAL CONSIDERATIONS 57 of the tibia weakens the bone much more than does removal of a piece of the anteromedial cortex. A twin saw or a single saw may be employed. In operating on the upper extremity reliable assistants ean hold the limb after the insertion of the graft. In fracture of the femur a special fracture table is almost indispensable, so that the splint may be appled without disturbing the graft. Success depends largely upon attention to details. With a fresh fracture one carries the incision down to the bone, incises the periosteum longitudinally, strips 1t back enough to permit approximation of the fragments, and saws out a gutter in the cortex. In old compound fractures the stripping back of the periosteum will occasion more difficulty. It is not necessary to remove all the scar tissue in these cases, but the ends of the bones must be bared, so that the scar tissue no longer lies between them. Both marrow canals must be opened, so that the blood vessels in each can make their way into the graft. Some operators emphasize the importance of stitching the periosteum of the graft to that of the receiving bone. Others do not find this necessary. The great advantage of the dowel in fresh fractures is its function as a splint, when it is properly fashioned, but its greatest availability is in old fractures of the femoral neck. In old fractures of the shafts of bones the inlay graft is much to be preferred. With an old infected compound fracture it is advisable before operating to allow an interval of two or three months after all suppuration shall have ceased. With war wounds the injection of antitetanic serum should precede the operation. 58 INFLAMMATION IN BONES AND JOINTS Fic. 29.—Low power photomicrograph of stained slide from a tibial graft used in an Albee spine operation two years before death from intercurrent disease. The graft was united firmly to the vertebral spines. Note the different staining reactions of the live and dead bone, the empty lacune, and the blood vessels pushing in from the surrounding soft tissue. As far as possible the employment of all non-absorb- able substances, such as metal nails, screws, or wire, should be avoided. Other materials have been employed as substitutes for bone in these operations, notably, ivory and the somewhat GENERAL CONSIDERATIONS 59 cheaper walrus tooth.* They are not as satisfactory as bone. Besides its employment in the treatment of fractures, the bone graft has many uses, notably in the treatment of diseased and flail joints to produce ankylosis, and in the Fic. 30.—Low power photomicrograph of a pseudarthrosis between a bone graft and the bone into which it is doweled. The graft is received into a cup-shaped cavity lined by fibrous tissue. At the surface of the fibrous tissue is a tissue, provided with villi, not to be distinguished from a synovial membrane. The bone of the dowel, as well as that of the receiving cup, is dead. Albee operation for tuberculosis of the spine. It has been recommended also for a variety of other conditions, and enthusiasts predict its wide availability in the future. When bone covered with cartilage is buried in the soft tissues, the cartilage persists in good condition long after ** KoeniG, Frirz: “ Ueber die Implantation von Elfenbein zum Ersatz von Knochen-und Gelenkenden,” Beitraege zur klinischen Chirurgie,’ 1913, Ixxxv, 19. 60 INFLAMMATION IN BONES AND JOINTS the bone has died. It seems to derive sufficient nourishment from the surrounding tissue and does not suffer from being cut off from a direct blood supply. Considerable work has been done experimentally in the transplantation of carti- lage, but ne practical results ever have been obtained in grafting it where its presence is of real importance, on the joint surface of the end of the bone. Reports of the transplantation of joints have been made.” ‘The results of one case were so good for a while that great hopes of the operation were raised, but the hopes were not fulfilled, and joint transplantation has given place to other measures. ANKYLOSIS The word ankylosis, or anchylosis, is derived from the Greek agkulos, crooked, but the meaning of the term as generally employed, is stiffness or loss of motion in the joint. Asarule we do not employ it to describe the stiffness * (a) Renn, Epwarp: “ Regeneraton des Knochenmarks. . . bei Gel- enktransplantation,” von Langenbeck’s Archiv., 1921, xevii, Heft 1.557. (b) “Epiphysentransplantation.” Miinchner medicinische Wochenschrift, 1911, viii, 2586. AxHauseEN, G.: “ Ueber den histologischen Vorgang bei der Transplanta- tion von Gelenkenden.” Archiv. fiir klinische Chirurgie, 1921, xcix. 1. Lexer, “Ueber Gelenktransplantation,” Verhandlungen d. deutsch. Gesell. f. Chir., 1910, ii. Medicinische Klinik, 1908, 817. Krapp, R.: “ Ueber Umpflanzung von Gelenkenden,” Archiv. fiir klinische Chirurgie, 1911, xcvi, 386. Hetrericn: “Zur Frage der Transplantation des Intermediirknorpels,” Miinchner medicinische Wochenschrift, 1911, lviii. 2796. Haas, S. T.: “The Transplantation of the articular end of bone, etc.” Surgery Gynecology and Obstetrics, 1916, xxiii, 301. “The Experimental transplantation of the epiphysis, etc.” Journal of the American Medical Association, 1915, Ixv. 1965. Heiter, E.: “ Versuche ueber die Transplantation der Knorpelfiige.” Archiv. fiir Klinische Chirurgie, 1917-18, cix. 1. GENERAL CONSIDERATIONS 61 present as a physical sign of'an active joint inflammation, but only that remaining after the inflammation has run its course. ‘The subject has received various classifications, of which the following is perhaps the best: A true ankylosis is one in which the impairment of mobility is caused by change in the joint tissues themselves; in false ankylosis it is caused by change in the tissues outside the joints. The term contracture is gradually replacing the latter. Complete ankylosis means an absence of motion, incom- plete means a restriction of motion. The former is always bony, though a dense fibrous ankylosis may simulate it clinically. An incomplete ankylosis may be due to fibrous adhesions between the bones, or between one or both of them and the capsule, as in the first great type of chronic arthritis, or it may be due to a change in the shape of the bone ends so that they no longer fit each other, as in the second great type of chronic arthritis. In order to treat a case of ankylosis intelligently, it is advisable for the surgeon to have a fairly clear idea of the anatomical changes as well as of their cause, and of all the peculiarities of the various joints. No absolute standard of treatment has been established, and every case must be judged on its merits. We do not get much help here from animal experiments. It is almost as hard to produce bony ankylosis in a dog’s knee as it is to prevent union of a simple fracture of the shaft of one of his bones.”° The opinion is general that bony ankylosis follows a resection of a jointinman. It often follows resection of the knee, if care be taken with subsequent immobilization. I think the hip is rather hard to ankylose. Bony ankylosis 1s not to be expected after resection of the ankle or the * Exry, Leonarp W.: “Experimental Resection of the Dog’s Knee Joint,” Annals of Surgery, 1919. 62 INFLAMMATION IN BONES AND JOINTS shoulder, and it is notoriously hard to secure in resection of the elbow. Exact information is lacking in the toe joints, Fig. 31.—Bony ankylosis of wrist following an old closed infectious arthritis of unknown etiology. but the end of the metatarsal may be cut off in cases of hallux valgus with little fear of ankylosis, though some stiffness may remain. GENERAL CONSIDERATIONS 63 It is easier to stiffen the joint of the adult than that of the child. Normal joints become stiff after immobilization. The exact anatomical cause of this stiffness is hard to determine. Some say that fibrous adhesions form in the joint, and hasten to remove splints in fracture cases and to carry out early active and passive motion. Others maintain that a normal joint will never become perma- nently ankylosed, no matter how long it may be immobilized, and that the restriction of motion is caused by contraction of the tis- sues outside the joint. It is hard to say where | the truth lies. Neither | mae side seems to have any =~ : oa actual proof. In former tr..scint. | One can easily realize the chest of any times I held the latter treatment other than operative upon a joint like this. view very strongly, but I am not quite so sure as I was. As to the treatment of ankylosis, competent authorities agree that no attempt should be made to mobilize a joint which is the seat of an active inflammation. Motion is the worst possible thing for such a joint, and we should assist nature in her efforts to provide rest. Pain is nature’s great conservative symptom. If a joint is painful, its owner will try to keep it at rest. When all evidences of active inflam- mation are absent, the case is different. Two things are important to know in a case of ankylosis. The first is its type, whether it is complete or incomplete, and whether caused by adhesions between the ends of the bones, or by their distortion. This is determined by an t 64 INFLAMMATION IN BONES AND JOINTS examination of the joint, and by the Rontgen picture. The second thing is the probable cause of the ankylosis. This is determined by a careful history, and by the examination of the patient himself as well as of his joint. Ankylosis from distortion of the bone ends is usually caused by the second great type of chronic arthritis, or by old joint fractures. Fibrous ankylosis results from tuber- culous, gonococcic, syphilitic, staphylococcie, streptococcic arthritis, and from other forms of arthritis also. Strepto- cocci and staphylococci may also cause a bony ankylosis. Syphilis probably never does. Simple intraarticular fract- ures may result in bony ankylosis probably through the building of a bony bridge in the capsule. A rare form of bony ankylosis has been described in the elbow, following a slight injury, without any evidence of fracture. It seems to have been essentially an ossification of the capsule. I have seen it follow an unreduced dislocation of the hip in an elderly man. According to Ollier®* and Mauclaire,*” after a bony ankylosis, the structure of the bone at the site of the former joint changes. ‘The diameter slowly lessens, the spongy bone is absorbed, the cortical bone thickens, the proximal and distal medullary canals extend until sometimes they join, the lymphoid marrow gives place to fatty mar- row, and finally a typical section of a shaft of a long bone may be established. I have never had the oppor- tunity to examine a specimen in the laboratory, but I have watched with the Rontgen rays the changes in the archi- tecture for as long as ten years after knee joint resections, pon * Maucrarre: “Noveau Traité de Chirurgie,” Paris, 1909. Ankyloses, p. 235, 65 GENERAL CONSIDERATIONS Fic. 33.—Tuberculous knee ten years after resection. 4 * a ‘ i — a ~ cr 7 66 INFLAMMATION IN BONES AND JOINTS and have seen the bone remodelled along these lines, but apparently not completely canalized. Complete canaliza- tion takes a long time. Spongy bone has been observed Fra. 34.—Ankylosis caused by new bone in the joint capsule. Mo- tion was restored in this case by the removal of the bone, and the insertion of a fascial flap over its base. two and a half years after the resection of a tubercu- lous knee.** THE TREATMENT OF ANKYLOSIS naturally falls under the head of that of the diseases which cause it, but certain aspects of it may be considered here. 3 WacstraFr, Mr.: Path. Soc. Trans., 1868-69, xx, 264: GENERAL CONSIDERATIONS 67 If there be reason to believe that tuberculosis was the cause, most authorities advise that the ankylosis be left absolutely alone. Eiven many years after all active symp- toms have subsided, foci of infectious material may remain locked up in the bone marrow, or in the fibrous adhesions of the joint, capable, if they be set free, of lighting up the disease afresh. The ankylosis following joint fracture may sometimes be improved by remodelling the bone ends by operation. Each case must be judged on its merits. Sometimes what appears to be a firm ankylosis turns out to be a plate of bone in the capsule continuous with one of the articulating bones. If it be removed, and a flap of fat or of fascia be swung over its base, free motion may be restored. In dealing with the knee joint it is well to find out if the tibio- femoral articulation, or the femoro-patellar, or both joints together, are involved. When the ankylosis is caused by fibrous adhesions, these may be broken up forcibly under an anesthetic (brisement forcé), and then the joint may be immobilized in a dif- ferent attitude. It may be necessary to repeat the manceuvre several times. In point of fact not much can be expected of this method. Physical therapy—baking, massage, hydrotherapy, gentle active and passive motion, etc.—at present has quite a vogue. Fibrolysin is more or less of a medical relic.** ARTHROPLASTY The modern attempts at forming a new joint are usually dated from Ollier. Helferich followed Oller. In this country the operation was first strongly advocated by Murphy. The subject has been investigated and de- * SriporENKO, P.: “ Experimentelle und klinische Untersuchungen ueber die Wirkung des Fibrolysins etc.” Deut. Z. f. Chir., 1911, cx, 89: 68 INFLAMMATION IN BONES AND JOINTS veloped by Payr, Sumita, Allison and Brooks, Baer and many others. The simplest form of the operation of arthroplasty 1s the division of ankylosing tissue, possibly supplemented by a shaping of the bones. Little is to be expected from this. Its poor results gave rise to attempts to supplement it with the interposition of various substances, organic and inor- ganic. Oller turned in periosteum between the two bones. Others interposed muscle flaps, fat and fascia flaps, animal membranes of various kinds, and even morganic sub- stances. The flap of fat and fascia is the one now most employed. Most writers affirm that temporomaxillary arthroplasty gives the best results. Perhaps this is because the operator on this articulation has but one object, to mobilize it. In other joints the fear of instability enters into the calcula- tion. An unstable knee, for instance, is much worse than a stiff one, though many knees have been mobilized without losing their stability. The hip offers a better prognosis than the knee. é Tuer OpErRATION.—Artificial ischaemia is not advisable, though Murphy employed it. ‘The joint is opened so as to provide free access to it. In the case of a fibrous anky- losis, all the fibrous adhesions are dissected away, and also the contracted and cicatricial capsule. ‘This is important. In a bony ankylosis the bone is divided at the site of the former joint, and the bone ends are trimmed to a shape as near their former shape as possible. Plenty of the bone nust be removed. In old fibrous ankylosis also, the bones should usually be reshaped. All bleeding must be checked. The tissue to be interposed is then sutured carefully over one articulating surface. If an attached flap is used, it is partially dissected from its bed in the neighborhood, and GENERAL CONSIDERATIONS 69 swung between the bones to be sutured. The wound is closed. The period of the subsequent immobilization is a ques- tion of circumstances, and largely of opinion. It is possible to err on either side. Obviously motion should begin as soon as practicable, but not soon enough to disturb the healing of the wound. Payr begins motion in about one week, using traction after the first forty-eight hours. Baer puts his cases up in plaster of Paris for about four weeks. I incline to an average of ten days to two weeks. Active as well as passive motion should be carried out. Electrical stimulation and massage of the atrophic muscles may begin almost immediately. Small hamatomata should be aspirated. The patient’s codperation is almost a sine qua non, and patience and interest on the part of the oper- ator also. In knee operations long medial and lateral incisions are the favorite. A separate long incision from near the proximal end of the lateral incision lays bare the fascia almost up to the trochanter. A strip of this about 10 cm. wide and 20 cm. long is then incised on its proximal, anterior and posterior margins, dissected clear of the vastus lateralis with care, and still attached at its distal border, is drawn through a tunnel made between this inci- sion and the first lateral one. It is sutured carefully over the entire end of the femur, so that it lies between the femur and the tibia, and between the femur and the patella as well. Before the wound is closed all bleeding must be stilled. Corner’s long anterior incision®® with splitting of the ** Corner, E. M.: “ The Surgery of the Knee.” Journai of the American Medical Association, 1914, Ixiii, 1069. 70 INFLAMMATION IN BONES AND JOINTS patella, should be admirably adapted to this operation. (Fig. 96.) Kirschner’s*® has also been recommended. In many cases of knee ankylosis, the tibio-femoral joint is normal and the entire trouble resides between the femur and the patella. The flap then would be interposed solely between these two. | In hip joint operations Baer favors the anterior in- cision, running distally from the anterior superior spine, about 15 cm. long between the tensor fasciz late and the sartorius. Sprengel’s incision®’ or Smith-Peterson’s slight modification of it,?> which add to the anterior incision one running from the anterior superior spine along the ilium just distal to the crest, gives a better exposure. (Fig. 91.) Murphy favors a large lateral U-shaped incision five inches wide with its base proximal and its convexity distal. (Fig. 92.) The trochanter occupies the centre of the flap. The flap includes the skin, fat and fascia lata and is reflected proximally. A threaded curved needle, passed around the trochanter draws a Gigli saw after it, and the trochanter is then divided and drawn proximally. This gives an excel- lent exposure of the joint. A flap of fat and fascia is dis- sected from the large original flap. © In the elbow, medial and lateral incisions may be em- ployed or a long posterior one with transverse sawing of the olecranon and its subsequent wiring or suturing. In the shoulder, the ordinary anterior incision will be found useful, between the deltoid and pectoralis major, or the posterior incision of Kocher.*® *° KirscHNeER: “ Kin neues Operationsverfahren zur schonenden Eroeffnung des Kniegelenks.” Beitr. z. klin. Chir., 1910-1911, Ixxi, 703. *7 SPRENGEL: “Zur operativen Nachbehandlung alter MHiiftresectionen,” Archiv. f. klin. Chir., 1898, lvii, 837: *8 SmirH-Pererson, M .N.: “ A new supra-articular, sub-periosteal approach to the hip-joint.”. American Journal of Orthopedic Surgery, 1917, xv. 592. * Kocuer, Tueopor: “ Mittheilungen aus der chirurgischen Klinik in Bern.” Arch. f. klin. Chir., 1888, xxxvii, 777. GENERAL CONSIDERATIONS 71 In temporomaxillary arthroplasty, Murphy*® advo- cated an L-shaped incision, the perpendicular arm about 4.cm. long running immediately in front of the ear, from the zygoma, and the horizontal about 2 cm. long, along the upper border of the zygoma. He removed about 1 cm. from the head and neck of the bone, and employed a fascial flap from the temporal muscle. BIBLIOGRAPHY BONE GRAFTING ALBEE, Frep H.: “ Bone-graft surgery.” Phila. and London, W. B. Saunders Co., 1915. AxseEE, Frep H.: “ An experimental study of bone growth and the spinal bone transplant.” J. A. M. A., 1913, lx, 1044. AxseE, Frep H.: “ The fundamental principles involved in the use of the bone graft in surgery.” dm. Jour. Med. Sci., 1915, exlix, 313. AxHAusEeN, Gerorc: “Arbeiten aus dem Gebiet der Knochenpathologie und Knochenchirurgie.” Arch. f. klin. Chir., 1910-11, xciv, 241. AXHAUSEN, GeEorG: “Die histologischen und klinischen Gesetze der freien Osteoplastic.” Arch. f. klin. Chir., 1908-09, lxxxviii, 23. AxHausen, Geore: “ Histologische Untersuchungen iiber Knochentransplan- tation am Menschen.” Deutsche Ztschr. f. Chir., 1907-08, xci, 388. AxHausen, Grorc: “ Ueber den Vergang partieller Sequestrirung transplan- tirten Knochengewebes.” Arch. f. klin. Chir., 1909, Ixxxix, 281. AxHauseEN, Geore: “ Ueber plastische Operationen am Knochensystem.” Fort- chr. d. Med., 1909, xxvii, 369. Bancrort, Frepertic W.: “The use of small bone transplants in bridging a bone defect.” Ann. Surg., 1918, Ixvii, 457. Bartu: “ Knochenimplantation.” Beitr. z. path. Anat., 1895, xvii, 65. Bartrn: “ Ueber Osteoplastik.” Arch. f. klin. Chir., 1908, Ixxxvi, 859. BascuKkirzen, N. J., ano Perron, N. N.: “ Beitrage zur freien Knocheniiber- pflanzung.” Deutsche Ztschr. f. Chir., 1912, exili, 490. Berceman, W.: “Wie lange nach dem Tode oder nach der Amputation bleibt der Knochen transplantationsfaehig.” Arch. f. klin. Chir., 1909, Cx, 2t9. Bercer, Hermann, UND Scuwas, M.: “ Knochen und Gelenktransplantation- en.” Deutsche med. Wehnschr., 1912, xxxviii, 2029. Bier, Aveust: “ Beobachtungen iiber Knochenregeneration.” Arch. f. klin. Chir., 1912-18, ¢, 91. Bitrner, WirHeEtm: “ Ueber Knochenplastik nach Resektion an langen Rohren- knochen.” Zentrlbl. f. Chir., 1910, xxxvii, 571. © Mourrny, Joun B.: Journal of the American Medical Association. 1914, xii, 1785. 712 INFLAMMATION IN BONES AND JOINTS Brooxs, Barney: “Studies in bone regeneration.” Ann. Surg., 1917, Ixvi, 625. Brooxs, Barney: “Studies in bone transplantation; A study of a method of increasing the osteogenetic power of a free bone transplant.” Ann. Surg., 1919, lxix, 1138. Brooks, Barney: “ Studies in regeneration and growth of bone.” Ann. Surg., 1917, Ixv, 704. Brooks, Barney: “Studies in bone transplantations, etc.” Archives of Surg., 1920, i, 284. CopMan, Ernest A.: “ Bone transference.” Ann. Surg., 1909, xlix, 820. Davis, Joun S.: “A comparison of the permanence of free transplants of bone and cartilage.” Ann. Surg., 1917, lxv, 170. Davis, Joun S.: “Partial epiphysial transplantation for defect in fibula.” Ann, Surg., 1916, lxiv, 519. Davis, JouN S. anp Huwnnicutt, Joun A.: “The osteogenic power of periosteum.” Johns Hopk. Hosp. Bull., 1915, xxvi, 69. ENpERLEN: “Zur Reimplantation des resecirten Intermediirknorpels beim Kaninchen.” Deutsch Ztschr. f. Chir., 1899, li, 574. Gauge, W. E.: “The history of a bone graft.” Am. Jour. Orth. Surg., 1914, xii, 201. Gautiie, W. E., anp Rozgertson, D. E.: “ Repair of bone.” Brit. Jour. Surq., 1919, vii, 211. Gauuie, W. E.: “The transplantation of bone.” J. A. M. A., 1918, Ixx, 1134. Groves, Ernest W. Hey: “ Methods and results of transplantation of bone in the repair of defects caused by injury or disease.” Brit. Jour. Surgq., 1917-18, v, 185. Haas, S. L.: “ The experimental transplantation of the epiphysis.” J. 4. M. 4., | 1915, Ixv, 1965. . HIAAS COs Lassa Free transplantation of bone into the phalanges.” J. A. M. 4., 1914, lxii, 1147. Iletrertcu: ‘“ Versuche iiber die Transplantation des Intermediarknorpels wachsender Réohrenknochen.” Deutsche Ztschr. f. Chir., 1899, li, 564. Henverson, M. S.: “The use of beef-bone screws in fractures and bone transplantation.” J. 4. M. A., 1920, Ixxiv, 715. Hociunp, Emin J.: “ New method of applying autogenous intramedullary bone *transplants.” Surgery, Gyn. Obst., 1917, xxiv, 243. Jost, Orro: “Beitrige zur Osteoplastik an den Extremitaten.” Beitr. z. klin. Chir., 1914-15, xev, 86. Kauscu, W.: “Zur Frage der freien Transplantation toten Knochens.” Zentribl. f. Chir., 1909, xxxvi, 1879. Konic F.: “ Erfolgreiche Gelenkplastik am Ellbogen durch Implantation einer Elfenbeinprothese.” Miinch. med. Wehnschr., 19138, |x, 11386. Konic, F.: “ Ueber die Implantation von Knochen und Gelenkenden.” Beitr. z. klin. Chir., 1918, Ixxxv, 91. Karp, R.: “Fall von ausgedehnter Knochentransplantation.” Deutsche Ztschr. f. Chir., 1900, liv, 576. GENERAL CONSIDERATIONS 73 Lawen: “Zur Histologie des frei transplantirten periostgedekten Knochens beim Menschen.” Arch. f. klin. Chir., 1909, xc, 469. Lexer, Ericu: “Die praktische Verwendung der freien Transplantation.” Miinch. med. Wehnschr., 1913, Ix, 2059. Lexer, Ertcu: “Ueber Gelenktransplantation.” Arch. f. klin. Chir.,, 1909, xc, 263. Mac Avstanp, W. R., anv Woon, B. E.: “Transplantation of the fibula.” Surg. Gynec. Obst., 1912, xiv, 380. McWitiiams, Ciarence A.: “ Bone transplantation.”4 nn. Surg., 1916, Ixiii, 185. McWrtutams, Crarence A.: “Transplantation of bone.” Med. Record, 1916, xc, 498. Mourpny, Joun B.: “ Contributions to the surgery of bones, joints and tendons.” J. A. M. A., 1912, lviii, 985, 1094. Morpny, Joun B.: “Osteoplasty.” Surg., Gynec. Obst., 1913, xvi, 493. Norsske, K.: “ Ueber den plastischen Ersatz von ganz oder teilweise verlorenen Fingern. . .” Miinch. med. Wehnschr., 1909, lvi, 1403. Petrow, N. N.: “Zur Frage nach der Quelle der Regeneration bei Knochen- iiberpfianzung.” Arch. f. klin. Chir., 1914, ev, 915. Puemister, D. B.: “The fate of transplanted bone and regenerative power of its various constituents.” Surg., Gynec. Obst., 1914, xix, 303. Puemister, D. B.: “Necrotic bone and the subsequent changes which it under- goen. JA. M.A., 1915, Ixiv, 211. Rewn, Epvuarp: “Zur Regeneration des Knochenmarks bei der homoplastichen Gelenktransplantation im Thierexperiment.” Arch. f. klin. Chir., 1912, xcvii, 35. ScHEWANDIN: “ Endresultate der Lexer’schn Arthrodese am Sprunggelenk.” Arch. f. klin. Chir., 1913, ci, 1009. Strepa, A.: “ Beitriige zur freien Knochenplastic.” Arch. f. klin. Chir., 1911, Iciv, 831. Stuckey, L.: “ Ueber die freie Knochentransplantation bei der Pseudarth- rosenbehandlung.” Beitr. z. klin. Chir., 1912, Ixxx, 83. Tovyo, Tsunenaru: “The growth of free bone transplants.” Surgery, Gyn. Obst., 1917, xxiv, 701. ARTHROPLASTY Orurrr, L. X. E. L.: “ Traité experimental et clinique de la régenération des os.” Paris, 1867, Masson. Herrericu: “Tin neues Operationsverfahren zur Heilung der knoechernen Kiefergelenksankylose.” Arch. f. klin. Chir., 1894, xlviii, 864. Hetrericu: “ Ueber operative Nearthrosis.” Miinch. med. Wcehnschr., 1913, Ix, 2769. Morpnuy, Joun B.: “ Ankylosis. . . Arthroplasty, clinical and experimental.” Joa. 4, L905, xliv,. 15738. Morpuy, Joun B.: “ Arthroplasty.” Ann. Surg., 1918, lvii, 593. Morpny, Joun B.: “ Arthroplasty for intra-articular bony and fibrous anky- losis of temporomaxillary articulation.” J. A. M. A., 1914, Ixii, 1783. 74 INFLAMMATION IN BONES AND JOINTS ' Payr, E.: “Ueber die operative Behandlung von Kniegelenksankylosen.” Arch. f. klin. Chir., 1912, xcix, 681. Payr, E.: “Ueber dic operative Mobilisierung ankylosierter Gelenke.” Miinch. med. Wcehnschr., 1910, lvii, 1921. Payr, E.: “ Weiter Erfahrungen ueber die operativer Mobilisierung anky- losierter Gelenke. . .” Deutsche Ztschr. f. Chir., 1914, cxxix, 341, Payr: “Ueber die blutige Gelenkmobilisierung. . .’ Wien. m. Wnsch., 1915, lxv, 1102. Sumrra, Masao: “Experimentelle Beitrige zur operativen Mobilisierung ankylosierter Gelenke.” Arch. f. klin. Chir., 1912, xcix, 755, Au.ison, NATHANIEL, AND Brooxs, Barney: “ Ankylosis: an experimental study.” Surg. Gynec. Obst., 1914, xix, 568. Auuison, NarHaniet, aNd Brooxs, Barney: “ Arthroplasty: experimental and clinical methods.” Am. Jour. Orth. Surg., 1918, xvi, 83. Auuison, NaTHANIEL, AND Brooks, Barney: “The mobilization of ankylosed joints: an experimental study.” Surg., Gynec. Obst., 1913, xvii, 645. Barr, Wiiu1am S.: “ Arthroplasty with the aid of animal membrane.” Am. Jour. Orth. Surg., 1918, xvi, 1, 94, 171. Barer, Witu1am S.: “A preliminary report of the use of animal membrane in producing mobility in ankylosed joints.” Am. Jour. Orth. Surg., 1909- 1910, vii, I. AxHAusEN, G.: “ Ueber den histologischen Vorgang bei der Transplantation von Gelenkenden, insbesondere iiber die Transplantationsfahigkeit von Gelenkknorpel und Epiphysenknorpel.” Arch. f. klin. Chir., 1912, xcix, 1. Briar, V. P.: “Operative treatment of ankylosis of the mandible.” Surg. Gynec. Obst., 1914, xix, 436. Cramer, F.: “ Ueber die Lésung der verwachsenen Kniescheibe.” Arch. f. klin. Chir., 1901, Ixiv, 696. Exry, Leonarp W., ann Cowan, Jonn Francis: “ Experimental resection of the dog’s knee joint; Bone and joint studies, 1.” Stanford University, California. Published by the University. 