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Year : 1964  |  Volume : 12  |  Issue : 1  |  Page : 1-13

Adenwalla Oration-Riddle of Glaucoma

Institute of Post-Graduate Medical Education and Research, Chandigarh, India

Date of Web Publication13-Feb-2008

Correspondence Address:
Tulsi Das
Institute of Post-Graduate Medical Education and Research, Chandigarh
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How to cite this article:
Das T. Adenwalla Oration-Riddle of Glaucoma. Indian J Ophthalmol 1964;12:1-13

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Das T. Adenwalla Oration-Riddle of Glaucoma. Indian J Ophthalmol [serial online] 1964 [cited 2024 Feb 27];12:1-13. Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?1964/12/1/1/39064

Table 3

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Table 2

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Table 2

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Table 1

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Table 1

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The earliest mention of a disease resembling acute congestive: glaucoma is in Sushrata. It is described in the supplement (Uttar Tantar) 4th Chap­ter and 11th, 12th and 13th stanzas. The 11th gives the common features of the four types of Adhimanth (Vataj, Pitaj, Kaphaj and Rahtak), whereas the 12th and 13th stanza gives the descriptions of Vata (the description resembling acute congestive glaucoma). The 20th stanza tells us that this leads to loss of sight in 6 days if not pro­perly treated. When the person be­comes blind due to this disease it is called Hat Adhimanth

The original text of Vataj Adhi­manth is : -­

In this disease of Vataj Adhimanth, the patient is in acute agony, feels as if his eyes are being torn apart, as if some churning is going on inside his eyes resulting in friction (sensation of grinding) and heat, piercing and stab­bing pain, stony feeling, hazy media, the eyes don't open properly on account of glare, bursting of the eye-ball, fullness of the eye-ball, and generalized feeling of discomfort and acute pain in the same side of temples and eye-brows (half headache). This Vataj Adhimanth usually follows Vataj Abhi Shyand which has the following symptoms : -

Piercing pain, hardness or stiffness of the eye-ball, general goozing of the skin, feeling of irritation and friction, stony feeling, half-headache, dryness of the eye, cold tearing of the eyes.

The diagnosis of Glaucoma once made is one of the most difficult to reverse, as in the lay mind the word Glaucoma has a most sinister conno­tation. The simplest definition of Glaucoma (primary) is a disease in which intraocular pressure is elevated to a degree which the eye cannot tole­rate without damage, to its structures.

Aetiology of this disease had so far eluded all human efforts. Almost every year voluminous literature is pro­vided to study the various facets of the disease yet we are no way near the solution of the problem. It is behaving just like Essential Hypertension. Glau­coma has posed a challenge to the Ophthalmologist and the number of seminars, symposia and experimental research directed to the solution of the problem indicate that the Ophthalmo­logist has not only accepted the chal­lenge but is in grips with the grim realities of the ever-growing complexity of this problem.

In this laboratory era of Medicine so much stress has been laid on the mechanical aids and the animal ex­periments that the clinical aspects are comparatively ignored. It is well said that a glaucomatous eye is a sick eye in a sick body and to concentrate all efforts on a particular segment of the eye is to ignore the disease and the man.

One cannot but admire the efforts of the leaders in Ophthalmology who have devoted all their time to the study of the anatomy and the physiology of the angle of the anterior chamber and the hydrodynamics of the aqueous to unravel the mystery of this disease. These lopsided efforts have no doubt yielded wonderful results but the mystery remains as unsolved as ever.

The increase in pressure may be due to faulty secretion, faulty composition and or faulty absorption or outflow of the aqueous humor.

To my mind, the word drainage is rather unfortunate; aqueous is too pre­cious to be just drained out of the eye. There is actual re-absorption of the useful components of the aqueous just like the valuable components of urine are getting reabsorbed in the urinary tubules of the kidneys. This conten­tion of mine is further supported by the anatomy of the limbus. I think it is very important for us to be familiar with the anatomy of this important area and reorientate our thinking about its exact nature.

