Ординатура / Офтальмология / Английские материалы / Comprehensive Ophthalmology_Khurana_2007

8.Peripheral field defects. These appear sometimes at an early stage and sometimes only late in the disease. The peripheral nasal step of Roenne's results from unequal contraction of the peripheral isopter.

9.Advanced glaucomatous field defects. The visual field loss gradually spreads centrally as well as peripherally, and eventually only a small island of central vision (tubular vision) and an accompanying temporal island are left. With the continued damage, these islands of vision also progressively diminish in size until the tiny central

island is totally extinguished. The temporal island of the vision is more resistant and is lost in the end leaving the patient with no light perception.

Diagnosis of glaucoma field defects on HFA single field printout. Glaucomatous field defects should always be interpreted in conjunction with clinical features (IOP and optic disc changes). Further, before final interpretation, the fields must be tested twice, as there is often a significant improvement in the field when plotted second time (because patients become more familiar with the machine and test process).

Criteria to grade glaucomatous field defects. The criteria to label early, moderate and severe glaucomatous field defect from the HFA central 30-2 test, single printout is depicted in Table 9.2.

Note. For proper understanding of Table 9.2, evaluation of the Humphrey single field printout described on page 485 should be revised.

Ocular associations

POAG may sometimes be associated with high myopia, Fuchs’ endothelial dystrophy, retinitis pigmentosa, central retinal vein occlusion and primary retinal detachment.

INVESTIGATIONS

1.Tonometry. Applanation tonometry should be preferred over Schiotz tonometry (see page 479).

2.Diurnal variation test is especially useful in detection of early cases (see page 215).

3.Gonioscopy. It reveals a wide open angle of anterior chamber. Its primary importance in POAG is to rule out other forms of glaucoma. For details (see page 206 and 546).

4.Documentation of optic disc changes is of utmost importance (see page 216).

5.Slit-lamp examination of anterior segment to rule out causes of secondary open angle glaucoma.

6.Perimetry to detect the visual field defects.

7.Nerve fibre layer analyzer (NFLA) is a recently introduced device which helps in detecting the

glaucomatous damage to the retinal nerve fibres before the appearance of actual visual field changes and/or optic disc changes.

8.Provocative tests are required in border-line cases. The test commonly performed is water drinking test. Other provocative tests not frequently performed include combined water drinking and

tonography, bulbar pressure test, prescoline test and caffeine test.

Water drinking test. It is based on the theory that glaucomatous eyes have a greater response to water drinking. In it after an 8 hours fast, baseline IOP is noted and the patient is asked to drink one litre of water, following which IOP is noted every 15 min. for 1 hour. The maximum rise in IOP occurs in 15-30 min. and returns to baseline level after 60 minutes in both normal and the glaucomatous eyes. A rise of 8 mm of Hg or more is said to be diagnostic of POAG.

DIAGNOSIS

Depending upon the level of intraocular pressure (IOP), glaucomatous cupping of the optic disc and the visual field changes (Fig. 9.14) the patients are assigned to one of the following diagnostic entities:

1.Primary open angle glaucoma (POAG).

Characterstically POAG is labelled when raised IOP (>21 mm of Hg) is associated with definite glaucomatous optic disc cupping and visual field changes.

However, patients with raised IOP and either typical field defects or disc changes are also labelled as having POAG.

2.Ocular hypertension or glaucoma suspect. Either of these terms is used when a patient has an IOP constantly more than 21 mm of Hg but no optic disc or visual field changes (for details see page 224).

3.Normal tension glaucoma (NTG) or low tension glaucoma (LTG) is diagnosed when typical glaucomatous disc cupping with or without visual field changes is associated with an intraocular pressure constantly below 21 mm of Hg (For details see page 224).