1916. Exry, Leonarp W.: “ Experimental resection of the dog’s knee joint.” Ann. Surg., 1919, Ixx, 586. Henperson, M. S.: “ What are the real results of arthroplasty.” Am. Jour. Orth. Surg., 1918, xvi, 30. Horra, A.: “Die Mobilisierung knéchern verwachsener Gelenke.” Ztschr. f. Orth. Chir., 1906, xvii, 1. Horrmann, H.: “Ueber Kieferegelenksankylose mit ‘ Vogelgesicht’ Bildung.” Beitr. z. klin. Chir., 1914, xcii, 92. Hormann, M.: “ Weitere Untersuchungen und Erfahrungen iiber Periost- transplantation bei Behandlung knécherner Gelenkankylosen.” Beitr. z. klin. Chir., 1908, lix, 717. Houmeter, F., ann Macnus, G.: “Zur Frage der Weichteilimplantation bei Geienkresectionen.” Beitr. z. klin. Chir., 1914, xciv, 547. Krapp: “ Ueber Umpflanzung von Gelenkenden.” Arch. f. klin. Chir., 1912, xcvi, 386. GENERAL CONSIDERATIONS 75 Kiescuner, Martin: “Ein neues Operationsverfahren zur schonenden Eroffnung des Kniegelenkes.” Beitr. z. klin. Chir., 1910-11, Ixxi, 703. Konie, F.: “Erfolgreiche Gelenkplastik am Ellenbogen durch Implantation einer Elfenbeinprothese.” Miinch. med. Wehnschr., 1915, 1x, 1136. Kurrner, Hermann: “Die Transplantation aus der Leiche.” Beitr. z. klin. Chir., 1911, lxxv, 1. Lexer, Erntcu: “ Ueber freie Transplantationen.” Arch. f. klin. Chir., 1911, xcv, 827. Lrxer, Ertcu: “ Ueber Gelenktransplantation.” Arch. f. klin. Chir., 1909, xc, 263. MacAvstanp, W. R.: “ Ankylosis of the elbow.” J. A. M. A., 1915, Ixiv, 312. Nerr, James M.: “ Arthroplasty.” Surg, Gynec. Obst., 1912, xv, 529. Puemister, D. B., anp Miter, E. M.: “The method of new joint formation in arthroplasty.” Surg., Gynec. Obst., 1918, xxvi, 406. Renn, Epvuarp: “Die Fetttransplantation.” Arch. f. klin. Chir., 1912, xeviii, 1. Rerner, Hans: “Ueber die funktionellen Resultate der Resektion des Ellbogengelenks. . .” Deutsche Ztschr. f. Chir., 1910, civ, 209. Scumerz, H.: “Ueber operative Kniegelenksmobilisierung und Function- serstellung durch Amnicninterposition.” Beitr. z. klin. Chir. 1911, Ixxvi, 261. Srecate, Carto: “ Experimentelle Untersuchungen iiber die Regeneration der Kniegelenkkapsel nach Totalexstirpation.” Beitr. z. klin. Chir., 1918, Ixxxvii, 299. Srcare, Carto: “Ueber die Regeneration der Synovialmembran und der Gelenkkapsel.” Beitr. z. klin, Chir., 1913, lxxxvii, 259, et SECTION II. mi = ACUTE OSTEOMYELITIS AND ARTHRITIS CEPA re ilbe ACUTE SUPPURATIVE HAMATOGENOUS OSTEOMYELITIS Or the four usual causes of inflammation, mechanical, thermal, chemical, and bacterial, the last two only are of great importance in inflammations of the bone marrow. Its situation protects it from ordinary degrees of heat and cold, and also from all injuries except fracture. After a simple fracture the changes in the marrow are essentially those incidental to the repair of the bone. Injury seems to do little permanent damage to the marrow. If the marrow be curetted from the shaft of a laboratory animal it quickly regenerates, and, after a com- paratively short time shows no trace of the injury. It is important to remember this fact, on account of the per- sistent tendency to ascribe to trauma a leading role in most diseases, acute and chronic, of bone as well as of other tis- sues. As our knowledge becomes more exact, trauma usually sinks more and more into the background. As to the influence of chemical agents, the evidence for one, such as phosphorus, is positive, that for others, such as toxines, is largely presumptive. The cause of osteomyelitis in an overwhelming propor- tion of cases is infection, and the chief bacterial infectious agents are the staphylococcus and streptococcus pyogenes, the tubercle bacillus, the bacterium coli commune, the gonococcus, the treponema pallidum, the diplococcus, the typhoid bacillus, and the pneumococcus. *Extreme low temperature may, of course, cause necrosis of the marrow. ?Exy, Leonarp W.: “Regeneration of the bone marrow. Bone and Joint Studies I.” Stanford University 1916, Published by the University. 79 80 INFLAMMATION IN BONES AND JOINTS It is customary to divide cases of osteomyelitis into acute and chronic, and this division, while by no means exact, is convenient and will be adopted here. Some cases are acute from the start, run a typical course, and end in recovery or in death. Others are essentially chronic. Still others start with all the earmarks of an acute disease, and then settle down into a chronic stage, to last indefinitely, or possibly to recover under appropriate treatment. Again, what has been from the beginning a chronic disease may at any time take on all the appearance of an acute one. ACUTE OSTEOMYELITIS The one great cause of acute osteomyelitis is infection. The infection may be carried in from the outside, as with compound fractures; it may make its way into the bone from neighboring tissues, as with*acute arthritis or deep suppurations; or it may be blood borne. The last consti-- tutes a special disease of itself, with a well defined clinical picture, and will be considered first. What is commonly known as osteomyelitis, or acute osteomyelitis, is a suppurative inflammation of the bone marrow, occurring almost always in children or in ado- lescents, with an acute onset, febrile course, and marked constitutional reaction, and ending in the death of a greater or less amount of marrow and of bone. Its cause is usually the staphylococcus pyogenes aureus, less often the staphy- lococcus pyogenes albus or the streptococcus pyogenes, and rarely the bacterium coli commune. The organism may exist alone, or the infection may be a mixed one. With invasion by streptococci a marked tendency to involve- ment of the neighboring joint has been noted. In many instances the organism can be cultivated from the blood. Occasionally the offending organism is brought from HAMATOGENOUS OSTEOMYELITIS 81 some known suppurating focus somewhere else in the body, usually its place of origin is not known. Its favorite port of entry has been assumed to be an abrasion of the skin, however small, and the fact that the staphylococcus albus is the most common infecting agent lends color to this assumption. ‘The tonsil has been under suspicion, not only on account of the occasional sequence of the disease on scarlet fever, but also because of the causal relation of the tonsil to acute and to chronic arthritis. The importance of trauma as a contributing cause has been much debated. The results of animal experiments are contradictory. Clinical opinion can be found on both sides of the subject. At present we must consider the question as not proved. The sequence of the disease upon an infectious disease, especially upon scarlet fever, has been noted, and also its sequence upon chilling of the surface. As has been said, acute osteomyelitis is essentially a disease of childhood and adolescence. It is most frequent in the second decade of life, and many cases occur in the first and third decades. lLexer taught that its location in the bones was dependent upon the arrangement of the blood-vessels about the epiphysial line. Klemm? considers acute osteomyelitis as simply a suppurative inflammation of lymphoid tissue, similar to that of lymphoid tissue any- where else in the body, and only modified and aggravated by the rigid bony shell in which it runs its course. I ad- vanced this reason for the occurrence of marrow tubercu- losis ten years ago.* Acute osteomyelitis almost invariably begins in the *Kremm, Pavr: “Die Osteomyelitis des Kindesalters,” Berlin, Verlag von S. Karger, 1914. ‘Err, Leonarp W.: “Joint Tuberculosis,” William Wood and Company, 1911. 6 82 INFLAMMATION IN BONES AND JOINTS metaphysis’ of one of the long bones, especially in that of the femur and of the tibia, less often in that of the humerus. The purulent inflammation spreads in the spongy bone, killing the marrow and the bone as it goes, and the process then adopts one of four different courses. 1. THe Typical SEVERE SPREADING OSTEOMYELITIS. —The inflammation travels widely in the spongy bone in the general direction of the central marrow canal, gains this, and involves its marrow for a greater or smaller dis- tance, sometimes reaching the epiphysial line at the other end of the bone. It also passes through the minute canals in the cortex, and comes to the under surface of the peri- osteum. It runs along between the cortex and the periosteum, dissecting them apart. If an operation has not been undertaken by this time, or death has not inter- vened, the pus breaks through the periosteum, burrows in every direction, and finally makes its way to the surface. We have then the necrotic shaft—the sequestrum—filled with pus, and lying within the periosteum, bathed in pus, and connected with the surface by sinuses. Death, from sepsis, from ulcerative endocarditis, or from metastases in the kidneys or in other organs, would probably have closed the scene; if not, then with the free discharge of pus, the disease settles down to the chronic stage. In areas the periosteum may become adherent to the necrotic bone beneath it. After a few weeks, bone formation begins in or under the periosteum, and proceeds until the necrotic shaft is enclosed in a more or less com- plete shell of bone (the involucrum) perforated by holes for the discharge of pus—cloace, sewers. A stage is thus reached which, without outside aid, will last indefinitely. The dead shaft, locked up in its rigid 5The metaphysis is that portion of the spongy bone which lies shaftward from the epiphysial line. HAMATOGENOUS OSTEOMYELITIS 83 case, is incapable of absorption, and remains permanently as a foreign body. In the end the patient may die from the effects of the prolonged suppuration. Not always does the disease reach the extreme limits detailed above. It may be halted at any point by nature’s protective reaction in the marrow, usually by a fibrosis. The wall of defence may slowly be reinforced by bone, and this, with the periosteal bone, forms a perforated box, in which lies the cylinder of sequestrated shaft, more or less continuous with it in structure. 2. THe SupeERFICIAL Form.—In this the disease, starting as in the preceding form, near the epiphysial disc, and probably near the cortex, never reaches the central marrow canal, but breaking through the thin cortex near the end of the bone, gains the under surface of the periosteum, and spreads shaftwards beneath it. It kills the superficial part of the cortex, and filling the space between it and the periosteum with pus, lifts the periosteum off, perforates it, and then, burrowing through the soft tissues, makes its way to the surface. This form of the disease is wont to be less severe than the preceding. 3. THE CIRCUMSCRIBED F’‘orm.—Brodie’s abscess.° In this form the disease remains localized in the metaphysis. An abscess forms, usually not of great diameter, and becomes walled off by dense bone. It may remain indefi- nitely stationary, or, according to some writers, may break out later, and spread through the bone, like the other ms. During its existence it may give rise at any time to a sterile effusion in the joint, as may the other three forms. It is said to be one of the causes of the so-called inter- mittent synovitis, or hydroarthrosis. Presumably Brodie’s abscess is caused by bacteria of a low degree of virulence. ° See an interesting article by Watrer M. Brickner: “Chronic medullary abscess in the long bones,” Annals of Surg., 1917, lxv, 483. 84 INFLAMMATION IN BONES AND JOINTS 4. Tue ArricuLArR Form.—Starting at or near the same place as the three preceding, the disease shows a marked tendency to spread towards the joint, perhaps spreading shaftward also. It may perforate the epiphy- sial cartilage, and involve the epiphysis, and then, having killed the joint cartilage, in whole or in part, break into the joint and become an arthritis. This is the “ acute epiphy- sitis ” of some writers. The epiphysis may be separated by the inflammation beneath it. The disease may break directly into the joint without perforating the epiphysial cartilage. In either case, the result is the same. Accord- ing to most writers, this type of case is usually caused by the streptococcus, less often by the pneumococcus or the typhoid bacillus. It is seen therefore that all four forms of the disease are the same in their pathological characteristics. They differ only in their details. Their course may be checked, modified, or changed by operative interference. OSTEOMYELITIS (PERIOSTITIS) ALBUMINOSA (SEROSA) is a rather rare form of the disease, usually occurring in the femur, with an acute and severe onset, and then a milder and chronic course which may last for several months. Suppuration does not result, but sequestra form, and when at length the fluctuating swelling is opened, the fluid is found to be thin, serous, synovia-like. The disease is caused by the same organisms as the other forms. SYMPTOMATOLOGY.—Acute osteomyelitis usually be- gins suddenly with the customary symptoms of an acute infection, chill, high fever, rapid pulse, etc. Sometimes the onset is preceded for a few days by headache, malaise, and pain in the limbs. The patient complains of severe pain in the vicinity of a joint, most often the knee, but not in the joint itself. Motion of the joint is usually not very pain- HAMATOGENOUS OSTEOMYELITIS 85 ful, but pain is caused by prolonged pressure over the af- fected region, or by percussion. Redness and swelling, often oedematous, soon appear, and the cedema may con- tinue distal to the seat of trouble. As soon as the process breaks through the cortex, a fluctuating swelling appears. The neighboring joint sometimes fills with fluid, which in the majority of cases is sterile. The leucocyte count is very high, and cultures of the offending organisms may often be made from the blood. ‘The subcutaneous veins are prominent, the adjacent lymph nodes are enlarged. The patient rapidly becomes worse, and often sinks into the so-called typhoid state, with coated tongue, delirium, ete. The fever as a rule is continuous. A fluctu- ating temperature is a sign of metastases. The urine is concentrated, and often contains albumin. Cutaneous eruptions may be present. Such a picture is comparatively easy to recognize. On the other hand, swelling may be absent, as may all local physical signs of disease, and the delirium and coma may be so early and so profound that the patient is not in a position to complain of pain. If the disease breaks into - ‘the joint, the evidences of an acute arthritis are added. THE DIAGNOSIS in most cases is easy. ‘The acute onset, with high fever, usually with a chill, the painful swelling in the neighborhood of a joint, extremely sensitive to pres- sure, with dilated superficial veins, and local cedema, present a characteristic picture. When the disease is in the region of the hip, buried deeply in the muscles, its recogni- tion is not so simple. ‘The appearance of the fluctuating swelling removes all doubt. The X-rays give us, as a rule, little help during the first week. After that, changes in the bone are evident. These show in the increased permeability of the bone to the rays, 86 INFLAMMATION IN BONES AND JOINTS Fic. 35.—Acute, suppurative, hamatogenous osteomyelitis of the femur in the chronic stage. HAMATOGENOUS OSTEOMYELITIS 87 more or less irregular, of course. In the later stage the new. bone in the periosteum can be seen on the plate, and the sequestra surrounded by rarefied areas. The effusion into the neighboring joint, occasionally occurring in the early stages of an acute osteomyelitis, the Fic. 36.—Acute, suppurative, hematogenous osteomyelitis of the clavicle, in the chronic, stage. so-called sympathetic synovitis, is usually sterile. Aspira- tion will determine this. An acute suppurative arthritis shows a swelling in the joint itself, and possibly for a short distance on each side of it, rather than on one side alone. Motion is much more painful. Fluid in the joint is an early phenomenon of acute arthritis, and can be found by aspiration. When pus is found, operation reveals its source in either instance. Acute inflammatory rheumatism is differentiated by its fleeting nature; by involvement of several joints in 88 INFLAMMATION IN BONES AND JOINTS succession, the first clearing up as the next is attacked; by the acid sweats; and by its reaction to salicylates. The severe cases, with few evidences of local disturb- ance, but with marked constitutional involvement, early delirum and rapidly deepening coma, offer the greatest difficulty. Sometimes only the necropsy clears up the origin of what has been diagnosed as a pyemia of un- known origin. Typhoid fever has a characteristic onset, with a de- lirium usually not appearing early, intestinal symptoms, a Widal reaction, and an absence of leucocytosis. ‘The typhoid state is rather late in typhoid. To occasion any confusion in osteomyelitis 1t would need to appear early. THE PROGNOSIS AS TO LIFE, as well as to the time of complete recovery, depends largely upon the promptness of treatment and its thoroughness. With early operation the majority of patients recover. Some patients die quickly from toxemia, even before the formation of pus. Others die after a short time from sepsis, ulcerative endo- carditis, metastases in the kidneys, ete.; others after a longer time from the effects of the prolonged suppuration, amyloid degeneration, or metastases in other bones. ‘The persistence of bacteremia after thorough drainage is a bad sign, but not necessarily a fatal one. THE TREATMENT is invariably operative, at the earliest possible moment, as soon as the diagnosis can be made, and without waiting for fluctuation. Under complete narcosis the long incision is made de- liberately in the muscle planes down to the periosteum, and this is sit open. If pus be found it must be followed up as far as it has traveled. With involvement of the marrow beneath, the cortex usually loses its glistening appearance and shows dead white, while pus, instead of blood, oozes HAMATOGENOUS OSTEOMYELITIS 89 from the minute apertures of the Haversian canals. Later, the cortex turns a dirty brown or blackish. In no circumstances must fear of infecting the marrow induce one to stop here. A long strip of the cortex should be removed, the marrow canal should be inspected, and if it be found infected, the removal of the lid of bone over it should be continued until the limits of the disease have been reached. It is not enough to open simply the central marrow canal. ‘Themetaphysis, where the process started, must be opened as well. In the early stages the marrow may be found only intensely congested, perhaps with yellow streaks running through it; later it will consist of yellow or greenish pus. If we have reason to suspect pocketing of the pus under the periosteum on the side of the bone opposite to that opened, counter openings should be made. Authorities differ as to the next step. Some operators stop here, either leaving the wound open or stitching the skin to the periosteum, to ensure its staying open. Some curette the marrow. Some not only curette, but also pack the cavity. Some immediately resect all the diseased bone. Most operators postpone the bone removal. The Carrel-Dakin treatment seems particularly appro- priate after operation. Nichols advises that the bone be not removed until new bone formation in the periosteum, the involucrum, has well begun. ‘This time can be determined by thrusting a needle into the periosteum, or more accurately by exam- ining a piece of it under the microscope. ‘The new bone imparts a crackling sensation, with a slight resistance. In the forearm and in the leg, where the diseased bone has a splint in the other bone, Nichols sets the time as about two months after the first operation; in the femur and in the 90 INFLAMMATION IN BONES AND JOINTS humerus, where no such splint is present, the time should be somewhat longer. Other operators wait longer before removing the sequestrum, but they all agree that too long an interval must not be allowed to elapse. If we wait too long, the bone in the involucrum becomes very dense. The repara- tive processes in dense bone are very poor, and in cases that have been postponed ‘too long, the cavity left by the removal of the sequestrum may remain indefinitely. If early sequestrotomy be practiced, a splint should be applied, on account of the danger of fracture of the involu- crum, a fracture that sometimes will not unite. If time for the formation of a solid involucrum be permitted to elapse, the removal of its steep sides at operation will hasten healing. When it comes to removing the sequestrum, the dead bone is not as a rule found perfectly separated, but united at its ends to the live bone and here and there adherent to the periosteum. These attachments must be divided. Sometimes, also, a considerable amount of bone must be chiseled from the involucrum, to permit of the removal of the sequestrum. When the disease has involved only the superficial part of the cortex, the problem is much simpler. In such a case the sequestrum may be in the form of a long sliver of bone ~ which can be removed easily. After the removal of the sequestrum the disease settles down into its chronic stage, and it is customary to allude to this stage as chronic osteomyelitis. It really is the stage of repair of the acute disease, a stage of repair which is pro- longed by mechanical conditions incident to the presence of the bony shell which prevents healing, as well as to the presence of pieces of dead bone unavoidably left behind. HAMATOGENOUS OSTEOMYELITIS 91 In favorable cases during the healing of the wound small sequestra are thrown out. After healing has taken place, to the accompaniment of slight pain and increase of temperature, pus pockets may form in and near the scar, and, rupturing, heal again after discharging small seques- tra. ‘This may go on indefinitely, but the ordinary period may be said to be a year. ‘The most troublesome cases are those in which, after a reasonable time, the processes of repair come to an end, leaving a cavity in the bone, with sclerosed walls, which will not fill in. Sometimes if the steep walls of this cavity be removed, giving it a shallow cup shape, repair will start up again, and will be completed. In other cases this procedure fails, especially when the cavity is near a joint, where its obliteration is difficult. The problem is then a difficult one, and has been attacked in various ways. Schede’ recommended filling the cavity with an asep- tic blood clot, followed by almost complete closure of the wound and the application of a protective tissue be- tween it and the voluminous dressing. It is difficult or impossible to prevent infection of the blood clot, and in the hands of others than its originator, this treatment has not been successful. Hamilton’s® sponge graft seems to have no advocates nowadays, nor Senn’s” decalcified bone chips. Good results have been obtained with Neuber’s'’ oper- ™Scuepe: “Ueber die Heilung unter dem feuchten Blutschorf.” Dtsch. med. Wochensch., 1886, xii, 389. ’Hamirron, D. J.: “On sponge grafting.” Hdin. Med. Jour., 1881, xxvii, 385. ®Senn, Nicnoras: “ Healing of aseptic bone cavities.” Am. Jour. of Med. Sci., 1899, xcviii, 219. © Nevser: “Zur Behandlung starrwandigen Ho6hlenwunden.” Arch. f. klin. Chir., 1896, li, 683. 92 INFLAMMATION IN BONES AND JOINTS ation. Neuber cleaned out the bone cavity, trimmed off its steep walls as much as possible, and turned in flaps of skin and soft tissue, securing them to the bone by nails, straps and invagination sutures. Perhaps the most promising procedure is, after trim-. ming the walls of the cavity and rendering them, as far as possible, aseptic, to fill them with some special form of paste. The exact chemical combination of the paste is probably not a matter of great importance. As von Mosetig-Moorhoff ** says, the “ plombe ” is merely a tem- porary substitute. Von Mosetig-Moorhoff, after thorough disinfection and drying of the walls of the cavity, filled it with a paste composed of a sterile mixture of iodoform 40 parts, and oil of sesame and spermaceti 30 parts each. He then closed the wound.” | The treatment of the superficial form of the disease is usually much simpler than that of the preceding. As a rule only the superficial portion of the bone is killed, and this only in a limited area. Healing follows slowly after the removal of the dead bone. Tue CircumscriseD Form or OsTEOMYELITIS— Bropie’s Axpscess.—The abscess should be cleaned out thoroughly, and its sclerosed walls should be chiseled away. The employment of some paste may be advisable to promote the healing in of the cavity, e.g., Mosetig- Moorhoff’s, Beck’s or “ bipp.” The formule of Beck’s two pastes are: No. 1, bismuth subnitrate (arsenic free) 33 per cent., vaselin 67 per cent. No. 2, bismuth subnitrate 30 per cent., vaselin 60 per cent., paraffin (120° melting point) 5 per cent., white wax 5 per cent. The formula for % Von Moseric-Moornorr, Dr. R.: “The elimination of cavities in opera- tive wounds.” Surgery, Gynecology and Obstetrics, 1906, iii, 547. “See also Cropron, M. B.: “The diagnosis and treatment of osteomy- elitis.” Surgery, Gynecology and Obstetrics, 1915, xx, 6, HHMATOGENOUS OSTEOMYELITIS 93 bipp is: Lodoform 16 ounces, bismuth subnitrate 8 ounces, liquid paraffin 8 fluid ounces, or a sufficient quantity. If Beck's paste or bipp be used, one must be on the lookout for symptoms of bismuth poisoning.’* ‘The possibility of iodoform poisoning with bipp and Mosetig-Moorhoff’s pastes must not be forgotten. Perhaps vaselin and paraffin, without iodoform and bismuth, would be as effi- cacious as with them. In operations on old sterile bone abscesses, the wound may be closed immediately. * Beck, Emit G.: “ Bismuth paste in chronic suppuration.” St. Louis C. V. Mosby Co., 1915, 182. DrersMANN: “Ueber Wismuthvergiftung.” Miinch. med. Wehnschr., 1901, xlvili, 238. Exy, Leonarp W.: “A fatal case of bismuth paste poisoning.” Med. Record, 1912, Ixxxi, 119. Fremicn, Exris B.: “ Bismuth poisoning following bismuth paste injec- Mia 04 Mo 4. L917, Ixvill,111. Mayer, Leo, ann Barur, Georce: “ Bismuth poisoning.” Surg., Gynec. and Obst., 1912, xv, 309. Morison, RutTuHerForp: “The treatment of infected suppurating war wounds.” Brit. Jour. Surg., 1916-17, lv, 660. Mvuuie, F.: “ Ueber Wismuthvergiftung.” Miinch. Med. Wchnschr., 1901, Ixviii, 592. Sicmunp, Erpuermm: “ Ueber Wismutintoxikation bei Behandlung nach der Methode von Beck.” Wien. klin. Wehnschr., 1912, xxv, 749. Vaccarezza, Raut F.: “Las intoxicaciones por el subnitrato de bismuto.” La Semana Med., 1919, xxvi, 366. CHAPTER II ACUTE SUPPURATIVE HA MATOGENOUS ARTHRITIS Lue ArticuLar Form.—It is quite likely that the infectious material may be carried to the synovial merm- brane in the first place, and thus that a suppurative Fic. 37.—Photomicrograph of bone and cartilage from a section of acute suppurative arthritis, following operation on a case of suppu- rative inflammation on the shaft of the tibia. Degenerating cartilage on the right, bone marrow on the left. Observe how the inflamma- tory process in the marrow is eating its way into the cartilage, and how it has already consumed most of the bone Only a few small trabecule are left. arthritis may precede the osteomyelitis, or may exist alone without involvement of the bone. The result in either case - is much the same, though if the synovial membrane alone be aifected, the treatment may be different. 94 HEMATOGENOUS OSTEOMYELITIS 95 In the treatment of these acute suppurative arthritides the problem is not, as in an uncomplicated osteomyelitis, a simple one of thorough drainage, but we are led to take risks by the hope of a movable joint. Again, in the case of Fig. 38.—Suppurative inflammation in the bone marrow in the region of the joint. T, T, T trabecule; C, colony of pus cocci in a small vessel. We know that in this case the bone is rapidly being destroyed, but the margins of the trabecule present an appearance typical of what is usually described as productive ostitis. a child, we must not do any more injury than is absolutely necessary to the epiphysial cartilage. Thorough drainage is demanded here as in the other forms of the disease, but it is well not to be too radical about gouging out the bone, especially about the epiphy- 96 INFLAMMATION IN BONES AND JOINTS sial cartilage. If constitutional symptoms be not severe, and if aspiration of the joint have revealed only a few leu- cocytes or even a few cocci, we may postpone opening it, possibly following Murphy’s advice,’ washing it out and injecting its cavity with a 2 per cent. solution of formalde- hyde in glycerin. The injection may perhaps be repeated once or twice if the constitutional symptoms and the local physical signs justify it. If the joint be full of pus, containing many cocci, little is to be gained by temporizing. It should be opened and thoroughly drained. Any drains which we insert must be left in, of course, as long as necessary, and yet we must remember that joints which have had tubes in them for any length of time usually become ankylosed. On the other hand, it is not likely that a joint, invaded by an osteo- myelitis in the vicinity serious enough to damage the cartilage badly, will ever possess enough function to justify much risk for its preservation. Cartilage scraped off from limited areas of the articular surface of animals’ bones sometimes reforms, but nothing that I have ever seen in my specimens makes me think that it is replaced after it has been destroyed by disease. We come back, then, to the principle that an acute hematogenous sup- purative arthritis requires free drainage. In disease of the knee or hip, traction may promote the comfort of the patient, and possibly may help in the treat- ment. Later on some such splint as the Thomas may be of service when the lower extremity is affected. It is sometimes impossible in an acute hematogenous suppurative arthritis to decide whether the synovial mem- brane alone is involved or whether the infection springs *Mureuy, Joun B.: “Metastatic gonorrheal arthritis of the knee.” Surgical Clinics of John B. Murphy, 1912, i, 825. HAMATOGENOUS OSTEOMYELITIS 97 from a marrow focus in the immediate vicinity. If the bone involvement is so minute as to escape detection, it may be ignored. A SUPPURATIVE HA MATOGENOUS ARTHRITIS 1S occa- sionally caused by the diplococcus of pneumonia. ‘The disease comes on during a pneumonia or in early conva- lescence, and is often fatal.” It may arise in the course of a general infection, and very rarely it is primary. Its treatment is the same as that of the preceding, but cures by aspiration have been reported. If the constitutional symptoms warrant it, this should be tried before more radical measures. A H&%MATOGENOUS ARTHRITIS occasionally is observed as a sequel of certain acute infectious diseases, notably scarlet fever, measles, smallpox and influenza.