THE LIBRARY 
 
 OF 
 
 THE UNIVERSITY 
 OF CALIFORNIA 
 
 LOS ANGELES 

 
 COMA 
 
 A HANDBOOK FOR THE GENERAL PRACTITIONER
 
 GLAUC O MA 
 
 A HANDBOOK FOR 
 
 THE GENERAL PRACTITIONER 
 
 M.D., B S. I.OXD., SC.D. EDIX. F.K.C.S. EXG. ETC. 
 
 LlECT.-COLOXEL I M.S. (RETIRED) 
 
 LATE SUPERINTENDENT OF THE GOVERNMENT OPHTHALMIC HOSPITAL, MADRAS ; 
 LAI E PROFESSOR Of OPHTHALMOLOGY, MEDICAL COLLEGE. MADRAS ; AXD LATE FELLOW 
 
 OF THE UNIVERSITY OF MADRAS ; 
 
 HONORARY FELLOW OF THE AMERICAN ACADEMY OF OPHTHALMOLOGY AND 
 OTO-LARYNGOLOGY. 
 
 PAUL B. HOEBER 
 
 67 & 69 EAST 59TH STREET 
 
 NEW YORK 
 
 1917
 
 Printed in England.
 
 
 So 
 E. C. I. E.
 
 00 
 SYDNEY STBPHENSON, M.B., C.M., F.B.C.S., D.O. 
 
 THIS 
 
 BOOK IS DEDICATED 
 
 IN GRATEFUL ACKNOWLEDGMENT OF THE^VERY GREAT 
 SERVICES WHICH HE HAS RENDERED TO OPHTHALMOLOGY 
 IN GENERAL, AND TO THE STUDY OF GLAUCOMA IN PAR- 
 TICULAR, IN THE PAGES OF "THE OPHTHALMOSCOPE," 
 DURING THE FOURTEEN YEARS OF THE VERY SUCCESSFUL 
 APPEARANCE OF THAT JOURNAL
 
 PREFACE 
 
 DURING the last ten years a very extraordinary amount 
 of interest has been taken in the subject of glaucoma. 
 At no time in the history of ophthalmology has this been 
 equalled, save possibly in the ten years which followed 
 the declaration of von Graefe's great discovery. Between 
 these two periods of interest in glaucoma, dating from 
 the start of each, nearly half a century elapsed. Though 
 this period was marked by no spectacular event in con- 
 nection with this particular subject, it was none the less 
 a time of steady progress and of fruitful speculation. 
 Some of the questions which puzzled von Graefe can be 
 answered by a student to-day, and yet we are far from 
 having attained finality. There are still many matters 
 on which authorities are at variance. There are, for- 
 tunately, many more on which they are in agreement. 
 
 It is not the purpose of such a work as this to discuss 
 the former. Space and common sense alike forbid such 
 a course. The aim which I have kept before me has 
 been to be of service to the busy medical practitioner. 
 The importance of the subject appears to me to demand 
 the publication of a monograph. My object has been to 
 writo the book simply and concisely, so that all may 
 understand it, shortly, so that all may have time to 
 read it, and without bias, so that all may feel its appeal. 
 
 Discussions of disputed joints have been avoided; the 
 views expressed are those which are current amongst 
 the great majority of ophthalmologists. Names of 
 
 vii
 
 viii PREFACE 
 
 authorities have been purposely omitted. A certain 
 amount of dogmatism has been inevitable. 
 
 The material for a much more exhaustive treatise on 
 the same subject lies on my desk to-day. The appeal 
 of that work will be to the scientific ophthalmologist. 
 In it subjects will be discussed at length, and authorities 
 freely quoted. Its aim will be widely different from that 
 of this little book, but the world-conflict makes the 
 publication of such a work an impossibility at present. 
 It was to have been issued first, and this book was to 
 have followed it. Circumstances have been too strong 
 for the carrying out of this intention; and now that the 
 data for the larger work are all ready to hand, there is 
 nothing to hinder the publication of the small one, which, 
 after all, is but an epitome of the former. The book is 
 addressed to the busy general practitioner in the hope 
 (1) that it will put him on his guard, so that he may not 
 overlook cases of glaucoma when he meets them ; (2) that 
 it will teach him to make sure of his diagnosis in case 
 of doubt ; and (3) that it will serve to indicate to him the 
 latest lines along which the treatment of the disease is 
 conducted to-day. 
 
 54, WELBECK STBEET, 
 
 CAVENDISH SQUARE, W., 
 January, 1917.
 
 CONTENTS 
 
 CHAPTER PAQK 
 
 I. INTRODUCTORY- - 1 
 
 II. THE ANATOMY OF THE PARTS CONCERNED IN GLAUCOMA 3 
 
 III. THE INTRA-OCULAR PRESSURE, AND THE TENSION OF 
 
 THE EYE 
 
 IV. THE PATHOLOGICAL ANATOMY OF GLAUCOMA - 
 V. THE CAUSES OF GLAUCOMA 
 
 VI. THE DIAGNOSIS OF GLAUCOMA- 
 VII. THE SIGNS AND SYMPTOMS OF GLAUCOMA 
 VIII. THE TREATMENT OF GLAUCOMA 
 IX. SECONDARY GLAUCOMA - 
 X. CONGENITAL AND JUVENILE GLAUCOMA 
 
 INDEX - - - - 58
 
 LIST OF ILLUSTRATIONS 
 
 no. 
 
 1. THE FILTRATION ANGLE (ARTHUR THOMSON) - Frontispiece 
 
 MM 
 
 2. MERIDIONAL SECTION THROUGH THE ANTERIOR POR- 
 
 TION OF THE EYE - - facing 3 
 
 3. THE OPTIC NERVE ENTRANCE - - 6 
 
 4. THE ANGLE OF THE CHAMBER, OPEN AND CLOSED facing 14 
 
 5. CUPPING OF THE OPTIC DISC - - facing 27 
 
 6. DEVICE TO EXPLAIN THE APPARENT ALTERATION IN 
 
 THE DIRECTION OF THE VESSELS AS THEY EMERGE 
 
 FROM A GLAUCOMATOUS CUP - 28 
 
 7. PHYSIOLOGICAL, GLAUCOMATOUS, AND ATROPHIC CUP- 
 
 PING OF THE OPTIC DISC - - 29 
 
 8. THE VISUAL FIELDS IN GLAUCOMA - 32 
 
 9. THE SCHIO'TZ TONOMETER - 33 
 
 10. LAGRANGE'S OPERATION - facing 40 
 
 11. HOLTH'S PUNCH FORCEPS 41 
 12 A. SCLERO-CORNEAL TREPHINING - - 42 
 
 12B. SECTION OF EYE TO SHOW PARTS CONCERNED IN TRE- 
 PHINING - - - - - 43
 
 GLAUCOMA 
 
 CHAPTER I 
 INTRODUCTORY 
 
 THE term " glaucoma " is not the title of any one single 
 disease. It is rather a convenient clinical label for a 
 large group of pathologic conditions, the distinctive 
 feature common to all of which is a rise in the intra- 
 ocular pressure. 
 
 The causes of these conditions are many and varied, 
 the pathological findings are most diverse, and the 
 difference in the symptoms presented is so extraordinary, 
 that very careful study is required to detect the bond 
 which serves to unite these very dissimilar manifestations 
 of disease in a common category. 
 
 When we speak of the hardness of a glaucomatous eye, 
 or of its rise in tension, we are referring to the outward 
 manifestations of an increase of the fluid pressure within 
 the globe. To this increase all the causes of glaucoma 
 lead up; on it every sign and symptom of the condition 
 depend. 
 
 If the rise in pressure can be traced to the action of 
 some antecedent local disease, we speak of the glauco- 
 matous condition as secondary ; failing this we term it 
 primary. 
 
 The presence of an increase in intra-ocular pressure 
 necessarily brings about some measure of interference 
 with the free escape of blood from the interior of the eye 
 
 1
 
 2 INTRODUCTORY 
 
 to the surface. So long, however, as such interference 
 does not give rise to obvious congestion of the eye or of 
 its conjunctiva, we speak of the condition as " simple 
 or non-congestive glaucoma." When evidence of inter- 
 ference with the venous return makes its appearance, 
 the disease is said to be congestive. The term "in- 
 flammatory," though often used in this connection, is 
 erroneous and should be dropped. 
 
 The classification of all cases of glaucoma into three 
 groups viz., the acute, the sub acute, and the chronic 
 has been productive of much confusion, owing to the 
 difference in the way in which these terms have been 
 used by writers on the subject. 
 
 Any case which presents the signs and symptoms of 
 severe congestion, as a result of a steep rise in intra- 
 ocular pressure, may reasonably be spoken of as acute; 
 similarly with eyes presenting the signs of siibacute 
 congestion. To define a chronic case is more difficult. 
 All that the term really implies is that the condition has 
 lasted for some time; but, in the accepted use of the 
 term, it is also understood that the case is not in an 
 acute or subacute stage. Any glaucomatous eyeball, 
 whether of the simple or of the congestive type, may 
 fall into this category. The point to be emphasized is 
 that there is no such thing as acute, subacute, and chronic 
 glaucoma. Any glaucomatous eye may be in an acute, 
 a subacute, or a chronic stage, and may readily pass 
 from one to another of these stages, and back again into 
 that from which it sprang; but to speak of acute, sub- 
 acute, and chronic glaucoma, as if we were dealing with 
 so many clinical entities, is wrong and misleading.
 
 CHAPTER II 
 
 THE ANATOMY OF THE PARTS CONCERNED 
 IN GLAUCOMA 
 
 BEFORE we can study the processes of disease in an 
 organ, or the methods of combating them, it is essential 
 that we should make ourselves acquainted with certain 
 anatomical details of the structures concerned. 
 
 The ciliary body and the parts adjoining it are " the 
 cockpit " of glaucoma. A study of the two illustrations 
 given will make a number of important points clear; a 
 few of the more essential anatomical features demand 
 some notice. 
 
 The Conjunctiva. It will be noted in the illustration 
 (Fig. 2) that the subconjunctival tissue is continued well 
 in advance of the sclero-corneal junction. It is along 
 this layer that we work in " splitting the cornea " in the 
 operation of trephining, and the looseness of the tissue 
 just referred to explains the ease with which that 
 manoeuvre is conducted. 
 
 Schlemm's Canal (Figs. 1 and 2) lies at the junction 
 of the cornea and solera, close to the inner surface of the 
 corneo-scleral envelope. It is separated from the aqueous 
 chamber only by the loose open network of the pectinate 
 ligament (Figs. 1 and 2). Fluid can pass readily from 
 the chamber to the canal through the open spaces of 
 this mesh work. 
 
 The Scleral Spar (Fig. 1) lies between the pectinate 
 ligament anteriorly and some fibres of the ciliary muscle 
 
 3
 
 4 GLAUCOMA 
 
 posteriorly. A contraction of these fibres will pull back 
 the spur and tend to open wide the canal of Schlemm. 
 As soon as muscular contraction ceases, the pectinate 
 ligament being elastic, will draw the scleral spur back 
 into place, and so close the canal of Schlemm (Arthur 
 Thomson). It is suggested that the pump action above 
 described is repeatedly in action during life, drawing 
 the fluid from the anterior chamber into the canal of 
 Schlemm, and then sweeping it on again from the canal 
 into the neighbouring veins. 
 
 The Angle of the Chamber (Fig. 2) is at the best of times 
 a narrow space. Inasmuch as the outflow of the aqueous 
 fluid takes place in this neighbourhood, it is most im- 
 portant that the angle should remain widely open. Its 
 patency may be infringed in several ways. 
 
 1 . Extreme dilatation of the iris, by crowding the mem- 
 brane out to its periphery, tends to fill up the angle, and 
 so to impede the passage of fluid through it. 
 
 2. The ciliary body may become swollen by congestion 
 with blood. If it does so, its apices move forward. A 
 glance at the illustration (Fig. 2) will show that, if this 
 happens, these apices will press upon the base of the iris, 
 and push the latter forward against the cornea, thus 
 closing the angle. A second point may be learnt from 
 the diagram. If the apices of the ciliary body move 
 forward, the attachments of the suspensory ligament 
 of the lens do the same; this, obviously, will allow the 
 lens to advance, and so to press on the base of the iris. 
 
 3. As life advances, the lens enlarges, whilst the tunic 
 of the eye remains stationary in size. The swollen lens 
 tends to press the iris forward, and so to occlude the 
 angle, just as in the previous case. 
 