MANAGEMENT

General considerations

Baseline evaluation and grading of severity of glaucoma. The aim of treatment is to lower intraocular pressure to a level where (further) visual loss does

Fig. 9.14. Triad of abnormalities in disc, field and intraocular pressure (IOP) for the diagnosis of glaucoma.

not occur. The management thus requires careful and regular periodic supervision by an ophthalmologist. Therefore, it is important to perform a good baseline examination with which future progress can be compared. The initial data should include: visual acuity, slit-lamp examination of anterior segment, tonometry (preferably with applanation tonometer); optic disc evaluation (preferably with fundus photography), gonioscopy and visual field charting.

American Academy of Ophthalmology (AAO) grades severity of glaucoma damage into mild, moderate and severe (Table 9.3).

Table 9.3: Severity of glaucoma damage

Degree Description

Source : AAO 2000a

Therapeutic choices include:

Medical therapy,

Argon or diode laser trabeculoplasty, and

Filteration surgery.

A. Medical therapy

The initial therapy of POAG is still medical, with surgery as the last resort.

Antiglaucoma drugs available are described in detail on pages 423-427.

Basic principles of medical therapy of POAG

1.Identification of target pressure. From the baseline evaluation data a ‘target pressure’ (below which glaucomatous damage is not likely to progress) should be identified for each patient. The target pressure is identified taking into account the severity of existing damage, the level of IOP, age, and general health of the patient. Although it is not possible to predict the safe level of IOP, however, progression is uncommon if IOP is maintained at less than 16 to 18 mm of Hg in patients having mild to maderate damage. Lower target pressures (12-14 mmHg) are required in patients with severe damage.

2.Single drug therapy. One topically instilled antiglaucoma drug should be chosen after due consideration to the patient’s personal and medical factors. If the initial drug chosen is ineffective or intolerable, it should be replaced by the drug of second choice.

3.Combination therapy. If one drug is not sufficient to control IOP then a combination therapy with two or more drugs should be tried.

4.Monitoring of therapy by disc changes and field changes and tonometry is most essential on regular follow-up. In the event of progress of glaucomatous damage the target pressure is reset

at a lower level.

Treatment regimes. There are no clear-cut prescribed treatment regimens for medical therapy of POAG. However, at present considerations are as follows :

I. Single drug therapy

1. Topical beta-blockers are being recommended as the first drug of choice for medical therapy of POAG in poors and average income patients. These lower

IOP by reducing the aqueous secretion due to their effect on beta - receptors in the ciliary processes. Preparations. In terms of effectiveness, there is little difference between various beta-blockers. However, each offers a slight advantage over the other, which may help in choosing the particular medication as follows:

Timolol maleate (0.25, 0.5% : 1-2 times/day) is most popular as initial therapy. However, it should not be used in patients having associated bronchial asthma and/or heart blocks.

Betaxolol (0.25% : 2 times/day). Being a selective beta-1 blocker it is preferred as initial therapy in patients with cardiopulmonary problems.

Levobunolol (0.25, 0.5% : 1-2 times/day). Its action lasts the longest and so is more reliable for once a day use than timolol.

Carteolol (1%: 1-2 times/day). It raises triglycerides and lowers high density lipoproteins the least. Therefore, it is the best choice in patients with POAG having associated hyperlipidemias or atherosclerotic cardiovascular

disease.

2. Pilocarpine (1, 2, 4%: 3-4 times/day). It is a very effective drug and had remained as the sheet anchor in the medical management of POAG for a long time. However, presently it is not being preferred as the first drug of choice or even as second choice. It is because of the fact that in younger patients it causes problems due to spasm of accommodation and miosis. Most, but not all, older patients tolerate pilocarpine very well; however, axial lenticular opacities when present precludes its use in many such patients. Therefore, presently pilocarpine is being considered only as an adjunctive therapy where other combinations fail and as second choice in poor patients.

Mechanism of action. Pilocarpine contracts longitudinal muscle of ciliary body and opens spaces in trabecular meshwork, thereby mechanically increasing aqueous outflow.

3. Latanoprost (0.005%: once daily). It is a prostaglandin by nature and decreases the IOP by increasing the uveo-scleral outflow of aqueous. Presently, it is being considered the drug of first choice for the treatment of POAG (provided patient can afford to buy it). Therefore, it is a very good

adjunctive drug to beta-blockers, dorzolamide and even pilocarpine when additional therapy is indicated.