The present study of limbus will re­veal that it plays a dominant role in the etiological complex of glaucoma. Its structure neither corresponds to that of the cornea nor to that of the sclera so that it could not be termed a true transitional zone between the two. Cornea is avascular, sclera is al­most so. On the other hand this limbus partakes of the characters of ciliary body and iris. It should rightly be termed a transitional uveal zone situated between the ciliary body and iris, as it is a highly vascular and cellular, more like the ciliary body than iris. It has atleast three tiers of vascular plexus, such as: 1. deep scleral. 2. intra scleral. 3. episcleral.

It is significant to note that the long posterior ciliary arteries and anterior ciliary arteries form the major arterial circle, just behind the junction of the iris with the ciliary body. Three struc­tures receive their blood supply from this circle. ciliary body behind, iris in front and limbos outwards.

Any inflammation of anterior sclera is associated with uveitis and in a number of cases is followed by glau­coma. It, therefore, means that the inflammation of limbus (wrongly call­ed corneo-sclera) is really the inflam­mation of that part of the Uvea, which at present is not considered a part of the uvea. This concept may resolve some of our main difficulties regarding the open angle glaucoma. It may be a very quiet inflammation of this silent part which may be more of the nature of a uveitis than anything else. This may account for the vascular or tra­becular changes or both, in this area responsible for the decrease in outflow of aqueous.

The word outflow of aqueous is used, because the fluid is going out of the eye. It is well and truly a process of re-absorption through the endothelium, lining the angle of the anterior chamber, the corneo-scleral mesh-work (uveal and scleral) canal of Schlemn, the three vascular plexuses (mention­ed above) before the fluid is accept­able to the veins of the anterior ciliary system. Recent study has shown that there are peripheral sympathetic ganglia and rich net-work of nerves which locally control the absorption or outflow of aqueous. It is also a well re­cognised fact that the endothelial cells of the cornea, the trabeculae and the iris have a selective absorptive capacity just like the epithelium of the cornea. It has also been proved that aqueous nourishes the cornea in front, lens in the centre and the vitreous be­hind and through it goes posterior also and is then absorbed into the in­traocular veins. There is a local re­flex mechanism which regulates the volume of outflow of aqueous accord­ing to the production of aqueous by the ciliary body which vary according to the daily needs of the eye. Even diur­nal variations of intraocular pressure support this view.

  Role of Composition of the Aqueous Top

It is now agreed that ciliary body actively secretes the aqueous and that aqueous is not just a dialysate. The normal composition of the aqueous is admirably suited for the biochemical needs of the three avascular structures such as vitreous, lens and the cornea, out of which, lens entirely depends on the quality of the aqueous for its optimum nourishment. The moment aqueous of wrong quality is produced as in a severe case of uveitis the posterior cortex of the lens develops lenticular opacity. Even in glaucoma it appears that the composition of aqueous is changed as it leads to posterior polar cataract i.e. a complicated cataract. The chemical studies of aqueous carried at the Institute of Post-­Graduate Medical Education and Re­search, Chandigarh, although the series is small, show changes of pH towards acidic side in cases of glau­coma. The pH of normal human aqueous being 7.21, in two cases of secondary glaucoma due to uveitis it was found to be 6.8 and 6.3 and in one case of acute congestive glaucoma it was found to be 6.4. The work is being continued and would be the subject matter of a subsequent paper.

Not only its quality varies, even the quantity of secretion is determined by the needs of the eye usually. It is only where adjustment fails that intraocular tension rises either due to faulty ab­sorption, which is more usual or over­production or faulty production of aqueous. In epidemic dropsy glau­coma there is an over secretion due to capillary vascular paresis.

