Chapter V Glaucoma | Operating Microscopes

Glaucomatous affections are characterized by increase of the intraocular tension, which excess the pressure gives rise to the following phenomena:

The eyeball becomes harder and firmer; the existence of this hardness mat be proved by the sense of touch or by various instruments, such as the tonometers of donders, dor, weber, Priestley Smith, Maklaloff, but these instruments are not in very general use, because they are somewhat difficult to apply.

The anterior chamber becomes shallower, because the iris and lens are pushed forwards. The lens may become less convex by the tension of its ligament, and this condition explains the fact that the eye becomes slightly hypermetropic. Less frequently it becomes myopic by the advancement of the lens.

the ciliary nerves lose their conductility from the excessive pressure, and thus ensue dilatation and immobility (presbyopia and any latent hypermetropia becoming manifest), and anesthesia of the cornea. This membrane shows more or less insensibility on being touched with a feather or small roll of paper, which is the article generally used to make this investigation.

The strain on the ciliary nerve also explains the violent neuralgic pains which accompany any sudden increase of intraocular pressure. The proof that we have here the true explanation of his phenomenon is to be found in the fact that the pains disappear immediately on our performing paracentesis of the anterior chamber (von Graefe).

The posterior circulation of the eye becomes disturbed, especially in the vasa vorticosa, which are compressed as they pierce the sclerotic. In consequence of this mechanical obstruction the venous blood from the eye is carried to the anterior ciliary veins, and thus we find the subconjunctival veins choked with blood, tortuous and forming many anastomoses.

the arteries of the optic papilla are seen to pulsate, either spontaneously or on the slightest pressure on the eyeball. The reason of these pulsations, which may also be produced of firmly compressing a normal eye, must be sought in the resistance which the tension of the eye gives to the circulation of the blood.

The flow of blood into the eye can only take place when the propelling power is greater that the intraocular pressure. In the normal condition, the arterial pulsations characteristic of glaucoma do not exist, because the tension of the arterial system is greater that the intraocular pressure, consequently the blood enters the eye in a continuous stream.
The optic papilla is pushed back through the opening in the choroid and sclerotic ring, sometimes even behind the level of the sclerotic (Fig.81). The intraocular pressure acts, it is true, with equal power on any point of the membrane which encloses the vitreous body; but the optic papilla; less resisting, yields more readily, and the lamina cribrosa, with the vessels and nerve fibres, is pushed backwards (excavation of the papilla).

At the papilla we therefore find a cavity with an overhanging superior margin, the bottom of which is formed by the lamina cribrosa and the optic nerve fibres and vessels. To the ophthalmoscope the appearance of glaucomatous excavation is very characteristic (Fig.82); the margin of the excavation, with perpendicular edges, is clearly seen, and hides from us the peripheral portion of the bottom, which it overlaps. Thus, on following the course of the vessel from the point where they emerge from the optic nerve, we see them at first running along the cavity and suddenly interrupted when they reach the periphery. The retina vessels, when they reach the margin of the papilla, stop as if cut short, or go over it like a hook. There is thus an apparent solution of continuity between the papilla and those of the retina, since we cannot see that past of the vessel which is on the side of the excavation and hidden by its border.

To make sure of the difference of level between the retina and the bottom of excavation, we must give slight lateral movements to the bi-convex lens generally used in the indirect method. We then notice that the margin of the excavation, which corresponds with the level of the retina, comes in front of the margin of the papilla. On examining in the same way a vessel in the fundus of the eye, we find that the portion of the vessel situated on the retina undergoes a greater displacement than that on the bottom of the excavation. This difference (parallactic displacement) is greater in proportion to the dept of the excavation.

Besides these phenomena, we also observe that the point of emergence of the vessels of the optic nerve is nearer the margin of the papilla, whilst in the normal state it is placed almost at the centre. The veins are engorged and flat, but the arteries are diminished in caliber by the resistance which they meet as they emerge. Again, we should mention the peculiar appearance of the papilla, on which we can easily distinguish the meshes of the lamina cribosa, and the white ring which surrounds the margin of the excavation. This ring is due to the atrophy of the choroid in the neighborhood of the optic nerve (Schweigger).