4.Dorzolamide (2%: 2-3 times/day). It is a recently introduced topical carbonic anhydrase inhibitor which lowers IOP by decreasing aqueous secretion. It has replaced pilocarpine as the second line of drug and even as an adjunct drug.

5.Adrenergic drugs. Role in POAG is as follows:

i.Epinephrine hydrochloride (0.5, 1, 2%: 1-2 times/ day) and dipivefrine hydrochloride (0.1%: 1-2 times/day). These drugs lower the IOP by increasing aqueous outflow by stimulating beta recepters in the aqueous outflow system. These are characterized by a high allergic reaction rate. Their long-term use has also been recognized as a risk factor for failure of filtration glaucoma surgery. For these reasons, epinephrine compounds are no longer being used as first line or second line drug. However, dipivefrine may be combined with beta-blockers in patients where

other drugs are contraindi-cated.

ii.Brimonidine (0.2% : 2 times/day). It is a selective alpha-2-adrenergic agonist and lowers IOP by decreasing aqueous production. Because of increased allergic reactions and tachyphylaxis rates it is not considered the drug of first choice in POAG. It is used as second drug of choice and also for combination therapy with other drugs.

II. Combination topical therapy

If one drug is not effective, then a combination of two drugs—one drug which decreases aqueous production (timolol or other betablocker, or brimonidine or dorzolamide) and other drug which increase aqueous outflow (latanoprost or brimonidine or pilocarpine) may be used.

III. Role of oral carbonic anhydrase inhibitors in POAG

Acetazolamide and methazolamide are not recommended for long-term use because of their sideeffects. However, these may be added to control IOP for short term.

B. Argon or diode laser trabeculoplasty (ALT or DLT)

It should be considered in patients where IOP is uncontrolled despite maximal tolerated medical therapy. It can also be considered as primary therapy where there is non-compliance to medical therapy.

Technique and role of ALT in POAG. It has an additive effect to medical therapy. Its hypotensive effect is caused by increasing outflow facility, possibly by producing collagen shrinkage on the inner aspect of the trabecular meshwork and opening the intratrabecular spaces. It has been shown to lower IOP by 8-10 mm of Hg in patients on medical therapy and by 12-16 mm in patients who are not receiving medical treatment.

The treatment regime usually employed consists of 50 spots on the anterior half of the trabecular meshwork over 180°.

Complications. These include transient acute rise of IOP, which can be prevented by pretreatment with pilocarpine and/or acetazolamide; and inflammation which can be lessened by use of topical steroids for 3-4 days. Less commonly haemorrhage, uveitis, peripheral anterior synechiae and reduced accommodation may occur.

C. Surgical therapy

Indications

1.Uncontrolled glaucoma despite maximal medical therapy and laser trabeculoplasty.

2.Non-compliance of medical therapy and nonavailability of ALT.

3.Failure with medical therapy and unsuitable for ALT either due to lack of cooperation or inability to visualize the trabeculum.

4.Eyes with advanced disease i.e., having very high IOP, advanced cupping and advanced field loss should be treated with filtration surgery as primary line of management.

5.Recently, some workers are even recommending surgery as primary line of treatment in all cases.

Types of surgery

Surgical treatment of POAG primarily consists of a fistulizing (filtration) surgery which provides a new channel for aqueous outflow and successfully controls the IOP (below 21 mm of Hg). Trabeculectomy is the most frequently performed filtration surgery now-a-days. The details of filtration operations are described on page 237.

OCULAR HYPERTENSION

Ocular hypertension or glaucoma suspect, either of these terms is used when a patient has an IOP constantly more than 21 mm of Hg but no optic disc or visual field changes. These patients should be carefully monitored by an ophthalmologist and should be treated as cases of POAG in the presence of high risk factors

High risk factors include:

Significant diurnal variation, i.e., a difference of more than 8 mm of Hg between the lowest and the highest values of IOP.