  Role of Neuro-Endocrine System in the Aetiopatho­genisis of Glaucoma Top

Certain cells of the central nervous system, particularly those of the cere­bral ganglia in invertebrates and of the diencephalon in vertebrates, show a considerable degree of light sensiti­vity: the dual function of the pineal body, sometimes optical, sometimes endocrinal, is an example of the same association. It is not surprising, there­fore, that nerve cells in these regions should sometimes respond by the se­cretion of hormones to the direct sti­mulus of light and at other times to indirect stimulation through the eyes. In general terms the neuro-endocrine system exercises a controlling influence over (a) ocular and skin pigments, (b) growth, (c) development of gonads and regulation of the reproductive cycle (d) a number of processes of in­termediate metabolism principally af­fecting water, salt, oxygen and carbo­hydrates. In human beings this neuro­endocrine system is composed of the Hypothalamus-pituitary axis control­ling especially the suprarenals and the gonads in both sexes and thus control­ling the mechanism of production of aqueous. The various hypothalamic nuclei exercise a supervisory control over the pituitary and most of the other endocrine organs. They take direct control of the pituitary In addition they exercise a quick-stimula­tion of the adrenal medulla through the sympathetic and through the me­dium of the pituitary they exercise a slow working control over a host of endocrine activities. A relationship, still vague though undoubted, exists between the intraocular pressure and the endocrine system particularly the hypothalamic - hypophysial complex and that diencephalic disturbance is related to the disturbance in intra­ocular pressure. Duke Elder believes that a hypothalmic centre exercises some control over the intra-ocular pressure. It is an influence which is responsible for the cyclic diurnal varia­tion in the normal intra ocular pressure and in part perhaps for the exaggera­tion of these variations that charac­terise primary glaucoma but whether this action is mediated by nervous or hormonal factors or both is still un­known. The reported association of hypotony with Hypopituitarism, pre g­nancy and progestational phase of menstrual cycle is suggestive. Similarly the association of hypertony with oestrogenic phase of post-menstrual period or oestrogenic treatment of en­larged prostate or after delivery is further corroborative.

Schonerl and Steinberg claim that the spinal fluid of rabbits contains two substances secreted by the posterior pituitary, one acting on parasympathe­tic and one on sympathetic, the former raising and the latter lowering the intra-ocular pressure. They also state that rabbits being a nocturnal animal the I.O.P. is said to increase during light and to fall during dark i.e. just the reverse of man (a diurnal animal). The knowledge of central or hormonal control, however, is still in a very ele­mentary stage.

  Relevant Anatomical Features of the Eye in the Study of Glaucoma Top

Secondary role is played by the anatomical varieties of the two scleral foramina viz. anterior and posterior. The chief characteristics of each are as follows: -

I. Anterior scleral foramen : Its size varies with the two main groups of glaucoma viz. angle closure and, open angle glaucoma.

(a) Angle Closure Glaucoma:

1. Cornea is small.

2. Anterior chamber is shallow.

3. Angle of the anterior chamber is narrow.

4. Iris is usually thick and more anterior, the roll of Fuchs is more highly developed.

5. Pupil is usually small and iris therefore has a firmer and larger contact with the lens

6. Lens is usually large.

7. Ciliary body is thick and hypertrophied and the attach­ment of iris to ciliary body is anterior.

8. Refraction is usually hyper­metropic.

(b) Open Angle Glaucoma:

The features are almost opposite to what are described above, except that in a small percentage the angle may be narrow but there too the root of iris is thin and there is no prominent roll of Fuchs. An angle less than 20 degrees is considered narrow. The angle opening may be of five grades : -

1. Wide open angle, ciliary body visible on gonioscopy, as well as other structures namely scleral spur, canal of Schlemn, posterior and anterior trabeculae and the Schwalbe's line.

2. Medium open angle : Ciliary body not visible but scleral spur and other structures noted above are visible.

3. Narrow open angle : here ciliary body and scleral spur are not visible but the trabeculae spe­cially the anterior trabeculae are visible.

4. Slit open angle : only line of Schwalbe is visible and the rest of the angle is obscured by the roll of Fuchs.

5. Closed angle : No details of the angle seen.

Narrow and slit types of angles are prone to angle closure, re­sulting in peripheral anterior synechae formation when the condition is called combined or mixed type of glaucoma, wherein open and closed angle mecha­nism operate together or the latter is superimposed on the former.