It is important to distinguish glaucomatous excavation from physiological and atropic excavations. Physiological excavation (fig.83), as a rule, only affects the center of the papilla, round the point of emergence of the vessels, and never invades the entire nerve as does the glaucomatous excavation. On one side or another it is always separated from the margin of the papilla, but gradually rises to the level of the retina, its margin is not interrupted-at most they are slightly bent. It is not extremely and no other symptom of glaucoma. I have myself seen a very striking example of it with full vision which never ended in glaucoma. Probably the effect is congenital.

As to the functional conditions of refraction which have already been mentioned, the ischaemia of the retina and the compression of the optic nerve give rise to diminution of the central vision, and to an irregular contraction of the field of vision, beginning almost always with the nasal side. Perception of colors, as a rule, remains normal, but the sense of light seems to become weaker. Patients affected with glaucoma often complain of colored circle round the flame of a candle, the most external bluish-green.

This phenomenon has been attributed to irregular refraction of the lens, rendered more sensible by the dilatation of the pupil (Donders). It may also depend on imperfect transparency of the cornea, the aqueous or the vitreos. Moreover, this phenomenon also occurs in some affections of the cornea where there is no glaucomatous complication.

The different manifestations of increased intraocular pressure which we have just described fall into one of two groups, according as the pressure increase suddenly, or by slow degrees. By this we may distinguish acute glaucoma.

A. ACUTE GLAUCOMA.

In the majority of cases (70 to 75 per cent.), acute glaucoma is preceded by certain very characteristic prodromata. These symptoms consist, in the first place, of a sudden diminution in the power of accommodation (presbysopia increasing, or a latent hypermetropia becoming manifest), in the appearance of colored circle round flames, in temporary difficulties of vision, which may last from a few minutes to several hours and during which the patient sees objects as if though a fog.

The phenomena chiefly occur when the head is congested, as after taking food, after a sleepless night, emotions, etc. the patients also sometimes complain of acute pain in the bones forming the orbit. If, at the moment when these phenomena occur, the eye is examined, we find a slight haziness of the cornea and aqueous humor, changing the color of the iris and the black reflection of the pupil, which is somewhat dilated and sluggish. These symptoms soon disappear, and everything again assumes the normal condition. Then, after a few weeks or months, they reappear, and so return after intervals of complete remission. This return of the eye to its normal state is characteristic of the incipient period of glaucoma, which may last one, two, or even more, years. Yet glaucomatous attacks may supervene suddenly, without any of the forwarnings which we have just described. It sets in during the night, and is characterized by acute pain in the eye, radiating to the head, with well-mared subconjunctival injection, lachrymation and chemosis.

The aqueous humor is muddy, and sometimes forms deposit on the posterior surface of the cornea; the iris is discolored, the pupil irregularly and widely dilated, giving a grayish-yellowish reflection. The eyeball becomes exceedingly hard, and the cornea insensible to touch.

Vision is more or less affected; it may be almost entirely destroyed, so that the patient cannot bee the brightness of a lamp placed before the eye; or it may be partially preserved, the patient being able to distinguish night from day. Photopsia is almost always present.

During the glaucomatous attack we are unable to make an ophthalmoscope examination, because of haziness of the cornea, aqueous and vitreous.

The beginning of the disease is marked by a general febrile condition, sometimes with obstinate vomiting, which may cause us to think that we have to deal with a gastric affection or severe migraine.

Rarely does a first attacked of glaucoma completely and permanently destroy vision. As a rule, after being present for a time varying from a few hours to a few days, the symptoms which we have enumerated diminish in intensity, by slow degrees vision results, and after some time there remains no trace of the attack except a slight increase of tension, alight diminution in the acuteness of central vision, and a slight contraction of the field of vision.