Significantly positive water drinking provocative test.

When associated with splinter haemorrhages over or near the optic disc.

IOP constantly more than 28 mm of Hg.

Retinal nerve fibre large defects.

Parapapillary changes.

Central corneal thickness < 555 µm.

Other risk factors include:

Significant asymmetry in the cup size of the two eyes, i.e., a difference of more than 0.2.

Strong family history of glaucoma.

When associated with high myopia, diabetes or pigmentary changes in the anterior chamber.

Treatment

Patients with high-risk factors should be treated on the lines of POAG (see page 222). The aim should be to reduce IOP by 20%.

Patients with no high risk factors should be annually followed by examination of optic disc, perimetry and record of IOP. Treatment is not required till glaucomatous damage is documented.

NORMAL TENSION GLAUCOMA

Definition and prevalence

The term normal tension glaucoma (NTG), also referred to as low tension glaucoma is labelled when typical glaucomatous disc changes with or without visual field defects are associated with an intraocular pressure (IOP) constantly below 21 mm of Hg. Characterstically the angle of anterior chamber is open on gonioscopy and there is no secondary cause for glaucomatous disc changes. NTG is varient of POAG which accounts for 16% of all cases of POAG and its prevalence above the age of 40 years is 0.2%.

Etiopathogenesis

It is believed to result from chronic low vascular perfusion, which makes the optic nerve head susceptible to normal IOP. This view is supported by following association which are more common in NTG than in POAG :

Raynauld phenomenon i.e., peripheral vascular spasm on cooling,

Migraine,

Nocturnal systemic hypotension and overtreated systemic hypertension.

Reduced blood flow velocity in the ophthalmic artery (as revealed on transcranial Doppler ultrasonography).

Clinical features

As described in definition the clinical features of NTG (disc changes and visual field defects) are similar to POAG, but the IOP is consistantaly below 21mm Hg. Other characterstic features of NTG are some associations mentioned in the etiopathogenesis.

Differential diagnosis

1.POAG. In early stages POAG may present with normal IOP because of a wide diurnal variation. Diurnal variation test usually depicts IOP higher than

21mm of Hg at some hours of the day in patients with POAG.

2.Congentical optic disc anomalies such as large optic disc pits or colobomas may be mistaken for acquired glaucomatous damage.Acareful examination should help in differentiation.

Treatment

1. Medical treatment to lower IOP. The aim of the treatment is to lower IOP by 30% i.e., to achieve IOP levels of about 12-14 mm of Hg. Some important facts about medical treatment of NTG are:

Betaxolol may be considered the drug of choice because in addition to lowering IOP it also increases optic nerve blood flow.

Other beta blockers and adrenergic drugs (such as dipiverafrine) should better be avoided (as these cause nocturnal systemic hypotension and are likely to affect adversely the optic nerve perfusion).

Drugs with neuroprotective effect like brimonidine may be preferred.

Prostaglandin analogues, e.g., latanoprost tend to have a greater ocular hypotensive effect in eyes with normal IOP.

2.Trabeculectomy may be considered when progressive field loss occurs despite IOP in lower teens.

3.Systemic calcium channel blockers (e.g., nifedipine) may be useful in patients with confirmed peripheral vasospasm.

4.Monitoring of systemic blood pressure should be done for 24 hours. If nocturnal dip is detected, it may be necessary to avoid night dose of anti-hypertensive medication.

PRIMARY ANGLE-CLOSURE

GLAUCOMA

It is a type of primary glaucoma (wherein there is no obvious systemic or ocular cause) in which rise in intraocular pressure occurs due to blockage of the aqueous humour outflow by closure of a narrower angle of the anterior chamber.

ETIOLOGY

(A) Predisposing risk factors. These can be divided into anatomical and general factors:

I. Anatomical factors. Eyes anatomically predisposed to develop primary angle-closure glaucoma (PACG) include:

Hypermetropic eyes with shallow anterior chamber.