 4. When the iris and cornea are brought into close 
 apposition in one of the ways above described, their 
 adjacent surfaces are apt to be glued together by the
 
 THE ANATOMY OF THE PARTS 5 
 
 exudate they throw out. In this way a permanent 
 obliteration of the angle may be brought about. 
 
 The Iris. On the anterior surface of this membrane 
 are found pit-like depressions, the crypts of the iris 
 (Fig. 2), which lead to the depth of the iris stroma, and 
 which place its tissue spaces in free communication with 
 the cavity of the aqueous chamber. In this stroma the 
 fluid comes into intimate contact with the thin-walled 
 iris veins, and passes into the latter by osmotic action. 
 The crypts are of importance when the angle of the cham- 
 ber is in an early stage of closure, for the fluid from the 
 chamber can enter through them and find its way along 
 the iris stroma to the neighbourhood of the pectinate 
 ligament, across which it then passes to enter Schlemm's 
 canal. 
 
 The Ciliary Body. Whilst few authorities now accept 
 the suggestion that there are definite tubular secretory 
 glands in this body, it is believed that its lining cells 
 have the power of taking up fluid transuded into their 
 neighbourhood from the capillary vessels, and passing 
 it across on to the free surface by a definite act of secretion. 
 
 The fluid thus poured out passes by two streams, one 
 backward into the vitreous, and the other inward and 
 forward into the posterior division of the aqueous 
 chamber; thence it finds its way through the pupil into 
 the anterior division of that chamber, and flows outward 
 all round to reach the angle. 
 
 The ciliary body presents a large surface of attachment 
 to the sclera. This is of interest in connection with the 
 operation of cy do-dialysis, the purpose of which is to 
 tear the former structure away from the latter over the 
 area marked out by a limited incision; the pectinate 
 ligament is obviously divided during this step. The 
 object aimed at is to open up a communication between 
 the anterior chamber in front and the suprachoroidal
 
 6 
 
 GLAUCOMA 
 
 space behind, by means of the detachment of the ciliary 
 body. 
 
 The vessels and nerves which supply the ciliary body and 
 iris pass forward between the choroid and the sclera. 
 In this course they are exposed to the full force of the 
 intra-ocular pressure, since they lie against the hard 
 unyielding scleral coat. 
 
 There is a free communication between the vascular 
 system in the interior of the eye and that on its surface 
 through the perforating vessels, which pierce the sclera 
 close behind the cornea. Both here and in the neigh- 
 bourhood of the vasa vorticosa, the evidence of con- 
 gestion within the eye is to be looked for when present. 
 
 FIG. 3. OPTIC NERVE ENTRANCE. (Drawn by E. E. from a lantern 
 
 projection of a slide.) 
 R, Retina ; 8, Sclera ; O, Optic nerve ; V, Central vessel. 
 
 The whole of the choroidal and retinal circulation lies 
 between the fluid contents of the eye and the unyielding 
 sclera, and must suffer whenever the pressure within the 
 eye is increased. The arterial and venous circulations 
 react differently. The pressure diminishes the amount 
 of blood entering the eye through the arteries, and also 
 that leaving it through the veins. The effect is to 
 diminish the arterial supply and to establish a condition
 
 THE ANATOMY OF THE PARTS 7 
 
 of venous congestion. If the pressure rises slowly, the 
 circulation can adapt itself to the change of conditions, 
 and the glaucoma remains simple. If. on the other hand, 
 the increase in pressure is a rapid one, no such adapta- 
 tion is possible, and an attack of congestive glaucoma is 
 the result. 
 
 The optic nerve entrance, being the weakest part of 
 the eye, is the first to yield under a rise of pressure, 
 hence the cupping of the optic disc. The whole nerve- 
 head, including the lamina cribrosa, is pushed backward 
 Owing to the fact that the fibres of the optic nerve lose 
 their medullary sheath as they pass through the scleral 
 coat, the bulk of the nerve diminishes from without 
 inward; consequently a section through this part shows 
 the nerve presenting roughly the appearance of a trun- 
 cated cone, with its base at the external surface, and its 
 truncated end at the fundus (Fig. 3). The channel in 
 which it lies has the same form. This explains the shape 
 of an advanced glaucoma cup, the overhanging edges 
 seen in the cup, and the apparent interruption in the 
 continuity of the bloodvessels which emerge from it (vide 
 Fig. 5, on p. 27, and Fig. 7s, on p. 29).
 
 CHAPTER III 
 
 THE INTRA-OCULAR PRESSURE AND THE 
 TENSION OF THE EYE 
 
 BEFORE we can understand the aetiology or pathology of 
 glaucoma, we must study the mechanism whereby the 
 healthy eye is kept of its usual shape, and at a normal 
 tension. 
 
 The tension of an eye is a measure of the state of 
 distension of its tunic, and is a factor which can be 
 estimated either by the fingers or by means of a special 
 instrument, known as a tonometer. 
 
 The intra-ocular pressure, on the other hand, is the 
 level of pressure at which fluid stands within the eye; 
 this is constantly varying, and can only be measured by 
 introducing the needle of a manometer into the globe, 
 a procedure which for clinical purposes is manifestly out 
 of the question. 
 
 Practically we measure the tension, and then seek to 
 arrive at the intra-ocular pressure ; but we must remember 
 that the tension of a globe depends on other factors 
 beside the pressure, the most important of these being 
 the thickness and distensibility of the ocular tunic. We 
 must therefore be very careful to keep the two terms 
 distinct in our minds. 
 
 THE PHYSICAL CONDITIONS EEGULATING INTRA-OCULAR 
 
 PRESSURE 
 
 The sclero-corneal coat of the eye constitutes a more 
 or less unyielding tunic, which is, however, endowed 
 with a degree of distensibility and of elasticity, properties
 
 THE INTRA-OCULAR PRESSURE 9 
 
 which are best marked in the young organ. The major 
 part of the contents of the globe consists of the intra- 
 ocular fluid. This fluid is constantly being changed; 
 fresh quantities are always being poured out by the ciliary 
 body, and a like amount is as constantly being drained 
 away at the angle of the chamber, and from the surface 
 of the iris. In this way a measure of equilibrium is kept 
 up. Passing through this fluid, and freely bathed by it, 
 are the bloodvessels of the eye. 
 
 It is probable that the intra-ocular fluid is poured out 
 as the result of a combination of filtration under pressure 
 and active cell secretion. As a result of the former, 
 fluid is expressed from the capillaries of the ciliary body, 
 and is accumulated in the neighbourhood of the epithelial 
 cells lining the surface of that organ (vide Fig. 2); these 
 in turn pass it through their bodies by a process of active 
 secretion. The greater the difference between the capil- 
 lary blood-pressure within the eye and the intra-ocular 
 pressure, the more rapid will the transudation be. More- 
 over, a freer supply of blood to the ciliary body will 
 excite its cells to a more active secretion. 
 
 The fluid finds its way back again into the circulation 
 through the pectinate ligament, and the crypts of the 
 iris (vide Fig. 1), which both lead into the veins of the 
 eye. This return is effected partly by osmosis, and partly 
 by a pump action, of which the motive power is supplied 
 by the ciliary and iris muscles. These pull open the 
 canal of Schlemm each time they contract, whilst the 
 elastic rebound is furnished by the pectinate ligament 
 and the scleral spur (Arthur Thomson). 
 
 There are thus two simultaneous and closely inter- 
 dependent circulations going on within the eye viz., 
 (1) the vascular, and (2) that of the intra-ocular fluid. 
 The latter is fed by, and returned to, the vessels of the 
 former system.
 
 10 GLAUCOMA 
 
 The pressure of the intra-ocular fluid (known as " the 
 intra-ocular pressure ") depends on the volume of the 
 total fluid (blood plus intra-ocular fluid) in the eye at 
 any given time. If secretion is increased, or if excretion 
 is impeded, and still more if both these factors are active, 
 the volume of the intra-ocular contents increases, and 
 can only then be accommodated by means of a slight 
 but distinct distension of the external coat of the eye; 
 to this distension there is opposed the elasticity of the 
 ocular tunic. The pressure of the contents conse- 
 quently rises, until the limit of distensibility and of 
 elasticity is reached, when the eye becomes " stony 
 hard." * 
 
 Traced back to its first cause, the intra-ocular pressure 
 depends on the blood-pressure within the eye. As in 
 all other organs, this pressure is highest in the arteries 
 as they enter the globe, and lowest at the points of exit 
 of the veins therefrom. Speaking generally, the intra- 
 ocular blood-pressure rises and falls with the general 
 or systemic blood-pressure, but wide variations from this 
 rule may occur. 
 
 It has already been pointed out that the difference in 
 level between the capillary blood-pressure in the eye 
 and the intra-ocular pressure (i.e., the pressure of the 
 free fluid within the eye) determines the freedom of 
 secretion of the intra-ocular fluid. Therefore a rise in 
 the capillary pressure will cause an increase in the volume 
 of intra-ocular fluid, and vice versa, always provided that 
 the intra-ocular pressure remains stationary. Con- 
 versely, a rise in the intra-ocular pressure will lower the 
 rate of secretion, by tending to level up the capillary and 
 intra-ocular pressures, and again vice versa. 
 
 It is essential to make it very clear that, though the 
 systemic blood-pressure is of great importance, and is, 
 indeed, the foundation element, it does not dominate
 
 THE INTRA-OCULAR PRESSURE 11 
 
 the whole situation. This will be better understood if 
 we first consider certain side-influences. 
 
 1 . Any factor which obstructs the outflow of fluid from 
 the angle of the chamber tends to increase the volume of 
 the intra-ocular contents, and so to raise the pressure 
 within the eye. 
 
 2. Any factor which facilitates the outflow from the 
 angle of the chamber must have the opposite effect. In 
 this connection it is important to remember that there 
 is evidence that, when the intra-ocular pressure rises 
 under physiological conditions, fresh channels of excretion 
 open, or else the existing ones enlarge, and so the removal 
 of the excess of fluid is facilitated, thereby relieving the 
 pressure within the eye. It is highly probable that the 
 same thing occurs under pathological conditions. 
 
 3. A rise in the intra-ocular pressure will tend to close 
 the lumina of the veins at the points where their pressure 
 is lowest viz., just where they are passing out of the 
 eye; for the pressure here is only a little above that of 
 the surrounding intra-ocular fluid. We know this is so, 
 because if we press lightly with a finger on the globe, 
 whilst using an ophthalmoscope, we can see the lumina of 
 the veins close up at their proximal ends. We infer that 
 under ordinary conditions the pressure in the veins is 
 kept at such a level that the current of blood can still just 
 escape from the globe. The closure of the venous exits 
 will result in a rise of the venous pressure, until the ob- 
 struction is overcome . Such a rise will work back through 
 the capillaries towards the arteries. An obstruction to 
 venous exit will therefore in the first instance bring 
 about a rise in capillary blood-pressure. Vice versa, a 
 fall in venous exit pressure will cause a fall in capillary 
 pressure. Now, a rise in capillary blood-pressure favours 
 an increase of secretion, provided other things are equal; 
 whilst a fall in it cuts down secretion.
 
 12 GLAUCOMA 
 
 If these elements of the situation are once grasped. 
 it is easy to understand how the intra-ocular pressure is 
 normally maintained at a steady level, for each factor 
 that would tend to raise or lower the pressure within the 
 eye carries with it compensating influences. How, then, 
 does it come about that the pressure of the eye ever 
 rises far above the normal ? A rise in intra-ocular 
 pressure, as has been shown, closes the venous exits, and 
 so raises the capillary blood-pressure. This should lead 
 to an increased escape of fluid from the eye, but if, owing, 
 to the condition of the excretory channels, it cannot do 
 so, the volumetric contents of the eye rise instead of 
 fall, as they normally should. Once again the venous 
 exits tend to become closed, and once again, in response, 
 the venous blood is dammed back until the vascular 
 pressure behind it suffices to force the obstruction. Each 
 time this occurs, the capillary pressure rises correspond- 
 ingly. Relief may come to the eye either (1) by the 
 opening up of fresh channels for the escape of the intra- 
 ocular fluid, or (2) by a diminution of the fluid secretion, 
 brought about by the fact that the levels of the vascular 
 pressure and of the intra-ocular pressure have become 
 more nearly equalized. If no such succour is forth- 
 coming, what happens to the eye ? Step by step the 
 venous pressure mounts upwards, and with it the capil- 
 lary pressure, until the whole system of vessels within 
 the eye reaches the blood-pressure level of the arteries 
 at their entrance into the globe; then circulation must 
 cease altogether. 
 
