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EDITORIAL
Year : 1966  |  Volume : 14  |  Issue : 1  |  Page : 44-54

Editorial


India

Date of Web Publication12-Jan-2008

Correspondence Address:
S N Cooper
India

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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Cooper S N. Editorial. Indian J Ophthalmol 1966;14:44-54

How to cite this URL:
Cooper S N. Editorial. Indian J Ophthalmol [serial online] 1966 [cited 2019 Jun 26];14:44-54. Available from: http://www.ijo.in/text.asp?1966/14/1/44/38565

Table 1

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Table 1

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In the course of the year, so many papers on glaucoma have been sub­mitted for publication that the editors have thought of piecing them together in the form of two "glaucoma numbers". Quite a few aspects of glaucoma have been covered, some of them very familiar, but many considerations have not been touched. In this editorial we have critically evaluated data from the articles presented and commented on some of the current problems on glaucoma, in an attempt to clear some of the haze that shrouds the mystery of glaucoma.

The problem of glaucoma which at one time appeared to be a simple imbalance between production and drainage of aqueous has now developed into so complex a condition, thanks to accelerated modern research, that new points for consideration keep on developing, many of which have still remained unsolved. The progress in the knowledge of glaucoma is punctuated with definite landmarks. It first originated with the concept of what we call acute congestive glaucoma. Subsequently the so-called non-congestive or simple glaucoma was added to this symptom-complex and later the primary and secondary varieties were distinguished.

In India another variety of glaucoma has been recognised, which is called epidemic dropsy glaucoma', as a result of ingestion of the active principle of argemon oil which is used for adulterating cooking oils.

Undoubtedly a series of chain reactions have been started in different research laboratories in both the worlds, all too interesting and all too impor­tant, with the aim of solving the cause and nature of unstable ocular tension which finally ends in constantly raised intra-ocular pressure (TOP), but this `international investigation bureau' is left with several disconnected links and controversial results yet to clear that shroud of mystery.

To begin with, the classification and theories of glaucoma have defied a satisfactory solution. There is no difficulty over terms like haemorrhagic, secondary, absolute, congenital etc. For the other varieties questions are asked: should there be gonioscopic, clinical or etiological classification? Inspite of tonography, biomicroscopy, histopathology, microangiography and electron microscopy we find some classifying as congestive and non-congestive and others as open angle and closed angle and yet others as wide angle and narrow angle. Low tension glaucomas add further to the confusion. For the reason that these terms are used as pet ones by certain schools, the editors have not insisted on one or the other terminology.

In the anatomical approaches to this problem considerable progress has been made. Anatomically, it was first discovered that the drainage mechanism in primates is different to that found in animals which has introduced special problems in anatomical aspects of this question. A controversy is still raging as to the actual site and mechanism of obstruction in cases where an anatomical obstruction is supposed. A description of aqueous veins gave a further spurt in the evaluation of the importance of these veins. Recent studies with the use of neoprin casts and injections of dyes have consolidated the anatomical approach. A good account of the position today can be had from the book "Clinical Glaucoma" by R. J. H. Smith. reviewed in the previous number.

On the physiology side, the problem is still undecided as to the nature of production of the aqueous and although the secretion-diffusion concept of the formation of aqueous has been accepted with reasonable certainty, our knowledge has not yet advanced to a stage to determine how far and in what way variations from the normal process is responsible for raising the ocular tension and utilise this knowledge for the relief of glaucoma.

On the etio-pathological side two distinct schools are at the moment in existence, 1) the anatomical and 2) the vascular, or neurovegetative each advancing proofs, clinical and experimental, to support their own pet theories. A compromise between the two schools appears to be the only way out of this confusion and was achieved in a form at the International Symposium on Glau­coma (1954).

With the advent of topography and exact tonometry, all glaucomas are attributed to angle defects, especially by the American and Swiss schools, thus pinning the condition to one and one cause only, a faulty drainage. The English school draws attention to the huge vascular network in the choroid and ciliary body and rightly wants a fair consideration of the vascular factors involved in the overall picture. According to them the controlling mechanism is a neuro-hormonal one over the tonus of the sympathetic which regulates the vascular circulation of the eyeball. Certainly the phasic variations, catas­tropic attacks and exacerbations of the congestive clinical varieties, failure of drainage operations to normalise tension in a few instances, control of tension by adrenergic drugs in some instances, suggest a possible disturbance of this neuro-hormonal control in glaucoma and offer a challenge to the mechanical obstruction to drainage theory. However, recent work on these catacholamines like noradrenalin shows that they act by increasing the outflow and thus one more piece is removed from the `vascular' pan and added to the `mechanical-obstruction' pan in the balance of evidences. The observations and arguments advanced by opposing schools appear equally convincing to the clinician and therefore appear to him annoyingly confusing.