* The inflammation may consist of a mild synovitis, single or *Bezancon, F. anp Grirron, V.: “Arthritis expérimentales a pneu- mocoques par infection générale et sans traumatisme articulaire.” Soc. d. Biol. Comp. Rend., 1899, li, 709. Cave, Epwarp J.: “ Pneumococcic arthritis.” Lancet, 1901, i, 82. Dunn, L. A. Rosrnson, H. BetHam anp Fietcuer, H. Mortey: “ Five cases of purulent pneumococcic arthritis in children.” Lancet, 1903, ii, 316. Ey, Leonarp W.: “A case of pneumococcus infection of the hip.” Med. News, 1905, lxxxvi, 930. Herrick, James B.: “ Pneumococcic arthritis.” dm. Jour. Med. Sci., 1902, cxxiv, 12. Horsratt, C. E., Campsett: “ Pneumococcus arthritis; vaccine treat- ment; recovery.” Lancet, 1918, ii, 556. Pasteur, W. anv CourtTauLp, L.: “Primary pneumococcal arthritis.” Lancet, 1906, i, 1747. Raw, Naruan: “ Pneumococcus arthritis with notes of seven cases.” Brit. Med. Jour., 1901, i, 1803. SecreTtan, W. Bernarp, anp WrancHam, Wriiiiam: “ Pneumococcic arthritis.” Brit. Med. Jour., 1906, i, 915. * Fritscus “ Ueber Gelenkerkrankungen bie Scharlach und Masern.” Beit. z. klin. Chir. 1911, Ixxii, 101. Scuvuretter, Max: “Ueber Bacterien bei metastatischen Gelenkentziind- ungen.” Archiv. f. klin, Chir., 1884-5, xxxi, 276. - / 98 INFLAMMATION IN BONES AND JOINTS multiple, which soon clears up entirely, or it may be more severe, with a plastic exudate. This latter form is fre- quently seen after influenza, and may result in almost complete ankylosis, from the dense adhesions in the joint. The arthritis may be suppurative, and not to be distin- guished from the acute streptococcic form already described. Its treatment is the same. CHAPTER III SUPPURATIVE OSTEOMYELITIS FOLLOWING COMPOUND FRACTURE THE suppurative osteomyelitis which follows infection from a compound fracture differs m its course and in its clinical manifestations from the hematogenous form, but the fundamentals of the pathological process of the two are much the same. The infection, of course, is always a mixed one, and, starting from any part of the bone, it spreads in every direction. In former days it was fre- quently fatal, but since the introduction of the modern methods of treatment of compound fractures, except: in war wounds it is rarely seen. Otherwise its manifestations are often mild in their nature. THE TREATMENT in the first place is prophylactic. A compound fracture which is considered clean may be treated expectantly, but at the first sign of infection, it should be thoroughly opened up. All foreign material and necrotic or loose bone fragments should be cleaned out, but bone fragments still attached to the periosteum should be left. Their presence is said to promote the union of the fracture. Provision should be made for drainage, and pos- sibly some form of wound disinfection should be installed— Carrel-Dakin. If in spite of our efforts, the infection spread, amputation may be necessary. Non-union frequently follows infected compound fractures. It is well not to undertake any operation for this until after the wound has been healed for several months. Otherwise we run the risk of lighting up the infection afresh. 99 CHAPTER IV TYPHOID OSTEOMYELITIS AND ARTHRITIS TyPuHoip OsTEoMYELITIS.—It appears from the inves-. tigations of Fraenkel’ and others that the bone marrow is a favorite domicile of the typhoid bacillus, after clinical recovery as well as during the actual course of the disease. Sometimes it causes an osteomyelitis which is wont to affect the superficial portion of the cortex, and may or may not result in suppuration, ‘The infection may be a simple one or it may be mixed. The shafts of the long bones, especially of the ribs or of the tibia seem to be affected by preference, but the disease is by no means rare in the spine. It is commonly called a periostitis when it occurs in the shafts of the long bones. Typhoid osteomyelitis usually develops in the third or fourth week of the disease, or at any time after the typhoid has run its course, and its onset is manifest ordinarily by a rise of temperature and a painful swelling of the bone. If suppuration results, the abscess should be thoroughly cleaned out and drained. The milder cases of a pure typhoid infection often disappear spontaneously, and need no other treatment than rest and protection from injury. TYPHOID ARTHRITIS An arthritis is an occasional complication of typhoid fever, coming on in the late stages of the disease, or during convalescence. ‘The fluid in the joint may be sterile, or it may contain typhoid bacilli, alone or mixed with pus cocci.” 1FRAENKEL, Eva.: “ Ueber Knochenmark and Infektionskrankheiten.” Muenchener medicinische Wochenschrift, 1902, xlix, 561. *Exxis, A. G.: “ As Experimental Study of Joint Affections Induced by the Typhoid Bacillus,” Jour. of Infect, Dis,, 1909, vi, 181. 100 TYPHOID OSTEOMYELITIS AND ARTHRITIS 101 Marrow involvement is probably, as a rule, slight. The chief pathological changes appear to be in the syno- vial membrane. Typhoid arthritis most often occurs in the hip, and usually is not very painful. Dislocation of' the hip is a rather frequent result. THE TREATMENT consists in rest and protection. In order to avoid a dislocation of the hip, the attitude of ex- treme flexion and adduction is to be avoided. If the joint be much distended with fluid it should be aspirated. With secondary infection by pus germs an operation becomes necessary, though, as the infection is probably synovial alone, it may possibly be checked by washing out the joint cavity with normal salt solution, and then injecting it with a mild antiseptic such as a solution of formaldehyde. TypHoID sPpINE.—This is an acute affection of the spine, coming on in the late stages of a typhoid, or during convalescence, and generally in vigorous young men. Its pathology has not been definitely established, for no case ever has come to necropsy, though in Rugh’s case a necropsy was done nine years after the attack. Osler taught for many years that it was a neurosis, but the clinical picture, the Roéntgen plate, and the occurrence of a kyphosis in one or two cases indicate that it is essentially an osteomyelitis, perhaps with an arthritis as well. No case ever has gone on to suppuration, and we assume that the offending organism is the typhoid bacillus. The disease may be mild and insignificant, and may pass as a “ lumbago ”’ practically unnoticed; it may be very severe. Its onset may be sudden or slow. Usually, in the late stages of a typhoid or during convalescence, the patient 102 INFLAMMATION IN BONES AND JOINTS complains of stiffness in his back and of pain in the lumbar region. ‘The pain in the severe cases is horrible, and is imcreased by the slightest motion. The patient is unable to turn in bed and cries out if the bed is only slightly jarred. The pain often comes in paroxysms, preceded perhaps: by a rise in temperature. It may remain localized in the back, or it may run around the abdomen, or into the ex- tremities. It may shift. 7 With the symptoms of an actual bony lesion may go those of a neurosis, or even of a marked hysteria—pares- thesias, muscular contractions, changes in the reflexes, etc. After a longer or shorter interval the symptoms slowly subside, and the patient recovers completely within a year. The milder cases run a short course. THE TREATMENT may be summed up in one word— rest. The severe cases demand recumbency, possibly with the immobilization reinforced by a gas-pipe frame, covered with canvas, to which the patient is strapped. Morphine, or even a whiff of chloroform or of ether may be necessary to quiet the paroxysms of pain. For the milder cases, and for the later stages of the severe ones, sufficient immobilization is furnished by a light steel spinal brace, or by a plaster jacket. The white-hot thermo-cautery, flicked quickly over the lumbar region, relieves the late pain and stiffness, and its application is relished by the patient. CHAPTER V GONOCOCCIC OSTEOMYELITIS AND ARTHRITIS THE gonococcus can cause an inflammation of the bone marrow, or of the synovial membrane, or of both. Practi- cally all authorities speak of a gonorrheal periostitis. I believe that this is not correct. The inflammation is in the superficial portion of the bone marrow and not in the periosteum. On account of the difficulty of recovering and growing the gonococcus, our observations on the disease are largely clinical. The corollary to this is that much difference of opinion prevails in regard to the disease. ‘The cause of gonorrheal arthritis is of course the gonococcus, but the diagnosis is made far more often without the demonstra- tion of the organism than with it. The disease, as would be — expected, seems to be more common in men than in women. _ It is customary to speak of acute and of chronic gono- coccic arthritis and to teach that while its incidence is usually in the florid stage of the urethral infection, at about the time of invasion of the deep urethra, it may nevertheless come on at any time during the course of an old chronic infection in the deep urethra. I think that this is an error; that a gonococcal arthritis is always an acute arthritis, and that it almost invariably, if not invariably, comes on during the acute stage of the urethral infection. I have never seen the gonococcus recovered from a case of chronic arthritis, and believe that in the old cases of chronic arthritis caused by a lesion in the deep urethra, the streptococcus is the offending organism. Baer,’ however found the gonococcus Barr, W. S.: “ Painful heels.” Johns Hopkins Hospital Bulletin, 1905, xvi, 264. 103 104 INFLAMMATION IN BONES AND JOINTS in a number of old spurs under the calcaneus. In acute arthritis the organism has a fleeting life; one day aspiration of the joint, especially immediately after an acute exacer- bation, detects it; the next day it may be gone. One might take either side of a wager on its presence or absence. On account of a paucity of pathological material we know little of the finer changes in the bone and joint. In the region of the joint the bone usually shows rarefaction under the X-ray. Farther from the joint, immediately under the periosteum, bone absorption and bone production go hand in hand. ‘This often results in irregular spurs and exostoses. The synovial membrane is inflamed, succulent, con- gested and villous. The exudate in the joint, while occasionally purulent or possibly serous, usually is fibrinous or plastic. It results sometimes in dense fibrous adhesions, which limit or abolish joint motion. The typical and characteristic invasion of the disease, not by any means invariable, however, is as follows: For a day or two several joints swell up and become slightly painful, one clearing up as the next is involved. Then, suddenly, the disease attacks one or perhaps two Joints and stays there. ‘The swelling and pain are great, with an increase of local temperature and marked sensitiveness. The joint is distended with fluid. QU’dema of the tissues in the neighborhood may be said to be almost characteristic. Constitutional symptoms as a rule are not marked. High fever with pronounced constitutional symptoms, usually spells mixed infection. The large joints are more frequently involved than the small ones. Everyone has his own ideas as to the relative frequency of involvement of the various joints. Person- ally I look for it in the man most often in the knee or ankle, GONOCOCCIC OSTEOMYELITIS AND ARTHRITIS 105 in the woman most often in the wrist, but then I have not seen many cases in which I was sure of the diagnosis. Sterno-clavicular involvement is most suggestive of the gonococcus. The disease has no definite course. Recovery may take place after a longer or shorter time, either complete or with much or little remaining stiffness. Endocarditis, iritis and “gonococcic septicemia” accompany the arthritis quite frequently, possibly because they all are an evidence of a severe infection, or of a high degree of vulnerability on the part of the patient. THE DIAGNOSIS as a rule is not difficult. The presence of an acute urethral infection is strong presumptive evi- dence. The patient rarely attempts to hide this, as he does achronic one. Acute inflammatory rheumatism has a fleet- ing nature, acid sweats, and usually a ready reaction to the salicylates. In acute suppurative hematogenous osteomy- elitis the start of the process is outside the joint. From acute suppurative hematogenous arthritis the disease may be differentiated by aspiration. The fluid from a gono- coccic joint is sterile or contains gonococci. TREATMENT.—Some authorities recommend immobil- ization, others maintain that immobilized gonococcic joints are more likely to become ankylosed. Hot applications are grateful to some patients, cold applications to others. Good results have followed washing out the joint with normal salt solution, or with a solution of protargol or argyrol. In aspirating or washing out a joint it is well to incise the skin and superficial fascia with a scalpel, and then use a large calibre needle or a trocar. Specific antigonococcic sera and vaccines have been employed often during the past ten years, and have been 106 INFLAMMATION IN BONES AND JOINTS highly praised. Apparently they are of great value. Re- cent investigations, however, indicate that the specificity is of no importance. The result of the use of non-specific proteins is said to equal that of specific proteins. Whatever local treatment be instituted, the prime indi- » cation in these cases is the treatment of the primary focus Fic. 39.—The so-called gonorrheal periostitis of the tubercle of the calcaneus. in the genito-urinary tract. It is a strange thing that the urethral symptoms often lessen as the joint becomes in- volved, to reappear as the joint condition improves. A peculiar condition sometimes is seen in old cases of deep urethral infections. ‘The patient complains of pain in the soles of his feet, where the plantar fascia is inserted into the tubercle of the calcaneus. Standing and walking are painful. Pressure by the thumb brings out the sensi- tiveness very prettily. The gait is characteristic. ‘The GONOCOCCIC OSTEOMYELITIS AND ARTHRITIS 107 patient walks as if he were treading on eggs. The Réntgen rays may or may not show a roughening of the calcaneal tubercle. Baer recovered the gonococcus from the tubercle in one or two cases. Attention to the lesion in the deep urethra usually causes a prompt disappearance of the symptoms. Vesicu- lotomy is often necessary. Massage of the prostate may be tried. Possibly strapping, or a sole plate sharply arched up under the anterior part of the calcaneus, may also be of benefit. Some surgeons advise an operation. The incision may be made on the medial aspect of the heel. It is carried down to the bone, and the suspected tissue is scraped out. Opera- tion is rarely necessary if the deep urethra be cleared. up. A similar condition of painful heels, not so marked nor so characteristic, is occasionally observed in patients with a focus of infection in their teeth or tonsils. Patients with flat feet also may complain of painful heels, but they have not the “egg-walking” gait. A spur is occasionally seen in the Rontgen picture of normal calcanea. It gives no symptoms, and requires no treatment. CHAPTER VI ACUTE INFLAMMATORY RHEUMATISM Strictly speaking, this is not a joint disease, but a general disease characterized by painful joint swellings and a marked pyrexia. Its cause never has been demonstrated. Numerous investigators’??*?°"5” have isolated organ- isms from the blood and from the joints, but have not succeeded in proving their causal relationship. Some believe that the disease is a toxemia or a mild form of pyemia. A modern view is that it is essentially an anaphylactic reaction, similar to that, for instance, against diphtheria antitoxin, but more severe. A strong array of evidence points to the tonsil as the seat of the infection, whatever it may be. Acute inflammatory rheumatism is characterised by a *AcHaAtME, P.: “Sur un signe de diagnostic précoce des attaques et des rechutes de rhumatisme articulaire aigu.” Arch. Gén. de Méd., 1902. exc, 257. * Beaton, R. M., ann Waker, KE. W. A.: “The Etiology of acute rheu- matism and allied conditions.” Brit. Med. Jour., 1908, i, 237. * Beatriz, James M.: “A contribution to the bacteriology of rheumatic fever.” Brit. Med. Jour., 1906, ii, 1781. 4Beartiz, James M.: “The Micrococcus rheumaticus. . ,” Brit. Med. Jour., 1904, ii, 1511. ° Lewis, Morris J.. aNd Loncopr, Warrietp T.: “ Experimental Arthri- tis and endocarditis...” Assn. Am. Phys. Trans., 1904, xix, 457. ® Poynton, Freprrick J.. AND Paring, ALExANDER: “The etiology of rheumatic fever.” Lancet, 1900, ii, 861, 932. 7Pornron, F. J.. anp Parner, ALExANDER: “Some further investigations and observations upon the pathology of rheumatic fever.” Lancet, 1910, i, 1524. 5 Rosenow, E. C.: “The Etiology of acute rheumatism, articular and muscular,” Jour. Infec. Dis., 1914, xiv, 61. ®TrRIBOULET AND Coyon: “Recherches bactériologiques concernant un cas de rheumatisme fébrile mortal. . .” Soc. de Biol. Comp. Rend., 1897, xlix, 1000. 108 ACUTE INFLAMMATORY RHEUMATISM 109 high, irregular, remittent temperature, a high colored acid urine, and sweats. ‘The larger joints as a rule, suffer most. They swell, one after another, and are exquisitely sensitive to motion and to touch. ‘The swelling is circumarticular as well as articular. The adjacent tendon sheaths may also be involved. The joint is red and hot. ‘The great peculi- arity of the disease is its fleeting nature. It flits from joint to joint, one joint clearing up as the next becomes involved. Another marked feature is its reaction to the salicylates. Acute inflammatory rheumatism is rarely overlooked when it is present. Its features are so characteristic that they can hardly be ignored. ‘The diagnosis is employed too often rather than too seldom. Many lives have been lost by failing to recognise an acute suppurative arthritis, and treating it as “ rheumatism.” It is a good rule never to diagnose anything as rheumatism, until every thing else has been ruled out. THE TREATMENT belongs in the realm of internal medicine. Splinting may alleviate the pain. There is a history of frequent sore throat, and the tonsils are diseased. These organs should be removed. Not infrequently the disease lights up after tonsillectomy, probably on account of the entrance of organisms through the raw surface. CHAPTER VII HYDRARTHROSIS INTERMITTENS Intermittent Synovitis, Intermittent Joint Hydrops THis rare and somewhat mysterious lesion was de- scribed by Perrin.’ It consists of a periodic effusion into one or more joints, usually into the knee. The fluid re- mains for a few days and then disappears. The cause is unknown. It has been regarded as a syphilitic manifestation, as a neurosis, and as a reaction of the synovial membrane to a focus of infection in the end of the bone, or in some other part of the body. Coincident disease of the thyroid gland has been noted, and vasomotor disturbances elsewhere. Some observers consider it as a passive effusion, others as a synovitis. It occurs with about equal frequency in men and women. The joint fluid is usually serous, and contains flakes of fibrin. The synovial membrane shows its customary reac- tion to the presence of fluid in the joint cavity, and becomes thickened and villous. The swelling usually comes on rather suddenly, in- creases for a few days, and then subsides, to return after an interval which may vary in length. Pain, if present, is not usually severe. Fever, dizziness, headache, pain in the limbs, vasomotor disturbances and other constitutional symptoms have been observed. In women a certain relation to the menses has been noted. If several joints are attacked, they may be attacked coincidently or one after another. Occasionally the affection leaves one joint and attacks an- 1 Perrin: Journal de. Médecine. Par. 1845, iii, 82. _ IIO HYDRARTHROSIS INTERMITTENS 111 other, like acute inflammatory rheumatism. Sometimes the patient can foretell the exact date of his next attack, but again cases which have been regular in their recur- rence may become irregular, and vice versa. In women the attacks sometimes have subsided during pregnancy. ‘TREATMENT.—Immobilization, apparently, is of no avail. As to internal medication the best results seem to have been obtained with quinine and arsenic, although no malarial basis ever has been found for the disease. On the chance that it may be caused by a focus of infection in the bone end, or possibly may be an “anaphylaxis” to a distant focus, a search for a focus should be instituted, and if one be found, it should be removed. ‘The only patient with this affection I ever saw, had evidences of infection in both teeth and tonsils, whose eradication she would not permit. CHAPTER VIII TRAUMATIC ARTHRITIS Traumatic Synovitis A SIMPLE traumatic arthritis may be caused by an in- jury to the joint capsule, or by an intraarticular fracture. In either case blood is poured out into the joint cavity, and probably, by its mere presence, irritates the synovial mem- brane. ‘The membrane becomes thickened, infiltrated, succulent and villous, encroaching somewhat on the carti- lage at its border. When the effusion has been absorbed, and the capsule or bone has healed, the synovial membrane returns to normal. A bloody or fibrinous exudate often leaves adhesions behind, with some stiffness which persists for a while. THE DIAGNOSIS is usually quite simple. An acute arthritis immediately following an injury is practically always a traumatic arthritis. It is not always easy to dif- ferentiate between the injury to the capsule—a sprain— and one to the bone—a fracture. Excluding the Rontgen rays, perhaps the two most valuable helps are the ecchy- mosis and the point tenderness on the bone in fracture. False point of motion and crepitus are hard to elicit unless the fracture is a severe one, and then there will be little difficulty in the diagnosis. THE TREATMENT of the arthritis complicating fracture is that of the fracture itself, except that if the amount of fluid in the joint be excessive, and cause great pain and possibly difficulty in the reduction of the fragments, it may be aspirated under strict asepsis. 112 TRAUMATIC ARTHRITIS | 113 The continued pain and stiffness which follow the healing of a fracture with misplaced fragments in a healthy person, are probably due to the constant spraining of the damaged joint apparatus, viewed as a machine. It is doubtful if any permanent changes are set up in the bone thereby. If, for instance, from an old stiff wrist, following a carpal fracture, the offending fragments be removed, good function often returns. On the other hand, marked stiffness and disability frequently follow a well reduced fracture, especially in an elderly person. In such case a careful examination of the patient, and especially of his other joints will probably reveal evidences of preéxisting bone changes. It is likely that the fracture simply con- verted a walled-in chronic infectious osteomyelitis into a chronic arthritis, which will be improved by prompt atten- tion to the teeth. | A SPRAIN is the tearing of a ligament, but the term in- cludes also the traumatic arthritis which results, and in the knee this is so dominant that we are wont to allude to the injury as a synovitis, whereas in the ankle we never should think of calling it anything but a sprain. The cardinal symptoms are pain and restriction of motion, especially of motion in one direction. The joint is swollen and its contour is changed. It contains fluid, which can easily be demonstrated in the knee and in the elbow, with more difficulty in the hip, ankle and spine. In the knee, the fluid floats the patella off the condyles; in the elbow fluctuation is to be sought posteriorly at the sides of the triceps tendon. ‘The pain is made worse by motion which puts the damaged ligament on the stretch. Usually the joint is held in semiflexion. THE DIAGNOSIS with the help of the Rontgen rays usually is simple. Without it, it is often impossible. The 8 114 INFLAMMATION IN BONES AND JOINTS main thing to establish is that the joint was normal at the time of the injury, in order that one may exclude a disease that was simply aggravated by it. TREATMENT.— The first indication is to restrict as much as possible the formation of the exudate in the joint, — especially in a joint that has a capacious cavity like the knee. This is done by rest, pressure, strapping, bandaging on a splint, etc. Ice bags, or hot compresses also are use- ful. ‘These measures may be continued for a few hours. Later the important indication is rest, not necessarily rest for the whole joint, but rest for its damaged part. In the later stages, to overcome stiffness, physical therapy —baking, hydrotherapy, massage—may occasionally be advisable. THE KNEE is usually sprained in its medial ligament, and especially when it is in flexion. Far less often is a crucial ligament torn. ‘Therefore the chief indication, after the acute symptoms have subsided, is to hold the joint in extension, in which position it is rarely injured. This is accomplished by diagonal criss-cross strapping with overlapping strips of adhesive plaster about ten inches in length and an inch or two in width, quite firmly applied over the front and sides of the knee, reaching from a point below the joint to one above the top of the quadriceps pouch. This strapping not only prevents flexion but also exerts pressure. The patient is encouraged to go about, preferably with a cane. His comfort is a good indication of the efficacy of the treatment. If he suffers pain the treatment is not sufficient. Then immobilization probably will be necessary, and subsequent physical therapy. If a semilunar cartilage be torn, the semidetached piece becomes pinched between the tibia and femur, and the joint is sprained. It fills with fluid, and an attack of “synovitis” TRAUMATIC ARTHRITIS 115 results. Often the knee “locks” in semiflexion, and only can be released by manipulation by the patient himself or by a bystander. Sometimes the deformity is fixed, and cannot be overcome. When the knee has been straightened, it usually swells for a while and is painful. ‘The symptoms slowly subside, and the joint returns to normal. No further trouble may be experienced, but as a rule the accident re- curs, possibly many times, and each time it is followed by the symptoms of joint irritation, usually not so severe as those following the first attack. The cause is a twist of the knee when it is in semiflexion. It is a frequent accident among athletes, especially among football players. The medial meniscus is much the more frequently torn. THE DIAGNOSIS as a rule is not difficult. The Rontgen picture is negative. ‘The patient gives the history of the attacks of locking. If sensitiveness of the anterior portion of the medial meniscus be present in addition, the diagnosis is fairly certain, though surgeons who have often opened the knee agree that absolute certainty is not possible. TREATMENT.—Various manipulations by the patient are successful in reducing the deformity—shaking the leg on the thigh, while the patient is erect or lying on his face, swimming motions carried out on the floor, ete. The surgeon may aid by shaking the flexed leg with the patient prone, or by flexing, extending and rotating. Jones’ recommends “ acute flexion, lateral deviation, and rotation inwards and full extension.” Sometimes it is hard to tell whether the cartilage has been reduced or not. The patient may be able to give us the required information, but there is a peculiar feel that may clinch the matter. If, with the patient supine, the knee be passively flexed and extended, attempted full extension comes to a sort of springy stop as * Jones, Rosert: “ Notes on derangement of the knee.” Annals of Surg., ° 1909, i, 969. ' 116 INFLAMMATION IN BONES AND JOINTS long as the cartilage is out of place, whereas with a normal knee, the stop is sudden and definitive. If all attempts at reduction fail, it is sometimes wise to send the patient home for 24 hours, to see what he can do by himself. If he fail, — operation is practically imperative. When the cartilage is first torn and has been reduced, the knee should be splinted, at least partially, and should be treated with the idea of healing the torn cartilage. There is a reasonable chance of success by these means. With each succeeding slip the chances grow smaller. Most authorities agree that recovery is not to be expected after the cartilage has been out two or three times, but cases have been observed (I have had a personal experience with one) in which recovery has ensued after numerous attacks. 'This is rare, and there is always an element of risk in the acci- dent. ‘There are times when a simple fall in the street from locking of the joint might be fatal. Most surgeons do not operate after the first slip, especially as the diagnosis is not a matter of certainty. ‘The oftener the accident recurs after this, the stronger is the indication for operation. JONES'S OPERATION, with the knee flexed, has attained a wide popularity. Strict asepsis is of the first importance. Not even a gloved finger should touch the wound. All sponges should be on holders. Artificial ischaemia is to be employed. The patient’s legs hang over the end of the operating table, and the operator sits facing them. The incision is a curved one. It starts from a point just proximal to the distal border of the patella, and about a centimetre medial to its medial border, runs distally to a point about a centimetre distal to the tibial margin, and then curves sharply medialwards for about two centimetres. It is about eight centimetres long. ‘The incision through the capsule is about half as long. The edges of the wound TRAUMATIC ARTHRITIS _ 117 are retracted, and the torn piece of cartilage is cut off with a knife, and without traction on it. Jones never ties ves- sels, always uses a tourniquet, and never drains. The wound is sutured in layers. The joint is immobilized for eight or ten days, and then passive motion and massage are begun. THE ANKLE is usually sprained by a twist of the foot inward, tearing the external lateral ligament. An excel- lent treatment, perhaps after twenty-four hours of hot or cold applications, is that with the Cottrell (sometimes erroneously called the Gibney) strapping. TREATMENT.—The foot is held in dorsal flexion and marked eversion. ‘The plaster, in strips one inch wide, and in two lengths, eight and twelve inches, is to be ready at hand. The first strap (eight inch) starts just behind the metatarsophalangeal joint of the little toe, runs around behind the heel, and ends in the region of the medial mal- leolus. The second (twelve inch), starts about the middle of the lateral surface of the calf, passes down the leg, under the heel near its posterior part, and ends near the medial malleolus. ‘The third overlaps the proximal half of the first, the fourth the anterior half of the second, and so on until about eight have been applied. A few criss-cross straps reinforce these where they cross at the ankle, and a snug bandage holds them all in place. The immediate relief afforded by this dressing is often remarkable, when it is properly applied. SPRAIN OF THE ELBOW is rare and demands rest. The same may be said of the shoulder. Subacromial bursitis, with its painful rotation and abduction, is to be suspected in painful injuries about the shoulder. SPRAINS OF THE WRIST also are probably quite rare, and should be diagnosed only when other lesions have been ruled 118 INFLAMMATION IN BONES AND JOINTS out. In this connection three things especially must be borne in mind: Ist, Fractures of the radius or of the carpal bones. The Rontgen rays will detect these. 