 The important lesson to learn is that the great factor 
 which dominates every other, and which ultimately 
 decides the level at which the intra-ocular pressure is 
 to stand, is that of the volumetric contents of the eye. 
 This in its turn is determined by the relative rates of 
 secretion and of excretion of the intra-ocular fluid.
 
 CHAPTER IV 
 THE PATHOLOGICAL ANATOMY OF GLAUCOMA 
 
 IN our search for the causes of a disease, we turn naturally 
 to a study of its pathological anatomy. In the case of 
 glaucoma this method is very unsatisfactory, as all our 
 material is obtained from globes far advanced in the 
 morbid condition. In such, the changes which cause the 
 rise in tension are obscured and overlaid by those which 
 result from the condition. Consequently, we are unable 
 to distinguish between cause and effect, and are there- 
 fore thrown back largely on clinical observation. The 
 difficulty is heightened by the fact that a large number 
 oi widely different conditions are grouped under the 
 heading of glaucoma, because a rise in the pressure 
 within the eye is the leading feature in all alike. 
 
 We may dismiss, as unworthy of serious consideration, 
 the view that changes in the vortex veins are an im- 
 portant factor in causing the disease. We may also deal 
 summarily with the idea that glaucoma is primarily a 
 disease of the vessels; for we now know well that the 
 familiar vascular changes are a result, and not a cause, 
 of the increase in intra-ocular pressure. Again, we can 
 jettison the view that the cupping of the disc is due, not 
 to an increase in the intra-ocular pressure, but to an 
 active atrophy of the optic nerve itself. It remains to 
 deal with the suggestion that the cause of the condition 
 is to be sought in a change in the tissues of the eye, 
 brought about by the deposit in them of waste acid 
 
 13
 
 14 GLAUCOMA 
 
 products with the result that they take up moisture 
 more readily than natural, and swell up in consequence. 
 The evidence available is all against such a view. 
 
 Fibrosis of the Pectinate Ligament. It has been shown 
 that, as life advances, the fibres composing the pectinate 
 ligament become thicker and thicker. This causes them 
 to encroach upon the spaces of the open network of the 
 ligament. It has been suggested (T. Henderson) that 
 this change opposes an obstacle to the free passage of 
 aqueous fluid from the anterior chamber to the canal of 
 Schlemm, since the current finds its way along these 
 open clefts or spaces. Again, the view has been brought 
 forward (A. Thomson) that the changes in the ligament 
 may interfere with the pump action, whereby fluid is 
 supposed to be sucked from the chamber into the canal, 
 since the rebound after each stroke of the muscular (iris 
 and ciliary muscles) action is dependent on the elasticity 
 of the ligament. That both these factors are to be taken 
 into account is accepted, but it must be remembered that 
 the changes in the ligament are said to be invariably 
 found as life advances, whilst glaucoma is far from being 
 so widespread as this. They may be taken to be con- 
 tributory, but no more. 
 
 Closure of the filtration angle is caused by the iris 
 base being pressed against the periphery of the cornea. 
 At first the closure is simply mechanical, the two sur- 
 faces merely lying in close apposition. Later a plastic 
 exudation is thrown out, which causes the two membranes 
 to become adherent to each other. Later still the iris 
 tissue becomes firmly compressed, and eventually under- 
 goes atrophy. The final stage is a retraction of the 
 ciliary processes which drags the iris back with them, and 
 may even tear through the adhesions between it and the 
 cornea. 
 
 During the earlier stages of the process, fluid can still
 
 PATHOLOGICAL ANATOMY 15 
 
 find its way along the meshes of the iris, to escape by 
 the drainage channels; but as compression asserts itself 
 such a flow is very severely interfered with. At the 
 same time, the pressure to which the parts are subjected 
 interferes with the circulation of blood, and paves the 
 way for atrophy to follow. 
 
 The closure of the filtration angle is brought about by 
 different factors in different cases. In congestive glau- 
 coma, the ciliary processes are enlarged owing to engorge- 
 ment by blood, and consequently push the iris base 
 forward in front of their expansion. At the same time 
 their forward movement permits the lens to advance, and 
 this, again, in its turn thrusts the iris forward. 
 
 In .simple glaucoma, the displacement forward of the 
 iris is a result of the enlargement and advance of the 
 lens which take place as life progresses. The action is 
 much slower than that met with in congestive cases, 
 and the tendency to the formation of adhesions is much 
 less. It only remains to add that the changes in the lens 
 just discussed are also operative in congestive cases, but 
 their role is then a subordinate one compared with that 
 of ciliary congestion. 
 
 The changes we have been describing naturally lead 
 to a shallowing of the anterior chamber. The latter is 
 well known to be a leading feature of glaucoma. 
 
 The Dimensions of Glaucomatous Eyes. The eyes of 
 glaucomatous persons are, as a rule, smaller than those 
 of the non-glaucomatous. The measurement of the 
 transverse diameter of the cornea furnishes the best 
 indication of the size of the eye. The factor of real 
 importance is the relationship between the size of the 
 eye and that of its contained lens. The lens grows con- 
 tinuously throughout life, whilst the cornea of the foatus 
 has nearly attained its full dimensions at birth, and the 
 sclera ceases to grow before the rest of the body does.
 
 ltj GLAUCOMA 
 
 Since the lens grows larger and larger as life advances, 
 whilst the globe stands still, it is clear that the older the 
 eye becomes, the more likely is it that the lens will 
 become too large for safety; and, again, the smaller the 
 globe is, the earlier in life will this disproportion occur 
 (Priestley Smith).
 
 CHAPTER V 
 THE CAUSES OF GLAUCOMA 
 
 HAVING reviewed the pathological anatomy of the 
 subject, we now pass on to its astiology. 
 
 1. Age takes precedence over all known causes of the 
 disease. In the earlier decades of life glaucoma is rare; 
 its frequency increases slowly in the fourth decade, more 
 rapidly in the fifth and sixth, remains stationary in the 
 seventh, and then diminishes again. How does the 
 advance 01 life cause glaucoma ? 
 
 (a) By bringing about alterations in the anatomical con- 
 ditions of the parts. Amongst such we may class (i.) en- 
 largement of the lens, (ii.) advancement of the lens due 
 to slackening of its zonule, and (iii.) fibrosis of the pecti- 
 nate ligament. 
 
 (6) By the influence of degenerative changes, which may 
 lead either to an increase in the volume of fluid secreted 
 by the eye, or to a change in the constitution of that 
 fluid making it less suitable for ready nitration. 
 
 (c) By rendering the eye liable to auto-intoxication and 
 all the consequences which flow therefrom. 
 
 (d) By interference with that free and even working 
 of the vascular system which is a characteristic of healthy 
 youth. 
 
 2. Sex. Congestive glaucoma is nearly twice as com- 
 monly met with in the female as in the male. The 
 unstable condition of the female nervous system at the 
 time of the climacteric probably accounts for the disparity- 
 
 17 2
 
 18 GLAUCOMA 
 
 On the other hand, non-congestive glaucoma is rather 
 more frequent in men than in women. 
 
 3. Heredity. The influence of heredity is revealed both 
 in the race and in the family. Jews, Egyptians, and 
 certain races of negroes, are believed to be especially 
 liable to the disease. 
 
 4. Errors in Refraction. The idea that the myope is 
 immune from glaucoma, whilst the hyperope is especially 
 liable to it, is a myth. Errors in refraction probably 
 play a very small part in the aetiology of the disease. 
 
 5. Mydriasis. Anything that dilates the pupil tends 
 to block up the angle of the chamber, and so, by causing 
 an obstruction to the outflow of intra-ocular fluid, pre- 
 disposes the eye to glaucoma. The causes of dangerous 
 mydriasis are (i.) the abuse of drugs; (ii.) the exclusion^ 
 of light from the eye; (iii.) the influence of violentor 
 exhausting emotions; and (iv.) the effects of depressing 
 disease. On this subject one word of warning is de- 
 manded. There is no drug which produces mydriasis 
 which can be safely instilled into an eye predisposed to 
 glaucoma, unless very careful safeguards are employed. 
 
 6. Nerve Shock and Strain. family bereavement, 
 haunting fear, business anxiety, long fatiguing anxious 
 night-watches, prolonged mental overwork, sleeplessness, 
 and such-like conditions, are often the factors that 
 determine an attack of glaucoma. 
 
 7. Febrile Diseases. These may act in one of two 
 ways : (a) by exhausting the vital energies of the patient, 
 or (6) by a toxic interference with the vascular arrange- 
 ments of the eye, or with the integrity and efficiency of 
 the secretory and excretory mechanisms of the globe. 
 
 8. Injuries. Very slight injuries of the eye or head 
 sometimes determine an attack of glaucoma. Faute de 
 mievx, we fall back on the explanation of an interference 
 with the vasomotor mechanism of the eye.
 
 CHAPTER VI 
 THE DIAGNOSIS OF GLAUCOMA 
 
 IN the great majority of instances, it is an easy matter 
 to make a correct diagnosis in a case of glaucoma. The 
 danger of a failure to do so does not arise from any 
 inherent difficulty, but rather from the surgeon's forget - 
 fulness of the possible occurrence of the disease in hi* 
 practice. Difficult cases are undoubtedly met with, and 
 over these even experts may differ ; but their very nature 
 is such as to provoke a suspicion of glaucoma in the mind 
 of any practitioner. Under these circumstances, it is 
 not difficult for him to put the responsibility on to other 
 shoulders. The essential point is that he should be fore- 
 warned, and therefore forearmed. Every patient he 
 meets with failing vision should make him think of the 
 possibility of simple glaucoma. Every case of severe 
 headache he is called in to treat should arouse in his 
 mind a suspicion of congestive glaucoma, especially if it 
 is accompanied by vomiting. 
 
 Early diagnosis, always important, has become much 
 more so since modern methods have made the disease 
 easier and safer to handle. Congestive glaucoma is 
 a surgical emergency, whilst the simple disease is a 
 dangerous pitfall of Medicine. 
 
 There is no such thing as prodromal glaucoma. The 
 disease must be divided into three stages: (1) the early, 
 the time of election for treatment; (2) the established, 
 when decisive action is urgently called for; and (3) the 
 late, often, alas ! too late. 
 
 19
 
 20 GLAUCOMA 
 
 Glaucoma is divided into two classes: (a) the simple, 
 or non-congestive, which presents no evidence of marked 
 vascular disturbance; and (6) the congestive (incorrectly 
 termed " inflammatory "), in which an obstruction to 
 the efferent veins at their points of exit from the eye 
 causes a damming up of blood within the organ. A 
 case may be simple throughout, or congestive throughout, 
 or the one form may pass into the other and back again 
 into that from which it first sprang. We may even meet 
 with simple glaucoma in one eye, and with the con- 
 gestive condition in its fellow. The essential feature, 
 however, in all cases alike is an obstruction to the out- 
 flow of fluid from the interior of the eye into its excretory 
 channels. Whether a congestive element enters into the 
 case is largely a matter of chance, in which the anato- 
 mical configuration of the organ, defective development 
 of the excretory channels, and the suddenness of the 
 onset of the changes which obstruct excretion, all play 
 a part. 
 
 The Clinical Course of an Attack o Simple Primary 
 Glaucoma. The onset is gradual, the signs of congestion 
 are absent, there is no pain and little subjective evidence 
 of any kind; but the visual field shrinks, so that the 
 patient complains that he feels as if he were looking 
 clown a tube (tube-vision), and therefore is unable to 
 avoid objects with which he meets. Visual acuity often 
 falls, and cupping of the disc is soon well marked. We 
 may speak of these as the essential triad of glaucoma 
 signs, and put them shortly as (1) contraction of the 
 field, (2) cupping of the disc, and (3) failure of visual 
 acuity. So gradually may the symptoms come on that 
 the patient may only discover their existence when the 
 first eye is lost entirely, and the second has begun to 
 fail. In the great majority of cases the pupil is dilated 
 and sluggish. Later still it is immobile, and surrounded
 
 THE DIAGNOSIS OF GLAUCOMA 21 
 
 by only a narrow margin of iris ; rarely it may be of normal 
 size until quite late in the disease. Sometimes moderate 
 or even good central vision is retained for a long time. 
 An increase in the tension of the globe is undoubted^ 
 present from the first dawn of the disease, but it is not 
 always recognized, and this for two reasons viz., (1) that 
 an increase in the intra-ocular pressure may be inter- 
 mittent, and therefore not always in evidence; and 
 (2) that, as compared with congestive glaucoma, the rise 
 in tension is quite moderate in early cases, and may 
 escape detection by digital examination, though it will 
 be revealed by the use of the tonometer. 
 