Even if we concede that there is obstruction to the outflow mechanism, it has not been clarified whether the block is proximal to, within or distal to Schlemn's canal and what is the nature of the obstruction.

The table below illustrates the confusing ideas that prevail out of which we seek clarification.[Table - 1]

It is unfortunate that the imagination of not many in India has been teased enough to probe into the mysteries of glaucoma. It must be confessed however that the problem is a complex one and our means in India are limited to explore such an approach. Nobody however has any original ideas on the subject except perhaps Hakim who has done some original work on the so-called Bengal Glaucoma, which fortunately has been licked and is now an extremely rare customer even in Bengal.

In his extensive studies on the pharmacological action of Argemon Mexicana, it has been established that plants and seeds of the papaver group which contain alkaloids like those found in argemone plants and seeds can produce the same type of glaucoma as argemone. In other words certain toxic poisons from plants can produce a type of glaucoma. The extensive distribution of such poisonous plants over the grain-fields of the world may be responsible for such poisons getting into the systems of many, either directly through adulteration or indirectly through milk of animals grazing on such plants. This affords an interesting and new approach to the theory of glaucoma.

The work of the Aligarh school on the association of trachoma with glaucoma is another original observation which needs exploring.

One feels however, that the role of malnutrition in India in glaucoma has received scant attention. One remembers too well the sudden rush of glaucoma cases in the Sindhi evacuees at the time of "the Partition." Here again one wonders whether it was malnutrition or emotional anxiety or both which were responsible.

We had undertaken many years ago, a study of the nutritional status in subjects of chronic simple glaucoma. The relation was not found to be unequivocal for although some of the cases showed definite hypo-proteinoemia, none of the cases showed a reversal of the albumin-globulin ratio.

Clinical proof in this direction is furnished by two of our cases where an operation was avoided by simply putting the patients on hospital diet. One of these patients returned a month later with increased tension once again. The hospital diet again reduced the ocular tension. Naturally, a high protein diet is not expected to reduce ocular tension in established cases where angle changes have become irreversible.

The experimental evidence afforded in this connection by the experi­ments of Hakim are again interesting. While studying the toxicity of argemone in rats he observed that retinal damage was found in chronic toxicity in old rats kept on low protein diet or were not protected against argemone toxicity by BAL. Thus BAL and a good protein diet seem to have a protective action against argemone or allied toxicity. Undoubtedly hypo-proteinoemia therefore seems to contribute indirectly to the overall condition of glaucoma and may not be discovered in all cases, though present in some, especially in India.

The influence of female hormones in glaucoma affords an interesting study. Following the beneficial effects of progesterone in glaucora recorded by some workers, we too have used it as a depot therapy in a limited number of some obstinate cases particularly after failure of surgery. The results have been heartening in some at least.

On the other hand estradiol, the estrogenic hormone in the ovary is reported to have increased the IOP to 35 mm. in a patient who was getting it for carcinoma prostate.

With topography, the influences of the different hormones are being scientifically evaluated in other laboratories and no doubt will afford a con­structive approach in the treatment of glaucoma. For the present it has been found that 'progestron' (not its synthetic counterpart Norlutin) causes a con­sistent drop in IOP, more so in post-menopausal subjects and in subjects over 50 years of age.

Belaxin, a special hormone present during the later weeks of pregnancy increases the outflow facility only in the presence of estrogen.

From the above considerations, we can get an idea of the complex factors at work by considering the glaucoma problem in the form of a star with five rays: - (1) resistance to outflow. (2) disturbance of the neuro-hormonal control mechanism of the ocular vasculature. (3) toxy-infective factors. (4) malnutrition. (5) Protective influence of female hormones. With all this there is an element of heredity, for glaucoma does seem to run in families and the paper on blood grouping in glaucoma by Carg and Pahwa in the last issue offers a new approach.