Eyes in which iris-lens diaphragm is placed anteriorly.

Eyes with narrow angle of anterior chamber, which may be due to: small eyeball, relatively large size of the lens and smaller diameter of the cornea or bigger size of the ciliary body.

Plateau iris configuration.

II. General factors include:

Age. PACG is comparatively more common in 5th decade of life.

Sex. Females are more prone to get PACG than males (male to female ratio is 1:4)

Type of personality. It is more common in nervous individuals with unstable vasomotor system.

Season. Peak incidence is reported in rainy season.

Family history. The potential for PACG is generally believed to be inherited.

Race. In caucasians, PACG accounts for about 6% of all glaucomas and presents in sixth to seventh decade. It is more common in South-East Asians, Chinese and Eskimos but uncommon in Blacks. In Asians it presents in the 5th to 6th decade and accounts for 50% of primary adult glaucomas in this ethnic group.

(B) Precipitating factors. In an eye that is predisposed to develop angle closure glaucoma, any of the following factors may precipitate an attack:

Dim illumination,

Emotional stress,

Use of mydriatic drugs like atropine, cyclopentolate, tropicamide and phenylephrine.

(C) Mechanism of rise in IOP. The probable sequence of events resulting in rise of IOP in an anatomically predisposed eye is as follows:

First of all due to the effect of precipitating factors there occurs mid dilatation of the pupil which increases the amount of apposition between iris and anteriorly placed lens with a considerable pressure resulting in relative pupil block (Fig. 9.15A). Consequently the aqueous collects in the posterior chamber and pushes the peripheral flaccid iris anteriorly (Iris bombe) (Fig. 9.15B), resulting in appositional angle closure due to iridocorneal contact (Fig. 9.15C). Eventually there occurs rise in IOP which is transient to begin with. But slowly the appositional angle closure is converted into synechial angle closure (due to formation of peripheral anterior synechiae) and an attack of rise in IOP may last long.

In some cases a mechanical occlusion of the angle by the iris is sufficient to block the drainage of aqueous. For this reason the instillation of atropine in an eye with a narrow angle is dangerous, since it may precipitate an attack of raised IOP.

CLINICAL PRESENTATION

On the basis of clinical presentation, the PACG can be classified into five different clinical entities. Previously these were considered progressive stages of PACG. However, now it has been well established that the condition does not necessarily progress from one stage to next in an orderly sequence. In clinical practice following clinical presentations are seen:

Fig. 9.15. Mechanism of angle closure glaucoma:

A, relative pupil block; B, iris bombe formation; C, appositional angle closure.

Latent primary angle-closure glaucoma (primary angle-closure glaucoma suspect).

Subacute (intermittent) primary angle-closure glaucoma.

Acute primary angle-closure glaucoma.

Postcongestive angle-closure glaucoma,

Chronic primary angle-closure glaucoma, and

Absolute glaucoma

Latent primary angle-closure glaucoma

The term latent primary angle-closure glaucoma (Latent PACG) is now used for the eyes which are anatomically predisposed to angle-closure glaucoma. Therefore, the preferred term is primary angle-closure glaucoma suspect i.e., eyes with shallow anterior chamber associated with an occludable angle. The suspect of latent angle-closure glaucoma is made:

On routine slit-lamp examination in patients coming for some other complaints, and

In fellow eye of the patients presenting with an attack of acute angle-closure glaucoma in one eye.

Clinical features

Symptoms are absent in this stage.

Signs. In suspected eyes following signs may be elicited:

1.Eclipse sign. Eclipse sign, which indicates decreased axial anterior chamber depth, can be elicited by shining a penlight across the anterior chamber from the temporal side and noting a shadow on the nasal side (Fig. 9.16).

2.Slit-lamp biomicroscopic signs include:

Decreased axial anterior chamber depth,

Convex shaped iris lens diaphragm, and

Close proximity of the iris to cornea in the periphery.