 It cannot be too strongly impressed on the practitioner's 
 mind that a diagnosis of glaucoma should not be made on 
 any one sign alone. Every possible scrap of evidence, 
 historic or clinical, should first be gathered; a broad 
 view should be taken, and judgment should then be 
 formed. In the early stage a decision may be impossible ; 
 careful watching of the patient is then indicated. Later, 
 when glaucoma is established, the most ordinary care 
 suffices, whilst later still no medical man could mistake 
 the condition for anything else. 
 
 The Clinical Course of an Attack of Primary Con- 
 gestive Glaucoma. A pronounced, attack of congestive 
 glaucoma may begin without warning of any kind. 
 More often it is heralded by the appearance of the so- 
 called " prodromata," or is engrafted upon and compli- 
 cates an attack of apparently simple glaucoma. Such 
 variations, of course, are very numerous. 
 
 In most cases, the patient has observed that from 
 time to time his sight has become misty for short periods, 
 generally for a few hours at a time. With this has been 
 associated some degree of pain in the eye, and headache, 
 together with the appearance of rainbow rings around 
 bright lights viewed in the dark. Flashes of light are
 
 22 GLAUCOMA 
 
 frequently seen before the eyes, and are variously de- 
 scribed as resembling summer lightning, rolling balls of 
 light, sudden flashing luminous points, fireflies, etc. 
 During the attacks the pupil is dilated, the eye con- 
 gested, the anterior chamber shallow, and the cornea 
 steamy. Exhaustion, sleeplessness, fatigue, or worry, 
 bring on the crises, whilst rest, food, warmth, and sleep, 
 cause them to pass away. They are frequently noticed 
 either in the early morning, or in the late afternoon or 
 evening. Sooner or later the early condition passes into 
 the phase of established glaucoma. The transition from 
 one to the other may be gradual and imperceptible, or, 
 on the other hand, the new phase may be ushered in by 
 a crisis, whose severity is such that the patient, quite 
 erroneously, dates the onset of his disease/frtmi ft: The 
 leading symptoms are (1) severe trigeminal neuralgia, 
 usually referred to the eye and forehead, but sometimes 
 to other parts as well; (2) a rapid fall in vision; and (3) a 
 marked contraction of the visual field. The eye is very 
 congested, as also are the lids. Chemosis may be present. 
 The cornea is steamy and insensitive ; the pupil is widely 
 dilated and often oval; the anterior chamber is shallow; 
 the iris appears discoloured; and the lens has a peculiar 
 green look (ry\avic6$ = sea-green). The eye is very tender 
 and painful, and is felt to be extremely hard. After 
 a varying period the attack passes off, leaving the eye 
 permanently damaged and in a condition of chronic 
 glaucoma, usually of a congestive type, though almost 
 all the signs of interference with the blood-stream may 
 pass away. The downward path of the eye is punc- 
 tuated by the more or less frequent occurrence of con- 
 gestive exacerbations of the disease. It will thus be 
 seen that the early attacks may pass gradually into the 
 more severe ones, or the latter may be the first to make 
 their appearance. The eye is grachially drifting towards
 
 THE DIAGNOSIS OF GLAUCOMA 23 
 
 an established condition of chronic congestive glaucoma. 
 The visual acuity is impaired; the field of vision is con- 
 tracted; the tension is above normal; circumcorneal 
 congestion, with distension of the perforating vessels, is 
 present; the cornea readily clouds over, and is losing its 
 sensitiveness; the anterior chamber is very shallow; the 
 pupil is wide and oval, and acts sluggishly; the iris is 
 changing in colour, and atrophic patches are appearing. 
 If the media are clear, we can see in the fundus (a) the 
 cupped disc surrounded by a ring of atrophy, (6) the 
 constricted arteries, (c) the congested veins, and (d) the 
 vascular pulsation, all of which are characteristic of 
 glaucoma. 
 
 Finally we come to the " late stage of glaucoma," often 
 spoken of as that of " absolute glaucoma." All sight is 
 lost, though the patient may protest that at times he sees 
 as well as ever, a delusion to which the name " memory 
 sight " may be applied. The green reflex, the stone-like 
 hardness of the eye, the degenerative changes which 
 mar the cornea, and the porcelain-like colour of the sclera, 
 with the dilated vessel standing out on its surface, com- 
 plete the picture already drawn of the earlier stage. 
 Even now there are possibilities of harm to be added, 
 since the patient may suffer from " blind painful eye- 
 ball," from perforation of the globe, or even from panoph- 
 thalmitis. 
 
 Let us pause for a moment to lay emphasis on certain 
 points in connection with this disease, be the type what 
 it may. 
 
 1. It is bilateral, and therefore complete blindness is 
 threatened. 
 
 2. In the vast majority of cases, it is relentless and 
 progressive. 
 
 3. Its keystone is a rise of pressure within the eye. 
 
 4. Its fundamental causes are protean.
 
 24 GLAUCOMA 
 
 5. One and all of them act by upsetting the balance 
 between the secretion and excretion of the intra-ocular 
 fluid. 
 
 6. The entry of the congestive factor into the drama 
 is an accident, though one of the very gravest pro- 
 portions.
 
 CHAPTER VII 
 THE SIGNS AND SYMPTOMS OF GLAUCOMA 
 
 WE shall take the structures of the eye seriatim, and 
 consider the evidence of glaucoma afforded by each. 
 
 The Conjunctiva and Solera. The only change seen in 
 simple glaucoma is a slight enlargement of the anterior 
 ciliary vessels, especially where they perforate the sclera. 
 
 In congestive attacks, the condition present may vary 
 from slight circumcorneal congestion to intense reddening, 
 and even to chemosis. In the intervals between attacks, 
 a permanent enlargement of the anterior veins is always 
 left. 
 
 In late glaucoma, the sclera has a bluish- white, porce- 
 lain-like appearance, against which the distended anterior 
 ciliary veins stand out in marked contrast. 
 
 The Cornea. There are two symptoms occurring from 
 the earliest stage of congestive attacks viz., (1) mistiness 
 of vision, and (2) haloes round lights. These are due to 
 two causes : (a) an overstretching of the cornea (the result 
 of an increased intra-ocular pressure), which interferes 
 with the refraction of the membrane; and (2) an actual 
 oedema of the corneal layers, the result of an obstructed 
 circulation. 
 
 The mistiness is often seen in the mornings, and gives 
 the erroneous impression of a fog or of smoke in the 
 atmosphere. The haloes round lights are best seen at 
 night, and are clearest around yellow flames. At least 
 two colours are &oen, an inner blue and an outer red. 
 
 25
 
 26 GLAUCOMA 
 
 Anaesthesia of the cornea becomes increasingly marked 
 as glaucoma progresses. A corneal haze makes its appear- 
 ance in some cases, and in late stages permanent opacities 
 of the cornea are found. 
 
 The Anterior Chamber is always shallow during con- 
 gestive attacks; later it becomes permanently so. The 
 depth of the chamber can best be estimated by looking 
 at it obliquely from the opposite side, under good illumina- 
 tion, with a loupe or an ophthalmoscope. The contents 
 of the chamber are often turbid in congestive cases. 
 
 The Iris. Dilatation of the pupil is found in most cases 
 of glaucoma. Exceptions are rare. It is usually well 
 marked. The pupil is often oval in form, with the long 
 axis vertical. In congestive cases the iris may be dis- 
 coloured. At a late stage atrophic patches appear in it, 
 through which the red reflex can be seen on ophthalmo- 
 scopic examination. In the very late stages, ectropion 
 of the uveal pigment appears, giving the edge of the 
 pupil a velvety black line. 
 
 The Ciliary Body. Weakness in accommodative power, 
 shown by an abnormal increase in presbyopia, is the 
 earliest evidence of involvement of the ciliary body. It 
 is an important point, since the need to change his glasses 
 soon may be the first thing to drive a glaucoma patient 
 to seek medical advice. Later a congestion of the circum- 
 corneal zone shows an engorgement of the ciliary body 
 with blood. 
 
 The Lens. Owing to the advance of the lens system, 
 as the anterior chamber shallows, a tendency to myopia, 
 or to lessening of existing hyperopia, is in evidence. 
 The weakening of the ciliary muscle, at the same time, 
 tends to bring about presbyopia, as above indicated. 
 These factors act in opposition, but the latter is the 
 stronger and therefore the prevalent one. 
 
 A form of cataract not infrequently complicates glau-
 
 F IG . 5. CUPPIKCJ OF THE OPTIC Disc (GLAUCOMATOUS). 
 
 Note (1) the sharp scleral spur on the right side ; (2) the overhanging edges ; 
 and (3) the retinal vessels hiding under the latter. x20. (From micro- 
 photograph kindly supplied by Mr. Chesterman. ) 
 
 [To face p. 27.
 
 THE SIGNS AND SYMPTOMS 27 
 
 coma. It has to be distinguished from cataract occurring 
 as an accidental complication of the condition. In some 
 cases cataract is the first morbid condition present, and 
 the glaucoma is secondary to it. The history and ap- 
 pearances of the eye will decide which condition is 
 present. 
 
 The green reflex in the pupil, which has given glaucoma 
 its name (from y\avK6s = sea-green), is produced by the 
 dilated pupil, combined with some want of transparency 
 in the lens, in the aqueous humour, and in the cornea. 
 
 The Optic Nerve and Retina. The changes found are 
 
 (1) pallor of the disc this is partly due to a constriction 
 of the blood-supply, and partly to advancing atrophy ; 
 
 (2) a depression of the floor of the disc, the so-called 
 cupping of the disc : (3) an alteration in the apparent 
 direction of the vessels as they pass from the disc on to 
 the surrounding fundus; (4) the presence of pulsation in 
 the retinal vessels ; (5) a change in the size of the retinal 
 arteries and veins. 
 
 The cupping of the disc is the best-known and most 
 easily detected sign of the disease. It is due to the 
 nerve entrance being the weakest spot in the globe, and 
 therefore yielding first under the increased pressure 
 within the organ. The important points to grasp are, 
 (a) that the whole of the disc is depressed in the great 
 majority of cases; (6) that, as each vessel passes from the 
 disc on to the retina, it shows a kink as it bends over 
 the lip of the cup ; and (c) that some of the vessels when 
 traced from the floor of the disc on to the retina seem to 
 change their direction somewhat, and so to emerge 
 parallel with what might have been expected to be their 
 course. The last-named phenomenon is frequently ill 
 understood by students, but is very easily made clear 
 by the aid of the following simple device. 
 
 Take a half-sheet of note-paper, 7 inches long by 4|
 
 28 
 
 GLAUCOMA 
 
 wide (the exact dimensions are unimportant), and join 
 the corners by drawing two diagonal red lines (Kg. 6, A). 
 thus making a multiplication sign, whose four arms are 
 
 A. The red lines are to represent blood- 
 vessels. The dotted lines indicate 
 where the paper is to be folded the 
 first time. 
 
 B.~ The first folding 
 of the paper shown 
 complete ; the dotted 
 lines show position 
 of the second fold. 
 
 
 
 C The second fold- 
 ing of the paper 
 shown completed. 
 
 Si 
 
 I). The double flaps raised in 
 concertina fashion, to show 
 the overhanging edge of the 
 disc and the apparent altera- 
 tion in the direction of the 
 vessels, as they emerge, on 
 the plane of the retina. 
 
 FIG. 6. 
 
 designed to represent four emerging vessels. Fold each 
 edge of the paper forward towards the centre, so that 
 the two edges meet each other over the centre of the
 
 29 
 
 multiplication sign (Fig. 6, B). Take each edge in turn 
 and fold it backward to meet the first folds (Fig. 6, C). 
 Then raise the two double flaps so made, forward in a 
 concertina-like fashion, and look down on the device 
 from above (Fig. 6, D). The unfolded part of the paper, 
 lying flat on the table, diagrammatically represents the 
 floor of the disc ; from the first fold to the second on each 
 
 ,s.sp. 
 