  Pain in Glaucoma Top


Physiology of pain in Glaucoma. We know of cases in glaucoma when the tension is as high as 70 or 80 mm. Hg. but the patient does not complain of pain, for example in epidemic dropsy glaucoma. There are others where the tension may be no more than 25 or 30 and yet the pain may be severe. This proves that the pain is not the result of increased tension in glaucoma but is a trigeminal pain as in ciliary congestion, from other causes like iritis or hypopyon and results from a reflex response of the ciliary vessels to the presence of acid metabolites and degeneration and toxic products within the eye as in the case of hmmorrhagic glaucoma. One proof of this fact lies in its treatment. Carbamynoylcholinechloride i.e. carbachol, Morryl, Dorryl and other similar products, Priscol etc. when injected retrobulbar will cause relief of pain within an hour without relieving the tension, and so is a useful physiological fact to remember when pain is an indication to do enucleation in case of congestive glaucoma, and if the patient is to be spared an enuclea­tion. We have found this extremely useful in haemorrhagic glaucoma, parti­cularly after an injury. It is very important to know that it must be injected retrobulbar in Tenon's capsule and NOT subconjunctivally (not even a drop) as then extreme stimulation of the para-sympathetic causes severe miosis and an unbearable increase in pain.


  Diagnosis Top


Surveys: Of late, there has been a lot of talk about mass screening for the detection of the potentially glaucomatous. Many surveys have been subsidised by substantial funds to carry out field surveys in certain popu­lations in the search for missed and potential glaucomas. This almost door to door search appears to us a little wasteful of the financial and energy resources of a nation. The reports of these surveys, do not appear very convincingly useful to us, though many may disagree. In the first place, such a study must be followed up by a later survey to see how many of the suspected cases developed glaucoma or got examined and treated and how many new cases can be discovered which were missed in the first survey. On an average the overall incidence of all glaucomas is about 10% and that of missed, dubious and borderline glaucoma is at the most a quarter of this 10%, let us say in all 2.5% maximum. To take a whole army of `diviners in search of a 2% of the population, involving such an expense of time, energy and money appears to us to be bordering on the ridiculous. Besides many of these do find their way to a hospital because of symptoms and are trapped if they come to the eye department.

In support of such surveys an argument is raised that they make the population glaucoma conscious. Certainly it does that but it raises a glaucoma hysteria as well. Not lon ago, in Bombay a talk on glaucoma was given by an ophthalmologist on the radio. For about two months our practice noticed a slight spurt in the number of patients who visited us thinking they had glaucoma. The excellent paper of Dr. Pollack in this issue gives a very sober idea of such a survey in which all the implications are clearly discussed.

To our mind a practical approach for such a screening programme would be to screen all hospital attendances over the age of 40 years and screen every patient over the age of 40 that comes to us for private consultation by taking his tension on a tonometer even though the eye feels normal on digital pressure. The same must be made applicable in the case of subsidised eye-camps. Thus, there can be continuous screening of large populations daily under very favourable and inexpensive conditions. Tensions over 22 mm. Schiotz are then refered for a detailed study to establish glaucoma, reject it or keep a doubtful case under observation.

Selective screening of near relatives of glaucoma patients is advisable in view of the fact that glaucoma tends to run in certain families.

Tonometry: Should tonometry be left to non-opthalmologists. For mass screening, one cannot find a better person, In the consulting room the secre­tarial staff learns it easily and gives it interest and pleasure in sharing the work of the chief. The borderline cases are of course checked by the ophthalmo­logist. Such paramedical staff can even do perimetry and scotometry. It would even be an advantage to entrust them with these examinations, because their results would be free from any bias.

What kind of tonometer should one use in practice? In India, with the mass of eye work and because of import restrictions, one has to have a practical approach. As against the good old Schiotz tonometer we have to-day applana­tion tonometers, electronic tonometers and other newer and newer devices, some of them quite expensive. Again we have to distinguish between a clinical tonometer for every day use and tonometer for research purposes. It is impossible to dilate on the qualities and theories about accuracy of the different devices and tests in these few pages. One must not get lost in these newer devices and forget the good old Schiotz tonometer with weights, which has now been standardized and must answer the requirements of these standards. Applanation and electronic tonometters, though very useful in the boarderline cases and for research, are not indispensible and we feel that with accurate tonometry and scotometry, charting out the blind spot and Siedl's scotomas one can unmask the true pathology of a dubious glaucoma even more effectively.

It must be remembered that tonometrically the normal variation is of a fair degree and no tonometer can give an absolute value of the TOP or the normal for an individual which differs from person to person. It is necessary to make an allowance on the higher side of the normal IOP for patients over 55 years of age. For comparing tensions between the two eyes and on two occassions in the same eye however, it has its maximum usefulness. What is useful to remember is that the same tonometer must be used for comparing values, the tension is best taken in the clinostatic or supine position, there must be a proper fixation device so that the eye looks straight up and there should be no blepharospasm because the action of extraocular muscles can considerably increase the IOP.