In a survey of 6000 normal persons it was found that 90% of the people had widely open angles incapable of closure, that only 10% had narrow anoles and of these only 2% were in critical danger of occlusion. The inci­dence of glaucoma as seen at Institute of Post-Graduate Medical Education and Research, Chandigarh, is shown in [Table - 1] below:­

The break-up of these cases of Glaucoma is shown in [Table - 2] where the angle closure of glaucoma accounts for 43.5% of the cases and open angle glaucoma constitutes 54.38% of cases.

A comparative incidence of primary Glaucoma from Gandhi Eye Hospital, Aliigarh and V. J. Hospital, Amritsar, is shown in [Table - 3] which almost con­forms to the patern seen at Chandigarh.

  Mechanism of Production of Angle Closure Glaucoma Top

In angle closure glaucoma, the role of the pupil is rather significant. Its anatomical features as outlined earlier in the text are distinctive and help in the mechanism of pupillary block which is a major factor in the patho­genesis of acute congestive glaucoma. With age, the lens and ciliary body both grow in size, the lens more so. This results in further narrowing of the anterior chamber and its angle. The iris is anatomically pushed forwards by the swollen lens. This results in a more intimate contact between the thick iris and the lens. The circum­lental space is also getting reduced because of the growing ciliary body and lens approaching upon it from the two sides. This eventually hinders the free flow of aqueous through the pupil and some of it may be dammed back and may push the periphery of the iris forwards (peripheral iris bombs) and may allow the scroll of Fuchs to come in contact with the lateral walls of the angle near the Schwalbe's line and thus further block the outflow. This sets up a vicious circle, the aqueous is retained in the posterior chamber which has become smaller and as the fluid is not accepted anteriorly it may seep into the vitreous which swells and thus pushes the lens and the ciliary body further forward resulting in further augmentation of the block. So long as the trickle of fluid from the posterior to the anterior chamber is maintained, the acute or hyper-acute episode may not arise but the moment the connection between the two chambers is broken or sus­pended, the aqueous in the recess of the angle of anterior chamber is ab­sorbed, a vacuum is created and the iris is actively sucked forward and the peripheral iris synechia (of course phy­siological) completes the closure of the angle and the acute or hyper-acute episode results. This is aggravated by emotional upsets which result in larger secretion of aqueous by the ciliary body or at least results in marked dila­tation of the rich vascular bed of the ciliary body resulting in its oedema and further pushing of the iris and ciliary body forward and diminished pumping action of the ciliary muscle. This vascular action is responsible for the fulminant attack of acute conges­tive glaucoma.

  Posterior Scleral Foramen and its Importance in Open Angle Glaucoma Top

The pathology in open angle type of glaucoma is mainly confined to the posterior part of the eye i.e. the poste­rior opening, whereas in angle closure glaucoma the main pathology is wit­nessed in the anterior part. Both these openings are situated at the transitional sites, liable to various malformations or mal-adjustments peculiar to such areas.



1) Its size varies with the size of the eye, a small eye has a narrow posterior scleral foramen and the large eye has a wider foramen.

Inner dimensions 1.5 mm to 2 mm

Outer dimensions 2.5 mm to 3.5 mm

[Figure - 2]

2) Lamina Cribrosa is 0.7 mm behind the retina in hyper-metropics and 0.4 mm in myopics.

3) The physiological cup may be just evident or may be very large.

4) The optic nerve fibres may be crowded together or there may be no suggestion of over-crowding.

5) The bulk of optic nerve fibres ascend on the nasal side of the pos­terior-scleral foramen and the central retinal vessels ascend with them. The vascular supply of optic disc, lamina cribrosa and of the optic nerve just posterior to lamina cribrosa is very in­adequate. Neither the central artery of the retina nor that of the circle of Zinn supplies even a branch of third degree i.e. an arteriole to it. As proved by Das and Singh (1963) the main supply is through capillaries though rarely a small branch may be supplied by the central retinal artery. These vessels are liable to vascular sclerosis in this disease and the earliest effect will be noticeable in this spot which will suffer from full-fledged effects of vascular ischemia. There is no collateral cir­culation either. The vessels are too small to stand any rise of pressure. The result is:­

i) collapse of vessels and resultant atrophy of the optic nerve fibres,

ii) loss of capillary stud on the optic disc, and

iii) degeneration of glial tissue.