2nd, Ganglion. This is a rather small, tense, fluctuating swell- ing found usually on the dorsal aspect of the wrist, slightly - to the radial side, or less often on the volar aspect in the immediate vicinity of the radial artery. 3rd, The so-called tenosynovitis or tenovaginitis crepitans, a slightly painful, diffuse swelling, over the posterior and lateral aspect of the distal end of the radius. When the patient actively extends and abducts his thumb, a fine crepitation like the rubbing together of two pieces of silk, is communicated to the examining finger. Circular strapping with adhesive tape, about two inches wide is a good treatment for a sprained wrist. SPRAINS OF THE SPINE, especially of the spine already affected with a chronic arthritis, are quite common, though on account of the inaccessibility of the spinal joints, the diagnosis is never more than presumptive. Following a severe wrench, twist, or sudden strain, the patient ex- periences a sudden pain, usually in his lumbar region (“lumbago’’) or down his thigh (“sciatica”). The pain often is quite severe, and as a rule is accompanied by marked stiffness of the spine. Sometimes the patient is unable to bend forward at all, at other times forward bending is carried out with a lateral deviation. When the sacroiliac joint is involved, perhaps also when the lower lumbar spine is sprained, a Kernig sign is present. An Ely sign? occasionally may be elicited in lumbar arthritis or sprain. ?In certain irritative lesions of the lower lumbar spine, if the patient lie prone, and his knee be flexed, his pelvis will rise from the table. This is the Ely sign, and it is probably caused by the pull forward on the rigid lumbar spine by the rectus femoris muscle. TRAUMATIC ARTHRITIS 119 TREATMENT.—These cases ordinarily are treated with “antirheumatic ”’ remedies as “myositis,” “ fibrositis,” “Jumbago ” or “ sciatica.”” A Rontgen plate usually will show the evidences of a chronic arthritis, and the main efforts at treatment should be directed at this. (See the chapter on chronic arthritis.) In sacroiliac sprain the X-rays often show a subluxation of the pubic symphysis. In the simple cases, snug strapping about the sacroiliac joints, below the anterior superior spines may be all that is necessary. Physical therapy also has its advocates. Some- times the subluxated pubic joint must be reduced under an anesthetic. Superextension of the thigh on the affected side will usually be found the best manipulation. CHAPTER IX SUPPURATIVE ARTHRITIS FROM WOUNDS THE joint may be involved directly by the penetration of dirty foreign bodies, or it may be involved secondarily by the spread of an infection from a compound fracture opening into the joint. In the first case the marrow may become infected secondarily from the joint. The infection is of course always a mixed one. At its start it possesses peculiarities depending upon its place of origin, and the nature of the trauma, but once under way, its course is much the same as that of a hematogenous infection. The soft parts may become gangrenous at an early stage. Our ideas on the treatment of joint wounds have been greatly modified during the late war, and, while unanimity has by no means been reached, a fairly well-recognized standard of procedure has been adopted. This may be stated briefiy as follows: . | In the absence of any sign of infection penetrating joint wounds made by sharp instruments, supposedly fairly clean, may be treated expectantly with sterile dressings. This applies also to perforating wounds made by bullets of high velocity, especially in the absence of fracture. They must be watched carefully, however, and must be opened up at the first sign of an infection. Other wounds demand operation. THE OPERATION OF DEBRIDEMENT, as practised so ex- tensively, aims to remove not only the foreign body but also its infected track through the tissues. In wounds of the soft parts all devitalized tissue in the neighborhood is 120 SUPPURATIVE ARTHRITIS FROM WOUNDS 121 also excised, but this feature is not so prominent in oper- ations on joints. ‘The wound of entrance is excised down into the joint, and the foreign body is removed. If the projectile is imbedded in bone or soft tissue, this is removed with it. The track of the missile is excised, with chisel and gouge, with a curette only if necessary. All foreign bodies, such as shreds of clothing, and all loose fragments of bone are removed. If the joint has been so badly damaged that useful function is not to be expected, resection had best be done forthwith. | After lavage of the joint cavity with normal salt solu- tion, the capsule is sutured, and the wound of the skin also, unless its infection is suspected. If so, the wound in the skin is left open. Some surgeons recommend filling: the joint cavity two or three times with ether after lavage with normal salt solution. If the joint fills with fluid thereafter, it should be aspirated. No drains should be left in the joint. Early active and passive motion, as soon as the wound has healed, are very important. In this procedure one must always avoid infecting sterile tissue. Instruments which have touched infected tissue should be discarded for fresh ones, and the gloves must be changed as often as necessary. In the early stage of infected wounds the same treat- ment may be carried out tentatively, perhaps modified by drainage for a day or two. Payr maintains that in joint wounds without bone damage, the infection is often super- ficial in the synovial membrane, and can be controlled by irrigation (injection), with or without temporary drain- age, either simply through smal! openings in the capsule, or with a glass tube. With frank infections, after thorough debridement and cleansing, drainage of course is necessary. Willems 122 INFLAMMATION IN BONES AND JOINTS advises, in addition to the openings in the capsule, early active motion to accomplish drainage. Opinions differ as to the efficacy of this treatment. ‘The Carrel- Dakin treatment has its advocates. Whatever method of drainage be adopted, care must be taken that it - is thorough. It is not enough simply to make openings in the joint unless they actually drain it. If necessary, bone must be removed, and no recess must be left for the aceumu- lation of pus. Some surgeons advise resection, others have been disappointed with the results of the operation. Amputation often will be necessary. CHAPTER X HAEMOPHILIAC JOINTS HeEmorruacE into the joint, especially into the knee, is a fairly frequent occurrence in that interesting condition known as the hemorrhagic diathesis or hemophilia. It is observed much more often in men than in women, as is the diathesis to which it is due. ‘The tendency to bleed un- controllably at the slightest scratch is hereditary, and is handed down through the female element. Addis’ in- vestigated a number of these families of “ bleeders ”’ and has added much to our knowledge of the subject of hemophilia. It is important to know the manifestations of the diathesis in the joints in order to avoid making a blun- der that may be fatal. As the result of a slight trauma, or, as some claim, with- out trauma, a joint of a bleeder, usually the knee joint, swells up, “like a balloon,” as one patient putit. Painasa rule is not a prominent symptom; the chief complaint is the interference with function from the presence of the fluid. Fluid can be detected in the joint, and sometimes a soft 1Appis, T.: “The effect of the adminstration of calcium salts and of citric acid on the: calcium content and coagulation time of the blood.” Quart. J. Med. 1908-09, v, 2. Appis, T.: “Coagulation time of the blood.” Brit. M. J., 1909, i, 1151. Appis, T.: “The coagulation time of the blood in man.” Quart. J. M., — 1908-09, ii, 305. Anvpis, T.: “ The coagulation time of the blood.” Brit. M. J., 1909, i, 1269. Avpts, T.: “ The coagulation time of the blood in disease.” Edin. M. J., 1910, tL aes Vv. D. Annis, T.: “ Hereditary hemophilia; deficiency in the coagulability of the blood the only immediate cause of the condition.” Quart. J. Med., 1910, v, 4:14. Avnis, T.: “The pathogenesis of hereditary hemophilia.” J. Path. and Bacteriol, 1910-11, v, 15: 427. 123 124 INFLAMMATION IN BONES AND JOINTS - crepitation. ‘The synovial membrane proliferates, some- times enormously, and its internal surface may become Fic. 40.—Hzmarthrosis of the knee in a “bleeder.’’ shaggy, with the enlarged villi branching like moss on a rock. The fluid may slowly be absorbed and the joint may return to normal, to be again attacked at a later period. HA MOPHILIAC JOINTS 125 Again layers of fibrin may be deposited upon the synovial membrane and possibly upon the cartilage. These layers of fibrin may become organized, and may give rise to dense adhesions, which cause a practically complete ankylosis. A sudden, fluctuating, comparatively painless swelling of a joint without history of injury, in the absence of physical signs of tabes, should always awaken the suspicion of haemarthrosis, and should occasion a search for a family Fria. 41.—Skiagram of a case of old fibrous ankylosis in a “bleeder.’’ history of bleeders, and for a personal history of profuse hemorrhage after slight injury. For THE TREATMENT of the acute attack, rest, pressure and cold applications are probably best. After the hem- orrhage has ceased and a little time has elapsed, hot appli- cations and gentle massage may possibly promote the absorption of the exudate. In case of need, blood trans- fusion may be done, or blood plasma may be injected.” The advantage of any such procedure is temporary only; * Personal note of Dr. Addis: “ Hot applications and gentle massage I should be afraid to use. I should prefer temporary immobilization with pressure. “Blood transfusion should only be used in case of danger to life. This would not arise in a hemorrhage confined to the joints.” 126 INFLAMMATION IN BONES AND JOINTS the coagulation time is shortened, but later is lengthened again, so that the patient is in greater danger than he was before. It is hardly necessary to emphasize the importance of avoiding in all circumstances and in every stage, any oper- ative interference with a joint hemorrhage in a bleeder. BIBLIOGRAPHY ACUTE SUPPURATIVE OSTEOMYELITIS Breck, Emit G.: “Sutureless skin-sliding method for the radical treatment of lung abscess and chronic osteomyelitis.” Surg. Gynec. Obst., 1918, Xxvi, 259. Cropton, Matvern B.: “The diagnosis and treatment of osteomyelitis.” Surg. Gynec. Obst., 1915, xx, 6. Dumont, Frirz L.: “Experimentelle Beitrige zur Pathogenese der akuten himatogenen Osteomylitis.” Deutsche Ztschr. f. Chir., 1913, exxii, 116. Estor, E., ann Errenne, E.: “La greffe graisseuse dans loblitération des cavités ostéomyélitiques.” Rev. d’orthopédié., 1913, 3s., iv, 193. Errenne, E., anp Armes, A.: ‘“ Ostéomyélite typique chez le nourrisson.” Progrés Méd., 1913, xli, 35. Evans, Arruur J.: “Excision of the diaphysis of the humerus with full functional recovery.” Brit. Jour. Surg., 1913-14, i, 632. FrRAENKEL, Evue.: “ Ueber Knochenmark und Infektionskrankheiten.” Miinch. Med. Wehnschr., 1902, xlix, 561. Gross, Hernricu: “Zur Kenntnis des osteomyelitischen Knochenabscesses der langen Rodhrenknochen, in besonderer Beriicksichtigung seines anatomis- chen Verhaltens.” Beitr. z. klin. Chir., 1901, xxx, 231. Hamant, A., ann Picacue, R.: “Ostéomyélite a infections mixtes” Gazz. d. Hop., 1918, Ixxxvi, 1158. Hamitton, Franx A.: “ Osteomyelitis with bone transplantation.” J. 4d. M. A., 1913, lx, 2030. Homans, Jonw: “ Osteomyelitis of the long bones,” Ann. Surg., 1912. lv, 375. Kennepy, Cuaries M.: “ Acute epiphysitis.” Brit. Med. Jour., 1912, ii, 114. Kirmisson: “Les ostéomyélites.” Progrés Méd., 1913, xli, 643. Kiemm, Pau: “Die akute und chronische infektidse Osteomyelitis des Kindesalters.” Berlin, S. Karger, 1914. Kiemm, Pavt: “ Ueber die chronische Form der sklerosierenden Osteomyelitis des Kindesalters.” Berlin, S. Karger, 1914. Kiemm, Pavt: “ Ueber die chronische Form der skelerosierenden Osteomyelitis und ihrer Varianten.” Beitr. .z. klin. Chir., 1912, Ixxx, 54. Kriemm, Pau: “Ueber die Gelenkosteomyelitis, speciell die osteomyelitische Coxitis.” Arch. f. klin. Chir., 1912, xevii, 414. HAMOPHILIAC JOINTS | 127 Kiemm, Pavut: “Ueber die Verinderungen der knéchernen Grundsubstanz bei Osteomyelitis und ihre Ursachen.” Deutsche Ztschr. f. Chir., 1913, exxiv, 309. Kocuer, THronor: “Die akute Osteomyelitis. . .” Ztschr. f. Chir., 1878-79, xi, 87. LANNELONGUE: “Des portes d’entrée de l’ostéomyélite.” Soc. de Chir. Bull, et mem., 1886, xii, 474. LANNELONGUE, ET AcHarp: “Des ostéomyélites a streptocoques.” Soc. de biol. Mem., 1890, 9 ser., ii, 298. LaNNELONGUE, ET AcHaARD: “Etude expérimentale des ostéomyélitis a staphylocoques et a streptocoques.” dnn, de l’Inst. Pasteur., 1891, v, 209. Le Conte, Roserr G.: “ Acute inflammation of long bones, with special reference to excision of the diaphysis.” Boston Med. Surg., Jour., 1911, clxiy, 771. Le Conte, Roserr G.: “ Acute inflammation of the long bones.” Ann. Surg., 1912, lvi, 150 McGume, R. Crarx: “Aberrant and recurrent osteomyelitis.” Brit. Med. Jour., 1913, i, 138. Nervuser, G.: “Zur Behandlung starrwandiger Hohlenwunden.” Avch. f. klin. Chir., 1896, li, 683. | Nicnuots, Epwarp H.: “ Acute, subacute and chronic infectious osteomyelitis.” J. A. M. A., 1904, xlii, 439. Park, Rosweti: “ Acute infectious processes in bone.” Bosivn Med, Surg., Jour., 1895, cxxxii, 425. Pueéur, J. A.: “L’ostéomyélite des os longs chez l’enfant et ladolescent.” These de Paris, 1912. Puemister, D. B.: “ Subperiosteal resection in osteomyelitis.” J. 4. M. A., 1915, Ixv, 1994. Puemister, D. B.: “ Osteomyelitis.” D. Appleton & Co., New York & London, 1922. Prince, Seton: “ Radical operation for chronic osteomyelitis.” Brit. Jour. Surg., 1913-14, i, 625. Rost, Franz: “ Experimentelle und klinische Untersuchungen iiber chronische, granulierende Entziindungen des Knochenmarks.” Deutsche Ztschr. f. Chir., 1913, cxxv, 83. Simmons, CuHannine C.: “ Localized osteomyelitis of the long bones.” Boston Med. Surg., Jour., 1913, elxviii, 637. Simmons, CuHanninoe C.: “The treatment of osteomyelitis.” Suwrg., Gynec. Obst., 1915, xx, 129. Srrone, G. R.: “Eight cases of osteomyelitis of the spine.” Lancet, 1912, ii, “1576. TrenveL: “ Beitrige zur Kenntnis der akuten infectidsen Osteomyelitis und ihrer Folgeerscheinungen.” Beitr. z. klin. Chir., 1904, xli, 607. Wuuiams, Gwynne: “ The localization of osteomyelitis, especially in adults.” Brit. J. Surg., 1914-15, ii, 97. CuvurcuMan, Joun W.: “Gentian violet in the treatment of purulent arthritis.” Jour. A. M. A., 1920, Ixxv, 583. 128 INFLAMMATION IN BONES AND JOINTS ACUTE GONOCOCCIC ARTHRITIS Corsus, B. C.: “Gonorrheal arthritis.” Medical Clinics of Chicago, 1917, ii, 1189. Cunver, Harry: “ Antibodies in gonococcal arthritis after the intravenous injection of specific and non-specific protein.” Jour. Lab. and Clin. Med., 191g at, Dvrour, M. H.: “Gaillard et Ravina: Sur les lésions des extrémités osseuses articulaires dans la polyarthrite gonococcique.” Bul. et Mem. d. l. Soc. Méd. des hopitaux de Paris, 1919, xxxv, 918. Harworrn, H. D.: “The treatment of gonococcal arthritis by sensitized gonococcal vaccine.” Brit. Med. Jour., 1918, i, 4. Marerrre Frxix: “ Antimeningococcic serum in the joint manifestations of gonorrhea.” New York Med. Jour., 1906, ciii, 1024. Rocers, Joun: “ The treatment of gonorrheal rheumatism by an antigonococcus serum.” J. Ad. M. A., 1906, xivi, 263. Rogers, Joun, AND Torrey, JoHN C.: “The treatment of gonorrhea! infections by a specific antiserum.” J. A. M. A., 1907, xlix, 918. Stockman, Ratpu: “The vaccine treatment of gonococcal arthritis.” Brit. Med. Jour., 1911, ii, 1465. Torrey, JoHn C.: “An antigonococcus serum effective in the treatment of gonorrheal rheumatism.” J, d. M. A., 1906, xlvi, 261. TYPHOID SPINE ALLAN, W., AND Squires, J. W.: “ Typhoid vaccine in a case of typhoid spine.” Amer. Jour. Med. Sciences, 1918, clvi, 11. Carnetr, J. B.: “Typhoid spine.” Annals of Surgery, 1915, Ixi, 456. Conxuin, C. B.: “ Typhoid spine.” Med. Record, 1914, Ixxxv, 157. Exy, Leonarp W.: “A case of typhoid spine.” Med. Record, 1902, xii, 966; 1904, Ixv, 655. Gauut, G.: “ Ueber spondylitis typhosa.” Muench. med. Woch., 1915, Ixii, 501. Lorp, Freprericx T.: “ Analysis of 26 cases of typhoid spine.” Boston Med, and Surg., Jour., 1902, cxlvi, 689. ; Oster, Wm.: “ Typhoid spine.” Canadian Med. Ass. Jour., 1919, ix, 490. Rueu, J. T.: “ Report of a case of typhoid spine.” dm. Jour. Orthop. Surg., 1915, xiii, 287. Rogers, Marx H.: “ Pathology of typhoid spine.” Boston Med. and Surq., Jour., 1913, elxviii, 348. Sirver, Davin: “Typhoid spine.” Amer. J. Orthop. Surg., 1907-8, v, 194, (bibliography). ACUTE INFLAMMATORY RHEUMATISM Fantus, Bernarp, Stmmonps, Warrer E., anv Moore, Jostan J.: “The effect of salicylates on experimental arthritis in rabbits.” Arch. Int. Med., 1917, xix, 529. LirppmMaNN: “Bactériologie du rhumatisme articulaire aigu.” Semaine Méd., 1900, xx, 77. HASMOPHILIAC JOINTS 129 Poynton, F. J., Acasstz, C. D. S., ann Taytor, J.: “A contribution to the study of the rheumatic infection.” Practitioner, 1914, xciii, 445. Poynton, F. J.. ann Patne, AteExanperR: Researches on rheumatism. London, J. & A. Churchill, 1913. Rotiy, Fr.: “Zur Aetiologie des akuten Gelenkrheumatismus.” Med. Klinik, 1916, xii, 1167. Rosenow, Epwarp C.: “ Elective localization of streptococci.” J. 4. M. A., 1915, Ixv, 1687. Swirr, H. F., ann Krnserra, R. A.: Bacteriologic studies in acute rheumatic fever.” Arch. Int. Med‘, 1917, xix, 381. Werntravup, W.: “Der acute Gelenkrheumatismus: Spezielle Pathologie und Therapic innerer Krankheiten.” Urban u. Schwartzenberg, Berlin, 1913. INTERMITTENT SYNOVITIS Brackett, E. G., ann Corron, F. J.: “Intermittent hydrops.” Boston Med. Surg., Jour., 1901, cxlv, 484. Lausir, A.: “L’Hydarthrose du genou et son traitement chez les blessés de guerre.” Jour. de méd. des Bordeaux, 1918, Ixxxix, 158. Linspercer, A.: “Ueber intermittierenden Gelenkhydrops.” Beitr. z. klin. Chir., 1901, xxx, 299. MacLetranp, R.: “Intermittent hydrops articulorum.” Lancet, 1919, i, 463. Seetincmutier, A.: “Hydrops articulorum intermittens.” Deutsche med. Wehnschr., 1880, vi, 52. Tavernier: “ Hydarthroses récidivantes du genou par coincements anatomi- ques.” Lyon Méd., 1918, exxvii, 433. SUPPURATIVE ARTHRITIS FROM WOUNDS Bristow, W. Rowtey: “Treatment of joint and muscle injuries.” London, Oxford University Press, 1917. Burcxuarpt, Hans unp Lanopors, Fenix: “ Erfahrungen uber die Behandlung inficierter Gelenke im Kriege. “ Beitr. z klin. Chir., 1915-16, xeviii, 358. Coox, Franx: “Gunshot wounds of joints, their pathology and treatment,” Lancet, 1917, i, 711. Denx, W.: “ Ueber Schussverletzungen der grossen Gelenke.” Beitr. z. klin. Chir., 1914, xci, 394. ; E1senpratH, Danret N.: “Injuries of the joints in war and in civil life.” Surg., Clin. Chicago, 1919, iii, 497. Jones, Rosert: “Injuries to the joints.” London, Oxford University Press, 1915. Morpny, Joun B.: “ Contribution to the surgery of bones, joints and tendons.” J. A..M. A., 1912, Iviii, 1254. Oscoop, Roserr B.: “Gunshot injuries to the joints.” Jour. Orth. Surg., 1919, i, 304. Payr: “ Arm-und Beinschussbriicke; Gelenkschusse; Gelenkeiterungen.” Beitr. z. klin. Chir., 1915, xcvi, 529. 9 130 INFLAMMATION IN BONES AND JOINTS Payr: “ Gelenkverletzungen, Gelenkeiterungen und ihre Behandlung.” Miinch. med. Wehnschr., 1915, Ixii, 1321. Payr: “Gelenkverletzungen, Gelenkeiterungen und ihre Behandlung.” Miinch. med. Wehnschr., 1915, Ixii, 1282. Payr: “Gelenkverletzungen, Gelenkeiterungen und ihre Behandlung.” Miinch. med. Wehnschr., 1915, Ixii, 1241. Poot, Evcene: “ War wounds.” J. A. M. A., 1919, xxiii, 383. Poot, Evcenr H., ann Jorson, JonHn H.: “ Treatment of recent wounds of the knee-joint.” Ann. Surg., 1919, lxx, 266. Poot, E. H., Lez, B. J.. ann Dineen, P. A.: “Surgery of soft parts, bones, and joints, at a front hospital.” Surg., Gynec. Obst., 1918, xxvii, 289. Swan, Joceryn R. H.: “Severe infected gunshot injuries of the shoulder and elbow joints; early excision to secure mobility.” Lancet, 1917, i, 524. Witiems, Cu.: “Quelques résultats du traitement des lésions articulaires. par la méthode de la mobilisation active immédiate.” Soc. d. Chir. Bull. et Mém., 1917, xliii, 1784. H/EMOPHILIAC JOINTS Cruet, Pierre: “ Hémophilie articulaire.” Presse Méd., 1906, xvi, 578. DeriBERE-Descarpes, Pierre: “Des arthropathies chez les hémophiles.” Thése de Paris, 1910. Escanpbe, F., ann Tapre, J.: “Sur un cas d’hémophilie articulaire.” Jour. de radiol. et délec., 1919, iii, 298. Gayvet, M. G.: “ Arthropathies et hématomes diffus chez les hémophiles.” Gaz. Lebd. de Méd. et. de Chir., 1895, xxxii, 258. Gocut, Hermann: “ Ueber Blutergelenke und ihre Behandlung.” Arch. f. Klin. Chir., 1899, lix, 481. Konic, Franz: “Die Gelenkerkrankungen bei Blutern mit besonderer Ber- iicksichtigung der Diagnose.” Samml. klin. Vortr. Chir., 1890-94, v, 233. Lecrerc, F., anp CuHauier, J.: “ Hemophilie familiale.” Lyon Meéd., 1912, cxix, 589. . Mankiewicz: “Ueber Blutergelenke.” Berl. klin. Wehnschr., 1913, 1, 2174. Martin-Dvu Pan, Cuartes: “De larthropathie hémophilique.” Rev. Méd. de la Suisse Rom., 1915, xxxv, 547. Merry, H., Sarin, H., ann Wirzorts, A.: “Deux cas d@hémophilie familiale. Arthrite hémophilique simulant |’ ostéomyélite.” Soc. de pediat. de Paris, ‘Bull., 1913, xv, 86. Prouter, M. P.: “Les arthropathies hémophiliques.” Gaz. d. hop., 1902. Ixxv, 385. Rorn, Paut B.: “ Case of hemophilia with effusion into knee-joints.” Brit. Jour., Child. Dis., 1918, xv, 116. Weu, P. E., anv Boyt: “ Hémophilies humaine animale et expérimentale,” Cong. Internat. de Path. Comp., 1912, ii, 335. Youmans, Joun B.: “Report of case of hemophilia with joint involvement.” Wis. Med. Jour., 1919-20, xviii, 257. SECTION IIL. CHRONIC OSTEOMYELITIS CHAPTER I PHOSPHORUS NECROSIS INDIRECTLY, and consequent upon the changes in the bone produced by phosphorus, bacteria from the mouth may cause a chronic suppurative osteomyelitis in the maxilla or more often in the mandible. The disease is usually found in workers in phosphorus match factories, and especially among those who have bad teeth. With the introduction of sanitary precautions it has grown rare. Hand in hand with the suppuration and necrosis in the bone and in the marrow, goes the production of new bone not only in the periosteum, but sometimes in the bone itself. The teeth loosen and fall out, and the soft tissues become infiltrated and inflamed. The entire mandible may be killed, and its articulation may become ankylosed. Death often ‘results. After the removal of the mandible a new bone may be formed by bone production in the periosteum. The treatment is prophylactic and operative. ‘The mouth and teeth of match-makers should be kept scrupu- lously clean and in good condition. Factory employés should not eat nor drink in their work-rooms, and by atten- tion to their hands and to their finger nails should avoid carrying any phosphorus into their mouths. _Work-rooms must be kept clean and well-ventilated. Where proper precautions are observed, phosphorus necrosis will rarely be seen. The operative treatment consists in the resection of the diseased bone. The resection should be a free one, and all the affected tissue must be removed. As a rule new bone will be built up to replace that which is removed. 133 134 INFLAMMATION IN BONES AND JOINTS SCLEROSING OSTEOMYELITIS A rather rare form of osteomyelitis, the so-called scleros- ing osteomyelitis, has been described which has an acute or subacute onset and does not lead to the immediate formation of pus. More or less of the bone becomes very dense and | thickened. Sometimes small abscesses with sequestra are found in this mass of dense bone. Whether this disease should be included under the head of acute or of chronic osteomyelitis is doubtful. The treatment consists of eradi- eating any possible focus of infection in the body, and cleaning out any abscesses with the surrounding: scler- osed bone. Another rather bland form of chronic osteomyelitis is occasionally seen in workers in mother-of-pearl. It has no tendency to suppurate, and yields readily to the removal of its cause. CHAPTER II SYPHILIS THE bone manifestations of syphilis are very frequent. Not only is the infection carried to the bone marrow at an early period, but it remains there almost indefinitely. It manifests itself in the secondary and in the tertiary stages, and also after the subsidence of the active period of the disease in the form of the so-called “neurotrophic ” bone lesions. Congenital bone syphilis is fairly frequent, in fact its lesions are among the most characteristic in the body. It has been pointed out that congenital syphilis is really acquired syphilis, acquired in utero, and that its peculi- arities are due simply to the differences in foetal and infantile tissues from those of the adult. Hereditary syphilis probably is a misnomer, as implying an infection of the germ plasm. In studying syphilis of the bones and joints one is struck by the marked, and, at first sight, unaccountable difference of opinion that prevails on most phases of the subject, but the difference of opinion is not so strange as it seems. Until the last few years the cause of syphilis had not been identi- fied. Therefore the diagnosis rested upon the history, upon the presence of other known (or presumptive) evi- dences of syphilis, upon the therapeutic test, or upon all three. Even to-day the vast majority of clinical diagnoses is made without the demonstration of the spirocheta palli- dum, and in such cases the pathologist never receives any of the material for examination, for no operation is done. 135 ‘ 136 INFLAMMATION IN BONES AND JOINTS On the other hand the pathologist regularly performs necropsies upon the bodies of still-born foetuses and of young infants, in which he can demonstrate syphilis. With these cases the clinician is not brought into contact. The morbid processes observed by the pathologist and by the © clinician appear to be entirely different, but in point of fact they are quite the same, and differ only in location and details. ParuoLocy.—The characteristic lesion of syphilis in bone is a proliferative inflammation in the marrow—a syphiloma, a gumma. ‘This may occur in any part of the bone, though its situation is largely determined by the age of the patient. In congenital syphilis, as seen in infants and children, the ends of the long bones and the shaft of the bones of the hands suffer most; in the adult the shaft of the long bones is most often attacked. The resulting process depends largely upon the location. While certain peculiar types of osseous syphilis can be recognized as more or less standard, it is necessary to remember that they are by no means invariable, and that here as elsewhere in the body, the disease often manifests itself in most unusual ways. EARLY CONGENITAL SYPHILIS Although a few cases of congenital bone syphilis had been published, the disease was considered to be very rare, in infants and children, until the publication of Wegner’s article in 1870... Then quickly the investigations of Parrot? and of Waldeyer and Koebner,® in 1872, and of | *'Wecner, Georce: “Ueber heredidere Knochensyphilis bei jungen Kindern.” Archiv. f. Path. Anat. u. f. klin. Med,, 1870, i, 305. 7 Parrot, M. J.: “Sur une pseudo-paralyse ... de syphilis héréditaire.” Archives. d. Physiol. Normale e. Path., 1872, iv, 319, 470, 612. *'WaxtpeyerR u. Korpner: “ Beitrege zur Kenntnis der _ herediteren Knochensyphilis.” Arch. f. Path. Anat. 1872, lv, 367. SYPHILIS 137 Taylor,’ in 1874, established the fact that bone lesions in early congenital syphilis, so far from being infrequent, were among the most common manifestations of the disease. The peculiar lesion of congenital syphilis, the ‘“ osteo- chondritis syphilitica”” of Parrot is located immediately adjacent to the epiphysial cartilage on its shaft side, that is, in and near the zone of provisional calcification. It con- sists essentially in a syphilitic myelitis. The new granula- tion tissue in the marrow breaks up the regular formation of bone. Under the microscope one sees tongues of it pushing up into the epiphysial cartilage. The columns of calcified and calcifying cartilage matrix in the zone of pro- -visional calcification are, to a great extent, absorbed, so that the zone or a part of it may eventually consist of little else than granulation tissue, separating the epiphysis partially or completely from the shaft. Later the granu- lation tissue undergoes necrosis. The zone of provisional calcification becomes much wider than normal and appears as a fairly broad white or pinkish band, irregular in its outline, instead of as a thin, barely perceptible line. Later the tissue breaks down and becomes a mass of grayish-white, brittle, mortar-like material, either in a small area or running across the entire width of the bone and possibly separating the epiphysis from the shaft. The process in the marrow is not regular and sharply defined, but decidedly irregular, wavy, and notched. Vessels from the marrow push up into the epiphysial cartilage. The resulting irregular outline of the shaft side of the epiphysial cartilage, somewhat similar to that in rickets, is perceptible to the naked eye and appears also in the X-ray plate. The X-ray shows also a *Taytor, R. W.: “Syphilitic lesions of the osseous system in infants and young children, etc.” Am. J. Obstet., 1874, vii, 53, 177, 559. 