Occasionally an applanation tonometer records a higher tension when paired readings with a Schiotz do not show any abnormality of tension or scleral rigidity. Where applanation tonometry is possible it should be used as a more reliable method.

Newer and newer types of tonometers are being devised. One such has a pneumatic plunger to flatten the cornea. This device can be used without anesthesia. The awkward thing about it is that it is inventend and developed by optometrists and so will carry an unhealthy prejudice. Scientific progress should not be allowed to be hindered by such narrow-mindedness.

The Maklakov type of tonometer reported upon by Telang and Badlani in this number offers a very simple device for utilising the applanation principle (Imbert-Fick Law), which should not cost much, should be locally manufactur­able and easily sterilizable.

Talking about sterilization of tonometer foot-plates and plungers, perhaps the danger of infection being carried from eye to eye is overfeared. That does not mean that no steps should be taken to sterilize the instrument at all. The introduction of 'tonofilms' however, appears to us to be a commercial stunt Wiping the foot-plate and plunger with a weak solution of Cetavlon or Zephiran should be sufficient for all practical purposes.

Corning to the provocative tests, glaucoma begins with a loss of lability of resistance so that the eye compensates poorly to any change in ocular dynamics. It is only when such poor compensation prevails that the diagnosis offers a challenge and when provocative tests are helpful. Tonography does the same by determining the coefficient of outflow, but where tonography is not available as in many places in India, one or other of the tests should be useful. In this connection tonography with perilimbal suction cup device is a variation which has to be watched. Homatropin and water drinking tests are simple, but for the latter, to drink a 1000 cc of water at a time is not too inviting even on a hot summer day. Ingestion of 500 ml of water causes hardly any perceptible rise of tension. Juggular compression test is a favourite one with us and it certainly helps to make decisions. It is also important to remember at what time the water-drinking test should be done. It must not be done at the peak hour of diurnal variation as the difference will be least then. It will not be so in the case of juggular compression because the criterion is whether the tension is raised upto 30 mm. or more, irrespective of the initial tension. The modern tendency is to combine tonography with the water drinking test.

'When one scans the literature on the subject of diagnosis of glaucoma and the various ordeals a man has to put up with for a diagnosis to be established, these `tortures' appear to border on the ridiculous. In doubtful cases, the patient is admitted into the hospital and the tension is taken four to six times even waking him up in the early hours of the morning. Then an exhaustive perimetric and a scotometric tests are gone through. Tonography and tonometry with an ordeal of having a weighted tonometer for four minutes on each eye with the gaze directed straight up to the ceiling without blinking is the next torture, which if not revealing is to be repeated after drinking a 1000 cc of water. Then the ordeal of getting half-choked with a sphygmomanometer collar round the neck with the left hand placed in ice-­cold water nearly reminds us of the middle ages with their "trials by ordeal". As if this is not enough a contact glass is put in the eye and the angle is studied with a gonioscope. We dare say some patients enjoy these and feel awfully important and satisfied. Sometimes even after a long search one becomes no wiser and the patient is asked to come again. What we feel is that these tests must be tempered with reason and we for our part feel that if there are no scotomas, no enlargement of the blind spots and no nasal field defects to weak stimuli, there is no cause for alarm. A six monthly check on a perimeter and a scotometer and of the tension with a Schiotz tonometer with paired weights, is the least annoying of these tests, which can be done by one's receptionist if he or she is trained properly.

Gonioscopy: It may be noted that quite a large part of the angle may be covered with anterior synechiae before the tension becomes pathological, but a slight ballooning of the posterior fold of the iris can effect a more destructive angle closure.


  Clinical Varieties Top


Pigmentary glaucoma should raise special interest in our country because of the pigmented iris of our people. A study undertaken by one of us at the King Edward Memorial Hospital Bombay some years ago showed that there was no relation between pigmented iris and pigment in the angle and heavily pigmented eyes were no more susceptible to glaucoma than light-­coloured eyes.

Secondary glaucoma: The type most often come across is the one asso­ciated with iridocyclitis. A word of caution is necessary here. Sometimes in the acute congestive variety, an ischaemic necrosis of some of the uveal tissue causes a secondary chamber flare and corneal precipitates, which give the false impression that the glaucoma is due to irido-cyclitis. Depigmented patches on the iris are suggestive of the secondary role of iritis here. The use of mydriatics makes the condition disastrous; miotics are strongly indicated and are beneficial. Iridectomy is the operation of choice and there should be no hesitation to its performance even in the presence of keratic precipitates.