This state of matter may last for weeks of months, but suddenly another glaucomatous attack supervenes, similar to the one which we have just described, and again followed by a remission of all the symptoms. Then the attacks become more and more frequent, and the intervals between them shorter.

After each attack the loss of vision increases and portions of the visual field left intact by the previous exacerbation become more and more involved. The tension of the eyeball gradually increase, the cornea by degrees loses its transparency and sensibility, that anterior chamber becomes shallower, the iris is discolored, both iris and lens are pouched forward towards the cornea. The pupil becomes very large and fixed, and presents a grayish or greenish reflection.

If during one of the periods of remission, after a few such attacks, we make an ophtalmoscopic examination, we find a diffuse haze of the cornea and vitreous humor, the characteristic alternations of the optic papilla (see p.245), arterial pulsation and, exceptionally, ecchymoses of the retina and choroid.

Even after vision is completely destroyed (absolute glaucoma), the glaucomatous process may make progress, leading to the disorganization of all the structures of the eyeball. The cornea still further losses its transparency and becomes the seat of ulceration; the tissue of the iris continues to atrophy till it is opaque, soften and swells, and there supervenes hemorrhage into the anterior chamber, the vitreous body, and the parenchyma of the deep structures of the eye; this hemorrhage still further increase the excessive tension of the eyeball. The dirty-colored, grayish sclerotic at last yields to the pressure, forming ectasie in the equatorial region and in the anterior portions of the eyeball.

The eye may remain for some length of time in this condition, hard as a piece of marble, and the conjunctiva furrowed with the large ciliary veins which anastomoses around the cornea. In other cases, there are signs of a slow atrophy, which may also take place as a consequence of purulent choroiditis or after separation of the retina (Arlt, Schwegger).

Still we must not think that all eyes affected with glaucoma follow precisely the course that has just been describe. Acute glaucoma, losing its intermittent character and even the most of its inflammatory symptoms, may become transformed into chronic glaucoma.

B. CHRONIC GLAUCOMA

We may distinguish two forms of chronic glaucoma-

Chronic glaucoma with inflammatory symptoms.
simple chronic glaucoma

chronic inflammatory glaucoma is distinguish from the acute variety by the uninterrupted presence of the characteristic symptoms, which are periodically increased by slight inflammatory exacerbations, it begins with the prodromata common to it and to acute glaucoma, and these first symptoms become more and more pronounced, and finally become permanently and progressively established.

The cornea loses its brilliance and its sensibility, the anterior chamber becomes shallower, the aqueous becomes slightly turbid, the iris and lens advance towards the cornea, the sclerotic assumes a grayish tint, and the subconjunctival veins increase in number and volume. The eye becomes more and more hard till it feels like a piece of tone. On ophtalmoscopic examination, we find progressive excavation of the papilla with arterial pulsations. The vision continues to decrease, the visual field becomes contracted, generally from within outwards, and ultimately the patient becomes quite blind.

In the course gradual and slow progress, which may occupy a very variable space of time, acute exacerbations supervene, during which the inflammatory symptoms becomes more marked. The patients then complain of very acute ciliary pain. The hardness of the ball suddenly increase, the cornea becomes perfectly insensible, the dilatation of the pupil is grater, as is also the turbidity of the cornea and aqueous humor, and the patients sees everything as through a thick fog.

These exacerbations sometimes supervene without any obvious cause, more frequently when the head is congested by some passing condition. They may disappears in a few hours or last for several days, and the eye regain its previous condition, except that there is a greater diminution of the visual acuteness than the chronic disease would give rise to in the same length of time uncomplicated with a exacerbation.

It may also happen that the course of chronic glaucoma is suddenly interrupted by a true sub acute attack, and that afterwards it maintains the character of acute glaucoma. It may thus pass through all the stages which we have already described, and end in the same way as acute glaucoma.