This atrophy of the nerve and glial tissue extending beyond the lamina-­cribrosa results in atrophy and shrink­age of axons with no anchorage pro­vided by glial tissue. This shrinkage leads to pulling back the optic disc and along with it the lamina cribrosa. It is, therefore, quite conceivable that whenever one finds a good pink optic disc it means that the vascular supply is adequate and that ischaemia is not there with the result that the disc can stand increase in tension. The collapse of capillaries with rise of tension may lead to ischaemia and anoxia. This is a disease of vascular sclerosis and may also be present in ciliary vessels and also the 3 plexuses of the corneo­scleral junction. The aqueous may, therefore, be produced either normally or may be slightly less than normal but there is no vascular instability and there is no question of hyper-secretion episodes. However the absorption through the three plexuses, deep, intra and episcleral, may be less with the result that although spaces in the trabeculae or the canal of Schlemm may not be affected, the drainage is not adequate. This defective absorption, therefore, is one main cause and its site may be internal or external to the Schlemn canal deuending on whether the pores or the collector channels i.e. the three plexuses (deep, intra and episcleral) are affected. Experimentally glaucoma has been produced in rabbits by closing the collector channels che­mically by the injection of phenol in 5% almond oil in all the four quad­rants of corneo-scleral junction. The same sclerosis may be present in anterior ciliary veins and venae-vorti­cosae.

  Etio-Pathogenesis of Congenital and Infantile Glaucomas Top

The development of the angle of the anterior chamber takes place from 25 mm stage of the embryo. At this stage there is a relatively deep anterior chamber, having an apparent angle far anterior to its final position. The margin of the optic cup is still further behind the circulus arteriosis iridis major, the canal of Schlemm and scleral spur are not developed. The angle is still far forwards to the cir­culus arteriosus. The angle is, however, extending backwards and the margin of the cup forming the ciliary body and iris cup is growing forwards till the final position of the angle is establish­ed, at the seventh month, when the canal of Schelmm and scleral spur are well anterior to the angle of anterior chamber. The development of the angle can arrest at any stage. Due to failure in cleaveage of the mesodermal tissue occupying the angle or say mal­absorption or atrophy of mesodermal tissue resulting in faulty backward movement of the angle of the anterior chamber results in forward insertion of the longitudinal and circular fibres of the ciliary muscle into the trabecular fibres. Contraction of these fibres, in­stead of opening the trabecular spaces and the canal of Schlemm, will rather compress them thus defeating the very purpose for which this muscle was created. The successful goniotomy operation results in dislocating back­ward the muscular insertion and thus increasing the aqueous outflow. This faulty insertion may result in infantile glaucoma at birth or coming up within the first year of life if the outflow is markedly inhibited. But if the outflow is partially impeded the eye-ball may gradually yield to slight rises of pres­sure at that tender age, resulting in progressive myopia. Later on in ado­lescence the eye-ball may refuse to yield further with the result that one may get juvenile glaucoma with myopia.

Cases have been seen in whom there is buphthalmos in one eye and only cupping of the disc with apparently normal other eye, but when tension is taken it is fairly high, say about 35 to 45 mm. In infants or young children before 5, one eye may show buphthal­mos, the opposite eye cupping with normal tension as the eye is still yield­ing to the small rises in pressure. Suspicion is aroused when there is a progressive myopia with marked physiological cups, or there may be loss of capillary stud and early cup­ping. Such a patient may come to the hospital with a complaint of dective vision only. There may be a slight increase in tension or it may be normal.

  Management Top

Angle Closure Glaucoma

Angle closure glaucoma may be called surgical glaucoma and is a dis­ease of symptoms which bring the patient early to the surgeon to render the early effective treatment and save the patient's vision which is of para­mount importance to him.