Another type of glaucoma that offers a challenge to one's judgement in treatment is the so-called phacolytic glaucoma. The lens looks dense white but has a muddy tinge, the iritis is severe, the chamber flare is markedly positive, even amounting to a hypopyon and the tension is very high. We have often seen such cases after a failed operation for detachment of retina. It requires courage to operate in the presence of such severe uveitis to save the eyeball though not the eyesight. Actually it is easy and once one has done it, he gains in confidence for similar subsequent challenges. Since the denatured lens matter is the cause of irido-cyclitis and glaucoma it stands to reason that such obnoxious matter be removed from the eye. The operation is done under general anesthesia after attempting reduction of tension by all available means for a day or two. The lens matter if it comes out extracapsu­larly is irrigated out in the usual way. A full iridectomy may be done. A surprisingly good recovery follows. The eyeball is saved. The subsequent redness is tackled by desensitization with lens proteins.

Another interesting form of secondary glaucoma is the so-called haemorr­hagic glaucoma. The paper by Labas in the previous issue draws attention that even an arterial occlusion can cause glaucoma. It must be remembered however that the eyes that do develop glaucoma after a vascular catastrophy are potentially glaucomatous. Once again we stress the value of carbaminoyl­cholinchloride injected into Tenon's capsule for the relief of pain and for saving an otherwise unescapable enucleation.

The question of iatrogenic glaucoma is well dealt with in the two papers on corticosteroid glaucoma. Here also a predisposition to glaucoma probably plays an important part in the selective incidence of such glaucoma.

In the case of unilateral glaucoma, particularly in young people two conditions have to be particularly remembered: (1) phacomatosis, similar to the case of unilateral buphthalmos in von Recklinghausan's in infants and children, (2) previous trauma to the eye even with full recovery.


  Medical Treatment Top


The search for newer drugs continues for the medical treatment of glau­coma because the results of surgical treatment are never uniformly happy.

For the acute congestive variety and for temporary relief of glaucoma, of recent years urea, mannitol and glycerol have come into vogue. Of these, much the simplest is the oral administration of glycerol on which three encouraging reports were presented in the previous issue. Its usefulness in reducing the previous ocular tension prior to intra ocular surgery is an added blessing.

Because mannitol does not enter inflamed eyes, it is more effective in lowering the tension in such eyes by osmosis, but it requires a larger volume of it.

Glycerol though most convenient to administer is too sweet to be palat­able and in diabetics must be avoided.

Acetazolamide is still holding its ground and its administration in a continuous release form is a useful variation in the mode of administration of this drug.

Question is often asked as to how long acetazolamide therapy can be continued with safety. If the patient is to be kept on a prolonged therapy it is important to increase the blood potassium levels in patients and it is necessary to estimate the electrolyte balance from time to time. With this safeguard the therapy may continue indefinitely.

Among the newer drugs that have drawn attention is echothiophate iodide (Phospholine). It is a cholinesterase inhibitor like eserin, but it has a much longer lasting action than eserin and so is gradually displacing it. Drops of 0.125 to 0.25% not only reduce the cellular cholinesterase but also plasma esterase and is therefore dangerous when a muscle relaxant is used like succinylcholine in general anaesthesia, because neutralization of this drug depends on serumcholinesterase.

For the present its main use is being confined to aphakic glaucoma. It is not yet freely available in India and it holds great promise to be a popular drug in glaucoma therapy.

Levo-epinephrin 2% continues to draw attention as an adjunct to the miotic therapy of glaucoma. In a pilocarpinised eye if one drop of I-epinephrin reduces the IOP after 45 minutes, it would he an indication to use it. The effect lasts for nearly 36 hours so that a drop of 2% solution morning and evening along with miotics would be sufficient. In view of the pupil dilatation and vasoconstriction effect of epinephrin it seems strange that it can reduce IOP by improving the facility of aqueous outflow, which it does.

Treatment of the so-called malignant glaucoma by the paradoxical mydriatic-cycloplegic therapy is well borne out by the cases reported in these issues. Evidently, it is due to a forward thrust of the lens-iris diaphragm due to laxity of the lens zonule and a swollen vitreous. A posterior sclerotony with letting out of vitreous is a sensible measure in this desperate condition. (see under surgical treatment also).