 FIG. 7. 
 
 A, physiological cup ; B, glaucomatous cup ; and C, cup of optic atrophy 
 (modified from Fucha). O.N., Optic nerve; I.e., lamina cribroso; 
 S. , sclera ; S.Sp., scleral spur, which is supposed to damage the retinal 
 fibres, as they bend over it ; a, a, retinal artery. 
 
 side represents the shelving wall of the disc; from the 
 second fold to the free edge represents the fundus level. 
 The apparent break in the continuity of the straight lines 
 originally made is very striking, and aptly illustrates our 
 point. 
 
 In late cases, the retinal vessels are sometimes seen 
 to be drawn over to the nasal side, in what looks like a 
 leash.
 
 30 GLAUCOMA 
 
 Pulsation of the Retinal Vessels. If the veins alone 
 pulsate, little stress need be laid on the phenomenon: 
 if, however, this pulsation is strong, and if a light pressure 
 on the globe with a forefinger causes the arteries to pulsate 
 as well, or if the arteries pulsate even when the globe is 
 untouched, there is a strong suspicion of a rise in intra- 
 ocular pressure. 
 
 A Change in the Size of the Vessels. The arteries tend 
 to become more constricted, and the veins larger and 
 fuller than natural. 
 
 Caution. A glaucomatous cup must be distinguished 
 from a physiological cup, from an atrophic cup, and from 
 a coloboma of the optic nerve (Fig. 7). 
 
 The physiological cup is rarely deep; it only involves 
 a part of the disc, usually the outer quadrant; some at 
 least of the vessels pass out without a kink; the main 
 part of, the papilla is of normal colour. 
 
 The atrophic cup is very shallow, the disc is grey, and 
 the- vessels are not kinked. 
 
 In coloboma the apparent disc is much enlarged and 
 the cup is of great depth. The history of the case may 
 be of value. 
 
 The Retina is starved of arterial blood, and the outflow 
 of venous blood is obstructed; it is also subject to direct 
 pressure; the circulation through the choroid too is im- 
 peded, and consequently the outer layer of the retina 
 has its nutrition interfered with. The result is a limita- 
 tion of the visual field, and the production of subjective 
 sensations of light. 
 
 The Size oi the Eye should always be noticed in glauco- 
 matous cases. It can best be judged of by measuring 
 the diameter of the cornea, which will often be found 
 to be below normal. The average horizontal diameter 
 of the cornea in healthy subjects is 11-6 mrn. (Priestley 
 Smith).
 
 THE SIGNS AND SYMPTOMS 31 
 
 Pain varies enormously in different cases, and is usually 
 a measure of the congestion present. A simple glaucoma 
 may be painless throughout, whilst an acute congestive 
 attack is marked by terrible suffering. There is severe 
 neuralgia not only in the eyes, but also in the head, teeth, 
 ears, and neck. The agony may be so great as to lead 
 to vomiting and pyrexia. In less acute cases, the pain 
 and headache are intermittent, or may be more or less 
 constant. Sleep, food, or rest, often relieve the pain. 
 
 Photopsise, or subjective sensations of light, are due 
 to interference with the retina. They may occur in other 
 affections of the retina and choroid, in some cases of 
 cerebral disease, in megrim and other nervous affections, 
 in neurasthenic patients, under conditions of cardiac 
 syncope, and in errors of refraction. In glaucoma they 
 are worse when the patient first lies down, and are 
 relieved after rest as the night advances, whilst in cerebral 
 cases they are often most troublesome later in the night. 
 
 Rainbows round lights have been already spoken of. 
 It remains to add that similar phenomena may be ob- 
 served in conjunctivitis owing to flakes of mucus on the 
 cornea; in some cases of early cataract; in eyes under- 
 going various forms of drug treatment (e.g., painting 
 with solution of silver nitrate); and habitually in the 
 eyes of certain apparently normal people. 
 
 A Diminution of Visual Acuity may be due to lesions 
 of the cornea, to opacities in the aqueous fluid, in the 
 lens, and in the vitreous, and to atrophy of the optic 
 nerve and retina . 
 
 The Visual Field is early affected, and affords one of 
 the most delicate tests of the presence and advance of 
 glaucoma. It undergoes a characteristic contraction, 
 the nasal portion usually suffering first (Pig. SA). The 
 colour fields are but little affected; central vision is 
 usually retained till quite late. The most delicate test of
 
 32 
 
 GLAUCOMA
 
 THE SIGNS AND SYMPTOMS 
 
 all is that devised by Bjerrum. It consists of examining 
 the field with a very small object (usually 1 mm. in 
 diameter) at the relatively great distance of 1 metre or 
 even 2 metres. When so tested, 
 it is found that the visual field 
 is much smaller than the nor- 
 mal, and that the scotoma due 
 to the blind spot is much en- 
 larged, and is continuous in one 
 direction with the loss of the peri- 
 pheral field (Fig. SB). Paracentral 
 scotomata are also observed, and 
 are considered to be of consider- 
 able importance in diagnosis. 
 
 Tonometry. The old method of 
 finger tonometry will always retain 
 its place in rough-and-ready work, 
 but is being steadily and rapidly 
 replaced amongst ophthalmologists 
 by the use of the Schiotz tono- 
 meter, or of some modification of 
 that instrument. Mechanical tono- 
 metry, when carefully carried out, 
 is of the greatest value. It is, how- 
 ever, a method for the specialist 
 
 FIG. 9. THE SCHIOXZ 
 TONOMETER. 
 
 rather than for the general prac- > sliding ro don which I, 
 
 the weight, is fixed ; 5, a 
 
 titioner. 
 
 hollow cylinder in which 
 a slides ; c, the collar on 
 which a moves by wheel 
 bearings ; f, foot-plate 
 which rests on the eye. 
 The rod a actuates the 
 lever above it, and so 
 records on the scale on 
 the arc. 
 
 DIFFERENTIAL DIAGNOSIS 
 
 A case of simple or non-con- 
 gestive glaucoma may be mistaken 
 for cataract, for an error in re- 
 fraction, or for an affection of the retina and choroid or 
 of the optic nerve. A careful examination of the case 
 will usually clear the matter up at once ; if not, it must be 
 
 3
 
 34 GLAUCOMA 
 
 kept under observation for a while, when the evolution of 
 the cupping of the disc and of the changes in the field will 
 settle the question. The point to insist strongly upon is 
 that in all such cases a routine examination of the media, 
 fundus, fields, and tension, is urgently demanded. 
 
 Congestive glaucoma, on the other hand, is often mis- 
 taken for conjunctivitis, for iritis, or for " bilious " or 
 other headache. 
 
 A case of conjunctivitis should easily be distinguished 
 from one of congestive glaucoma, since in the latter we 
 find (1) marked circumcorneal congestion; (2) steami- 
 ness of the cornea ; (3) dilatation of the pupil ; (4) a con- 
 siderable rise in tension ; (5) severe headache and neuralgia . 
 None of these signs are usually present in eyes suffering 
 from conjunctivitis. 
 
 In iritis the pupil is contracted, and the loss of pattern 
 and the change in colour of the iris are prominent features, 
 whilst the tension is not as a rule raised. 
 
 The diagnosis from bilious headache, gastric catarrh, 
 and other conditions associated with headache and 
 vomiting, can always be easily made by any surgeon 
 who will trouble to examine the eyes. So long as it is 
 borne in mind that these cases may possibly be glauco- 
 matous, there is not the least danger of a mistake in 
 diagnosis; the latter can only arise when the surgeon is 
 taken off his guard.
 
 CHAPTER VIII 
 THE TREATMENT OF GLAUCOMA 
 
 THE treatment of glaucoma falls naturally under two 
 headings: (1) the general and meiotic, and (2) the opera- 
 tive. These will be dealt with in turn. 
 
 The General and Medicinal Treatment of Glaucoma. 
 The patient, who is known to be suffering from glaucoma, 
 should be carefully warned to regulate his Me in such a 
 way as to avoid, as far as possible, anything which may 
 provoke a vascular storm in the eye. A list should be 
 given him of the following sources of danger: constipa- 
 tion, overfatigue either mental or bodily, anxiety and 
 business worry, sleeplessness, exposure to chill, and 
 any form of violent mental excitement. The use of 
 any form of mydriatic drug is strongly contra-indi- 
 cated, unless subsequent meiosis can be assured. 
 Even the instillation of cocaine may be dangerous. If 
 it is deemed necessary to use one of the milder mydriatics 
 for any purpose, the patient must not be allowed to pass 
 away from supervision until the pupil has contracted 
 again under the influence of a meiotic. It is a wise 
 precaution to provide the patient with a further supply of 
 weak eserine or pilocarpine drops, to be used should the 
 pupil tend to dilate again in the course of the day. 
 
 It is not enough to give general warnings. We must 
 never forget that the glaucomatous eye is a " sick eye 
 in a sick body." Every system of the body should be 
 overhauled with the thoroughness of an examination for 
 life insurance, special attention being paid to the vascular 
 
 35
 
 36 GLAUCOMA 
 
 and urinary organs. Any source of auto-genetic poison- 
 ing should be eliminated, and the diet and habits should 
 be carefully regulated. Alcohol should be forbidden, or 
 at least strictly limited. It is to be remembered that 
 infectious diseases, and amongst these we may especially 
 mention influenza, carry additional dangers to the victims 
 of glaucoma. 
 
 Meiotics. There are two entirely distinct conditions 
 under which meiotic drugs are used; these are (1) in 
 the congestive phases of glaucoma, to restore the eye to 
 its normal vascular condition, or at least to as near to 
 that as may be possible; and (2) in the absence of con- 
 gestion, as a substitute for operative treatment. We will 
 take these points in order. 
 
 In congestive attacks, the action of 1 per cent, solutions 
 of eserine or of pilocarpine should be boldly pushed, the 
 drops being instilled every few hours until a result is 
 obtained. With this should be combined free leeching, 
 active purgation, rest in bed, milk diet, and the ad- 
 ministration of morphia (unless the last-named is other- 
 wise contra-indicated). 
 
 If it is decided to employ meiotics over a long period 
 in chronic congestive cases, pilocarpine is preferable to 
 eserine, and the weakest solution that will keep the pupil 
 contracted should be used. As time goes by, the strength 
 of the drops may require to be augmented. To begin 
 with, half a grain to the ounce will probably suffice. Care 
 must be taken to counteract the tendency of these drugs 
 to produce chronic catarrh of the eye, and the patient 
 must be warned never to let his stock get stale or run out. 
 In this connection there are certain important warnings 
 to be given. 
 
 1. The treatment is merely palliative, not curative. 
 
 2. Meiotic treatment is useless in simple glaucoma. 
 Its only role is in cases of the congestive type.
 
 THE TREATMENT OF GLAUCOMA 37 
 
 3. The glaucoma patient should be kept under constant 
 observation, careful periodic examinations being made 
 of the field of vision, of the tension of the eye, of the 
 cupping of the optic disc, and of the visual acuity. The 
 above order is deliberate, and signifies the relative im- 
 portance to be attached to the four points. Should the 
 condition of the eye be deteriorating, operative treatment 
 should be substituted without delay for the medicinal 
 regimen. The latter has sometimes been spoken of as 
 " expectant treatment." If the patient is losing ground, 
 it can be expectant only of disaster. 
 
 4. Every authority on glaucoma from von Graefe 
 onwards has laid stress on the fact that, if an operation 
 is to be performed for the relief of glaucoma, the earlier 
 it is done, the better is the chance of success. Hesitation 
 is dangerous. Once we see that other measures are 
 failing, we must recommend and carry out an operation 
 with the least possible delay. 
 
 5. The exhibition of meiotics can only have a rational 
 basis so long as the contractility of the iris is unimpaired. 
 Therefore in late cases it is useless. 
 
 Massage. The great value of massage in glaucoma 
 does not appear to be sufficiently appreciated. The 
 tension of an eye can be quickly and sensibly reduced 
 by digital manipulation, and the patient can be taught 
 to perform the simple movements for himself. These 
 are two in number. The first consists in placing the tips 
 of the two index fingers on the upper lid over the globe 
 (the surgeon standing behind the patient), and pressing 
 with each finger in turn in the direction of the centre 
 of the eye. The movements should be slow at first, and 
 made more rapidly later, as the operator acquires skill 
 and the patient toleration; the subject must look down- 
 ward, and gently close the eyes. The period of massage 
 should be short at first (about half a minute), and should
 
 38 GLAUCOMA 
 
 be extended until it lasts three to five minutes, thrice 
 daily or more often. The second movement is a gentle 
 circular, smoothing action performed with three fingers 
 of one hand, through the gently closed lids. It serves 
 the same purpose as the wide smoothing movements used 
 after massage of other parts, and only needs to be done 
 for about fifteen or twenty seconds. 
 