Cases have also been observed in which the chronic glaucoma has lost all its inflammatory symptoms, and assumed the aspect of simple chronic glaucoma.
Simple Glaucoma.- in this variety of glaucoma the inflammatory symptoms are entirely absent, and the appearance of the eyeball does not materially differ from that in the normal eye. At most, we may find, after some exciting cause, a slight turbidity of the aqueous humor soon disappearing. In short, the patient does not complain of any pain, and the exterior of the eye preserves its natural appearance.

It is often difficult in the early stages, and even throughout the disease, to decide by the sense of touch whether the eye be harder than usual. This is all the more difficult that the physiological tension is subject to considerable variation.

To the ophthalmoscope the media of the eye seem to be completely transparent; but we find the characteristic excavation of the papilla, and the arterial pulsations, which are either spontaneous, or easily produced by slight pressure of the fingers on the eye.

Some time must elapse before the excavation is produced. The nerve fibres accommodate themselves for a certain length of time to the pressure (excavation of the papilla with out disturbance of vision), and do not really suffer till the pressure has exceed a certain amount. They then begin to artrophy, and the papilla takes the white color of atrophic degeneration.

As to the vision, the visual, the visual field begins to contract generally on the internal side, and this contraction gradually extends towards the center and round periphery. The central visual acuteness may remain for a long time relatively good, until the defect in the visual field end in complete blindness without the patient experiencing any pain, only the eyeball being a little harder than normally and the optic papilla excavated.

The progress of the disease is slow, and generally lasts for several years; it usually affects both eyes successively. It may also happen that simple glaucoma suddenly changes its character and becomes more like inflammatory chronic, or even acute, glaucoma.

Prognosis.- this disease was considered from the earliest times an incurable one, which sooner or later must produce absolute blindness.

The prognosis of glaucoma has considerably changed since the fortunate discovery by von graefe, that iridectomy is a sovereign remedy. The earlier in the course of the disease this operation is performed, the more likely it is to prove efficacious. If performed during the period of prodromata, it cuts short the disease and preserves, or even improves, the vision.

In acute glaucoma, complete restoration is obtained if the operation be performed at once; at a later period, if excavation of the papilla and marked contraction of the visual field have already taken place, we can only hope to preserve the vision in the same condition that exists at the time of operation. During the first few weeks after the operation, the vision may somewhat gain in acuteness and the visual field extend. When the eye has been blind for a length of time, operation can only be of service in relieving the patient of severe ciliary pain.

In chronic glaucoma, the operation arrests the progress of the disease, and the functional condition of the eye remains as it was at the time of the surgical interference. Nut, if the iridectomy is performed immediately after an acute exacerbation occurring in the course of the chronic variety of glaucoma, the vision returns to the condition in which it was before the last attack.

In simple glaucoma, the effect of operation (iridectomy or sclerotomy) is much less sure. It sometimes preserves the vision in status quo; more rarely it improves it. On the other hand, however, cases of simple glaucoma have been observe in which the operation did not arrest the progress of the disease; sometimes it has only arrested it for a time, and has had to be repeated; lastly, operation has also been fallowed by an immediate aggravation of the disease. Without considering the diminution of the vision due to the astigmatism, which can be corrected by cylindrical lenses, following the operation, it happens, in cases where the contraction of the field of vision has attained nearly the point of fixation, that the central vision is entirely lost after and notwithstanding the operation. It may be that in the last phases of the disease the operation does not prevent the amount of vision from diminishing, because the atrophy of the nerve fibres, produced by the compression to which they have been subjected, proceeds even after its exciting cause has been removed. Apart from such facts, there are other cases in which the operation, performed when there only remain as small portion of the visual field to the upper and outer aspects, has preserved this remaining portion for many years.

Etiology.- although at the present day it seems beyond all doubt that glaucoma consist of an increase of the intraocular tension, opinion is divided as to the cause of this increase. According to von Graefe, it must be sought for in an inflammatory alternation of the choroid and iris (serous irido-choroiditis), with hypersecretion of serous fluid, which increase the volume of the vitreous body.