Treatment of glaucoma by drops of synthetic acetyl choline (carbamy­noylcholinchloride 'Carbachol', 'Doryl', 'Moryl', 'Priscol' etc.) is going out unfor­tunately, because its action is not understood properly. Pupil contraction results as a liberation of acetyl cholin, but if there is no acetycholin libera­tion due to atrophy of the iris and its corresponding neuro-hormonal mecha­nism, pupil contraction can only be obtained by instillation of acetyl cholin or even more effectively by one of its synthetic forms because on the latter, cholinesterase is ineffective. It use is to be reserved only when there is iris atrophy, otherwise it produces some severe pain due to extreme miosis.


  Surgical treatment Top


Analysis of the results of surgical procedures stated in the different papers on this subject in this issue, clearly show that in all of them the initial lowering of tension is much lower than what one sees in later years. This is due to the tissue-shock of any surgical procedure, the final outcome of which can truly be assessed at least six months after the operation. When one sees the results in an unbiased atmosphere some six months later, the smile of earlier satisfaction settles to a scowl in many instances, especially in the case of open-angle glaucoma. In our experience surgical procedures are most satisfactory in juvenile glaucoma because in them the angle block is purely mechanical due to a congenital membrane (Barkan's membrane) blocking the angle. I have never seen it to fail, but it is very rare. In the older group of patients, although tonographically it can be proved that the "block" is in the angle, the nature of the block is still an unclarified mystery. It is a pathological process e.g. some kind of sclerosis that keeps on progressing even after a drainage operation by a most skilled and experienced surgeon. Is it an unsourmountable block? Is the block in the sclera beyond Schlemn's canal? Are there other unknown countributory factors which keep mounting even after surgery? Then what about the low tension glaucoma?

As regards the various surgical procedures, they are variations and com­binations of the different established techniques which when the surface is scraped seem to seek the same object with almost similar success. One always feels a personal bias in these studies in favour of one's own favourite technique.

Most surgeons have settled down to a combination of inclusion surgery with some form of sclerectomy. It is difficult to compare cases and results, because of the number of factors one has to take into consideration: (1) initial tension, (2) initial vision, (3) initial fields, (4) duration in each case, (5) initial facility of outflow. (6) excavation of the disc, (7) immediate results, (8) late results in which we must take into account not only the central acuity but also the fields. (9) Complications like cataract recurrence of high tension, hyphema, flat chamber, leaks and infection of the filtering bleb and posterior chamber block leading to malignant glaucoma.

In many cases even after surgery one has to have recourse to miotics and acetozolamide in a fair number of cases. Can we then confidently say that surgery is the answer for open-angle glaucoma even when medical measures have failed.

In some cases it is possible to rectify a filtering bleb which is threatening to close (1) by corticosteroids drops (2) by suction cup applied over the bleb, but in quite a few the bleb flattens out and the effect of the operation is lost.

The question of a flat chamber after sclerectomy is important. It is much more common when a thermal cautery is used to bore a hole in the sclera. How long is a flat chamber compatible with good functional results? Oral Diamox and glycerol perhaps help in its reformation, but the chamber forms by itself sooner or later in any case, and help given by the ocular hypotensive agents must remain a matter for speculation. Indeed one wonders whether it is advisable to reduce aqueous secretion by giving Diamox because the shocked ciliary body becomes ascretive or hyposecretive and is the cause of the flat chamber. In any case a chamber can remain flat for a fortnight without causing any undue effect though the chances of success are progressively reduced day after day. Drinking of plain water may be encouraged in such cases by way of hydrotherapy.

In failed surgery the only answer is cycloelectrolysis or cyclodiathermy. Even then the high tension tends to return and may require a repetition of the operation.

Finally, cataract in a glaucomatous eye presents a special problem. Should the two be tackled together or separately and if the latter, which should be tackled first. The tendency is to do the two together these days, combing some form of sclerectomy with or without iris inclusion, after extraction of cataract. It is a subject on which a play of imagination produces a fantastic number of procedures with no material difference between the results obtained.

In conclusion we ask how much wiser have we become in recent years on the subject of glaucoma. The answer is given in the lines of Omar Khayam:


"There was a Door to which I found no Key

There was a Veil past which I could not see".

There are many doors in the etiology, pathology and treatment of glaucoma for which no key has yet been found. Let us leave it to the Wise to keep on with the search. Let us relax with Khayam but without a glass of wine and conclude with apologies to the poet:


"Leave the Wise to wrangle and with us

The quarel over glaucoma let be:

And in some corner of the laboratory

Make game of that which makes game of Thee."



 
 
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