 Massage of the eyes should be just as much a routine 
 measure in the treatment of glaucoma as the use of 
 meiotics or the regulation of the patient's habits. Not 
 only so, but it is also a measure of very great value in 
 augmenting the effect obtained by operative measures, 
 when that proves to be on the short side. 
 
 The Operative Treatment of Glaucoma. We begin with 
 a short description of the various operative procedures 
 before the profession, leaving the reader to refer for 
 details to more lengthened treatises on the subject. 
 
 Iridectomy. This operation, introduced by von Graefe, 
 held sway for nearly fifty years, until its supremacy was 
 challenged by the procedures which aimed deliberately 
 at the formation of a filtering scar i.e., a scar which 
 allows the aqueous fluid to escape indefinitely from the 
 interior of the eye to the potential subconjunctival space 
 on its surface. 
 
 The removal of a portion of iris may relieve a glauco- 
 matous patient in several ways. 
 
 1. If performed quite early, before any adhesions have 
 formed between the iris base and the cornea, it establishes 
 a limited space over which the normal filtration can con- 
 tinue unimpeded either by dilatation of the iris or by 
 the formation of adhesions over the area of the coloboma. 
 
 2. The pressure within the eye is temporarily relieved. 
 The ocular circulation is permitted to resume its normal 
 character, and the patient, warned by the severe lesson 
 hejias received, may so alter his life habits as to protect
 
 THE TREATMENT OF GLAUCOMA 39 
 
 himself from another attack for a long time to come. 
 The predisposing factors of glaucoma are ever with 
 him, and are steadily, if slowly, increasing in their power 
 for harm, but, thanks to his care, the exciting causes 
 are as far as possible eliminated, and so an attack is 
 avoided. 
 
 3. A filtering cicatrix may be accidentally established 
 as a result of the operation, though this is not what was 
 deliberately aimed at. 
 
 Certain plain lessons are here to be learnt. 
 
 (a) If iridectomy is to be useful, it must be done at 
 the earliest possible stage of the disease. 
 
 (6) The incision must be peripheral, so as to admit of 
 the iris being removed as far back as possible. 
 
 (c) The incision must be large, so that the portion of 
 iris removed shall be as wide as possible; this insures a 
 wide area of the angle for free drainage. 
 
 (d) If we desire to produce a filtering scar, we should 
 employ an operation deliberately designed for the pur- 
 pose, and not one which causes it only by accident. 
 
 We shall now pass on to consider the various pro- 
 cedures which aim deliberately at the production of a 
 filtering scar, but before doing so we must make it quite 
 clear what we mean by this term. A filtering scar is 
 one which allows the intraocular fluid to pass through 
 the tunic of the eye into the subconjunctival tissue, and 
 there to be taken up by the lymph and blood vessels. 
 The ocular evidence of such a scar is a boggy or oade- 
 matous condition of the overlying conjunctiva. When a 
 probe is pressed over this area, marked pitting takes 
 place. It has been pointed out that a similar pitting 
 may be demonstrated in some normal, and in not a few 
 inflamed, eyes. It is necessary, therefore, to emphasize 
 the point that the pitting over a true filtering scar is 
 more marked, and usually much more fluid, than that
 
 40 GLAUCOMA 
 
 in the conditions above mentioned. The diagnosis rests 
 on the degree and fluidity of the cedematous condition. 
 
 An effort has been made to distinguish between a 
 " filtering scar " and a " fistulous scar." There is, 
 however, no anatomical basis for the view that it is 
 possible to establish a spongy filtering condition of such 
 a cicatrix, and it is safe to assume that all cicatrices 
 supposed to be of a spongy nature are in reality per- 
 meated by tiny fistulae. 
 
 Lagrange's Operation. Lagrange was the first to 
 remove a portion of the ocular tunic (sclerectomy) in 
 order to make sure of establishing a filtering scar. The 
 following are the steps of the operation. 
 
 1. A small shelving corneo-scleral flap is cut with a 
 Graefe knife, and a wide conjunctiva apron is added 
 thereto (Fig. 10A). 
 
 2. The conjunctival flap is turned down, and the cor- 
 neal lip of the wound is removed with scissors (Fig. 10B). 
 
 3. Iridectomy is performed, if required (Fig. lOc). 
 
 4. The flap is stroked into position and the wound 
 closed. 
 
 The result of the operation may be seen in Fig. 10D. 
 
 Herbert's Operations must be spoken of in the plural, 
 as the exact procedure has varied from time to time. 
 The underlying idea of all of them has been to obtain 
 a filtering scar by a modification of the operation of 
 sclerotomy. We shall take the procedures seriatim. 
 
 1. Has first attempt (1906) was to make the lips of a 
 small sclero-corneal incision as jagged as possible, in 
 order to prevent primary union, and so to obtain a 
 permanently weak scar. 
 
 2. In 1907 he introduced the wedge isolation operation, 
 the object of which was to isolate a wedge of solera close 
 to the limbus, and to leave it in situ, in the hope that, 
 being cut off from its blood-supply, it would shrink, and
 
 .4. Section of the Sclera and Conjunctiva. 
 
 B. Resection of the Sclerotic. 
 FIG. 10. ILLUSTRATING LAGRANGE'S OPERATION (A, B). 
 
 [To face p. 40.
 
 C. The Making of the Iridectomy. 
 
 D. The Result of the Operation. 
 FIG. 10. ILLUSTRATING LAGRANGE'S OPERATION (C, D). 
 
 [To face p. 40.
 
 THE TREATMENT OF GLAUCOMA 41 
 
 so allow of filtration from the interior of the eye into 
 the subconjunctival space around its margins. 
 
 3. Later he introduced his small flap operation, which 
 consisted in the making of a small keratome incision 
 from behind the limbus into the chamber, and then 
 carrying two or four cuts forward at right angles to this, 
 in order to form a trap-door flap of solera. The cuts 
 were made with special scissors. 
 
 4. Latterly he appears to have gone back to a pro- 
 cedure that he favoured in his earliest efforts namely, 
 the attempt to establish a fistula by tucking conjunctival 
 tissue into a scleral wound close behind the limbus. The 
 tuck is kept in place by a metal plug, sutured in position 
 and kept there for some days following the operation. 
 
 FIG. 11. HOLTH'S PUNCH FORCEPS. 
 
 The drawback to all these procedures is that, like their 
 prototype sclerotomy, they are apt to fail owing to 
 healing up of the wounds made. On the other hand, 
 it is only fair to add that Herbert's contention is that 
 the modern operations, which remove a definite piece of 
 sclera, are apt to do too much. 
 
 Holth's Operation. A sclero-corneal flap is cut with 
 a keratome, a conjunctival apron being fashioned by 
 entering the knife into the conjunctiva some distance 
 above the point of scleral puncture. Iridectomy follows, 
 and then the anterior lip of the wound has a tongue cut 
 out of it by means of a specially designed punch. The 
 flap is replaced in position. 
 
 Fergus's Operation. A conjunctival flap is dissected
 
 42 
 
 GLAUCOMA 
 
 up to the cornea, but not into it; a disc of solera is cut 
 out with a 3 mm. trephine, close up to the limbus; in 
 a certain number of cases a cyclo-dialysis is added; the 
 ciliary body is laid bare in the wound. Some stress is 
 laid on the opening up of a communication between the 
 anterior chamber and the suprachoroidal space. 
 
 Sclero-Corneal Trephining (the author's operation) has 
 sometimes been confused with the last-named operation, 
 with which it has little in common, beyond the fact that 
 
 wwwiA/yi/ 
 
 FlG. 12A. SCLERO-CORXEAI, TREPHINING. 
 
 sp, speculum ; ii, incision in conjunctiva ; c, cornea ; t, trephine-hole ; p, pupil ; 
 aa, uncut conjunctiva, which serves to allow filtering fluid from the neigh- 
 bourhood of the trephine-hole to pass into the rest of the subconjunctival 
 space. 
 
 a trephine is used in both of them. The object of the 
 procedure is to tap the anterior chamber, to drain it 
 permanently into the subconjunctival space, and, in 
 doing so, to avoid if possible any interference with, or 
 impaction of, the uveal tract. An incision concentric 
 with the cornea maps out a large conjunctival flap, which 
 is dissected down to the limbus, the whole thickness of 
 the tissue being taken up. The dissection is carried on 
 into the substance of the cornea for another millimetre,
 
 THE TREATMENT OF GLAUCOMA 43 
 
 the cornea being actually " split " over this area. This 
 flap being held down out of the way, a 2 mm. trephine 
 blade is next applied to the corneo-scleral margin, and 
 a disc is cut out in such a manner that it remains hinged 
 on the scleral side. At the same time the iris protrudes 
 
 FIG. 12B. DIAGRAM TO SHOW IN SECTION THE RELATION OF 
 THE PARTS IN A TREPHINED EYE. 
 
 a, normal position of conjunctiva; b, conjunctiva reflected on to the cornea, 
 after " splitting " of that membrane; ab, area of the crescent formed by 
 "splitting" the cornea; c, the piece of sclero-cornea removed by the 
 trephine (it is shown shaded); d, iris ; e, ciliary body ; /, lens ; y, cornea ; 
 
 k, sclera. 
 
 through the opening. The disc and iris are seized in 
 one grip of a pair of iris forceps, and cut off with a single 
 snip of the scissors. The iris is replaced, and the con- 
 junctiva is smoothed into position and sutured there. The 
 advantages claimed for this procedure are as follows. 
 Its technique is not difficult; the sclerectomy on which
 
 44 GLAUCOMA 
 
 drainage depends is the smallest possible, and is made 
 on an intact globe; consequently the dangers of vitreous 
 prolapse and of intra-ocular haemorrhage are reduced to 
 a minimum; finally, the operation can be repeated, if 
 need be. The accompanying illustrations (Figs. 12A, 
 12B) serve to make the steps of the operation plain. 
 Full details of the method are to be found in the author's 
 book on the subject.* 
 
 Thread Drainage. A number of operations have been 
 put forward in which a thread is introduced into the 
 anterior chamber, and its ends are buried in the sub- 
 conjunctival tissue. It has been supposed that they 
 would favour the spread of drainage under the flap. 
 If any of the modern operations are carefully performed, 
 there will be little difficulty in the diffusion of the drainage 
 fluid. On the other hand, the introduction of a piece 
 of thread, in free communication with the interior of the 
 eye, appears to be a needlessly dangerous procedure. 
 Recognizing this risk, Prince has substituted a gold 
 drain for the thread. If a drain is to be used at alL 
 this is certainly a preferable expedient. 
 
 Cyclo-dialysis, or the separation of the ciliary body 
 from its attachment to the solera, was designed to open 
 up a communication between the anterior chamber and 
 the suprachoroidal space. It is now very seldom re- 
 sorted to. 
 
 Two subjects remain to be discussed : (1) the operation 
 to be selected in any individual case; and (2) the argu- 
 ments that can be used against the undertaking of any 
 operative procedure. 
 
 1. The Selection o an Operation. There is at the 
 present time the greatest diversity of opinion amongst 
 
 * " Sclero-Corneal Trephining in the Operative Treatment of 
 Glaucoma" (second edition, 1914), by Lieut. -Colonel R. H. 
 Elliot. London: George Pulman and Sons, Ltd.
 
 THE TREATMENT OF GLAUCOMA 45 
 
 experts on this subject. There are those who would 
 perform iridectomy in all cases; there are others who 
 would always resort to one or other of the forms of 
 filtering operations; there are still others who would 
 select the operation according to the case. Much depends 
 upon the idiosyncrasy of the surgeon and on his past 
 experience. There is no rule to be laid down. The 
 practitioner will be well advised to leave such technical 
 matters to the judgment of the surgeon he calls in. At 
 the same time it should be said that there are a 
 very large number of surgeons who hold to the broad 
 general rule to perform iridectomy in acute and subacute 
 cases, and a filtration operation in chronic ones. The 
 author's personal view is that sclero-corneal trephining 
 is the safest, the easiest, and the simplest operation in 
 any and every case of glaucoma, with two exceptions. 
 These are (1) glaucoma secondary to the swelling of a 
 maturing cataract, and (2) that which follows any con- 
 dition which places the aqueous and vitreous chambers 
 in free continuity with each other. He can claim that 
 this view is founded on a large practical experience, and 
 that it is supported by that of a number of very able 
 surgeons; at the same time, he would freely admit that 
 many dissent from it. 
 