There are 3 phases of this disease: -

1) Acute angle closure glaucoma,

2) Sub-acute angle closure glau­coma,

3) Chronic angle closure glaucoma.

The patient is usually brought to the hospital in extreme agony. With the modern osmotherapy, carbonic anhy­drase inhibitors and miotics locally it is possible to break this pupillary block and restore normalisation of tension. If the patient comes early the angle is free of synechiae but if he has come later say after 48 hours or so, some of the adhesions though soft may remain behind leaving a patient pre-disposed to further onset of similar or milder episodes.

A sub-acute attack has the same mechanism but of a lesser intensity. If the sub-acute or acute attacks are not properly treated the result is a chronic malady, in which various degrees of rise of tension will permanently persist with increasing adhesions in the angle till it is completely blocked and ab­solute glaucoma supervenes. The pre­cipitating factor in most cases, there­fore, is vascular crisis of emotional, hormonal or allergic nature in which local and central controls play a pre­dominant role However dilatation of the pupil by any cause such as mydria­tics, dark room, prolonged near work in comparatively less illuminated sur­roundings may result in a sub-acute or acute attack.

The fulminant attack may lead to segmental necrosis of the iris which later on may develop into patchy degeneration and irregular dilatation of the pupil. This dilatation of the pupil may sometimes prove fortuitous in that it may break the pupillary block per­manently. This type of glaucoma in its acute crisis will usually yield to the treatment mentioned above but it is a surgical problem and with a mini­mum of surgery i.e. peripheral iridec­tomy will give cent-per-cent cure pro­vided : -

i) the angle opens completely with medical treatment,

ii) synechiae are absent,

iii) tension is normalized and stays normal with medical treatment for 48 hours.

During this period all investigations such as gonioscopy and tonography and fundoscopy are done. This case is ideal for peripheral iridectomy in the interval period which is utilized for proper investigation.

If after 8 to 10 hours the patient has a tendency to a rise of tension, opera­tion need not be delayed and whatever investigations are possible be done.

In case miotics, osmotherapy and Diamox fail to normalize the tension but it does not go beyond 30 mm of mercury, peripheral iridectomy will still restore normality but miotics may also be needed post-operatively. This operation is not an interval operation but the results with operation and miotics are good. If the tension stays above 30 mm and there are a few adhesions, paracentesis may be done to restore normality and if this helps, peripheral iridectomy and miotics may be instituted but sometimes an interval fistulising operation such as iriden­cleisis or Scheie's sclerectomy with cauterisation of the margins of wound may serve the purpose.

In some severe cases this operation may fail. It will have, however, served some purpose as peripheral iridectomy has established a direct passage be­tween the anterior chamber and pos­terior chamber and has relieved pu­pillary block partially. A second ope­ration is, however, called for.

Rarely a fulminant case may result in complete blindness inspite of all the treatment undertaken for its relief if the patient has come late. There may be partial relief of tension but the vision may not be there either due to macular hemorrhage or damage to the already severely inadequate capillary supply of the disc, lamina-cribrosa and the immediate portion of the extra bul­bar part of the optic nerve.

The sub-acute attack will respond to the medical treatment but one should not overdo it and surgical treatment be instituted as soon as the eye is quiet. Peripheral iridectomy is the treatment of choice but sometimes iridencleisis is necessary.

In chronic angle closure glaucoma usually the medical treatment will not result in opening of the angle and a fistulizing operation will be the answer.

The modern trend is towards iriden­cleisis or Sheie's sclerectomy but a careful trephine should produce the same results. The various modifications of iridencleisis are a testimony to the poor results of this operation or for that matter of any other filtering ope­ration. Failures from 10 to 25%, are reported in competent hands. As in this variety patient reports to the hos­pital early, better prognosis with all fistulizing operations can be predicted. Even 90% results have been reported. More anterior the incision in Corneo Sclera, the better are the results as it avoids corneo sclera (really a part of uvea).