3.Gonioscopic examination shows very narrow angle (Shaffer grade I i.e., pigmented trabecular meshwork is not visible without indentation or manipulation in atleast three of the four quadrants) (see page 205 Fig 9.2)

4.Van Herick slit-lamp grading of the angle may be used with a fair accuracy when a gonioscope is not available. Here, the peripheral anterior chamber depth (PACD) is compared to the adjacent corneal thickness (CT) and the presumed angle width is graded as follows (Fig. 9.17):

Grade 4 (Wide open angle): PACD = 3/4 to 1 CT

Grade 3 (Mild narrow angle): PACD = ¼ to ½ CT

Grade 2 (Moderate narrow angle): PACD = ¼ CT

Grade 1 ( Extremely narrow angle): PACD < ¼ CT

Grade 0 (closed angle): PACD = Nil

Fig. 9.16. Estimation of anterior chamber depth by oblique illumination : A, normal; B, shallow.

Clinical course

Eyes with latent primary angle-closure glaucoma, without treatment, may follow any of the following clinical courses :

Intraocular pressure may remain normal, or

Subacute or acute angle-closure glaucoma may occur subsequently, or

Chronic angle-closure glaucoma may develop without passing through subacute or acute stage.

Diagnosis

Diagnosis is made by:

Clinical signs described above, and positive provocative tests

Provocative tests. Provocative tests for PACG suspects have been designed to precipitate closure of the angle in the ophthalmologist’s office, where it can be treated promptly.

1.Prone-darkroom test is the most popular and best physiological provocative test for PACG suspects. In this test baseline IOP is recorded and patient is made to lie prone in a darkroom for one hour. He must remain awake so that pupils remain dilated. After 1 hour, the IOP is again measured. An increase in IOP of more than 8 mm Hg is considered diagnostic of PACG.

2.Mydriatic provocative test is usually not preferred now-a-days because this is not physiological. In this test either a weak mydriatic (e.g., 0.5% tropicamide) or simultaneously a mydriatic and miotic (10% phenylephrine and 2% pilocarpine) are used to produce a mid-dilated pupil. A pressure rise of more than 8 mm Hg is considered positive.

Inferences from provocative tests

A positive provocative test indicates that angle is capable of spontaneous closure.

A negative provocative test in the presence of a narrow angle of anterior chamber does not rule out a possibility of spontaneous closure. So, patient should be warned of possible symptoms of an attack of PACG.

Treatment

Prophylactic laser iridotomy should be performed in both eyes of all the patients diagnosed as latent angle-closure glaucoma. If untreated, the risk of acute pressure rise during the next 5 years is about 50%.

Fig. 9.17. Van Herick method of slit-lamp grading of angle width: A, Grade IV; B, Grade III; C, Grade II; and D, Grade I, and E Grade 0. PACD = Peripheral anterior chamber depth;

CT = Corneal Thickeners

Subacute or intermittent primary angle-closure glaucoma

In subacute primary angle-closure glaucoma (Subacute PACG) there occurs an attack of transient rise of IOP (40-50 mmHg) which may last for few minutes to 1-2 hours. Such an attack in a patient with occludable angle is usually precipitated by :

Physiological mydriasis is e.g., while reading in dim illumination, watching television or cinema in a darkened room, or during anxiety (sympathetic overactivity); or

Physiological shallowing of anterior chamber after lying in prone position.

Clinical features

Symptoms. The episode of subacute PACG is marked by experience of unilateral transient blurring of vision, coloured halos around light, headache, browache and eyeache on the affected side.

Self-termination of the attack occurs possibly due to physiological miosis induced by bright light, sleep or otherwise.

Recurrent attacks of such episodes are not uncommon. Between the recurrent attacks the eyes are free of symptoms.

Signs. Usually during examination the eye is white and not congested. However, all the signs described in latent primary angle-closure glaucoma can be elicited in this phase also (see page 226).

Clinical course

Eyes with subacute primary angle-closure glaucoma without treatment may have variable course :

Some eyes may develop an attack of acute primary angle-closure glaucoma and

Others may develop chronic primary angle-closure glaucoma without passing through acute stage.