138 INFLAMMATION IN BONES AND JOINTS rarefaction of the bone corresponding to the irregular area of the disease, on the shaft side of the epiphysial cartilage. The broken down syphilitic granuloma may later break through the periosteum and communicate with the surface and become secondarily infected, or resolution may take place under appropriate treatment. If the epiphysis have been separated, union usually is brought about by new bone laid down in and under the periosteum, and the growth of the limb is not retarded. The changes described above are often seen in still-born syphilitic foetuses. They may, however, be present in syphilitic children born alive or may appear during the first few months of life. They occasion swellings in the bone in the neighborhood of the joint, sometimes quite painful and sensitive to pressure, sometimes not so painful. The resulting condition is what Parrot described as “ pseudo- paralysis.” The limb hangs limply. The child refuses to move it, and cries when it is moved. With separation of the epiphysis, a false point of motion can be found, with a soft crepitus. When union has been brought about, the thickened periosteal bone, shaftward from the epiphysis ean be felt. The gross changes in and about the epiphysis are some- what similar to those seen in rickets, and the similarity 1s so great that certain observers in the past have thought that syphilis was the cause of rickets. The essential points in the diagnosis are: first, syphilis appears at an earlier age than rickets; second, with syphilis other marks of the dis- ease such as roseola, mucous patches, etc., are usually present, possibly also other changes in the shafts of the long bones and the skull; third, the changes about the epiphysis in syphilis usually, as far as clinical evidence goes, are single or at best are evident in only two or three SYPHILIS 139 places, whereas with rickets they are more or less general; fourth, syphilis is more painful than rickets. The changes in the region of the epiphysis in scurvy, are somewhat similar clinically to those of syphilis, but scurvy usually appears somewhat later, the irregular appearance of the zone of calcification and the bone absorption do not appear in the X-ray plate in scurvy, the onset is sudden, the pain perhaps is more severe, other signs of syphilis are absent, and signs of scurvy, such as hemorrhages from the gums are present. Besides this so-called syphilitic osteochondritis another notable marrow change is often met with in young syphilitic children according to Wegner, namely fatty degeneration of the vessels and cells of the marrow. 'This may be more or less diffuse, or may be circumscribed, and gives to the bone marrow a yellowish or pinkish yellow color. Perhaps to these extensive marrow changes is due the well known anemia of syphilitic children. In older children three syphilitic lesions are often found in the bones of the extremities: first, cortical changes similar to those of the adult, later to be described; second, disease of the bones of the hand, most often of the proximal phalanx, similar to the spina ventosa of tuberculosis; third, disease of the ends of the long bones with an accompany- ing arthritis. Syphilitic disease of the marrow of the bones of the hand is fairly frequent in children. It causes a rarefaction of the bone and an enlargement, more or less general, but especially marked at its proximal extremity. It shows little or no tendency to involve the joint, and quite often breaks through the cortex and the periosteum, communi- cates with the surface, becomes secondarily infected, and leads to the establishment of persistent sinuses. The 140 INFLAMMATION IN BONES AND JOINTS irritation of the disease in the marrow with the resulting destruction of bone in the interior, is said to cause the formation of new bone in the periosteum, perforated in one or more places for the discharge of the necrotic material within. A probe passed through one of these holes in the | shell of the bone easily enters the large cavity. This syphilitic dactylitis is as a rule not very painful. The swelling may be slight but usually is quite well marked, giving the bone twice or thrice its normal diam- eter. The length of the bone may also be slightly increased. Fie. 42.—Dactylitis, probably syphilitic but treated for a long time as tuberculosis. The general shape of the bone in its breadth is round, while it appears to have in its longitudinal direction an oval shape (Taylor). It is somewhat broader at its base than at its distal end, and the swelling begins quite perceptibly at the metacarpo-phalangeal joint, which it enlarges, and ends somewhat abruptly at the next joint, that is, of course, with disease of the proximal phalanx, the usual lesion. The integument is usually stretched and may or may not be reddened. : The Roéntgen rays show the irregular structure of the bone, and its enlargement, especially at the proximal end. This peculiar shape of the bone may help in the differentia- SYPHILIS 14] tion of syphilitic from tuberculous dactylitis, as may the presence of other syphilitic lesions in the body, and perhaps the reaction to anti-syphilitic treatment, but very often the problem cannot be solved without the aid of the microscope and the guinea-pig test. With syphilitic involvement of the marrow in the ends of the long bones in children a pathological process results in the bone and joint so similar to that of tuberculosis that the clinical differentiation may be extremely difficult or even impossible. .Not only are the essentials of the pathological process the same, but also the symptomatology and physi- eal signs. The realization of this fact alone will save one from humiliating mistakes. The differential diagnosis will be taken up under the head of tuberculosis. | One of the best known evidences of congenital syphilis in the child is the so-called “saber shin,” an anterior bowing of the tibia probably caused by a chronic syphilitic process in the marrow in the superficial part of the cortex. It gives to the child’s legs a characteristic appearance, not to be forgotten when once seen, and hardly to be confused with the outward bend of the ordinary bowlegs. BONE SYPHILIS IN THE ADULT Syphilitic osteomyelitis is frequent in the adult. The gummatous inflammation causes primarily, whatever its situation, a rarefaction, an absorption of the bone, and, if the process be very severe, death of the bone to a greater or less extent. The tissue breaks down and forms jelly- like or mucilaginous or cheesy masses, which may be absorbed under appropriate treatment, may be encapsu- lated, or may become secondarily infected and lead to the formation of sinuses. Probably this syphilitic inflammation can exist in any 142 INFLAMMATION IN BONES AND JOINTS part of the bone marrow, but it occurs in an overwhelming proportion in the superficial part of the cortex directly under the periosteum. The bone becomes spongy and later sclerosed in that locality, and new bone is produced in and under the periosteum. This new bone production dominates the clinical picture and gives the entire lesion its stamp, and it is customary to allude to this form of syphilis as a periostitis, and to regard bone production as the essen- tial factor. The great weight of authority is in favor of this view, but I believe it is an error, and consider the sequence to be: first, proliferative inflammation in the marrow; second, bone destruction; and third, bone formation. ‘This so-called syphilitic periostitis probably may occur almost anywhere in the body, but its favorite location in the ex- tremities, is in the shafts of the long bones, especially in that of the tibia. It may appear in the form of a more or less circumscribed swelling, or in a more diffuse and irregu- lar thickening of the entire shaft or of a portion of it. Again the new periosteal bone may be present in small patches. This cortical lesion possibly may occur in any period of congenital syphilis, but is considered more or less charac- teristic of the tertiary stages of the acquired form. It may be painless or comparatively so, but usually is quite pain- ful; in fact the boring pains of this form of bone syphilis, with their nocturnal aggravation, are notorious. Local sen- sitiveness 1s usually present. The overlying tissues may or may not be inflamed. If the gumma break down and become secondarily infected, a sinus is formed which may persist indefinitely, and in a general way may be said to resist treatment in proportion to the length of time it has existed. The openings of these sinuses are wont to be dark red, dirty, sluggish, undermined and ragged, not pale, puffy and pouting, like the tuberculosis sinus. SYPHILIS 143 X-rAyY Dracnosis.—Syphilis usually involves more than one bone; osteomyelitis usually only one bone. In syphilis there is rarely the extensive demineralization (so-called “ bone atrophy ”) which is a prominent feature of osteomyelitis. Syphilis involves especially the superficial part of the cortex, the only medullary involvement usually being by a smooth narrowing of the medullary canal, due to the thick- ening of the cortex at the expense of the medulla; whereas osteomyelitis begins as an.acute myelitis with secondary periostitis, of a less regular type. These points apply to active cases alone. Old lesions are frequently impossible to differentiate. Bone forming sarcoma of the periosteal type may be so characteristic as to be in little danger of confusion. ‘The fungoid, “hair on end” appearance (‘whiskers’), due to the vertically disposed bone “rays” serves to differentiate from other proliferations. Bone forming sarcoma pro- duces enlargement of the bone, which is locally more ex- tensive than the enlargement of lues or osteomyelitis, but which does not extend so far up or down the shaft. Also there is much less proliferation in comparison with the amount of enlargement. It is necessary to say that the X-ray diagnosis is sug- gestive, not final. I have seen a mixed series of cases thrown on the screen whose nature defied detection. Syphilitic disease of the marrow of the spongy bone of the spine and extremities, is not nearly so frequent as the preceding, that is as far as one can judge from clinical evidence. It causes a diffuse and more or less irregular absorption of the bone, as revealed by the Rontgen rays, very like that caused by tuberculosis, and sometimes not to be distinguished from it by clinical examination. ‘These lesions in the spongy bone do not show a marked tendency 144 INFLAMMATION IN BONES AND JOINTS to break down, are usually slow and chronic, are often painless, and, unlike tuberculosis, may exist indefinitely in the immediate neighborhood of the joint without involving it. | The X-ray picture is similar to that of the members of the first great type of arthritis, for new bone production ser nng Fig. 43.—Bone syphilis. The patient of whose radius this is a picture had been treated for a long time for tuberculosis, and recovered under appropriate treatment. in the periosteum is not always to be found in the neighbor- hood of the joint in this form of syphilitic myelitis. The diagnosis is made by the history, by the detection of other signs of syphilis in the body, especially new periosteal bone in other locations, by the Wassermann and Noguchi re- actions, and, of greatest importance, by the results of anti- syphilitic treatment. It isa safe rule to regard every case of suspected tuberculosis as possible syphilis until syphilis has been definitely ruled out. On the other hand, the rare SYPHILIS 145 eases of shaft tuberculosis are usually mistaken for syphilis. Radiologically the two are the same. A third and much rarer form of bone syphilis is a gum- ma of the central marrow canal. This usually results in the formation of a more or less circumscribed collection — of mucilaginous material in the medulla, about which the bone may or may not be sclerosed. This lesion, as a rule, is not very painful, but the reaction in the periosteum over the portion of the bone where it is situated causes a certain degree of local sensitiveness. The Rdéntgen picture may be quite similar to that of a bone cyst, but careful observation usually detects new bone production in the perios- teum over the gumma, whereas this bone production is absent in the ordinary bone cyst. esides the syphilitic ar- thritis resulting from disease in the marrow of the neighboring bone, another form of syphilitic arthritis is fairly frequent in the tertiary stages of the dis- 10 Fie. 44.—Syphilis of the shaft of the humerus. This case was operated on with anerroneous diagnosis of bone cyst. Note the reaction in the peri- osteum, which should have made a correct diagnosis easy. 146 INFLAMMATION IN BONES AND JOINTS ease. It is essentially a proliferative inflammation of the synovial membrane—a syphilitic synovitis—and shows little or no tendency at any stage to involve the bone marrow. ‘The synovial membrane proliferates and becomes | villous, and pours out a secretion which fills the joint. This syphilitic synovitis may be uniarticular or multiarticular, affects by preference one or both knees, is usually practi- cally painless, and responds promptly to treatment. ‘The skiagram is negative except for the swelling of the soft parts. Tabetic joints and bone lesions are an interesting manifestation of late syphilis. ‘They are probably degen- erations rather than inflammations. Whether or not they should be included in a book on bone and joint inflamma- tion, is doubtful. TREATMENT.—This, in its main features, is that of syphilitic lesions anywhere in the body, namely by ars- phenamin, mercury and the iodides. ‘The restoration of the normal structure of an apparently hopelessly damaged bone or joint is sometimes remarkable, but when secondary infection has taken place the treatment must often be continued for a long time. Of course operations should be avoided if possible, and this fact is well known. ‘The tendency of clean wounds to break down after operations on syphilitic bones is also well known. A peculiar fact, or possibly a theory, in the treatment of syphilitic arthritis is the lack of response to immobilization of the joint, and this fact is not without value from a diag- nostic standpoint. If a syphilitic joint be immobilized, pain does not decrease as a rule. Indeed, in contrast to tuberculosis, it may grow worse, and necessitate the removal of the dressing. CHAPTER III CHRONIC OSTEOMYELITIS OF UNKNOWN ORIGIN Unper this heading can be included a number of clini- eal forms of marrow inflammation whose identity is not firmly established, and whose differentiation is by no means definite or exact. Indeed that they are all marrow inflam- mations is not universally acknowledged. Three of them may be grouped. They possess in common certain patho- logical features, some of which may be regarded as an exaggeration of those ordinarily observed in the bones with the advancement of age. They are probably closely related, and probably are variations of the same process. They are Paget’s disease, or ostitis deformans, leontiasis ossea, and the so-called ostitis fibrosa. Eiven to find a name under which to group them is not easy, but for con- venience, we will call the group OSTEOMYELITIS FIBROSA The first and probably the fundamental change in the members of this group is a fibrosis of the marrow. With this goes an irregular production and absorption of bone, with or without the formation of osteoid tissue. Cyst formation is also a frequent accompaniment. These characteristics, as we shall see, are shared by the second great type of arthritis, and some writers with good reason have regarded the two diseases as essentially variations of the same pathological process. Others deny any relation between them. 147 148 INFLAMMATION IN BONES AND JOINTS PAGET’S DEFORMING OSTEOMYELITIS, OSTITIS DEFORMANS This disease was_ first established as a_ clinical entity by Sir James Paget, who, in a paper read before the Royal Medical and Chirurgical Society, placed five cases of it on record in such detail that little defi- nite has since been added to his description.’ Five years later he published seven more cases.” The disease is comparatively rare, though probably not as rare as is generally thought. Four or five cases are on record at Stanford. Mit1I0Locy. — Nothing definite is known as to this. The whole appearance of bone and marrow is that of a low grade chronic infec- tion, though no definite proof of an infection ever has’ been adduced [he theory that the disease was a manifestation of syphilis has been advocated, but has been Fic. 45.—Paget’s deforming osteomyelitis; Stanford Clinic Case No. 1. 1 Pacer, James: “On a form of chronic inflammation of bones.” Medico- chirurgical transactions, 1877, lx, 37. 2Pacet, James: “ Additional cases of ostitis deformans.” Med. Chir. Trans., 1882, lxv. 225. CHRONIC OSTEOMYELITIS 149 almost universally discarded. Several of Paget’s cases died of malignant disease, and Paget thought that there was same causal relation between the two, but other observers have not confirmed his observation. The similarity of Fic, 46.—Paget’s deforming osteomyelitis; Stanford Clinic Case No, 2, Paget's disease to the second great type of chronic arthritis might suggest the alveolar processes of the Jaws as a pos- sible atrium of infection. Paget’s disease is essentially a disease of middle and later life, though one case was observed at the age of 150 INFLAMMATION IN BONES AND JOINTS twenty-one. It is most commonly seen after forty, and the majority of patients have been men. A slight familial tendency has been noted. The bones most frequently and most severely affected in Paget’s disease are the tibia, the femur, the calvarium, Fic. 47.—Paget’s deforming osteomyelitis. Photograph of one of Doctor Ethan Smith’s patients. the clavicle, and the spine. Apparently almost all the bones of the body may be involved eaceu those of the face, which always escape. The disease begins in the superficial part of the bone cortex. Probably the initial macroscopic change is a rare- faction of the bone in this vicinity, a rarefaction which CHRONIC OSTEOMYELITIS 151 slowlyadvancesinward, Anirregular production of osteoid tissue and new bone, especially new periosteal bone, follows this, overshadows the initial rarefaction and clinically is by far the most prominent feature of the disease. The bones become thickened and deformed, and, composed as they are i } Fic. 48.—Paget’s deforming osteomyelitis. Skiagram of the skull of poorly formed bone tissue, yield to pressure and to strain. The head sinks between the shoulders, the clavicles become prominent, the spine bows and sinks together, and the femora and the tibias bow outward. ‘The skull may become enormously enlarged, sometimes with a smooth surface and sometimes with irregular nodules. As the result of the shortened trunk and the bowed extremities the arms appear disproportionately long. ‘This gives to 152 INFLAMMATION IN BONES AND JOINTS Fic. 49.—Paget’s deforming osteomyelitis. Skiagram of the bones of the legs. CHRONIC OSTEOMYELITIS 153 the patient an appearance which has been well likened to that of an anthropoid ape. Hisrotocy.—The marrow consists of a vascular con- nective tissue, more or less rich in cells. ‘Typical giant cells are often seen, sometimes in great numbers, and giant cell tumors are not rare in this disease. ‘The Haversian canals are widened,and are filled with vascular tissue, espe- cially in the superficial portions of the bone. ‘The whole Fie. 50.—Paget’s deforming osteomyelitis—Doctor Ethan H. Smith’s second case. This photograph was taken in 1906, and the disease then was presumably of about twenty years standing. Eight years later the femur was fractured at about the junction of its proximal and middle third. The fracture did not unite. Doctor Smith amputated about five months later. He ‘‘ pinched the neck of the femur off’’ between his thumb and forefinger. The bone must have been very soft. The next figure shows the specimen. architecture of the bone is changed. ‘The Haversian sys- tems as such are obliterated, the cortex is thickened and the central marrow canals or the diploé may be obliterated by the overgrowth of new bone and osteoid tissue. Some- times the new bone is of normal consistency, sometimes it cuts easily with a knife. At times greater or smaller islands of sclerosed bone tissue are formed in the midst of the other bone. ‘The osteoid tissue evidently may be ossi- fied later, or at times may itself fall a victim to absorption. The margins of the trabeculz often show the classic picture of rarefying ostitis—so-called osteoclasts in Howship’s lacune. Cysts have been observed in some cases. In 154. INFLAMMATION IN BONES AND JOINTS Paget’s cases “the medullary structures appeared to the - naked eye as little changed as the periosteum.” Strange to say, in spite of all the bone absorption, frac- tures do not often occur in Paget’s disease. SYMPTOMATOLOGY.—Pain may or may not be present. As a rule it is not severe. Frequently the first thing Fic. 51.—Distal two-thirds of femur, and proximal end of tibia of Doctor Smith’s second case, sawn sagittally. Note the disorganization of the extreme distal end of the femur, and the complete change from the normal architecture of the whole bone. The cortex cut easily with the knife in the laboratory. It consisted of rather open- meshed fibrous tissue containing scattered, slender bone trabecule. noticed by the patient is that he is compelled to wear a larger hat than formerly, and must increase its size as time goeson. When the bones of the lower extremity are first involved, then their bowing will be the first thing noticed. The X-ray picture will show a marked thickening of the affected bones, usually more or less irregular in structure. Border line cases may sometimes be hard to distinguish, but the typical case of Paget’s deforming osteomyelitis is easily recognized. The enlarged cranium, the bowed and CHRONIC OSTEOMYELITIS 155 shortened spine, the bowed lower extremities, the short neck and the ape-like build present a picture not easily confused with anything else. The disease is probably not as rare as has been thought, and escapes recognition only when one is not alive to the possibility of its occurrence. TREATMENT.—No treatment has ever been accepted for this disease. On the theory that the appearance of the marrow indicates a low-grade chronic infection as a causal factor, a search should be made for a focus of infec- tion anywhere in the body, especially in the teeth. If one be found, it should be removed. Following out what at present is little more than a theory, it will be well to search for the amoeba in the intestinal canal. LEONTIASIS OSSEA The pathological features of this disease are similar to those of the preceding. Its distinguishing characteristic, however, is a marked involvement of the bones of the face, giving to the patient the appearance of one with leprosy. It is of very infrequent occurrence. Besides the ordinary symptoms of pain and discomfort, the involvement of the facial bones may cause severe disturbance in the organs of special sense. Nothing is known as to the cause of leontiasis ossea, nor © . as to its treatment. On the chance that it may be caused by some obscure source of infection, any focus of possible infection should be sought and removed, especially in the jaws. OSTEOMYELITIS FIBROSA, OSTITIS FIBROSA Without the peculiarities of the two last named diseases, a form of chronic. osteomyelitis occasionally is seen, char- acterized by the change of the marrow to fibrous tissue. Giant cells are frequent in this fibrous tissue. ‘The disease 156 INFLAMMATION IN BONES AND JOINTS may be generalized or local. Cysts may form in the fibrous tissue, and the architecture of the bone is usually changed. The bone may be distended, but the thickened cortex and the periosteal reaction observed in syphilitic disease is absent. Pain may or may not be present. Fracture occa-_ sionally occurs. ‘The diagnosis is made with the Ront- gen rays. The cause of this disease also is not known, but it is probably some obscure form of infection, possibly in the jaws. ‘The tendency of the marrow to become fibrous as age advances, is to be borne in mind. TREATMENT.—Any focus of infection should be re- moved. Cysts may be cleaned out by operation. Giant cell growths in bone, the so-called giant cell sar- comata or benign myelomata are quite similar to the pre- ceding, are probably inflammatory, and should be classified with the chronic inflammation, but as they are usually regarded as new growths, they will be omitted from consideration. PULMONARY HYPERTROPHIC OSTEOARTHROPATHY Somewhat akin to the preceding diseases is a rather rare condition first described by Bamberger, and later, by Marie, whose bone manifestations apparently consist of a chronic osteomyelitis with a production of new periosteal bone. The name is a most unfortunate one in every re- spect, but until we know more about the disease, it is hardly worth while to change its name. In the first place, it is caused by other things than pulmonary lesions, and in the second place the disease apparently may exist without any bone or joint involvement whatever. /ETI0LoGy.—Four groups of causes may be enu- merated: CHRONIC OSTEOMYELITIS 157 1. Suppurative or gangrenous processes in the lungs or pleura. 2. Infectious diseases. 3. Valvular heart lesions, especially congenital. 4. Malignant tumors in the lung or in the mediastinum. SympromMaToLocy.—W hat has always been considered the distinguishing mark of the disease is a clubbing of the terminal phalanges of the fingers (the Trommelschlegel- finger of the Germans), together with a curving or beak- like deformity of the nails. The fingers are wont to be eyanosed as well. ‘The swelling of the end phalanges is entirely in the soft parts: The bone is not affected. Associated with this peculiar deformity may be a thick- ening of the rest of the fingers, and sometimes also of the forearm (or leg) as well. Examination shows that this thickening is due to new bone formation, which is plainly shown by the X-rays to be located on the outside of the cortex. TREATMENT.—This consists in the removal of the cause if possible. Definite improvement has been reported from successful treatment of the causal lesion. REFERENCES HYPERTROPHIC PULMONARY OSTEOARTHROPATHY Bampercer, E.: “Ueber Knochenverenderungen bei chronischen Lungen-und Herzkranken.” Zeitsch. f. klin. Med., 1890-91, xviii, 193. Janeway, T. C.: “Hypertrophic osteoarthropathy, etc.” Am. J. Med. Sci. 19038, n..s.. cxxvi. 563. Marte, P.: “De Vostéoarthropathie hypertrophiante pneumique.” ‘Revue de Med., 1890, x, 1. Horrman, V.: “Ein beitrag zur Kenntnis der Ostéoarthropathie hyper- trophiante pneumique (P. Marie).” Deut. Arch. f. kl. Med., 1919, cxxx, 201. Francenuemm, P.: “Die Ostéoarthropathie hypertrophiante pneumique; Neue deut. Chir.,” “ Band x. P. v. Bruns, Ferdinand Enke, Stuttgart, 1919. CHAPTER IV RICKETS, RHACHITIS RIcKETs is a constitutional disease of infancy and early childhood, whose chief anatomical changes appear in the bones. Good authority is behind the statement that the disease occasionally occurs in foetal life. Certainly its manifestations have been observed in very early infancy. The so-called “late rickets’ of adolescents is probably a misnomer. AK r10LoGy.—Nothing definite is known as to this. The marrow changes point strongly toward chronic infection as a cause, and various investigators have claimed to have produced the disease experimentally by the use of infec- tious agents, but their claims have not been substantiated. On account of the similarity of the bone changes in rickets and in syphilis, syphilis has been considered as a cause of rickets, but the two diseases are quite distinct. One does not cause the other. The cause of rickets is closely bound up with the proc- esses of nutrition. ‘The disease can be produced experi- mentally in animals, by surrounding them by unnatural conditions. ‘The essential element of these unnatural con- ditions is popularly thought to be an error in diet, an absence from the food of some essential element, but Leonard Findlay and others stress the importance of con- finement, and of the lack of fresh air. Perhaps all are but contributing causes. Rickets is more common in certain races than in others, and in certain climates than in others. People from 158 RICKETS, RHACHITIS 159 southern climates, transplanted to northern, are especially liable to the disease, possibly because they live more in-doors in their new domicile. On the other hand the Esquimaux are said to be exempt from the disease. It is much more frequent in the city than in the country. It is common in England and in Germany, and in our northern cities many severe cases are seen among negroes and Italians. Patrnotocy.—The bone changes alone interest us here, and it is hard to say which is the fundamental change. The fie. 52.—Rickets. Low power photomicrograph of the costochondral junction. Note the irregularity of outline of the cartilaginous disc on its left border. marrow becomes very vascular and undergoes a fibrous change. Islands of osteoid tissue appear in it, and the Haversian canals widen. In other words the marrow is the seat of a chronic inflammation. The most marked evidences of the disease are on the outside of the cortex, and in the region of the epiphysial disc; in other words, in those parts of the bone where growth is most active. The changes at the epiphysial line (as at the costo- chondral junction) are among the most characteristic. Masses of marrow tissue push in among the columns of cartilage cells in the zone of provisional calcification (Nichols). The zone of provisional calcification disap- 160 INFLAMMATION IN BONES AND JOINTS pears, the cartilage cells lose their typical arrangement, and the epiphysial disc becomes irregular and decidedly broadened. On its diaphyseal side masses of osteoid tissue imstead of bone, are laid down, and in this osteoid tissue islands of cartilage persist. In other words ossification is halted. Neither calcification nor ossification takes place. Layers of osteoid tissue form on the trabecule of the diaphy- sis, but whether or not there is ever a reversion of bone tissue to osteoid is doubtful. Prob- ably the process is best inter- preted as a failure to build up bone, rather than an actual tearing down of bone already built up, aside from the tear- ing down inseparable from the remodelling incidental to growth. The periosteum is_ thick- ened, and layers and arches of osteoid tissue instead of true bone are formed in it. Rare- faction of the cortex is pro- Fig. 53.