Treatment of the Fellow Eye

Some Surgeons always insist on prophylactic iridectomy in the second eye in angle closure glaucoma espe­cially when they find some symptoms suspicious of glaucoma or tonography or provocative tests warrant it. It is better to watch the result in the dis­eased eye and postpone the operation in the second eye for a week or so. I n this country the fellow eye may be operated at the same time, as the pa­tients hardly ever return in good time.

Chronic Simple Glaucoma

It is a betenoir of the ophthalmo­logist. It poses some of the most trying problems. Some of the normal eyes may be diagnosed as glaucoma and some of the y glaucomatous eyes may, for some time be diagnosed as normal. It is the most elusive type of eye dis­ease. Its diagnosis is late, prognosis is poor, and surgical treatment not un ­often unsatisfactory. It is a disease that runs a sinister and insidious course with no warning to the patient but with the unmistakable signs in the late stages when an irreparable damage has already been done to the eye. It may take 10 to 15 years to develop clinical signs in the optic disc. The patient usually reports with defective vision or for some other eye disease when an observant ophthalmologist has noticed a nasal shift of vessels or loss of colour or early cupping. It is a bilateral dis­ease. The patient may be hypermetro­pic or myopic, male or female, with shallow or normal anterior chamber, with normal or a little raised tension, needing a rapid change in his near glasses and has defective dark adapta­tion. The patient has become conscious of his eyes. A little later there may be discomfort or brow ache after work. The younger patients may see colour haloes round the light and may find cinema hall very discomfortable after seeing the picture.

The signs in the fundus as noted earlier are late and are very important from prognostic point of view, but de­finitely indicate that the patient had incipient glaucoma for atleast 5 years to produce nasal shift of blood vessels. So one must employ other ancillary methods for its early diagnosis. Tono­graphy plays a valuable role in this re­gard. Unfortunately in our quest for early diagnosis we have produced an­other type of glaucoma known as tonometric glaucoma. The tonometers at various hospitals are hardly calib­rated properly and there is no central organisation where this work could be undertaken although in many countries this is possible.

Tonometers are not manufactured in this country and the various qualities available are not all genuine. One who practices tonography should have at least 3 tonometers. Two should be in regular use, one acting as a check on the other and the third one kept in reserve to standardise the other two tonometers in daily use. The electronic tonometer and the applanation tono­meters are not readily available and may be used mostly for research pur­poses. Even in every ophthalmic hos­pital there should atleast be two tono­meters and readings be taken with 2 weights atleast before a judgment of glaucoma is given. There is no urgency in making a diagnosis of chronic sim­ple glaucoma if you are in doubt. To this may be added the variety of iatro­genie glaucoma resulting from use of medicines systemically for treatment of medical diseases e.g. prolonged admi­nistration of high doses of cortico­steroids and peparations containing belladonna alkaloids. The mechanism of causation of glaucoma in the former is not yet clear. It may be due to de­creased absorption due to constriction of vessels, or due to its effect on mucopolysaccharides in the angle of the anterior chamber, but the latter is due to angle closure caused by dilata­tion of pupil in the already pre-dispos­ed eyes. There may be rise of intra­ocular pressure when ganglion block­ing drugs are used for lowering pres­sure in hypertension as it interferes with the nutrition of the eye due to lesser blood flowing through the scle­rosed arteries.

  Treatment Top

With no satisfactory prognosis, the surgeon is chary of operating especially when surgery has its hazards and may not offer a better alternative to medical treatment.

If every eye is checked for tension with tonometer we may suspect this glaucoma in early stages and with tonography, gonioscopy, provocative tests and scotometry may not only confirm our diagnosis but may also be able to evaluate the medical treatment. If the patient in spite of medical treat­ment is losing field of vision and visual acuity and is not getting a normalisa­tion of tension, medical therapy needs implementation by the exhibition of stronger medicines or better combina­tions. If even this medical treatment fails, surgery should not be delayed.