According to Donders, this hypersecretion is due to an alternation in the nerves which regulate the secretion, so that the cause of the disease is external to the eye. Cusco and Coccius hold that the starting point of glaucoma is an inflammation of the sclerotic; the thickening and secondary contraction of the sclerotic tissue furnishing in such cases the mechanical cause of the intraocular, compression. Again, Weber and Knies say that there are anatomical changes in the tissues surrounding the canal of Schlemm and Fantanas’s space, which, by compression and obturation of the so-called angle of filtration, diminish or prevent the exist of the intraocular fluids; and de Wecker has stated his opinion that the efficacy of the operation in glaucoma is due to the formation of a cicatrix which promotes the filtration of these fluids.

Brailey, having examined a large number of glaucomatous eyes, has not always found the anatomical changes stated above, and has even found them, as have Pagenstecher and Schnabel, in cases when the tension of the eyeball was diminished; he regards as a chief factor in the pathology of glaucoma the distention of the blood-vessels, especially of the ciliary region, and the thinning of their walls; these conditions producing the increase of the quality of blood in the eyeball, and the hypersecretion of the intraocular fluids. Priestlet Smith believes that progressive increase in the size of the lens, which he has ascertained to occur as life advances, diminishes or obliterates the interval between the margin of the crystalline lens and the ciliary processes, blocking the passage of the intraocular fluids, and giving the starting point of glaucoma. Ulrich considers this passage impeded by alteration of the iris, and Stilling by alternation of the optic nerve.

Whatever be the difference theories as to the atiology of glasucoma and in our opinion this disease may be due to each of these causes in isolated or combined action, in so far as they hypersecretion or abnormal retention of the intraocular fluids, or both of them- age, and the rigidity of the sclerotic increasing with it, certainly occupy an important past. This disease is rarely found before the age of thirty, except in children with keratoglobus, and it most frequently occurs in persons of from fifty to sixty years of age. Gout and arterio-sclerosis seem to predispose; violent emotion, sorrow and depressing influences in general have been notice to precede the onset of acute glaucoma. Instillation of atropine in a predisposed eye is liable to bring on an acute attack. We have observed several cases of the same effect produces by general contusion of the eyeball with mydriasis.

Glaucoma seems sometimes to be hereditary, especially in its inflammatory varieties (von Graefe).

Lastly, not unseldom do we find glaucoma occurring in eye suffering from other diseases; and this variety, the symptoms of which are exactly the same as those of glaucoma in general, has received the name of secondary glaucoma.

In this complication we must distinguish those cases in which the primary disease predisposes to a glaucomatous attack, from those in which the glaucoma supervenes in a disease eye which would ultimately have become glaucomatous even if otherwise healthy. In the first group we must include all staphylomatous affections, in which a part of the envelope of the eye has yielded to the intraocular pressure- for example, staphyloma of the cornea, or, less frequently, of the sclerotic. In these diseases it may happen that the resistance of the surrounding membranes is increased with age, whilst the internal pressure remains the same. The pressures then acts on the weakest part, which corresponds to the optic papilla. Other affections of the cornea which become but seldom complicated with glaucoma are- diffuse keratitis, riband-like transverse infiltration, certain varieties of wide ulceration, and herpes cornea.

We should also here mention cases in which the iris or choroid is subjected to prolonged irritation, as when there is a cicatrix with adhesion of the iris, or when, after an injury of the lens capsule, the lens is increased in size by the swelling of its cortical substance, and thus processes on the iris. Again, after dislocation the lens may act as a foreign body and irritate the structures with which it is in contact; for the same reasons tumor of the choroid are sometimes accompanied with glaucoma.

We would also mention serous iritis and posterior synechie; in complete annular synechia the communication between that anterior chamber of the eye and the vitreos body is interrupted, so that the fluids accumulate behind the iris and cause an abnormal tension.

In all these cases glaucoma is more easily established the greater the resistance of the sclerotic, and the less it yields to the intraocular pressure from loss of elasticity, as in old and rheumatic people.