—Skeleton of rickety child. ceeding meanwhile, and the Haversian canals are widened and contain vascular mar- row. ‘The masses of osteoid tissue in the periosteum give to the bone a thickened appearance. ‘They are more prom- inent in certain situations than in others, especially upon the parietal eminences of the skull. In other parts of the skull absence of bone formation, as well as of osteoid tissue, is the prominent feature. This is best seen in the occipital RICKETS, RHACHITIS 161 bone, the so-called craniotabes. The bone is thin and parchment like, easily indented by pressure with the finger. This craniotabes is one of the most important diagnostic signs of rickets. Lack of bone formation in the cranial bones causes a persistence of the fontanelles, also an important diag- nostic sign. In gross the bones become soft and bent, and are broad- ened in the region of their epiphyses. Fractures are said to be frequent. Vascular, soft, spongy, grayish-red masses of tissue are seen in the medulla and on the cortex. The epiphysial line is broadened, and, instead of being sharply defined and approximately straight, is irregular. Medullary and osteoid tissue extends into it. The central medullary canal is widened. When the disease has run its course, calcification and ossification of the osteoid tissue take place, and the bones become denser than normal—sclerosed. 'The deformities may persist or they may disappear. Almost always in later life, the enlarged epiphyses and the peculiar shape of the head, remain as vestiges of the infantile disease. SyMPToMATOLOGY.—The constitutional manifestations of rickets are numerous and well known. Among them are the nervous symptoms, the convuisions, the laryngismus stridulus, the restlessness at night, etc. The patient is anemic and pasty looking, and is afflicted with sweating about the head. Usually he is pot-bellied and suffers from constipation. ‘Teething is late and the child does not begin to walk at the usual time. All these are quite important, but they do not justify a diagnosis of rickets. This is only to be made upon the bone changes. The two most important of these perhaps are the craniotabes and the epiphysial changes, the latter 1 162 INFLAMMATION IN BONES AND JOINTS including the changes at the junction of the ribs with their cartilage. Craniotabes is a very early sign, and by some is consid- ered as an invariable and pathognomonic sign of rickets, provided its presence is carefully sought. It may be more | or less general in the occipital bone, or small areas only may be involved. The enlarged epiphyses are easily detected. ‘The enlarge- ment of those of the wrist and ankle is most evident: = [ha enlargement of the costo-chon- dral junctions causes a line of knobby prominences on_ the chest wall, known as the rhachi- tic rosary. The - new bones?onsaane parietal eminences gives rise to a peculiar shape of the head— a squareness that is quite characteristic. The forehead is prominent. Some _ patients are dolichocephalic, not square-headed. The occiput is usually rather broad and flat. Fic. 54.—Rickets. Harrison’s groove, the concavity of the lower part of the antero-lateral chest wall, is often quite marked in rhachitic patients. While not directly caused by the dis- ease, its formation is evidently facilitated by the softness of the ribs. The concavity of the chest is in marked con- trast to the prominent belly. The spine usually has a long rounded convexity. ‘The RICKETS, RHACHITIS 163 deformity may appear more or less fixed, but, if the child be laid upon his face, and if his pelvis be lifted from the table by raising his heels in the air, pressure with the palm of the hand upon the curve will obliterate it. Many of the severe cases of rotary lateral curvature are probably rhachitic in their origin. The pelvis is often narrowed and deformed. The rhachitic pelvis in the female becomes of great interest in later life to the obstetrician. In the lower extremity the rhachitic deformity takes the form of knock knee or bow leg. In the former the deformity is usually in the femur, in the latter in the tibia. Probably the chief cause of these deformities is the inability of the bones of the extremity to bear the weight of the body without bending, but sometimes they may be quite marked in children who have never walked. ‘The popular idea that they are caused by too early walking, is of course erroneous, for the rickety child usually walks late, and any child will always walk as soon as he can. In the active stages of the disease, and roughly up to the end of the fourth year, these crooked bones have a more or less elastic feel when an attempt is made to bend them, but after that time they become quite hard and unyielding. As long as they are soft there is some hope of correcting the deformity with braces, but when they have become eburnated, little can be expected from conservative treatment. The diagnosis is made on the peculiar bone changes. The severe cases rarely give rise to doubt. The milder ones are often missed. The disease is very frequent in large cities, and, if one is looking for its manifestations, one will find them in a very heavy percentage of one’s cases. Scurvy has its painful swellings in the neighborhood of the joints, its more or less acute onset, and its hemorrhages. The rhachitic spine may simulate the tuberculous spine, but 164 INFLAMMATION IN BONES AND JOINTS it lacks rigidity, muscular spasm and pain. Other signs of rickets can be found, and these practically rule out tuber- culosis, for the association of active rickets and tuberculosis is at best very ‘rare. In chronic hydrocephalus the shape of the head is globu- lar rather than square, and the epiphyses are not enlarged. Fig. 55.—Rickets. Skiagram of a knee. TREATMENT.—Of the first importance in the active stages are a well regulated diet and plenty of fresh air. Findlay stresses the importance of exercise, but manifestly a child with rhachitic deformities in its lower extremities, should be kept off his feet as much as possible. Otherwise, unless he wear braces his deformities will increase. Most authorities, in addition to a proper diet, recommend the administration of cod liver oil. Some of them believe also in the efficacy of phosphorus. RICKETS, RHACHITIS 165 It is seen that the treatment of rickets as a disease, is along medical lines. ‘The deformities which follow the disease present a different problem. If they are attacked early, before the bones become sclerosed, their treatment usually is not very difficult.. The round back, or the scoli- otic spine, demands recumbency, preferably on some such apparatus as the Whitman-Bradford frame. Mild degrees of bow-leg or knock-knee may be treated by frequent manipulation. ‘The mother is shown how to bend the limb as if it were a crooked stick which she were trying to straighten. She should manipulate it fifty or a hundred times a day. In addition the sole of the shoe is raised about a quarter of an inch, on the inner side for knock-knee, on the outer for bow-leg. More marked cases demand brace treatment. Stand- ard forms of braces are in use, but it is not difficult for anyone with a little mechanical ability to devise one that will answer the purpose perfectly. Severe cases of bow-leg and knock-knee demand opera- tive treatment, as do moderate cases after the bones have become hardened, that is, after the end of about the fourth year. Osteotomy is not a difficult operation, and if done with ordinary care is comparatively free from risk. A sharp osteotome incises the tissues longitudinally down to, and through, the periosteum, at the seat of the greatest deform- ity. In bow-legs this is usually at the junction of the mid- dle and proximal thirds of the tibia, in knock-knee just proximal to the condyles of the femur. After the peri- osteum has been incised longitudinally, the blade of the osteotome is turned transversely and with blows of a mallet divides partially the bone. The fracture is completed by manual force. After every few strokes of the mallet the operator moves the osteotome back and forward to keep it -from wedging fast. 166 INFLAMMATION IN BONES AND JOINTS One or two sutures are inserted in the skin, a sterile dressing is applied, and the limb is put up in plaster of Paris in a slightly overcorrected attitude. The plaster of course extends well above and below the seat of the fracture, and remains on for about two months. If the © bones are still soft, braces should be applied when the plaster is removed. BONE SYPHILIS Bapin, Pauu-Vira: “ Syphilis osseuse héréditaire tardive.” Presse Méd., 1914, xxil, 240. Bacinsky, ApotpH: “ Bone lesions of hereditary syphilis in children.” Internat. Clin., 1899, 9 ser., iii, 224. Ex1y, Leonarp W.: “A case of bone syphilis masquerading as tuberculosis.” Med. Rec., 1912, Ixxxi, 1179. Fisuer, Arruur L., “Syphilitic bone and joint lesions simulating tuberculosis.” J. A. M. A., 1917, Ixviii, 366. FrrzwituiaMs, D. C. L.: “ Syphilitic affections of bones met with in childhood.” Brit. Jour. Child. Dis., 1912, ix, 97. GuszMAN, JoseF: “ Polyarthritis syphilitica acuta.” Wien. med. Wehnschr., 1915, Ixv, 186. Hazen, Henry H.: “Syphilis.” St. Louis, C. V. Mosby Co., 1919. Hocustncer, Cart: “Syphilis.” Pfaundler und Schlossmann Handbuch der Kinderheilkunde, 1910, ii, 487. Lone, H.: “Klinische und pathologisch-anatomische Untersuchungen iiber Skelettverinderungen bei kongenitaler Syphilis und ihre Heilungsvor- ginge.” Virchows Archiv., 1915, ccxx, 95. Miran: “Syphilis des os et des articulations.” Nouveau traité de Médicine, 1912, xxxix, 95. O’Rettty Arcuer: “Joint syphilis.” Am. Jour. Orth. Surg., 1913-14, xi, 431. Ortu, Jowannes: “Ein Beitrag zur Kenntnis der congenitalen Syphilis.” Dermat. Studien Von Unna., 1910, xx, 1. Owen, Sypnry A.: “Syphilitic diseases of joints and bones in childhood.” Med. Press and Circ., 1913. exlvii, 318 Parrot, M. Jules: “ Les lésions osseuses de la syphilis héréditaire.” Path. Soc. Trans., 1878-79, xxx, 339. Parror: “Deux cas de syphilis héréditaire avec lésions osseuses.” Soc. de. Biol. Mem., 872, iv, 119. Payr, E.: “Syphilis der Gelenke.” Lehrbuch der Chirurgie, Wullstein wu. Wilms, 912, iii, 521. Peritz, Grorc: “Ueber die Syphilis der Wirbelsdule.” Charité Ann., 1918, xxxvii, 65. RICKETS, RHACHITIS 167 Pick, Lupwic: “Zur Réntgendiagnose der angeborenen Knochensyphilis.” Deutsche med. Wcehnschr., 1919, xlv, 989. Pick, Lupwic: “Zur Rontgendiagnose der angeborenen Knochensyphilis.” Deutsche med. Wehnschr., 1919, xxxv, 953. Srotper, P.: “Ueber die Beziehungen zwischen Syphilis und Trauma.” Deutsche Ztschr f. Chir. 1902, lxv, 117. Taytor, R. W.: “Clinical observations on the syphilitic lesions of the bones of the hands in young children.” Arch. Scient. and Pract. Med., 1878, i, 354. Wattace, James O.: “Diagnosis of syphilis of bones and joints.” Jour. Orth. Surg., 1919, i, 258. PAGET’S DEFORMING OSTEOMYELITIS Connotiy, Harry W.: “A case of Paget’s disease.” Med. Jour. of Australia, 1916, i, 283. Czerny, V.: “Eine lokale Malacie des Unterschenkels.” Weiner med. Wehnschr., 1873, xxiii., 894. DaCosta, J. Cuatmers, Funx, Ermer H., Bercerm, Orar ann Hawk, Pur B.: “ Osteitis deformans.” Publications from the Jefferson Medical College and Hospital, 1915, vi, 1. 7 Daser, Paut: “ Ueber einen Fall von Osteitis deformans (Paget’s).” Miinch. med. Wehnschr., 1905, lii, 1634. Exsner, Henry L.: “Osteitis deformans (Paget’s disease) including a report of two cases.” New York State Jour. Med., 1910, x, 287. Ferris, AtpertT Warren: “A case of osteitis deformans.” Med. Rec., 1919. xcev, 852. Frencu, Herpert: “A case of osteitis deformans with pronounced affection of forearm.” Brit. Jour. Surg., 1919-20, vii, 425. GraFFNeR: “Ein Fall von Ostitis deformans (Paget).” Berliner klin. Wochenschrift, 1913, i, 1369. Haun, Reernartp G.: “ A case of osteitis deformans terminating with cerebral symptoms.” Brit. Med. Jour., 1910, i, 135. HartMann, Kari: “Zur kenntnis der Ostitis fibrosa (deformans).” Beit. zur. klin. Chir., 1911, Ixxili, 627. Heazurr Lepra: “Sarcoma complicating Paget’s disease of bone. Report of case.” New York State Jour. Med., 1917, xvi, 331. Hicser, Wir11am S., anv Exxis, Arter G.: “A case of osteitis deformans.” Jour. Med. Res., 1911, xxiv, 43. Kitner, Warrer J.: “Two cases of osteitis deformans in one family.” Lencet 1904, i, 221 Kutscua, Ernst von: “ Beitrag zur Kenntniss der Ostitis deformans (Paget’s).” Arch. f. klin. Chir., 1909, Ixxxix, 758. Lancrreavx, E.: “ Traité d’anatomie Pathologique.” 1889, 173. Lancereavux, E.: “ Traité de Vherpetisme.” 1883, 147. 168 INFLAMMATION IN BONES AND JOINTS Locke, Epwin A.: “Osteitis deformans with sarcoma of the humerus.” Med. Clin. N. A., 1917-18, i, 947. Macxey, Cuartes: “ A case of osteitis deformans with Huntington’s chorea.” Lancet, 1906, ii, 787. Marte, Pierre ET Lert, Anpres: “ Le crane dans la maladie osseuse de Paget.” Soc. Med. des Hopitaux, 1919, xxxv, 901. De Massary ET Lecuetres: “ Maladie osseuse de Paget localisée a un seul os long.” 1920, xxxvi, 134. Matsuoka, M.: “ Beitrag zur Lehre von der Pagetschen Knochenkrankheit. (Os- teomalacia chronica deformanshypertrophica nach Recklinghausen).” Deutsch. Zeitschrift f. Chir., 1909, cii, 515. PacKkarp, Frepericx A., STEELE, J. D., ann Kirxsring, T. S.: “ Osteitis defor- mans.” Am. Jour. Med. Sci., 1901, cxxil, 552. Pacer, James: “ Additional cases of osteitis deformans.” Med. Chir. Trans., 1882, Ixv., 225. Pacet, James: “On a form of chronic inflammation of bones.” Med. Chir. Trans., 1877, Ix, 37. Paine, F.: “Case of osteitis deformans.” Royal Jour. Med., 1913, vi, 72. Parry, T. Wirson: “A case of osteitis deformans.” Brit. Med. Jour., 1912, i, 879. Perkins, C. Wryrietp: “A Rontgenographic study of osteitis deformans —Paget’s disease.” American Jour. Réntgenology, 1919, vi, 151. Prernet, Grorce: “ Morphoeo-sclerodermia of the shins associated with osteitis deformans.” Brit. Jour. Dermatolagy, 1917, xxix, 110. Rarusun, Naruaniet P.: “Report of a case of osteitis deformans.” Am. Jour. Surg., 1911, xxv, 66. Stau., B. Franxuin: “Osteitis deformans, Paget’s disease, with reports of two cases and an autopsy in one.” Am. Jour. Med. Sci., 1912, cxxxxiii, 525. STivELMAN, B. ann Ray, E. L.: “ Paget’s disease of the bones.” New York Med. Jour., 1918, eviii, 678. Tuompson, W. Girman: “OsSteitis deformans (Paget’s disease).”Med. Rec., Ixxxiii, 832. Vocet, Kart M.: “A case of Paget’s disease. Med. Rec., 1911, Ixxx, 214. Wattace, Guy: “ A case of osteitis deformans.” Bellevue and Allied Hospitals. Med. and Surg., Rep., 1911-12, v, 7. Watson, Wii1AM T.: “A case of osteitis deformans.” Johns Hopkins Hospital Bulletin, 1898, ix, 133. Wiixs: “Case of osteoporosis.” Path. Soc. London Trans., 1868-69, xx, 273. OSTEOMYELITIS FIBROSA Buiooncoop, Josepu C.: “ Benign bone cysts, ostitis fibrosa, giant-cell sarcoma and bone aneurism of the long pipe bones.” An. Surg., 1910, lii, 145. BocKENHEINER, Pu.: “ Ueber die diffusen Hyperostosen der Schidel und Gesichtsknochen s. Ostitis deformans fibrosa.” Arch. f. klin. Chir., 1908, lxxxv, 511. RICKETS, RHACHITIS 169 Borr: “ Ueber Leontiasis ossea und Ostitis fibrosa.” Arch. f. klin. Chir., 1912, xevii, 515. Butiowa, Jesse G. M.: “ Osteitis fibrosa.” Med. Rec., 1915, Ixxxvii, 539. Burcuarp, A.: “Zur Diagnose der chondromatisen fibrésen und cystischen Degeneration der Knochen.” Fortschr. a. d. Geb. d. Réntgenstrahlen, 1912-13, xix, 113. CurscHMANN, H.: “Ueber osteomalacia senilis und tarda.” Med. Klinik, 1911, vii, 1565. Czerny, V.: “Eine locale osteomalacie des Unterschenkels.” Wiener Med. Wochsch., 1873, xxiii, 893. Fusu: “Ein Beitrag zur Kenntnis der Ostitis fibrosa mit ausgedehnter Cystenbildung.” Deutsche. f. Chir., 1912, exiv, 25. Gaucete, K.: “Zur Frage der Knochencysten und der Ostitis fibrosa von Recklinghausen’s.” Arch. f. klin. Chir., 1907, Ixxxiii, 953. Greic, Davin M.: “ Osteitis fibrosa.” Edinburgh Med. Jour., 1920, xxiv, 324. HarrmMann, Karu: “Zur Kenntnis der Ostitis fibrosa (deformans).” Beit. z. klin. Chir., 1911, Ixxiii, 627. Herneke, H.: “Ein Fall von multiplen Knochencysten.” Beit. z. klin. Chir., 1903, xl, 481. Jacosy, Martin, AND ScurotH: “ Ueber die Einwirkung von Calcium lacticum auf einen Fall von Ostitis fibrosa. . .” Mitteil. a. d. Grenzgel. d. Med. wu. Chir., 1913, xxv, 383. Karuoricky: “Ostitis deformans.” Wien. klin. Wochsch., 1906, xix, 1428. Kocu, Max: “Demonstration eines Schadels mit Osteitis deformans Paget.” Deutsche path. Gesell. Verhand., 1909, xiii, 107. Kouisxo: “ Ostitis deformans.” Wiener klin. Wcehnschr., 1906, xix, 1429. Laxe, Norman C., ann Scuuster, Noran H.: “A case of osteitis fibrosa.” Lancet, 1920, i, 546. Lorscu, Frrrz: “ Ueber generalisierte Ostitis fibrosa mit Tumoren und Cysten. . .” Arch. f. klin. Chir., 1915-16, cvii, 1. Moncxeserc: “ Ueber Cystenbildung bei Ostitis fibrosa. Verh. der. dent. Path. Gesell., 1904, vii, 232. Morzarp, AnD Bources: “ Un cas d’ostéite déformante.” Arch. de Méd. Exper., 1892, iv, 479. OrstreicH, R.: u. Slawyk, “ Riesenwuchs und Zirbeldriisen-Geschwulst.” Virchow’s Archiv. 1898, clvii, 475. PreirFer, C.: “ Ueber die Ostitis fibrosa und die Genese und Therapie der Knochencysten.” Beit. z. klin. Chir., 1907, liii, 473. Prince, Morton: “ Osteitis deformans and hyperostosis cranii. . .” dm. Jour. Med. Sci., 1902, xxiv, 796, Roru, Max, ann VorkmMAaNN Jou.: “Zur Kenntnis generalisierten Ostitis fibrosa.” Mitteil. a. d. Gremzgeb. d. Med. u. Chir., 1920, xxxii, 427. Surtron, Brann: “Leontiasis ossea.” Illus. Med. News, 1889, ii, 217. 170 INFLAMMATION IN BONES AND JOINTS RICKETS Conn, M.: “Zur Pathologie der Rachitis.” Jahrb. f. Kinderheilk., 1893-1894, xxxvii, 189. Comry, J.: “La radiographie dans le rachitisme.” Arch. de. Med. de enf., 1918, xxi. 549. Finptay, L.: “The etiology of rickets.” British Med. Jour., 1908, ii, 13. Finpiay, L.: “ Rickets: a historical note.” Glasgow Med. Jour., 1919, xci, 147. Finpiay, L.: “ Rickets in its relationship to housing.” Glasgow Med. Jour., 1918, Ixxxix. 268. Hu.tpscuinsky, K.: “ Die Ultraviolettherapie der Rachitis.” Strahlentherapie, 1920, xi, 435. Jackson, L.: “Demonstration of micrococci in the bones in rickets and scurvy.” Jour. Infect. Dis., 1918, xxii, 457. Kassowirz, M.: “Zur Theorie der Rachitis.” Wien. Med. Wcehschr., 1901, li, 17538, 1807, 1857. Lert, A. anp Becx, T.: “Le ‘ Petit rachitisme’.” Ann. de Med., 1919, vi, 449. Looser, E.: “ Ueber Spetrachitis und Osteomalacie.” Deutsche Ztschr. f. Chir., 1920, clii, 210. Metranpsy, E.: “ An experimental investigation on rickets.” Lancet, 1919, i, 407. Orume, C.: “ Ueber die Beziehungen des Knochenmarkes zum neugebildeten, kalklosen Knochengewebe bei Rachitis.” Beitr. z. Pathol. Anai., 1908, xliv, 197. Paton, D. N., anp Watson, A.: “The etiology of rickets.” Brit. Jour. Exp. Path., 1921, ii. 76. Paton, D. N., ann Finpuay, L.: “ Observations on the cause of rickets.” Brit. Med. Jour., 1918, ii, 6265. Scumonrt, G.: “ Ueber Rachitis tarda.” Deutsche Arch. f. klin. Med., 1905-1906, Ixxxv, 170. Scumort, G.: “ Die pathologische Anatomie der Rachitis.” Dresden. Gesellsch. f. Natur. u. Heilk. Jahresbericht., 1906-1907, xc. 95. Scumort, G.: “Ueber die Knorpelverkalkung bei beginnender und _ bei heilender Rachitis.” Deutsche Path. Gesellsch. Verhandl., 1905, ix, 248. Scuwarz, H.: “Craniotabes and beading of the ribs as signs of rachitis.” Am. Jour. Dis. Child., 1920, xix, 384. Suiptey, P. G., anp Parx, E. A.: McCartxium, E. V., ann Simmonpns, N.: “Studies on experimental rickets. No. iii.’ Johns Hopkins Hosp. Bull., 1921, xxxii, 160. Vicnow, R.: “Das normale Knochenwachsthum und die rachitische Stoerung desselben.” Arch. f. path. Anat. und Physiologie., 1853, v, 409. hd GA al “h et ik : ; SECTION IV. CHRONIC ARTHRITIS ; ¥ a y * t 1 : ce et ‘ aaa ‘0 : sj 4 ese ae ae oe ie a of CHAPTER I THE TWO GREAT TYPES JOINT TUBERCULOSIS IN GENERAL THE custom is almost universal to describe the chronic arthritides as separate from inflammations in the shafts. This custom has decided merit, for, when the joint is involved, the symptoms of the arthritis usually dominate the picture, and throw the symptoms referable to the bone decidedly in the background. The fact must not be forgot- ten however that the distinction is largely an artificial one, that no sharp dividing line can be drawn between an arthri- tis and a myelitis, that most arthritides are the result of a previously existing myelitis, and that a primary arthritis may easily spread into the bone and involve the bone marrow. The whole subject of chronic arthritis is a most confused one in all its aspects. Indeed this confusion exists not only as to its etiology and its pathology but also as to its classi- fication and nomenclature, so that often a student is baffled in his efforts to find out an author’s meaning. Until comparatively recently practically all these arthritides were grouped under the broad general name of chronic rheumatism, and were supposed to be due to some mysterious dyscrasia or diathesis, and even to this day we find some investigators taking refuge in the similar terms rheumatoid and metabolic. It is interesting in studying chronic arthritis to see how a firm structure of fact slowly has been built up by patient investigation. On the other hand at all times this structure of fact has been almost 173 174 INFLAMMATION IN BONES AND JOINTS buried in a flood of supposition and theory. One by one, various members of this group of diseases have been identi- fied and described, until now it may be said that the main features of the majority of them are fairly well known, and the pathological characteristics of the others. CLASSIFICATION.—The prevailing method of classify- ing the chronic arthritides is partly on an etiological, and partly on a pathological and clinical basis. Thus, most writers describe tuberculous, gonococcic, syphilitic and other forms of arthritis, and then classify the cases of unknown etiology according to some pathological or clinical feature which they deem most important. The disadvantages of this method are manifest. The ideal classification of course is an etiological one, but, as long as so much doubt hangs about the cause of several forms of chronic arthritis, it is well if possible to classify on a clinical or a pathological basis, preferably the latter. As has been said, the changes, especially the gross changes observed in the tissues of the joint are comparatively few in number, and on the basis of these it is possible to divide all cases of chronic arthritis into two great divisions or types, whose pathological features are sharply differenti- ated and whose clinical features usually are so well marked as to permit a distinction between them. ‘They may be differentiated almost invariably, or invariably, with the Rontgen ray. The first type is characterized by a pro- liferative inflammation in the synovial membrane and in the bone marrow, with a resulting rarefaction or death of the bone, and a perforation or death of the articular cartilage. This type probably includes all the bacterial arthritides, e.g., tuberculous, syphilitic, pneumococcic, ty- phoid and coccidioidal arthritis; and the cases of chronic JOINT TUBERCULOSIS IN GENERAL 175 arthritis supposed to be caused by diplostreptococcic infec- tion in the tonsil, in the deep urethra, and in other locations. The English often call these last cases “rheumatoid” ar- thritis, Goldthwait calls them “atrophic” and “infectious” arthritis, Nichols and Richardson call them “‘the prolifera- tive form,” and other writers have given them other names, almost without number. | An arthritis of this type may recover completely, or it may result in fibrous or in bony ankylosis. All the cases in this type are alike, clinically and radiographically. They all belong in the same family, so to speak. While the different members of the family can be often diagnosed clinically, a positive diagnosis can be made only in the laboratory. The second great type has been recognized as a clinical entity for a number of years, though its cause has never been established. Its gross pathological feature is the formation of new bone at the joint line, with the production of spurs and bony ridges at the lines of insertion of the capsule, but the essential original pathological change at the bottom of this bone production never has been deter- mined until recently. This is the senile type of arthritis, the “arthritis deformans” of the Germans, the ‘osteo- arthritis” of the English, the “hypertrophic arthritis” of Goldthwait, the “degenerative form” of Nichols and Richardson, and the “metabolic” arthritis of certain other writers. The joint becomes distorted and mechanically damaged, but union of the bones entering into it, whether by fibrous or bony tissue never takes place except in the spine. On the other hand the bony changes are permanent, and a joint once damaged by this form of arthritis probably never returns to a completely normal state. 176 INFLAMMATION IN BONES AND JOINTS Into one of these two great types falls every case of chronic arthritis. They can usually be distinguished clini- cally and always by the X-ray. While every chronically inflamed joint belongs quite definitely in one class or the other, nevertheless in rare instances a patient may show — signs of the one great type in certain joints, and of the other great type in others, but it is doubtful if the involve- ment 1s ever synchronous. JOINT TUBERCULOSIS IN GENERAL 177 THE FIRST GREAT TYPE OF CHRONIC ARTHRITIS TUBERCULOUS ARTHRITIS AM r10oLocy.—The exciting cause of joint tuberculosis is, in every instance, the tubercle bacillus. Authorities dif- fer as to the relative frequency of the bovine and human type of the organism as a causative agent. Except in the very rare instances of direct infection from the outside, practically unknown, the tubercle bacillus must be brought to the joint in the circulation.t The consensus of opinion is that it comes in the blood, either floating free in the blood stream or in the embrace of a leucocyte. Friedrich? main- tains that the infection may be through the lymphatics. Though occasionally an infected embolus may be the start- ing point of the disease, a macroscopic plug of infected tis- sue as a causative agent is probably a great rarity. Marrow tuberculosis may be easily produced in laboratory animals by the injection of a pure culture of tubercle bacilli into the nutrient artery,”* as well as by carrying them in on a platinum loop through a trephine opening in the cortex.”” CONTRIBUTING CaAusEs.—Heredity and environment may be considered together under this heading, for they are not always easy to separate in their influence. There is a type of physique considered prone to tuberculous *Kappis: “Beitrag zur traumatischen Tuberkulose.” Deut. med. Woch., 1910, xxxvi, 1310. * Friepricu: “ Experimentelle Beitraege. u.s.w.” Deut. Zeit. f. Chir. 1899, lili, 512. *Muvettrr: “ Experimentelle Erzeugung typischer Knochentuberkulose.” Cent. f. Chir., 1878-79, xi, 317. *“Hoeter: “Die experimentelle Erzeugung der Synovitis granulosa, etc.” Deut. Zeit. f. Chir., 1878-79, xi. 317, 330. ° Evy, Leonarp W.: “ Lymphoid marrow and tuberculosis; an experimental study.” J. A. M. A., 1915, lxv, 1868. ®Oxiver, Jean: “Early changes following the injection of tubercle bacilli into the metaphysis of the long bones of animals.” Jour. Ewpr. Med.. 1920, xxxii, 153. 12 178 INFLAMMATION IN BONES AND JOINTS infection—the so-called tuberculous diathesis—and_ the offspring of tuberculous parents is notoriously vulnerable to tuberculosis, but how much of this vulnerability is due to constitutional predisposition and how much to the infec- tion spread by careless tuberculous parents is still a subject | of debate. The same uncertainty exists as to the influence of en- vironment. ‘The disease is rather frequent in the dense population of the larger cities, and its frequency has been ascribed to the effect upon the constitution of general insanitary conditions, but the element of infection here also is probably of much greater importance than is the lowered vitality.’ TrauMaA.—As in most diseases of the bones and joints, so in tuberculosis, trauma has been considered an important element in the causation. The subject has been attacked from the experimental side with contradictory results.*° Clinicians differ markedly in their estimation of the impor- tance of injury. Some ascribe to it a very prominent role, others disregard it entirely. All authorities agree that a severe injury, such as a fracture or a dislocation, is prac- tically never followed by tuberculosis of the bone or joint. The injury is a slighter one, such as a “strain” or a sprain. Indeed, as we shall see, some writers have maintained that the vulnerability of the joints to injury determines the location of tuberculosis in their vicinity. On the other 7In this connection the experience of San Francisco is interesting. Huntincton, T.: “The early operative treatment of osteomyelitis in the femoral head and neck.” Surg., Gyn. Obst., 1906, ii, 409. °SuerMAN, H.: “ Report of focal operations in hip joint tuberculosis.” Cal. S. J. Med., 1907, v, 62. * ALBEE, T. H.: Surg., Gyn. and Obst., 1910 x, 256. TUBERCULOSIS OF THE HIP 289 head. ‘This permits a slight subluxation proximally, of the head of the femur. As much as possible of the carti- lage is removed from the femoral head together with a little of the bone underlying it. An assistant rotates the femur in and out, to facilitate this. ‘The wound is closed with superficial and deep sutures, and dressed. A long plaster spica is applied, with the hip in slight flexion and abduction. REsEcTION.