  Medical Treatment Top

i) Medical treatment consists in the administration of vascular dilators with miotics (mild ones). There is no place for strong miotics in the early stages. Pilocarpine alone 1-2% or combined with epinephrine 1-2% 2 to 3 times a day should normalize the tension and check the deterioration of field of vi­sion. This treatment is the treatment of choice if tension can be kept at 15 mm of Hg.

ii) If the above treatment fails, 3 to 4%, pilocorpine with or without epine­phrine 3 or 4 times daily may help. If the tension is normalised no surgery is indicated.

iii) If the above methods fail, stronger miotics i.e. physostigmine, phospholine iodide, demecarium bromide, D.F.P. may be tried provided the angle is wide as otherwise the congestion produced may set up pupillary block resulting in angle closure.

iv) If Diamox alone or along with other milder miotics is needed, tension may be normalized but surgery can­not be held back for long.

v) In old people above 60 to 65 years of age, medical treatment of various types may help them as the life ex­pectancy is not more than 5 to 10 years in such cases. However in younger patients surgery is the answer.

  Choice of Surgery Top

For the first two varieties of angle, trephining offers a better choice. You may combine it with sclerencleisis [Figure - 3] to ensure not only an addi­tional channel for normalisation of tension but also to provide protection to the conjunctival flap as well. Two filtering sites are thus available.

2) For the 3rd and 4th varieties of angles, fistulizing operation such as Iridencleisis if the Iris is not atrophic or Scheie's Sclerectomy with cauterisation of the margins of the wound will serve the purpose.

Pre-operatively all miotics must stop 48 to 72 hours earlier so that all sources of irritation and congestion are eliminated. Diamox has to stop 24 hours earlier as there is danger of flat anterior chamber afterwards.

The prognosis is excellent if the disc is pink, fields are good and the vision also is 6/ 12 or above. The prognosis is good even if the vision is 6/ 12 or high, cupping is mild, fields show Bjerrum Scotoma above or below but shows improvement with vasodilators and normalisation of tension.

The prognosis is fair if the vision is still preserved but the fields show Ronnes' step but no ring scotoma is present.

The prognosis is poor if ring sco­toma has already formed or Bjerrum has broken through to the periphery.

A tubular vision is considered by some as contra-indication but as the patient is sometimes very keen, sur­gery may be tried provided the posi­tion is explained to the patient. A vision of 6/60 offers a very poor prognosis.

  Congenital and Infantile Glaucoma Top

Infantile Glaucoma reeds goniotomy and gonio-puncture which may be combined at the very first sitting and can be repeated if required. In failed cases Scheie's operation is helpful. Corneo-scleral trephine or Iridencleisis usually do not prove successful. Juve­nile Glaucoma usually needs a fistu­lising operation.

  Summary Top

Two new concepts have been pre­sented for the solution of the etiopatho­logical explanation of primary Glau­coma: -

1) that Limbus is predominantly uveal in nature having an anato­mical structure resembling the ciliary body and not the corneo­aclera, or, as it does not partake of the character of either cornea or sclera and, therefore, is ac­tively associated with aqueous absorption and not a passive drainage channel.

2) the vascular supply of the optic disc Lamina Cribosa and the optic nerve fibre immediately behind the Lamina Cribosa is extremely poor and is mainly capillary in nature. Therefore most vulnerable to slight rises of pressure or arterio - sclerotic changes.

3) A brief resume of the manage­ment of the various types of Pri­mary Glaucoma is given.

4) A modification of sclerencleisis operation combining it with corneo-scleral trephining is des­cribed.[4]

  References Top

Berens (1949) The Eye and Its Diseases. Page 103. Saunders Company. Phila­delphia.  Back to cited text no. 1
Carpenter R. L. (1957) Amer. J. of Ophthal. 44, 220.  Back to cited text no. 2
Schmirl E. and Steinberg B. (1948) Amer. J. Ophthal. 31, 1097.  Back to cited text no. 3
Singh S. S. and Das R. (1963), Brit. J. Ophthal. 47, 651.  Back to cited text no. 4


  [Figure - 1], [Figure - 2], [Figure - 3]

  [Table - 1], [Table - 2], [Table - 3]


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