Hemorrhagic Glasucoma.- retinal hemorrages are sometimes followed by acute or subacute glaucoma, although no other relation can be traced between these two disease than those anatomical changes in the blood-vessels (arterior-sclerosis) which are the chief factors of both. Iridectomy in general seems of no avail in this form of the disease.

Treatment.-Our treatment is almost exclusively limited to the operation of iridectomy, which, according to von Graefe’s great discovery, permanently diminishes the increase intraocular pressure. Puncture of the sclerotic with exit of some vitreous (Mackenzie, 1830), paracentesis of the anterior chamber (Desmarres, 1841), diminish the pressure only temporarily, but donot prevent the progress of the glaucoma. Blood-letting and medication are of absolutely no use; and subcutaneous injections of morphia are only beneficial in so far as they soothe the pain for the time being till we are ready to operate.

Instillations of eserine (Weber, Laqueur) and polocarpine exercise an important influence on the diminution of intraocular tension. These alkaloids should be employed when we have reason to fear the onset of a glaucomatous attack (period of prodromata); when, in a glaucomatous attack, we are obliged to delay operation for some good reason; when the operation has given an insufficient result; or in cases of hemorrhagic glaucoma, in which one eye is already lost by glaucoma, freed of its glaucomatous symptoms by regular instillation of polocarpine; the visual acuteness, as also the field of vision, being greatly improved, and this improvement being maintained.

As to the method of performing the iridectomy, we would refer the reader to the article on iridectomy. Eserine or polocarpine have to be used previously in order to contract the pupil. The iridectomy must be made in the periphery, and a wide portion of iris must be removed.

According to the rules already laid down in the chapter on iridectomy, the best position for this excision is directly upwards or directly downwards. It is of importance during the operation to make the escape of the aqueous humor as slow as possible, for, if the diminution of tension be too sudden, we may have retinal hemorrhage, as has been observed after the iridectomy for glaucoma. After the operation, we must pay special attention to the consistence of the eyeball, the formation of the anterior chamber, and the process of cicatrisation.

Not unfrequently we find, on the day after the operation, a certain degree of tension, which gradually disappears in the course of a few days. This takes place when the formation of the anterior chamber is slow, allowing the iris to be brought into close contact with the cornea.

The use of eserine and perfect rest are then absolutely necessary, till the internal pressure is lowered to what it generally is after an iridectomy, and till the anterior chamber is re-established. When the eyeball preserves a marked hardness, even immediately after the operation, it is better not to use a pressure bandage, but merely to close the lids with strips of adhesive plaster (von Graefe). When there is pain, even although not severe, morphia must be administered by subcutaneous injections in the temple, or we may give chloral hydrate internally. Von Graefe was the first to describe a peculiar form of cicatrisation which is occasionally seen after iridectomy for glaucoma. In this form we find the cicatrix rising above the level of the conjunctiva, and assuming the appearance of a vesicle. Elongated in the direction of the incision, and filled with a whitish liquid (cystoid cicatrix). In such cases we may suppose that the conjunctiva wound has closed before the one in the scleroctic, so that the aqueous humor still escapes, and collects beneath the conjunctiva, which becomes raised like a blister.

As a rule, this form of cicatrix does not present any inconvenience; but, in presence of exceptional cases, in which, after remaining innocuous for years, it has been the starting point of an inflammation which endangered the eye, our attention should be directed to the means of avoiding this irregular cicatrisation, or of arresting its progress. As to arresting its progress, our only advice is to prolong the application of the compress and bandage, or to attempt, after the lapse of the sclerotic would by destruction of the vesicle.

As to the means of preventing the formation of the cystoid cicatrix, we only know one, namely, the methodical execution of the iridectomy, it is very reasonable to supposed that if the extremities of the iris flap are enclosed in the scleroctic wound, they will prevent the wound from uniting rapidly and regularly. The aqueous, especially when there is a certain degree of increase tension, will thus continue to escape, and will be collected beneath the conjunctiva, for the small wound made in the conjunctiva closes in a very short time. Hence we have a universal indication to excise the iris as carefully as possible to the very angles of the sclerotic incision, and to manipulate as already described in order to bring the margin of the artificial pupil within the anterior chamber. Still, we are forced to admit that, in spite of all precautions, a cystoid cicatrix will sometimes be formed even when the execution of the operation has left nothing to be desired.