 2. The Arguments against Operation. These are four 
 in number : 
 
 (i.) There are a certain number of cases of glaucoma 
 on record in which the status quo has been maintained 
 for years by ' medicinal treatment alone. These rare 
 instances have encouraged many surgeons to delay opera- 
 tion, and have caused a loss of sight out of all proportion 
 to the meagre gains which can be laid to the credit of 
 the " expectant treatment." 
 
 (ii.) Any operation for glaucoma, at a late or com- 
 paratively late stage of the disease, may be followed by
 
 46 GLAUCOMA 
 
 a considerable deterioration in visual acuity, associated 
 with a marked loss of field. The author believes that 
 such cases never occur if operation is undertaken early, 
 and that even in the late stage they are rare in modern 
 filtration operations, as compared with iridectomy. 
 Against this must be set the hopeless prognosis of the 
 very great majority of cases of glaucoma when left to 
 themselves. 
 
 (iii.) Much stress has been laid on the bad late results 
 that may follow an operation for glaucoma, and especially 
 on the danger of "late infection." By that term is 
 understood an infection of the eye through the operation 
 wound, long after the latter has healed, and quite inde- 
 pendent of the introduction of sepsis at the time of 
 operation. This accident has followed all forms of opera- 
 tive procedure, including iridectomy and sclerotomy, 
 but it is probably more frequent in those cases in which 
 a filtering scar has been deliberately produced. Much 
 may be done to lessen this danger by the use of a proper 
 technique at the time of operation. At the same time 
 it would be idle to belittle the danger. We must face 
 the question and deal with it in the large. The per- 
 centage of risk does not appear to be very high, especially 
 if suitable care be taken. On the other hand, the con- 
 dition for which we are undertaking operation is an 
 extremely serious one, and justifies us, up to a certain 
 point at least, in taking some chances. 
 
 (iv.) There is a hesitation amongst surgeons in under- 
 taking any new form of procedure. This attitude is not 
 merely comprehensible, but within limits it is justifiable. 
 Tune and a favourable experience alone will serve to 
 break it down.
 
 CHAPTER IX 
 SECONDARY GLAUCOMA 
 
 THE study of secondary glaucoma is of importance to 
 the general practitioner for three reasons. 
 
 1. It throws a valuable light on the aetiology of the 
 primary form of the disease. 
 
 2. It shows the need for early and careful diagnosis. 
 
 3. It emphasizes the fact that it is difficult to treat 
 cases of this kind, for the obvious reason that we must 
 not only strike at the rise in intra -ocular pressure, but 
 must also, and in the first instance, direct our attention 
 to the causative condition, which is not seldom very 
 intractable. 
 
 ^Etiology. The causes of secondary glaucoma may be 
 divided into two groups viz., (a) those which act by 
 bringing about a closure of the angle of the anterior 
 chamber, and thus shutting off the stream of fluid from 
 the excretory outlets in this neighbourhood; and (6) those 
 which owe their influence to a change in the constitution 
 of the intra -ocular fluid. Such change may be either due 
 to an alteration in the composition of the fluid (e.g., from 
 the presence of albuminous matter in solution therein), 
 or to the presence of epithelial or other debris therein. 
 Both these changes tend to block the excretory channels 
 mechanically, and so to impede the outflow of aqueous 
 fluid through them. 
 
 Secondary glaucoma may be brought about by any of 
 the following conditions. 
 
 47
 
 48 GLAUCOMA 
 
 Fistula of the Cornea. Whilst the fistula is open, the 
 ^interior chamber lies empty for a longer or shorter 
 period, with the iris base in contact with the cornea; 
 the formation of exudate, as a result of inflammatory 
 action, may agglutinate the two apposed surfaces, and 
 so cause obliteration of the angle of the chamber. When 
 the fistula heals, and the fluid can no longer escape 
 through it, the normal channels may be found to be 
 occluded, with the result that the intra -ocular pressure 
 rises. Later, staphyloma of the cornea may follow. 
 
 Anterior Synechia, following a fistula or a penetrating 
 injury, may cause such displacement forward of the iris 
 base as to effect an obliteration of the angle of the 
 chamber. Such a closure is usually partial in the early 
 stage, and may become complete later. 
 
 Posterior Ring Synechia leads to I' iris bombe, a condition 
 in which the iris is pushed forward by the fluid dammed 
 up behind it. The result is an obliteration of the angle 
 of the chamber, which adds to the difficulty already 
 caused by the want of a free circulation through the 
 pupil. 
 
 Anterior Dislocation of the Lens. Here the iris is found 
 wrapped round the posterior surface of the lens, and also 
 in close contact with the cornea peripherally, thus sealing 
 the angle all round. 
 
 Lateral Dislocation of the Lens acts much like anterior 
 synechia, only here the force that closes the angle is a 
 push from behind instead of a pull from in front. It also 
 resembles the latter condition in that the occlusion is 
 partial in the first instance at least. 
 
 Injury to tJie Lens. As a result of accidental trauma, 
 the capsule of a lens may be ruptured or pierced. In 
 either case the lens fibres swell up, with the result that 
 the lenticular mass increases in bulk, and so comes to 
 press upon the angle of the chamber and occlude it.
 
 SECONDARY GLAUCOMA 49 
 
 In addition, the lens masses tend to pass into solution, 
 and so to change the constitution of the aqueous, render- 
 ing it less able to pass through the meshes of the pectinate 
 ligament. We have thus a twofold tendency to secondary 
 glaucoma. 
 
 Operations. As a result of accidental injury during 
 operations, the same sequence of events, as has above 
 been outlined, may take place. Moreover, in the discis- 
 sion of soft cataracts the capsule is deliberately cut over 
 a limited area, with a view of letting in the aqueous 
 fluid; the swelling produced may sometimes outrun our 
 expectations or wishes, and then secondary glaucoma 
 follows. 
 
 After Cataract Extraction a dangerous form of secondary 
 glaucoma is sometimes met with. It may be due to 
 any of the following causes: (1) impaction of a tag of 
 capsule in the section ; (2) closure of the pupil by exudate ; 
 (3) the formation of a membrane behind the pupil, which 
 becomes impermeable to fluid, and so stops the passage 
 of the aqueous forwards; (4) the presence of a slow irido- 
 cyclitis, with all that this connotes; (5) the passage of 
 vitreous fluid forward into the angle of the chamber. 
 
 Intra-ocular Tumours. These set up a low form of 
 uveitis, as a consequence of the liberation of toxic sub- 
 stances by the growing organism. In this way the angle 
 may become sealed. 
 
 Cyclitis acts in two ways: (1) by sealing up the angle 
 of the chamber with exudate, and (2) by altering the 
 contents of the aqueous. The chemical constitution of 
 the fluid may be changed, rendering it less liable for 
 filtration ; or cellular contents may be added to it, which 
 tend mechanically to block up the meshes of the pectinate 
 ligament. 
 
 Intra-ocular Hcemorrhage adds suddenly to the volume 
 of the intra -ocular contents; it also makes the vitreous 
 
 4
 
 50 GLAUCOMA 
 
 more albuminous, and so promotes an osmotic flow into 
 it from without. 
 
 The Diagnosis ol Secondary Glaucoma. 
 
 In each individual case the signs and symptoms of the 
 primary disease must be carefully noted and their signifi- 
 cance weighed. The conditions which may give rise to 
 this form of glaucoma have already been sufficiently 
 indicated in the previous paragraphs. 
 
 The Treatment of Secondary Glaucoma. 
 
 In all cases in which the primary disease is still active, 
 it should be most energetically attacked, regard being 
 had not merely to symptomatic treatment, but above 
 all to the root-cause of the condition. To take one 
 instance, the treatment of glaucoma secondary to cyclitis 
 is incomplete if due attention be not paid to the possi- 
 bility that pyorrhoea, latent gonorrhoaa, syphilis, or 
 some other form of auto-intoxication, may be at the root 
 of the matter. 
 
 When the iris base is drawn forward, and the condition 
 is an early one, iridectomy is indicated. This is especially 
 the case in anterior synechia. 
 
 Pressure by a dislocated lens or by masses of lens matter, 
 following any form of trauma, demands the free evacua- 
 tion of the offending material. 
 
 Glaucoma secondary to the swelling of a maturing 
 cataract is best met by a prompt iridectomy. That due 
 to the formation of an impervious after-cataract may 
 sometimes be relieved by free discission of the obstructing 
 membrane. Glaucoma folio whig cataract extraction, in 
 the absence of any such membrane, often yields promptly 
 and permanently to trephining. Where, however, it is 
 due to the vitreous passing freely through the pupil into
 
 SECONDARY GLAUCOMA 51 
 
 the anterior chamber, and there proving too viscid to 
 allow of the natural escape of the fluid, it is doubtful if 
 anything can be done. 
 
 The presence of an intra -ocular tumour indicates the 
 need for an excision of the eyeball. 
 
 In haemorrhagic cases medicinal and general treatment 
 are probably the safest, though under desperate circum- 
 stances it may be permissible to trephine. 
 
 The treatment of iritis and cyclitis is on ordinary 
 lines; paracentesis, however, should always be kept in 
 reserve. 
 
 There are few more difficult things to decide than the 
 best method of immediate treatment of a case of acute 
 or subacute congestive glaucoma. The use of eserine, 
 which will open the angle, will at the same time increase 
 the congestion present. Atropine will reduce the con- 
 gestion, but will increase the difficulty opposed to the 
 outflow of the intra -ocular fluid. Operation in any form 
 is dangerous, though it may have to be undertaken. 
 There are cases in which the bold use of atropine or of 
 eserine, selected according to the exigencies of the in- 
 dividual case, may prove invaluable, and there are times 
 when operation must be undertaken and the fate of the 
 eye risked on the result of a single throw. The practi- 
 tioner will be well advised if, under such circumstances, 
 he places the responsibility on an expert, if possible. 
 In the meantime the patient should be kept in bed, the 
 forehead and temple should be freely leeched, and vigor- 
 ous fomentations applied. Free purgation should be 
 established, but not pushed after the first twenty-four 
 hours. Morphia should be used, if not otherwise contra - 
 indicated, to relieve pain and to obtain sleep, and the 
 patient should be kept quiet, in a shaded light. Needless 
 to say, all the individual indications previously dealt 
 with should be carefully attended to. The surgeon must
 
 52 GLAUCOMA 
 
 always remember that the aim of his treatment is not 
 merely to bring the patient through a painful period into 
 a condition of physical quiescence, but also, and above 
 everything else, to save as much vision as possible. If he 
 fails in this last respect, he has practically failed 
 altogether.
 
 CONGENITAL GLAUCOMA 
 
 BY this we understand glaucoma which is congenital in 
 origin. A large percentage of such cases are also con- 
 genital in their manifestation of the condition, though 
 the earliest signs of many such are undoubtedly over- 
 looked both by medical men and by parents. At the 
 other pole of life say from the age of forty onward 
 are found the cases of senile glaucoma. Intermediate 
 between the two, too late to be classed as congenital, 
 too early for the senile group, are a number which, 
 for convenience' sake, we call "juvenile." Speaking 
 generally, congenital glaucoma is due to defects in the 
 development of the excretory passages, whilst senile 
 glaucoma is to be attributed to degenerative and other 
 changes which accompany the advance of age. It is 
 probable that both elements play a part in the juvenile 
 cases, and the preponderance of one or the other in- 
 fluence determines whether the case is an early or a late 
 juvenile one, and so whether it is in danger of being 
 confused with those of the congenital or senile classes. 
 The terms " buphthalmos " and " hydrophthalmos " are 
 synonyms of congenital glaucoma . 
 
 Signs and Symptoms o Buphthalmos. 
 
 The condition is usually noticed at birth or before the 
 third year, and is bilateral in the great majority of cases. 
 Boys are more frequently affected than girls. 
 