—A simple resection of the femoral head in an uninfected case of hip tuberculosis can usually be relied on for a cure, whether the operator lets the great trochanter dislocate on the dorsum of the ilium, or shoves it into the acetabulum. The latter operation is not so apt to be followed by extreme and troublesome adduction, as the former. We do not know the exact reason why these simple operations, without any pretense of removing all the tuberculous tissue, are a success, and we shall not know until we have had the chance to examine specimens from cured cases in the laboratory. Probably the same change of the lymphoid marrow to fatty as follows an ankylosis, takes place here and the bone becomes dense. Dense bone is a poor location for tuberculosis. ‘The disease seems to require some space to thrive. Any one of a number of incisions may be employed for this operation.’ The wound should always be closed without drainage, and the hip should be put up in a long spica in rather marked abduc- tion. The plaster may be trimmed for 5 or 6 inches above, and at the knee, in about a month, and the patient may walk shortly thereafter. The anterior incision has already been described. It does not afford a wide view of the joint, and, if much ® Bracket, E. G.: “A study of the different approaches to the hip joint, with special reference to the operations for curved osteotomy and for arthrodesis.” Boston Med. and Surg., Jour., 1912, clxvi, 235. 19 290 INFLAMMATION IN BONES AND JOINTS obstruction to removing the head of the bone exists, it is not very satisfactory. The operator who employs it should take care to keep lateral to the sartorius muscle. If he carry his dissection medial to it he is likely to have trouble with branches of the femoral nerve. It is an excellent inci- sion for a simple case. SPRENGEL’S Inciston.°—This was brought out many years ago, and has recently been revived under the name of Smith-Peterson. It is very simple, very satisfactory for all ordinary cases, and has not attained the popularity it deserves. It has two arms. The longitudinal one starts from the anterior superior spine of the ilium, and runs distal about 15 centimetres just lateral to the tensor fascizw late. The transverse arm runs from the anterior superior spine backward along the outer lip of the crest of the ium for about half its length, and is carried down right through the periosteum to the bone. Keeping close to the bone, the operator Fic. se core Hs up int tl + ’ ? l= . e nary anterior incision’ E, A, then pushes with a blunt chisel the fibres B, Smith-Peterson incision. A : Prin E, A, D, Sprengel incision. of the glutei, medius and minimus, away S, sartorius muscle. T, tensor fascie femoris. The dotted from their attachment to the dorsum of lines C, A, shows the crest of the ilium. the ilium, and reflects backward the whole flap of skin, fascia, fat and muscle, until he reaches the antero-proximal border of the acetabulum. Meantime he has been carrying the longitudinal arm of the incision by intermuscular dissection down to the capsule of the joint. He opens the capsule and an assistant by exter- °SprenceL: “Zur operativen Nachbehandlung alter Hiiftresectionen.” Archiv. f. klin. Chir., 1898, lvii, 837. TUBERCULOSIS OF THE HIP 291 nal rotation turns the head out of its socket. It is best to remove it at the very base of the neck. If there be any diffi- culty in disarticulating, the removal of a little bone from the antero-superior border of the acetabulum overcomes it. My experience with this incision has been very satisfactory, and I recommend it for routine work. After removal of the head, the trochanter may be per- mitted to dislocate, or it may be shoved into the acetabulum. The wound is closed and dressed, and the whole limb is put up in a long plaster spica, in a position of ex- treme abduction. Kocuer’s [nctston.'°—Place the patient on his sound side in the latero-ventral position. Slightly flex the hip. Let an assistant grasp the leg so as to change the position of the thigh according to directions. Beginning at the posterior margin of the base of the trochanter major, make a cut in the proximal direction to the posterior angle of the summit of the trochanter. At this point change the direction of the incision, and cut prox- imally and backward towards the posterior superior iliac - spine, 2.é., cut parallel to the fibres of the gluteus maximus and expose that muscle. Split the tendon of the gluteus maximus in the direction of its fibres, and enlarge the deep wound proximally and backward by splitting the muscle itself. Retract the edges of the deep wound, exposing the gluteus medius at its insertion into the trochanter. Rotate the hip slightly inward, so as to make prominent the posterior part of the summit of the trochanter. Find the groove between the gluteus medius and minimus, prox- imally, and the pyriformis, distally. Beginning at this place separate with elevator or knife the insertions of the gluteus medius and minimus, along with the corresponding ** From Binnie’s Operative Surgery. 292 INFLAMMATION IN BONES AND JOINTS periosteum, from the trochanter, until the anterior inter- trochanteric line is reached. At this point separate the insertion of the ilofemoral ligament. While doing this flex the thigh and rotate it out. | Divide the capsule along the distal edge of the pyri- formis tendon. Flex the thigh and rotate it inwards so as to gain access to and divide the insertion of the pyriformis. With ele- vator or chisel (removing a thin shell of bone if desired) separate the inser- tions of the obturators and the gemelli. Murphy"’ employed a lateral U- shaped incision, with the trochanter in its centre, reaching from a point ten centimetres proximal to one five centi- metres distal to the tip of the trochan- ter. ‘The open end of the U is proximal and is twelve centimetres wide. He reflected proximally the U-shaped flap of skin, superficial fas- Murphy incisions ior resection cia and fascia lata. He then passed a of the hip. A,B, Murphy. C, (Eee Gigli saw about the base of the tro- chanter, and divided the trochanter. (This may be done with osteotome.) The trochanter, with its attached muscles, he turned proximally, and thus gained access to the capsule. REFERENCES TUBERCULOSIS OF THE HIP Auuison, NatHaniEeL: “Tuberculosis of the hip. An analysis of twenty-five selected cases.” Am. Jour. Orth. Surg., 1914-1915, xii. 622. ANNANDALE, T.: “On the pathology and operative treatment of hip disease.” Edinb. Med. Jour., 1875-1876, xxi, 410, 487, 591, 694. 1 MourpHy, Joun B.: Journal of A. M. A., 1905. TUBERCULOSIS OF THE HIP 293 Asnourst, J., and Tunis, J. P.: “Tuberculosis of the hip-joint.” Path. Soc., Phila., Trans., 1898, xviii, 2. Batty, R.: “Coxa vara tuberculosa.” Arch. f. klin. Chir., 1907, Ixxxiii, 648. Barker, A. E.: “The after-history of 41 cases treated by operation for destructive hip-joint disease.” Lancet, 1900, i, 1499. Becx, Emi G.: “ Treatment of tuberculous hip-joint disease with coexisting sinus by means of bismuth paste. . .” Western Surg., Ass. Trans., 1913, xxiii, 46. Brnpver. R.: “ Die conservative Behandlung der Coxitis u. s. w.” Ztschr. f. orthop. Chir., 1899, vii, 276. Buioopcoop, J. C.: “ Early exploratory operations in tuberculosis of the hip.” Johns Hopkins Hosp. Bull., 1900, xi, 11. Bowrsy, A. A.: “Nine hundred cases of tuberculous disease of the hip.” Brit. Med. Jour., 1908, i, 1465. Braprorp, E. H.: “Use of traction in hip disease.” dm. Jour. Orth. Surq., 1905-1906, iii, 199. Brackett, E. G.: “An experimental study of distraction of the hip-joint.” Boston Med. Surg., Jour., 1890, exxii, 241. . Bruns, P.: “ Ueber die Ausgiinge der tuberkulésen Coxitis bei conservativer Behandlung.” Arch. f. klin. Chir., 1894, xlviii, 213. Curpeautt, A.: “Coxalgie tuberculeuse limitée au ligament rond.” Soc. Anat. de Par., Bull., 1890, Ixv, 276. Coupray, P.: “ Coxotuberculose et son traitement.” Rev. de Chir., 1911, xiii, 420. Dirtte: “ Experimentelle Studien uber die Stellung bei Hiiftgelenkenzundung (Coxitis).” Ztschr. d. k. k. Gesell. d. Aerzte zu Wien., 1856, xii, 665. Enrincuavs, Orro: “Zur Aetiologie der Knochenatrophie bei tuberkuliser Koxitis.” Charite-Ann., 1910, xxxiv, 755. FroeticuH: “ Des coxitis et coxalgies frustes de l’enfance etc.” Rev. de Chir. 1917, lili, 307. Gavvain, H. J.: “Tuberculous disease of hip-joint.” Lancet, 1918, ii, 666 GisnrEy, V. P., WarermMan, J. H., ann Reynotps, W. G.: “A contribution to the study of hip-disease. On the ultimate results of the mechanical and operative treatment. . .” Ann. Surg., 1891, xxviii. 435, 454. Haperern, J. P.: “ Ueber Beckenabscesse bei Coxitis und ihre Behandlung.” Centribl. f. Chir., 1881, viii. 193. Hacen, W.: “ Zur Statik des Schenkelhalses.” Beitr. z. klin. Chir., 1908, lvi, 627. Jorrkowirz, P.: “Die Schleimbeutelentziindungen an der Hiifte in ihrer Stellung zu einen Trauma und hinsichtlich der Differentialdiagnose gegeniiber einer Coxitis.” Med. klin., 1918, xiv, 694. 294 INFLAMMATION IN BONES AND JOINTS Jupson, A. B.: “ Historical notes on the question of the value of traction in the treatment of hip disease.” NV. Y. Med. Jour., 1893, lviii, 649. KeEpplLer, W., AND Erxes, F.: “ Ueber den Wert der Tuberkulinherdreaktion fiir die Diagnose unklarer Hiiftgelenkserkrankungen.” Arch f. klin. chir., 1914, cic, 800. Kocuer, T.: “Arthrotomia coxe.” Arch. f. klin. Chir., 1888, xxxvii, 797. - Konic: “ Untersuchungen iiber Coxitis.” Deutsche Ztschr. f. Chir., 1873, iii, 256. Konic: “Die operative Entferung (Resektion) des tuberkulés erkrankten Hiiftgelenks.” Berl. klin. Wehnschr., 1909, xlvi, 429. Maracriano, D.: “La Remeralizzazione Chirurgica delle Coxiti tubercolari.” Riforma Med., 1919, xxxv, 292, 394. STeMPEL, W.: “Das Malum coxe senile als Berufskrankheit und in seinen Beziehungen zur socialen Gesetzgebung.” Deutsche. Ztschr. f. Chir., 1901, Ix, 265. CHAPTER IIT TUBERCULOSIS OF THE KNEE THE primary focus may be in the tibia, the femur, or the patella. Perhaps in rare instances, the disease may start in the head of the fibula. Most authorities agree that primary synovial tuberculosis is fairly frequent, and, while this theory is practically impossible of demonstration, I believe that it is correct, especially in adults. Sometimes the location of the primary focus can be detected with reasonable certainty, often it can only be surmised. The knee joint may be considered as comprising three articulations, two tibio-femoral, and one femoro-patellar, and this more or less complex arrangement, coupled with the presence of the synovial curtains, or partitions, is often responsible, in knee joint tuberculosis, for a peculiar dis- tribution of the disease which has not received the attention it deserves. ‘Thus one finds, for instance, cases with marked involvement of the quadriceps pouch, and with the tibio-femoral articulation practically intact, as if it had been walled off by adhesions in the same way as is the peri- toneum. Again one finds one tibio-condylar articulation badly diseased, and the other only slightly affected. Often of course the whole knee joint is equally involved. The joint cavity may be filled with a clear serous, a hemorrhagic, a turbid, or a flocculent fluid, or it may con- tain the so-called tuberculous pus. In the last case, the joint cavity constitutes a cold abscess. There is usually nothing characteristic about the appearance of the fluid in a tuberculous joint, unless it happen to be turbid and floc- culent. This is practically pathognomonic. In some 295 296 INFLAMMATION IN BONES AND JOINTS Be Fia. 93.—Old tuberculosis of the knee-joint. The heavy shadows in the plate are not to be interpreted as new bone, but as collections of calcified material. Note the decrease in the light zone between the bones, showing the disappearance of the articular cartilages. cases the joint contains no fluid at all. These are usually the slow, dry cases. In these the joint cavity may be ab- sent, and the bone ends may be bound tightly together by TUBERCULOSIS OF THE KNEE 297 fibrous adhesions, which run not only from bone to bone, but also from each bone to the capsule. When these adhe- sions are torn apart at operation they leave the bones with an irregular, torn, disorganized appearance, that is al- most diagnostic. | In some cases the synovial membrane is thickened, villous and succulent, giving a boggy, doughy feel to the articulation. ‘These usually contain a little free fluid, not always capable of detection clinically. : In the cases with free fluid, the patella floats; in the boggy cases, it can be moved with a sort of soft resistance; in the fibrous it is usually bound tightly down to the femoral condyles. | | The ends of the femur and of the tibia often appear to be enlarged, but they never are. ‘The swelling is in the circumarticular tissues. This swelling, in the cases with much proliferation in the synovial membrane, takes on a peculiar spindle shape, accentuated by the atrophy of the thigh and calf, and the skin, with veins dilated, becomes blanched, giving to the joint an appearance from which the disease derived its former name of “tumor albus” or “white swelling.” ‘The same thing is seen sometimes in the elbow, less often in the ankle, and rarely in the other joints. ~The knee is held in slight flexion, and the flexors, work- ing at an advantage over the large extensor, subluxate the tibia backward, at the same time rotating it outward. ‘The posterior portion of the capsule shrinks after a while, if the subluxation is permitted to remain, and prevents the return of the tibial head to its place under the condyles. If force be employed in the attempt to reduce the subluxa- tion, the tibial head is levered backward, and possibly one 298 INFLAMMATION IN BONES AND JOINTS of the soft bones may be fractured. This subluxation is perhaps most prominent in the cases with marked involve- ment of the quadriceps pouch, and in mild synovial cases is not to be looked for. Atrophy of the muscles of the thigh and calf is an early — and constant phenomenon, especially in the bony type of the disease. In this atrophy the bones of the thigh and leg take part. SYMPTOMATOLOGY The disease begins with pain in the knee, stiffness and a feeling of discomfort. ‘The patient limps. Swelling usually appears early. ‘The swelling may be fluctuating or boggy, the patella may float or it may not. In the late stages of the disease the mobility of the patella is almost always impaired. ‘The knee is in flexion, and its range of flexion and extension is limited. Sometimes the patient walks upon the toes of the affected foot. The flexion in the later stages may reach an extreme degree, and, with the peculiar outward rotation and general appearance of the joint, may make the identification of the disease an easy matter. In some cases however the patient may present a slightly swollen, painful joint, with nothing character- istic about it. Sensitiveness to pressure of the synovial membrane is usually present, best detected when the knee is in flexion. Abscess formation is fairly frequent, and, on account of the nearness of the joint to the surface, rupture of the abscess and secondary infection are hard to avoid. Luck- ily an infected abscess in a joint that is near to the surface is not as a rule so hard to heal as one in a deeper joint, like the spine and hip. TUBERCULOSIS OF THE KNEE 299 PROGNOSIS There seems to be a rather definite opinion that the prognosis in knee joint disease is better than in tuberculosis of other joints, and I believe this is correct, and that it is correct because the knee is easier to stiffen. Perhaps, on the other hand, it is because mechanical conditions make splinting more effectual. Conservative treatment requires two or three years at best, and under it children sometimes recover with a fair degree of motion, though always with the danger of a relapse threatening them, as with tuberculosis of any other organ. Some good authorities assert that the synovial form in adults often recovers with good function, but usually when good motion results, one views one’s diagnosis with scepticism. At best, under conservative treatment, in the adult one looks for a painless, stiff joint, and to attain this long continued treatment is necessary. The resulting ankylosis is fibrous. Unless a secondary infection has been added, bony ankylosis is rare, if it ever occurs. Under properly planned radical treatment, the disease can be brought to a standstill in about six months. Some patients, however, seem to possess no resistance to the disease. In them, in spite of treatment, the disease stead- ily advances, the operative wound breaks down, and a thigh amputation must be done to save the patient’s life. We see the same thing here as in pulmonary tuberculosis, but in this case we have a life-saving measure which we do not possess in that. TREATMENT Some surgeons recommend conservative treatment in patients of all ages, some radical in them all, but the trend of modern treatment, in which I heartily concur, is toward 300 INFLAMMATION IN BONES AND JOINTS invariable conservative treatment in children, and invari- able radical treatment in adults, as soon as a positive diagnosis is made. When we speak of a positive diagnosis we do not mean one that is made after a rapid examination, however experienced the examiner may be, but one founded on indisputable evidence. On the other hand, if physical examination, backed by the evidence accorded by the Ront- gen rays, shows that the joint is so badly damaged as to be incapable of good function, whatever the exact nature of the disease may be, positive proof of the presence of the tubercle bacillus 1s unnecessary, and we proceed to com- plete the task which nature has set for herself, and destroy the joint. _ A completely ankylosed, painless joint is better than a partially ankylosed, painful one, and far safer. ‘There is little hope that this method of treatment will ever become very popular among the laity. ‘The usual adult will resort to the surgeon who will promise him something bet- ter, but sooner or later he must submit to the inevitable. In spite of the claims that have been made for consery- ative treatment in children, if conditions were the same in. them as in adults we should probably be tempted to adopt radical measures, and spare them the long, tedious and uncertain course of conservative treatment, but in the knee, especially, radical treatment is to be shunned at all costs. Here are located two of the most important centres of bony growth in the body, and here unsightly postoperative deformity is notoriously difficult to avoid. Again, radical treatment is not followed by the almost certain cure that follows it in the adult. If my theory, whose truth has not yet been completely demonstrated, is correct, this is because lymphoid marrow is present in the shafts as well as in the ends of the bones, and its presence TUBERCULOSIS OF THE KNEE 301 is not dependent upon function. Resection does not cause its disappearance. In spite of all that has been said for many years against the radical treatment of tuberculous knees in children, its sporadic advocacy is perennial, and evidently cannot be killed. Only the opportunity to see, years afterward, the results of their treatment, causes its advocates to aban- don it, and their experience seems powerless to deter their successors. In this connection it may be said that Hibbs maintains that his ankylosing operation does not disturb the centres of growth, and hence does not cause shortening. CONSERVATIVE TREATMENT Precedent to the application of permanent apparatus, any deformity in the nature of fixed flexion should be corrected, and this may require patience, care and some skill. Not only the hamstrings are contracted, but also the posterior and lateral ligaments of the joint, and, if the tibia be simply straightened by direct force, its head will be levered backward with the lateral ligaments as a sort of fulcrum, perhaps fracturing the softened bone, and the tibia will be brought into a line parallel with that of the femur, but on a plane posterior to it. Various expedients have been devised to correct the deformity. Bilroth recommended two lateral hinges with long iron bars whose ends are provided with perforated pieces of tin for incorporation in plaster of Paris. The limb is put up in plaster piled quite thick in the popliteal space. When the plaster has set, it is divided at the knee joint, and a wooden wedge is driven in the crack posteri- orly, forcing it somewhat open. From time to time other 302 INFLAMMATION IN BONES AND JOINTS larger wedges are driven in, until the leg is straightened. Several plaster dressings may be necessary. The patient may be put to bed, perhaps with his leg in plaster, and then the leg may be put in a sling, and traction forward may be made on its proximal part by means of weight and pulley from a bar over the bed. The weight of the foot and of the distal part of the leg, tends to stretch the contracted ligaments, and to lever the tibial head out from under the femoral condyles. No marked flexion deformity at the knee should ever be corrected too rapidly and forcibly, on account of the danger of rupturing the popliteal vessels. Gangrene has been caused by rough manipulation. After the reduction of the deformity, the surgeon will have the choice of plaster of Paris or a brace. It is hard to say which is better. Some prefer one, some the other. Some employ both. If plaster be chosen, the knee should be fairly well, but not excessively, padded over a well fitting stockinette, and a little padding should be applied about the malleoli, and the proximal end of the thigh. The shape of the limb, that of an inverted pyra- mid, must be borne in mind, and the plaster must be molded carefully about the knee and calf to prevent it from sag- ging. At the knee the plaster should be less than 14 of an inch thick, and elsewhere less than half that. ‘The lighter the plaster is, consistent with strength, the less tendency it will have to sag. It is grotesque to see some plaster dressings put on to immobilize the knee, and reach- ing perhaps five or six inches above and below it. They should reach from the perineum to a line about one inch proximal to the tip of the lateral malleolus. Tue Tuomas Bracr.—lIf the surgeon elect a brace, he will probably find that the Thomas brace will serve his TUBERCULOSIS OF THE KNEE 303 purpose better than any other. It is one of the most use- ful braces that ever has been invented, and consists of a padded leather covered steel ring whose outline is that of a cross section of the proximal end of the thigh, and of two steel rods, running distal from the medial and lateral aspects of the ring. At their distal ends these steel rods are joined by a rubber shod sole piece. Two broad leather bands are provided to support the back of the thigh and calf, and the knee is held securely in place by a bandage, or by another broad leather band, which buckles over the front of the joint. Extension is fur- nished by straps fastened below to the foot piece, and running upward to _ buckles attached to adhesive straps on the leg. In measuring for the ring, about an inch should be allowed for the padding. ‘The uprights are the length of the limb from perineum to sole, plus about two inches, so 5. 9, the Thomas that the foot will be swung clear of the pore ground. The sole of the other shoe must be raised an equal amount to compensate. In the later stages of the dis- ease when traction is no longer necessary, and in the early stages as well, if we believe that fixation only is required, the uprights are fastened below to the sole of the shoe, and the high shoe on the other side is dispensed with. In any case, of course, the brace must be worn night and day. When all active symptoms have subsided, and when the joint seems well, whatever appliance the patient has worn should not be abandoned, but should be left off at first during the night, and then by degrees during the day. If there be any return of active symptoms, or any tendency to deformity, continuous treatment should be resumed. 304. INFLAMMATION IN BONES AND JOINTS Tuberculous knees that have healed in a faulty position of fixed flexion, may be straightened by linear osteotomy, or better yet by the removal of a wedge shaped piece of bone with its base forward. Osgood has devised a very ingenious operation for the correction ef this deformity.’ — OPERATIVE TREATMENT In operating on a tuberculous knee, the surgeon is guided by one of two principles; either he removes as much as possible of the tuberculous bone and synovial membrane, or he disregards completely the extent of the disease, and simply strives to produce a bony ankylosis. From reasons heretofore set forth at + length, I regard the latter procedure as correct. In either case, or with whatsoever theory the surgeon oper- ates, if he succeed in producing a bony ankylosis and in avoiding a secondary infection, he will cure the disease. The knee is an easy joint to ankylose: it is therefore an easy joint to cure. The approach to the knee 1s Fic. 95.—Thering ofaleft Thomas simple. The incision most often em- knee splint. C, B, the anterior portion, A, B; the perineal portion. ployed is a curved anterior, trans- verse one, convex distally, between the condyles, dividing the patellar tendon. Some surgeons make the incision with the convexity proximal, dividing the quadriceps ten- don just proximal to the patella. Some employ a straight incision, dividing the patella transversely with a saw. SR erence ne 1QOscoop, R. B.: “A method of osteotomy of the lower end of the femur in cases of permanent flexion of the knee joint.” Amer. J. Orth. Surg., 1913, xi, 336. TUBERCULOSIS OF THE KNEE 305 From this point the procedure varies with the surgeon's purpose. If he wishes to remove all the tuberculous tissue possible, he proceeds to a thorough dissection of all the synovial membrane he can reach, and to the removal of all the bone patently diseased. If his purpose is simply to ankylose, he flexes the knee acutely, dissects the soft tissues from the top of the head of the tibia, causes his assistant to retract the tissues from the head of the tibia and from the condyles of the femur, and saws off a thin slice from the head of each bone.*” In order to make the ankylosis more secure Hibbs* denudes the sides and back of the patella, and hooks it into a cavity gouged out of the head of the tibia, and the distal end of the femur. If fixed flexion was present before the operation, and if a portion at least of the lateral ligaments be spared, the joint locks fast when it is straightened. yr. 96.—teisions e en : the k inte AY :B; Deep and_ superficial sutures close the anterior longitudinal in. cision; C, D, the transverse Ane Solna Ee ees The end of the bones is usually sawn "°°? % the medial meniscus. off square. ‘The operator plans his saw cut so that when he brings the bone ends together, the bones will be in a straight line or slightly flexed as he wishes, and bowed neither in nor out. . The difficulty of getting the two flat bone surfaces together, and keeping them in apposition, prompts some *Evy, Leonarp W.: “Die Tuberkulose des erwachsenen Kniegelenks, etc.” Berl. klin. Woch., 1910, xlvii, 2062. *Ery, Leonarp W.: “Tuberculosis of the adult knee joint, etc.” Trans. Surg. Sect. A. M. A., 1910, 36. *Hrezs, R. A.: “ Tuberculosis of the knee joint in the adult, etc.” WN. Y. Med, J., 1917, cv, 922. 20 306 INFLAMMATION IN BONES AND JOINTS surgeons to practise the Fenwick operation, in which the distal end of the femur is sawn convex from before back- ward and the end of the tibia concave. This operation avoids one difficulty, and incurs another, and probably. greater one. It leaves the bone ends in the very best pos- sible shape for the formation of a new joint, which is Juss what we wish to avoid. Some operators wire the bones together with silver, others spike or plate them. Albee recommends a bone graft. Other things being equal, metal should not be bur- ied in the wound, on account of the danger of subsequent secondary infection. I have seen infection occur about an old spike that had been in for months, and then lost the patient eventually, after a thigh amputation. After the wound has been sutured and dressed, the limb is encased in plaster of Paris from perineum to toes. Including the foot is wont to make the pain less. In a week or two the plaster may be removed from below the malleoli. The limb should be immobilized for about six months. Bony union does not take place for about one year. REFERENCES TUBERCULOSIS OF THE KNEE Branves, Max: “ Uber das Endresultat radikal operierter Kniegelenkstuber- kulosen im Kindesalter.” Deut. Ztschr. f. Chir., 1912, exvii, 490. Do.iuimncer, Juuius: “ Das Zuriickbleiben im Wachsthume der kranken Ex- tremitat bei tuberkulésen Kniegelenksentziindung.” Cent. f. Chir., 1888, xv, 897. Dranor, M.: “Zur Behandlung der Kniegelenkstuberkulose mit besonderer Beriicksichtigung der Resektion.” Beitr. z. klin. Chir., 1905, xlvii, 737. Exs, Hernricu: “Ueber die Behandlung der Tuberkulose des Kniegelenks und ihre Erfolge.” Beitr. z. klin. Chir., 1913, Ixxxvii, 51. Garnier, P.: “ Beitrag zur chirurgischen und konservativen Behandlung der Gonitis tuberkulosa.” Deut. Ztschr. f. Chir., 1915, cxxxiv, 195. TUBERCULOSIS OF THE KNEE 307 Hernierns: “ Kniegelenkstuberkulose: vollstaendige Luxation.” Miinch. med. Wehnschr., 1911, lviii, 2308. Henverson, M. S.: “ Resection of the knee-joint for tuberculosis.” J. A. M. A., 1915, Ixiv, 140. Hiszs, Russert A.: “Tuberculosis of the knee-joint in the adult in which operations were done eliminating motion by producing fusion of the femur and tibia.” NV. Y. Med. Jour., 1917, cv, 922. Koenic, F.: “ Die specielle Tuberkulose der Knochen und Gelenke, 1. das Kniegelenk.” Berlin, 1896, Verlag von August Hirschwald. Konic: “ Bemerkungen zur Behandlung der Tuberkulose des Kniegelenks, u. S. W.” Arch. f. klin. Chir., 1895, i, 417. Leuspen, Friepricu Pers: “ Ueber die bei Tuberkulose des Kniegelenkes zu beobacktenden Wachsthumsverainderungen am Femur.” Deut Ztschr. f. Chir., 1899, li, 257. Linuart, A.: “ Beitrag zur Resektion des tuberkulésen Kniegelenkes.” Beitr. z. klin. Chir., 1909, Ixl. 455. May, Warren Anpreas: “ Ueber das Endresultat radikal operierter Knieg- elenks-tuberkulosen bei Erwachsenen.” Leipz., 1918, A. C. W. Vogel. Sever, J. W., anD Fiske, E. W.: “ Tuberculosis of the knee-joint in childhood.” Am. Jour. Orth. Surg., 1914-1915, xii, 597. Scuirtowsky, M.: “ Beitrag zur chirurgischen und konservativen Behandlung der Gonitis tuberkulosa.” Deut. Ztschr. f. Chir., 1915, cxxxiv, 242. (Gam CaNed bith ses ii" TUBERCULOSIS OF THE ANKLE AND TARSUS TUBERCULOSIS of the large joints of the extremities 1s peculiar. in that it shows no tendency to spread from the joint where it originates, through the bone, to the joint at its other end. In other words, it remains indefinitely in and about the original joint. ‘Tuberculosis of the joints of the ankle, tarsus and carpus does not share this peculi- arity. A focus in one bone may give rise to an infection of any joint of which that bone is a component. There- after the disease may spread to the other bone or bones making up that joint, and then to the other bones and joints of the region. It is this peculiarity which has made tuberculosis of the carpus and tarsus so difficult to treat. Its prognosis always has been bad. On the other hand the clinical fact has been noted that tuberculosis of the ankle has not a great tendency to spread to the other tarsal joints, and that disease of the calcaneus usually remains in the bone marrow, and does not spread to a joint unless a way is opened to it by unwise surgical procedure. THE ANKLE Tuberculosis of the ankle is much less frequent than tuberculosis of the spine, hip or knee, and this comparative infrequency has been adduced as an argument against the traumatic origin of joint tuberculosis, for the ankle is exposed to trauma more than almost any joint in the body. The relative frequency of the disease is said to be greater in adults than in children, like disease of the smaller joints in general, but this is open to question. 