Diagnosis and treatment

Same as described for latent primary angle-closure glaucoma (see page 227).

Differential diagnosis of coloured halos in PACG.

Coloured halos in PACG occur due to accumulation of fluid in the corneal epithelium and alteration in the refractive condition of the corneal lamellae. Patient typically gives history of seeing colours distributed as in the spectrum of rainbow (red being outside and violet innermost) while watching on a lighted bulb or the moon.

The coloured halos in glaucoma must be differentiated from those found in acute purulent conjunctivitis and early cataractous changes. In conjunctivits, the halos can be eliminated by irrigating the discharge. The halos of glaucoma and immature cataract may be differentiated by Fincham's test in which a stenopaeic slit is passed across the pupil. During this test glaucomatous halo remains intact, while a halo due to cataract is broken up into segments (Fig. 9.18).

Acute primary angle-closure glaucoma

An attack of acute primary angle closure glaucoma occurs due to a sudden total angle closure leading to severe rise in IOP. It usually does not terminate of its own and thus if not treated lasts for many days. This is sight threatening emergency.

Clinical features

Symptoms

Pain. Typically acute attack is characterised by sudden onset of very severe pain in the eye which radiates along the branches of 5th nerve.

Nausea, vomiting and prostrations are frequently associated with pain.

Rapidly progressive impairment of vision, redness, photophobia and lacrimation develop in all cases.

Past history. About 5 percent patients give history of typical previous intermittent attacks of subacute angle-closure glaucoma.

Signs (Fig. 9.19)

Lids may be oedematous,

Conjunctiva is chemosed, and congested, (both conjunctival and ciliary vessels are congested),

Cornea becomes oedematous and insensitive,

Anterior chamber is very shallow. Aqueous flare or cells may be seen in anterior chamber ,

Angle of anterior chamber is completely closed as seen on gonioscopy (shaffer grade 0),

Iris may be discoloured,

Pupil is semidilated, vertically oval and fixed. It is non-reactive to both light and accommodation,

Fig. 9.19. Clinical photograph of a patient with acute congestive glaucoma. Note ciliary congestion, corneal oedema and middilated pupil.

IOP is markedly elevated, usually between 40 and 70 mm of Hg,

Optic disc is oedematous and hyperaemic,

Fellow eye shows shallow anterior chamber and a narrow angle (latent angle closure glaucoma).

Clinical course of acute primary angle-closure glaucoma.

The clinical status of the eye after an attack of acute PACG with or without treatment is referred to post congestive glaucoma (details are given below).

Diagnosis

Diagnosis of an attack of primary acute congestive glaucoma is usually obvious from the clinical features. However, a differential diagnosis may have to be considered :

1.From other causes of acute red eye. Acute congestive glaucoma sometimes needs differentiation from other causes of inflammed red eye like acute conjunctivitis and acute iridocyclitis (see page 146-147).

2.From secondary acute congestive glaucomas such as phacomorphic glaucoma, acute neovascular glaucoma and glaucomatocyclitic crisis.

Management

It is essentially surgical. However, medical therapy is instituted as an emergency and temporary measure before the eye is ready for operation.

(A) Medical therapy

1.Systemic hyperosmotic agent intravenous mannitol (1 gm/kg body weight) should be given initially to lower IOP.

2.Acetazolamide (a carbonic anhydrase inhibitor) 500 mg intravenous injection followed by 250 mg tablet should be given 3 times a day.

3.Analgesics and anti-emetics as required.

4.Pilocarpine eyedrops should be started after the IOP is bit lowered by hyperosomtic agents. At higher pressureiris sphincter is ischaemic and unresponsive to pilocarpine. Initially 2 percent pilocarpine should be administered every 30 minutes for 1-2 hours and then 6 hourly.

5.Beta blocker eyedrops like 0.5 percent timolol maleate or 0.5 percent betaxolol should also be administered twice a day to reduce the IOP.