We must also mention the fact that not unfrequently we find a glaucomatous attack occurring in the healthy eye a few days after the operation on the other. Although the possibility of this accident should not prevent our operating when necessary, still it imposes on us the duty of forewarming the patient or his friends. This attack disappears rapidly and without return under the use of eserine, and does not require immediate operation.

When the operation has had no effect, we may be led to perform it a second time. In such cases, we select the opposite margin of the corneal periphery for the second operation. Thus, we perform it at the inferior margin if the first has been at the superior, and vice versa. In the same circumstance, the re-incition of the sclerotic, in order to open again the cicatrix of the first operation (cicatrisotomy of Wecker, or oulotomy of Panas) has been also employed.

Attemps have been made to replaceiridectomy, in the treatment of glaucoma, by section of the ciliary muscle. Hancock’s method of operation is as follows: a cataract knife is introduced at the inferior and external aspect of the corneal margin, at its junction with the sclerotic; the point of the knife is made to enter obliquely from before backwards and from above downwards, till the sclerotic fibres are obliquely divided for the eight of an inch; any effused blood is allowed to escape along the knife. This operation is seldom followed by any disagreeable symptoms. In only one of Hancock;s cases was there a little inflammation, which speedily disappeared.

Stellwag’s and de Wecker’s opinion, that the efficacy of iridectomy is not due to the excision of the iris, but to the incision of the sclerotic, has been put in practice by Cuaglino (1871) who has replaced iridectomy by sclerotomy. In order to avoid prolapse of the iris, eserine has to be used before and after this operation, which should not be performed if the pupil cannot be previously contracted to nearly pinhole size. The point of von Graefe’s cataract knife is entered into the anterior chamber as for the puncture in cataract extraction, but at the distance of 1 millimeter from the corneal margin. The counter-puncture is made at the corresponding point at the other side of the anterior chamber, and the section is enlarge by a sawing motion of the knife until only a bridge of tissue about 2 millimeter broad remains undivided (de Wecker). If, notwithstanding the use of eserine, the pupil be of irregular shape, the hard rubber of silver sptula should be introduced into anterior chamber to restore the pupil to its normal shape by gentle pushing of the iris. But, should this not prove satisfactory, or should there be an actual prolapse of the iris, it would be best to turn the sclerotomy into an iridectomy. Sclerotomy ha been praised in case of hemorrhage glaucoma, as a supplemental operation when iridectomy has been of no use, and in chronic simple glaucoma. For this last disease, we have had to record its failure many times, and the vision repeatedly lost in eyes operated on by means of a gold thread, also proposed by de Wecker for glaucoma, has not met with a favorable reception, and seems to have been given up even by its author.

After the iridectomy has been performed, we often find that the visual acuteness improves considerably under suitable treatment. This treatment consists in the administration of such mineral waters as act of the skin and kidneys, and in the frequent application of a dry cups and artificial leeches. Persistent neuralgia may be checked by 10-15 centigrammes (2-3 grains) of quinine three or four times daily. Badal and abadie have obtained in these cases immediate and lasting relief by the elongation of the external nasal nerve, and Brailey, by the same operation perfomed on the supraorbital nerve. If there by symptoms of active congestion, we prescribe derivation on the bowels (Carlsbad or Marienbad) leeches in case of cessation of menses or hemorrhoids, and if the head be also congested we can use wet cupping in the neck or heurteloup’s apparatus at the temples.

We should also advise our patients to observe great emotion exposes them, warming them of the danger to which any great emotion exposes them, and interdicting any axcessive use of the eye.

In cases of glaucoma, and even after vision has been lost for considerable time, it is better to free the patient of any source of pain by puncture of the sclerotic with escape of vitreous, by enucleating the ball, or by the neurectomia optocillaris.

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