 53
 
 54 GLAUCOMA 
 
 The eye enlarges slowly but steadily, and may attain 
 enormous proportions. The whole globe is uniformly 
 distended. Proptosis, lagophthalmos, and limitation of 
 ocular movement follow. The great enlargement of the 
 cornea is a striking and obvious feature. That membrane 
 may retain its lustre, or it may become scarred in various 
 ways. 
 
 The anterior chamber is greatly deepened. The sclent, 
 is evenly distended, and the uveal pigment shows through 
 the thin coat, making the white of the eye appear of a 
 bluish colour. The iris is tremulous; the pupil is round, 
 sluggish, and slightly dilated. The lens is normal in 
 size or smaller than natural, and is tremulous owing 
 to the overstretching of its suspensory ligament. The 
 vitreous may be clear or more or less cloudy. The 
 choroid is overstretched and atrophic. The retina is 
 overstretched, and detachment may take place. The 
 optic disc is cupped. The tension of the eye is raised, 
 sometimes very markedly so ; owing to the alteration in 
 the curve of the cornea, the ordinary tonometer cannot 
 be used, and we must rely on a finger examination. The 
 visual acuity is often much impaired owing to changes in 
 the media and in the optic nerve and retina. A moderate 
 myopia is usually present, often associated with astig- 
 matism, but its correction by glasses is difficult. .Nystag- 
 mus is common. The children are usually backward 
 and diffident, and their general health is often below par. 
 
 Clinical Course and Complications. 
 
 The great majority of cases go steadily downhill to 
 loss of vision, either through retinal degeneration or 
 opacification of the media, or both. A few cases stop 
 spontaneously; yet others, and these fewer still, retain 
 throughout comparatively normal functions. It has been
 
 CONGENITAL AND JUVENILE GLAUCOMA 55 
 
 suggested that the last class represent a gigantism of the 
 eye, for which the name " megalocornea " has been 
 proposed. This is a disputed question. The buphthalmic 
 eye is very liable to injury. In a few cases buphthalmos 
 is associated with an obscure condition termed " neuro- 
 fibromatosis." 
 
 Differential Diagnosis of Buphthalmos. 
 
 Buphthalmos must be distinguished from megalo- 
 cornea, juvenile glaucoma, keratoconus, keratectasia, 
 staphyloma, and exophthalmos. The first two condi- 
 tions have already been dealt with. In the remaining 
 four the diameter of the corneal base is not increased, 
 whilst in congenital glaucoma it is above the normal and 
 continues to enlarge. 
 
 The Pathological Anatomy and 2Etiology of Buphthalmos. 
 
 The leading points are as follows. (1) The cornea is 
 very liable to damage, especially on its posterior surface, 
 due to overstretching and consequent tearing of the 
 membrane of Descemet. This gives rise to characteristic 
 scars at the back of the cornea. (2) The anterior chamber 
 is very deep, and its angle appears to be widely open. 
 This appearance is often deceptive, as has been proved 
 by anatomical examination, for the angle is frequently 
 found to be closed by bands in this neighbourhood. 
 These represent a foetal condition of development. The 
 canal of Schlemm is often absent or insufficiently de- 
 veloped. It is this deficiency of the normal passages for 
 the excretion of intra -ocular fluid which is the paramount 
 factor in the aetiology of buphthalmos. The influence of 
 heredity is well marked, and is probably a question of the 
 inheritance of the above-mentioned defective develop-
 
 50 GLAUCOMA 
 
 ment. The next point of importance is the distensibility 
 of the young eye, which accounts for and permits the 
 great enlargement characteristic of the disease, and which 
 is not present in older globes. 
 
 Buphthalmos not seldom follows an injury or inflam- 
 mation of the eye. In most of these cases the condi- 
 tion is probably quite distinct from that of congenital 
 glaucoma ; they really are instances of secondary glaucoma 
 occurring in young and therefore distensible eyes. 
 
 JUVENILE GLAUCOMA 
 
 This group comprises a great variety of forms, some 
 of which are really congenital in origin (though their 
 onset may be delayed or may at first escape observation), 
 whilst others closely resemble the different forms of 
 senile glaucoma. Every variety of senile glaucoma may 
 be imitated, from the simple to the most acute. A very 
 interesting feature is the common association of juvenile 
 glaucoma with myopia. Another is the tendency for 
 the early stage of the disease to be prolonged owing to 
 the fact that the yielding of the young globes staves off, 
 for a time at least, the worst consequences of the rise in 
 intra-ocular pressure. 
 
 It cannot be too strongly insisted on, that there is no 
 essential difference between the various forms of glau- 
 coma. The best evidence of this is found in the following 
 facts. When glaucoma affects several successive genera- 
 tions, it tends to be of the senile type in the first genera- 
 tion, and more and more of the juvenile type in the later 
 ones. Again, in a single generation of one family in- 
 stances may occur of juvenile glaucoma in some members, 
 and of buphthalmos in others. Lastly, a single individual 
 may have buphthalmos in one eye, and juvenile glaucoma 
 in the other.
 
 The Treatment o Congenital and Juvenile Glaucoma. 
 
 The treatment of these conditions by medicine has 
 been very unsatisfactory. Inasmuch as some few of 
 them either never lead to serious symptoms, or else tend 
 to come to a full-stop by themselves, it is well to watch 
 each patient closely, and only to decide on active inter- 
 ference when the case is steadily going downhill. The 
 reliance to be placed on meiotic and similar treatment 
 is " expectant " only of disaster. If operation is decided 
 on, it should be undertaken at the earliest possible 
 moment. Iridectomy has been practically abandoned 
 as unduly dangerous in these conditions. 
 
 Many forms of operation have been tried, with varying 
 success. Sclerectomy has proved more satisfactory than 
 sclerotomy or anything else, and trephining appears to 
 have yielded the best results of any procedure. It 
 would, none the less, be idle to conceal the fact that, do 
 what we may, the prognosis of a case of buphthalmos is 
 not a very happy one. On the other hand, the dismal 
 certainties that attend inaction make it imperative that 
 we should not hesitate to shoulder our responsibilities 
 towards the patients and their relatives. The author's 
 personal experience has shown him that a certain number 
 of cases will yield results which, if not brilliant, are at 
 least highly gratifying, inasmuch as they enable a child 
 to see and to play a useful part in life. It is certainly 
 worth operating on ten cases to get five such results, 
 and that is, we think, somewhere near the probabilities of 
 the matter.
 
 INDEX 
 
 A. 
 
 ABSOLUTE glaucoma, 23 
 
 Acute glaucoma, 2, 45 
 
 Age, a cause of glaucoma, 17 
 
 Alterations in anatomical con- 
 ditions of eye, 17 
 
 Anaesthesia or cornea, 26 
 
 Angle of chamber, closure of, 4, 
 
 14, 47 
 obliteration of, 5, 48 
 
 Anterior chamber, shallowing 
 of, 15, 26 
 
 Anterior synechia, 48 
 
 Arguments against operating 
 for glaucoma, 45 
 
 Auto-intoxication, 17 
 
 B. 
 
 Bilateral disease, glaucoma a, 23 
 Bilious headache, 34 
 Blind painful eyeball, 23 
 Blood-pressure, intra-ocular, 10, 
 11, 12 
 
 systemic, 10 
 Buphthalmos, 53 
 
 aetiology of, 55 
 
 course and complications 
 of, 64 
 
 differential diagnosis of, 55 
 
 pathological anatomy of, 55 
 
 signs and symptoms of, 53 
 
 treatment of, 57 
 
 C. 
 
 Cataract extraction, glaucoma 
 
 following, 49 
 forms of, 27 
 Causes of glaucoma, 17 
 Chemosis, 22 
 
 Choroidal circulation, 6, 30 
 Chronic glaucoma, 2 
 
 Ciliary body, 3, 4, 5, 26 
 
 fluid secreted by, 5 
 glands of, 5 
 
 Ciliary nerves, 6 
 
 Ciliary processes, 15 
 
 Ciliary vessels, 6 
 
 Coloboma of disc, 30 
 
 Congenital glaucoma, 53 
 
 Congestive glaucoma, 2, 7, 15, 
 19, 20, 21 
 
 Conjunctiva, 3, 25 
 
 Conjunctivitis, 34 
 
 Cornea, 25 
 
 size of, at birth, 15 
 splitting the, 3, 43 
 
 Cupping of disc, glaucomatous, 
 
 7, 27 
 non-glaucomatous, 30 
 
 Cyclitis, 49 
 
 Cyclo-dialysis, 5, 44 
 
 D. 
 
 Degenerative changes in eye, 17 
 Device to explain cupping, 28 
 Diagnosis, difficulties in, 19 
 Differential diagnosis, 33 
 Dimensions of glaucomatous 
 
 eyes, 15 
 
 Distensibility of ocular tunic, 8 
 Distension of ocular tunic, 10 
 
 E. 
 
 Early operation, 37, 39 
 Elasticity of ocular tunic, 8, 10 
 Elliot's operation, 42 
 
 F. 
 
 cause of 
 
 Febrile diseases, a 
 
 glaucoma, 18 
 Fergus operation, 41 
 Fibrosis of pectinate ligament, 
 
 14, 17 
 
 58
 
 INDEX 
 
 Filtering cicatrix, 39 
 Filtration angle, closure of, 14, 
 
 15 
 
 Fistula of cornea, 48 
 Flashes of light, 21 
 
 G- 
 
 General treatment of glaucoma, 
 
 35 
 Glaucoma cup, overhanging 
 
 edges of, 7 
 Green reflex, 22, 23, 27 
 
 H- 
 
 Haemorrhage, intra-ocular, 49 
 Hsemorrhagic glaucoma, 51 
 Herbert's operation, 40 
 Heredity, influence of, 18, 55 
 Holth's operation, 41 
 Hydrophthalmos, 53 
 Hydrophyllic theory, 14 
 
 I. 
 
 Inflammatory glaucoma, 2 
 Injuries, a cause of glaucoma, 
 
 18 
 Intra-ocular fluid, direction of 
 
 flow, 5 
 
 drainage of, 9 
 source of, 9 
 vicarious channels of 
 
 excretion of, 11, 12 
 volume of, 10, 11, 12 
 Intra-ocular pressure, 1, 8, 10, 
 
 11, 12 
 
 conditions regulating, 8 
 Intra-ocular tumours, 49 
 Iridectomy, 38, 57 
 Iris bombe, 48 
 
 crypts of, 5, 9 
 dilatation of pupil, 4, 
 
 22, 26 
 Iritis, 34 
 
 J 
 
 Juvenile glaucoma, 53^ 
 treatment of, 57 
 
 L. 
 
 Lagrange's operation, 40 
 Late infection, 46 
 Lens, 26 
 
 advance of, 4, 15, 17 
 
 dislocation of, 48 
 
 growth of, 4, 15. 16, 17 
 
 injury to, 48 
 
 M. 
 
 Manometer readings, 8 
 Massage, 37 
 Meiotics, 35, 36, 37 
 Memory sight, 23 
 Mistiness of vision, 21, 25 
 Mydriasis, dangerous, 18, 35 
 
 N. 
 
 Nerve shock and strain, 18 
 Non-congestive glaucoma, 2, 19, 
 20 
 
 0. 
 
 Operative treatment, 38 
 Optic nerve, 27 
 
 atrophy of, 13 
 
 entrance, 7 
 Osmotic action in iris veins, 5, 9" 
 
 P. 
 
 Pain, 22, 31 
 
 Panophthalmitis, 23 
 
 Paracentesis, 51 
 
 Pathological anatomy, 13 
 
 Pectinate ligament, 3, 5, 9 
 fibrosis of, 17 
 perforating vessels, 6 
 
 Photopsiae, 31 
 
 Post-operative glaucoma, 49 
 
 Primary glaucoma, 1 
 
 Prodromata, 19, 21 
 
 Pulsation of retinal vessels, 30 
 
 Pump action of ciliary muscle, 
 4, 9, 14 
 
 Pyrexia, 31 
 
 R. 
 
 Rainbow rings, 21, 25, 31 
 Refraction, errors in, 18 
 Retina, 27, 30 
 Retinal circulation, 6, 30 
 Ring synechia, 48 
 
 S. 
 
 Schlemm's canal, 3, 5, 9, 14 
 Sclera, 25 
 
 cessation of growth of, 15 
 Sclera spur, 3, 9 
 Sclero-corneal trephining, 42 
 Secondary glaucoma, 1, 47 
 diagnosis of, 50 
 treatment of, 50 
 Selection of operation for glau- 
 coma, 44
 
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