308 TUBERCULOSIS OF THE ANKLE AND TARSUS — 309 As with other tuberculous joints, the proportion of per- sons afflicted shows a slight majority in favor of the male sex, but not enough to correspond to the greater liability to trauma. | «According to Sever,’ out of 7474 cases of bone and joint tuberculosis at the Children’s Hospital; Boston, only 213 were tuberculous ankles. Of these the right ankle was involved in 108, the left in 90, and both ankles in 15. Patruotocy.—The primary focus is said to be located most often in the talus, but may be in the tibia, or in the fibula. A synovial focus is assumed in some cases. The disease may spread through the talus, and involving one of the tarsal synovial membranes, may then attack the other tarsal bones, but, as has been said, this phenomenon probably is rather rare. Abscess formation is the rule in disease in this locality, and, because of the nearness of the joint to the surface, secondary infection is almost impossible to avoid. ‘The condition of “fatty osteomalacia” is seen often in disease of the tarsal bones. ‘They cut easily with the knife, and are little else but shells. SyMPTOMATOLOGY.— Pain, swelling and limp, are early symptoms, and muscular spasm, limitation of motion, and atrophy of the leg muscles are early physical signs. ‘The normal contour of the ankle is obliterated, the hollows behind and in front of the malleoli, and distal to them dis- appear, and the whole region becomes diffusely swollen. The swelling often assumes the classic spindle shape. ‘The foot is usually held in equinus, and the patient walks upon his toes, with his knee semiflexed. Sensitiveness to pres- *Srever, J. W.: “Tuberculosis of the ankle joint and tarsus.” Jour. A. M .A., 1910, lv, 2128. 310 INFLAMMATION IN BONES AND JOINTS sure is wont to be pronounced, perhaps localized more or less over the place of greatest involvement. DiFrFERENTIAL Diacnosis.—This is made on the gen- eral principles already set forth, and, with the exercise of reasonable diligence and care, rarely occasions much diffi- ' culty. A sprained ankle has the traumatic history, with the symptoms following immediately, and sensitiveness distal to the lateral malleolus. Fractures have the distinct traumatic history, with positive X-ray findings. Proanosis.—This is not particularly good. Children - often recover with a stiff joint after secondary infection. Resection gives a useful foot in adults, but in them second- ary infection usually spells amputation. TREATMENT.—Conservative treatment usually gives good results in children, and is not difficult to carry out. Its duration is shorter than that of disease of the hip and knee. The joint should be immobilized in a position of adduc- tion and right angle flexion, by a plaster of Paris dressing reaching from the bend of the knee to the toes. If sinuses be present, windows may be cut in the plaster at their openings. If the patient walk directly upon this dressing, he will soon break the plaster to pieces, therefore we are com- pelled to adopt stilting in addition. This is best done with the Thomas brace, and a high shoe on the other side. Inas- much as extension with adhesive straps is impossible in disease of the ankle, the brace is slung from the shoulders, by a looped strap, which attaches in front and behind to the thigh ring. The Bier treatment by passive congestion, and helio- therapy are still reeommended abroad particularly. They seem especially indicated in the treatment of the ankle, TUBERCULOSIS OF THE ANKLE AND TARSUS © 311 tarsus and wrist. Cutting operations are rarely advisable upon children’s ankles. OPERATIVE 'TREATMENT.—On acount of the marked tendency to abscess formation, with the risk of extension to the other tarsal joints, in disease of the ankle joint, operative measures should be undertaken in the adult as soon as a positive diagnosis is made, and here, even less than in most other localities, should one attempt the futile operation of scraping and pack- | ing. ‘To do this is to invite dis- aster, for, if the disease once spread through the talus into the tarsal synovial cavities, an exten- sive resection, or more probably an amputation, almost always will be necessary. Our object is to produce a bony ankylosis, but this is extremely difficult in the sh ml UE Oy i ona ane ankle. Usually all we can secure sion of the talus. is a fibrous one. Theoretically a bone dowel, driven up from the sole, through the talus, into the tibia, should answer the purpose well. The operation that has given the best results is ablation of the talus, with removal of the joint surfaces of the bones with which it articulates—the Whitman operation. The incision is a curved one with the convexity distal, starting proximal to the lateral malleolus, and behind it, and run- ning distal and forward to the anterior extremity of the talus. ‘The peroneal tendons may be divided and later sutured. In disarticulating the talus one must keep close to the bone on the medial aspect, in order to avoid damag- ing the vessels passing behind the medial malleolus. If the entire foot be subluxated backward, and if the sides 312 INFLAMMATION IN BONES AND JOINTS of the caleaneus be freshened for apposition to the fresh- ened malleoli, the stability of the result will be increased, and a serviceable member will be secured. In the adult as well as in the child in secondarily infected cases, before resorting to amputation, some surgeons believe in a prolonged course of passive hyper- emia, combined with the use of Klapp’s cupping, and heliotherapy. THE TARSUS The joints of the tarsus may be affected primarily, or secondarily by extension from the ankle joint, especially if the primary focus be situate in the talus. Secondary infection with pus producing organisms, and abscess forma- tion are the rule, and usually occur early. According to Hahn’ who has compiled statistics of 704 cases of tuber- culous disease of the foot, the frequency of the disease diminishes according to the distance of the affected bone from the ankle. The significant point in tarsal disease, besides the spongy structure of all the bones, is the extent and the ramifications of the synovial membranes. ‘There are six or seven separate synovial cavities. The bones are bound together by ligaments running in different directions, and these again are covered by tendons, nerves and blood ves- sels. 'To ascertain the extent of the disease in the bones and synovial membranes is a physical impossibility. To attempt to eradicate it without an amputation is difficult. The symptoms and physical signs are the same as in tuberculosis of other joints. The patient usually walks upon his heel, with his foot abducted to remove it from Haun, O.: “Ueber die Tuberkulose der Knochen und Gelenke des Fusses, u. Ss. w.” Beit. z. klin. Chir., 1900; xxvi, 525. TUBERCULOSIS OF THE ANKLE AND TARSUS — 313 strain. ‘Two important points in differentiating the affec- tion from painful flat foot are the local sensitiveness to pressure, and the signs of inflammation over the affected region. A skiagram will show roughening of the bone, with rarefaction, and irregularity of contour. Kohler’s’ disease is also to be remembered. TREATMENT.—In children this is almost invariably conservative. The reparative processes are vigorous, and fie. 98.—Tuberculosis of the tarsus. Talo-navicular joint laid open. Note the irregularity of the articular cartilage. a foot with discharging sinuses, which appears to be hope- lessly diseased, under conservative treatment often recov- ers and forms a useful member. ‘The temptation to operate is strong, but should be stoutly resisted. In cases with secondary infection, in which drainage is poor, the foot may be immersed in a bath of normal salt solution at a temperature of 105°-110°F’., for an hour or two daily. In adults, as well as in children, heliotherapy and passive hyperemia, supplemented by the employment of Klapp’s cups, may be given a faithful trial, though I am sceptical of the results in adults, and personally should not advise the treatment. 314 INFLAMMATION IN BONES AND JOINTS The mechanical treatment is best carried out with some such brace as the Thomas, and, if too many sinuses be not present, a plaster of Paris dressing in addition. The foot should be put up in adduction, at right angle flexion with the leg. If, on account of the sinuses, we are unable to - apply plaster, we may be obliged to permit the foot to remain in a faulty attitude until the sinuses are healed. Then the faulty attitude may be gradually corrected by plaster dressings. OPERATIVE TREATMENT.—In tuberculosis of the ankle in the adult the treatment, as in disease of other joints, is almost always operative. In a very early case, with a bone focus and no synovial involvement, an early excision might perhaps effect a cure. Later this will be difficult or impossible. | In tuberculosis of the navicular there may be involve- ment of two synovial cavities, one of them extensive and with a number of ramifications; in disease of the cuboid there may be involvement of three, in disease of the talus or caleaneus, of three. When two or three bones are diseased, four, five or six synovial cavities may be involved. The disease seems to run riot when once it has become diffused through the tarsus, and all temporizing measures are usually without avail. In uncomplicated cases in the adult, wide resections have given fairly good results. Theoretically a bone graft Jaid down right through the diseased region should be the ideal treatment. I have never had the chance to do this operation in tuberculosis of the tarsus, but have done it in the wrist with excellent results. *Ery, Leonarp W.: “An operation for tuberculosis of the wrist.’ Jour. A. M. A., 1920, Ixxv, 1707. TUBERCULOSIS OF THE ANKLE AND TARSUS 315 Fic. 99.—Tuberculosis of the calcaneus, with secondary infection. TUBERCULOSIS OF THE CALCANEUS This occurs fairly frequently in children, not so fre- quently in adults, and is peculiar in several respects. It affects, almost invariably, the anterior spongy part of the 316 INFLAMMATION IN BONES AND JOINTS bone, is characterized by the formation of a sequestrum, breaks down early, ruptures on the lateral aspect, and very rarely involves a joint. The disease is a stubborn one, and its treatment is most tedious. If secondary infection have taken place, the sequestrum should be removed. ‘The usual measures of passive hyperemia, Klapp’s cupping, heliotherapy, etc., may be tried, perhaps also plugging the cavity with an iodoform paste. Finotti has had good results with the operation of ablation of the calcaneus, and says that the ability to walk is not seriously compromised. If the ten- don sheaths are badly involved’ an amputation will prob- ably be necessary, according to Finotti.* REFERENCES TUBERCULOSIS OF THE ANKLE AND TARSUS Finortr, E.: “ Tuberkulose des Calcaneus.” Deut. Ztschr. f. Chir., 1895, xl, 450. Gauzin, E.: “Resection pour tuberculose osseuse.” Rev. de. Chir., 1905, xxxli, 342. Hann, O.: “ Ueber die Tuberkulose der Knochen und Gelenke des Fusses. u. Ss. w.” Beitr. z. klin. Chir., 1900, xxvi, 525. Maass: “Die Tuberkulose des Sprunggelenks.” Arch. f. klin. Chir., 1902, Ixv. 182. Ouse, E.: “ Ueber Dauererfolge bei Behandlung der Fusswiirzeltuberkulose durch Resektion mit vorderem und hinterem Querschnitt.” Beitr. 2z. klin. Chir., 1908, lvii, 276. Rocers, Marx E.: “ Prognosis and treatment of tuberculosis of the ankle in adults.” Boston Med. Surg., Jour., 1911, clxiv. 811. Sever, JAMES Warren: “ Tuberculosis of the ankle-joint and tarsus.” J. 4. M. A., 1910, lv, 2128. Spencier, E.: “ Ueber Fussgelenk-und Fusswiirzel Tuberkulose.” Deut. Ztschr. f. Chir., 1896-1897, xliv, 1. Wotrr, Oscar: “ Ueber ausgedehnte Resectionen am tuberkulésen Fuss.” Arch. klin. Chir., 1896, liii, 304. 4Finorti, E.: “ Ueber Tuberkulose des Calcaneus.” Deut. Zeit. f. Chir., 1895, xl, 450. CHAPTER V TUBERCULOSIS OF THE SHOULDER TUBERCULOSIS of the shoulder is rather rare, especially so in childhood. Roughly, two clinical forms of the dis- ease are recognized, one in which there is a production of soft granulation tissue, with formation of abscesses, and the other in which the slow tuberculous process in the mar- row eats away, so to speak, the bone in the humeral head, and destroys it without abscess. The latter is more fre- quent, and is known as “caries sicca.” The primary focus is usually located in the head of the humerus. In all my specimens this appears to have been the case. Pain is an early symptom, felt in the shoulder, and running down the arm. Limitation of motion is present, but, on account of the mobility of the shoulder girdle on the sterno-clavicular joint, the limitation may escape the patient’s notice for some time. In testing for it, the shoulder girdle should be held fast with one hand, while the humerus is moved about with the other. If the patient is simply directed to move his arm about, the vicarious motion at the sterno-clavicular joint may give a false im- pression to the observer. The chief limitation is in abduc- tion, and in rotation. Atrophy of the deltoid and of the other shoulder mus- cles, is an early and a very important physical sign, and is especially prominent in the dry cases. It gives to the shoulder a peculiar flattening. The roundness of the del- toid disappears, and is replaced by a more angular contour. Sensitiveness to pressure is quite marked. Fluctuation 317 318 INFLAMMATION IN BONES AND JOINTS may be detected in the moist cases. Abscesses appear at the. margin of the deltoid muscle, and, rupturing, may give rise to stubborn sinuses. Besides the other forms of shoulder. arthritis of the first great type, there are two lesions of this region which deserve especial mention, namely, subacromial bursitis and acromio-clavicular arthritis. The general principles of the differentiation of the other members of this type have already been set forth. Subacromial, subdeltcid or Duplays_ bursitis,” “periarthritis” of the shoulder is, as its name implies, an 2, 3, 4, inflammation of the bursa, about three centimetres in diameter, situated partly beneath the deltoid, partly be- neath the acromion, and between them and the tendon of the supraspinatus muscle. It is often traumatic in origin, but often its cause can only be surmised. It is closely simulated by lesions of the subjacent supraspinatus ten- don. The bursa may contain fluid, or its cavity may be obliterated by the tight fibrous adhesions which bind together its walls. Collections of lime have been described in it, but Brickner and others have shown that the lime is not in the bursa, but beneath it. The symptomatology of subacromial bursitis is similar to that of tuberculosis of the shoulder, or identical with it. The same pain, sensitiveness, limitation of motion, and atrophy are all present. The X-ray plate may show a * Brickner, W. M.: “ Pain in the arm: subdeltoid (subacromial) bursitis.” Jo A A LOL Te kix 212500 *Copman, E. A.: “On stiff and painful shoulders.” Boston Med. and Surg., Jour., 1906, cliv. 613. *Copman, E. A.: “ Bursitis subacromialis or periarthritis of the shoulder Joint.” Boston Med. and Surg., Jour., 1908, clix, 533. *Copman, E. A.: “Complete rupture of the supraspinatus tendon etc.” Boston Med. and Surg., Jour., 1911, clxiv, 708. TUBERCULOSIS OF THE SHOULDER 319 shadow corresponding to the location of the bursa, a col- lection of calcareous material in the same region, a slight irregularity at or near the insertion of the supraspinatus muscle, or perhaps a small tear of the greater tuberosity. Sometimes a distinct history of trauma can be obtained, such as a fall upon the shoulder, or an overstrain throwing a baseball, with the symptoms following immediately. In the absence of definite evidence a positive diagnosis between tuberculosis of the shoulder and bursitis is impossible at the first examination. If the pain and stiffness continue, sooner or later a tuberculous process, if present, will make itself known by rarefaction in the humeral head. In acromioclavicular arthritis the pain and sensitive- ness can be localized by careful examination, in the acromio- clavicular joint, as distinct from the shoulder joint proper. Abduction of the arm is limited and painful, but not rotation. ‘The X-rays make the positive differentiation. The frequency of lesions of this joint is not generally appreciated.° TREATMENT.—In children immobilization may be se-— cured by bandaging the arm to the side, and slinging the forearm from the neck. ‘The clothing should be worn over the dressing. ‘The author’s brace constitutes a ser- viceable appliance for the later stages of the disease.° Bony ankylosis is difficult or impossible to secure by operation, but resection usually gives good results, and is followed by tight fibrous ankylosis. The arm should be put up after the operation on an eroplane splint, to pre- vent the disabling adduction that ordinarily follows opera- * Severs, R.: “Ueber die Bedeutung des Akromialgelenkes, u. s. w.” Archiv. f. klin. Chir., 1914, ev, 418. *Ery, Leonarp W.: “A new brace for the shoulder joint.” Med. News, 1904, Ixxxv, 160. 320 INFLAMMATION IN BONES AND JOINTS tions on the shoulder. If ankylosis in abduction can be secured, the rotation of the scapula will permit excellent function in the joint. For the same reason immobiliza- tion in internal rotation should be avoided. Several operations for resection have been devised. The simplest and the best for routine work is perhaps that through the anterior incision with the arm in abduction on aboard. The incision, about twelve centimetres long, runs distal from the clavicle along the anterior border of the deltoid. The operator identifies the median cephalic vein, and retracts it or ties it between ligatures, carries his dissection between the deltoid and the pectoralis major, anterior to the biceps tendons, to the joint capsule, and slits the capsule widely at right angles with the line of the joint. He then dissects subperiosteally all the tissues from the head and from the tuberosities, the assistant rotating the arm meanwhile first in one direction, and then in the other. The assistant dislocates the head through the wound, and the operator saws it off. If he believe in the efficacy of the removal of tuberculous tissue, he removes all he can reach with knife, scissors, gouge and chisel; otherwise he contents himself with the removal of the head and the articular surface of the glenoid. The operator finally closes the wound with deep and superficial sutures, dresses it, and puts the limb on the splint so applied that, when the patient stands, his hand will be about on a level with his mouth. The splint should be worn for two or three months. Kocher’s posterior incision offers no particular advan- tages in tuberculosis of the shoulder, and is much more difficult. TUBERCULOSIS OF THE SHOULDER 321 REFERENCES TUBERCULOSIS OF THE SHOULDER Durtay: “Sur une forme particuliere d’osteo-arthrite tuberculeuse de Tepaule.” Semaine Med., 1897, xvii, 81. Konic, Wirnerm Vicror: “Die Tuberkulose des Schultergelenkes.” Deut. Ztschr. f. Chir., 1891-1892, xxxiii, 403. Monvan, ET Avupry: “Les Tuberculoses de l’epaule.” Rev. de Chir., 1892, xii, 224. Worrr, Oscar: “’Tuberkulose im Schultergelenk und Caries des Processus coracoideus.” Cent. f. Chir., 1898, xxv, 146. CHAPTER VI TUBERCULOSIS OF THE ELBOW THE disease is said to begin most often in the ulna, less frequently in the humerus, and least frequently in the head of the radius. Primary synovial disease seems to be fairly common. In one of my specimens the only bone lesion discovered was a bunch of tuberculous granulations sprouting up through the articular cartilage of the radius. Abscess formation is frequent, and bursting of the abscess ean with difficulty be prevented. The pain is felt in the elbow, and perhaps shoots down the forearm. Svwelling is an early symptom, and is us- ually diffuse. If fluid be present, it is manifest posteriorly at the sides of the triceps tendon. ‘The muscles of the arm and of the forearm shrink, and this atrophy, coupled with the swelling of the joint, causes the classic spindle shape of the elbow, so often seen in the elbow, knee and ankle. On the other hand, swelling may be absent entirely in the slow, dry, fibrous cases. The forearm is semiflexed, and midway between pro- nation and supination. All motions in the elbow may be limited, or the limitation may be confined to flexion and extension, rotation remaining free. In the latter case, the radio-humeral pouch is assumed to be intact. The differential diagnosis rarely causes much difficulty. Leaving out of consideration the general diagnostic points already detailed, for some unknown reason a slow, chronic, uniarticular lesion in the elbow joint is usually tuberculous. TREATMENT.—Here as in other joints, the treatment is conservative in children, radical in adults. 322 TUBERCULOSIS OF THE ELBOW 323 CONSERVATIVE 'TREATMENT.—Some surgeons put their trust in heliotherapy and passive hyperemia, slinging the forearm from the neck during the course of the treatment. Most surgeons rely upon immobilization in plaster of Paris. ‘The elbow is put up in plaster, in flexion ata right angle or slightly beyond, and is kept in plaster until it is well. This position, enabling the patient to get his hand to his face, is the most serviceable for the general run of patients, but the rule may be modified in certain circum- stances. Adults should choose the attitude in which a stiff elbow would be most useful to them in their business. In order to get the joint into the required position, ether or gas may be administered, or, better yet, the method of Thomas may be adopted. Thomas slung the wrist to the patient’s neck, pulling the sling tight enough to make him bend his neck down toward his hand. As this position is uncomfortable, the patient gradually straightens up his head, flexing his elbow to that extent. ‘This procedure is repeated daily until the required flexion has been secured. If sinuses be present, windows may be cut in the plaster. Carrying the plaster bandage repeatedly up and down the extensor surface of the arm and forearm, avoids the piling up of the plaster in the reentrant angle, which occurs with the ordinary method of application. The dressing reaches from the axilla to the wrist, and is reinforced by an ordi- nary sling about the wrist. OPERATIVE TREATMENT.—The operative treatment of a tuberculous elbow is not, as a rule, very satisfactory, and this is probably because the joint is a difficult one to anky- lose. A bony ankylosis in an attitude of right angle flexion, would give a serviceable member. The customary treatment is resection. ‘This gives a rather loose joint, which appears for a time to be well. ‘Then, with re-forma- 324 INFLAMMATION IN BONES AND JOINTS tion of the synovial membrane, the disease lights up afresh, and compels another resection, with the sacrifice of more bone. ‘The resection is repeated, perhaps several times, until at length, with the ends of the bones sclerosed and tied loosely together with fibrous tissue, cure results. A flail jomt is not very useful. If one expects nature to build up an elbow joint anew after a resection, as in Ollier’s © classic and oftquoted case, one will be disappointed. (See the section on bone formation in the first chapter. ) The resection is done subperiosteally, and the operator must beware to keep close to the bone throughout the operation, anteriorly especially to avoid the vessels and nerves, medially especially to avoid the ulnar nerve as it passes behind the medial condyle. Some surgeons employ two posterior incisions, some Kocher’s incision, and some the Z-shaped incision of Oller, but most prefer the single, long posterior incision. The single posterior incision, about twelve to fifteen centimetres long, is made over the middle of the olecranon, and is carried down to the humerus and ulna, opening the joint. The olecranon, the posterior surface of the ulna for a short distance distal to it, and the posterior surface of the distal end of the humerus are skeletonized. ‘The ole- eranon process is removed with a few strokes of the mallet and chisel, giving access to the joint. After the condyles of the humerus and the end of the ulna have been denuded of periosteum, they are removed with saw or chisel. The head of the radius can be reached through the opening in the lateral wall of the wound, and it also should be removed. The wound is closed with deep and superficial sutures. Some authorities have maintained that if the joint be put up in full extension for a week or so, and if the position TUBERCULOSIS OF THE ELBOW 325 then be changed to right angle flexion, bony ankylosis will ensue. ‘The custom is to put it up in flexion. There is a good opportunity, in disease of the elbow, for the employment of ingenuity to ankylose the joint with a bone dowel or inlay graft. At the suggestion of one of my students I attempted to drive a dowel through the olecranon into the medial condyle, but evidently missed the condyle, for motion was present when the plaster was removed six weeks later. It might be possible to run a strut from the olecranon to a niche just proximal to the olecranon fossa of the humerus. Of course, if the radio- humeral joint is intact, all ankylosing work should be done between the ulna and the humerus, so as not to compromise the important motion of rotation. To lay down a graft between the head of the radius and the lateral condyle should be a comparatively simple matter. REFERENCES TUBERCULOSIS OF THE ELBOW BarpeNHEvER: “Zur Frage der radikalen Friihresektion des tuberkulésen Ellenbogengelenkes iiberhaupt sowie besonders im kindlichen Alter.” Deutsche. Ztschr. f. Chir., 1906, Ixxxv, 1. Damianos, N.: “ Beitriige zur operativen Behandlung der Tuberkulose des Ellbogengelenkes.” Deutsche. Ztschr. f. Chir., 1904, Ixxi, 288. Lossen, W.: “ Beitriige zur extrakapsuliiren Radikal-resektion des tuberku- lésen Ellenbogengelenks.” Deutsche. Ztschr. f. Chir., 1905, xcii, 120. OscHMANN: “ Ueber die operative Behandlung des tuberkulésen Ellenbogen- gelenks und ihre Endresultate.” Arch. f. klin. Chir., 1900, Ix, 177 and 397. Retner, Hans: “ Uber die funktionellen Resultate der Resektion des EIl- bogengelenks mit Interposition eines Muskellappens nach Helferich.” Deutsche. Ztschr. f. Chir., 1910, civ, 209. Sever, J. W.: “Tuberculosis of the elbow.” Bost. Med. Surg., Jour., 1910, clxii, 666. Topp, T. W.: “The end result of excision of the elbow for tuberculosis.” Ann. Surg., 1913, lvii, 430. Watrer: “ Osteo-arthrite tuberculeuse du coude droit, ete.” Bull. et Mem. Soc. de Chir. de Paris, 1913, xxxix, 1544. CHAPTER VII TUBERCULOSIS OF THE WRIST TuBERCULOsIS of the wrist is rare in childhood, some- — what less so in the adult. The primary focus may be in any one of the bones entering into the formation of the joint, or possibly in the synovial membrane. The most frequent starting place is said to be the head of the radius. Owing to the great extent of the synovial membrane, and to its many ramifications, the disease, once started, tends to spread widely, and to involve the synovial cavities one after another in a manner described in the section on tuberculosis of the tarsus. | Abscesses form early and break down, leaving infected sinuses leading down to the joint. The tuberculous inflammation is especially likely to spread to the tendon sheaths passing over the joint, and the resulting tuberculous synovitis adds severity to the disease. The wrist is often swollen, and usually it is in slight flexion and in pronation. Sensitiveness is present over the site of the disease, and sometimes fluctuation and muscular atrophy. aPC ives Passing oa CER nena tarde Re OOUNS | hii 2 == _ S60 ESSE ———————————————————————————— aes detisnaaindncamamesaiel —<— = = — - —_ erenecorecs =~ pon rrr rere ganna eSSeanassSee pecans Secs Aree Rar SAL Serer SPST St edie pre <2 caer enis Seana? aA ES AOS STNG ENS SPSS Nie einen las eins pepeaar ansiasegeansOaesr WEAN SSAA aS NY AS nSSnnAS SSeS eeies = > —! nrnct amen nea reine meter oa << > ——— - ———— BS =a 0S @& SA — 2. 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