Primary angle closure glaucoma is a common disease that is frequently seen by ophthalmologists in Asia. The problem is made worse by late attendance, often days or weeks after onset, and the consequent medical unresponsiveness of this disease.¹ In Asia, the prevalence of primary angle closure glaucoma can exceed that of primary open angle glaucoma, whereas the reverse is true in many predominantly Caucasian countries.² The chronic condition develops insidiously, the patient often being unaware of the ocular problem until relatively late in the disease process.

In acute angle closure glaucoma, the rise in intraocular pressure is associated with infarction of the iris tissue and inflammation. Oedema of the corneal epithelium is typically present, and can be seen by the irregular scatter of light from the corneal surface (figure 1). In an acute attack, the pupil is mid-dilated. An oval appearance results from sectorial infarction of the iris sphincter with spiralling of the stromal fibres (figure 2).

Figure 1. Clinical appearance of acute angle closure glaucoma.

After an acute attack, the iris atrophy remains, and often sphincter pupillae action is lost. The patient in figure 3 has had a peripheral iridectomy; the pupil is irregular after sectorial infarction of the iris with spiralling of the remaining viable fibres and depigmentation secondary to atrophy of the iris stroma.
Raised intraocular pressure may cause necrosis of the anterior lens epithelium. After an acute attack of angle closure glaucoma, diffuse small white opacities are often seen in the anterior sub-

Figure 2. Characteristic oval, mid-dilated appearance of angle closure glaucoma.

Figure 3. Features of the pupil and iris in angle closure glaucoma.

capsular region (figure 4). Another aspect of acute glaucoma in Asian eyes is the frequency of very shallow anterior chamber, both centrally and peripherally, which differs from the disease behaviour described in a Caucasian population.¹

Glaucomflecken, virtually diagnostic of a previous attack of angle closure glaucoma, are seen to have an irregular amoeboid shape in high power view (figure 5).² A histological section of an affected lens (figure 6) reveals foci of the epithelial cell necrosis.

The optic disc maintains a normal appearance at follow-up provided the acute attack is rapidly controlled. If this is not achieved, damage occurs resulting in visible optic atrophy and corresponding field loss. Six months after an acute glaucoma attack, images of a normal left and involved right eye show 'flat' diffuse optic atrophy,

indicating neuronal and vascular damage to the disc from the acute attack (figure 7). If ocular pressure remains elevated, the optic nerve takes on a cupped appearance indistinguishable from that seen in open angle glaucoma. Acute infarction of the optic disc may also occur resulting in an appearance of anterior ischaemic optic neuropathy.¹

Figure 4. Discrete, granular opacities (glaucomflecken) and corneal oedema.

Figure 5. High power view of glaucomflecken.

Figure 6. Histological section of lens showing foci of epithelial cell necrosis.

Treatment for an eye with acute angle closure glaucoma involves reducing the intraocular pressure as quickly as possible by pharmacological means, after which a laser iridotomy is performed (figure 8).² In medically unresponsive cases, laser iridoplasty has been effective in stopping the acute attack, allowing for a reduction in invasive surgery.¹ The long-term prognosis for intraocular pressure control depends upon the extent of trabecular meshwork damage from ischaemia or the formation of synechiae during the acute attack.² The conversion rate to chronic angle closure glaucoma is 32% over an average period of 18 months.¹

Figure 7. Six-month follow-up after acute closure glaucoma: involved right eye (a) and normal left eye (b).
a	b

Figure 8. Successful laser iridotomy.

References

1. Wong JS, Chew PTK, Alsagoff Z, et al. Clinical course and outcome of primary acute angle-closure glaucoma in Singapore. Singapore Med J 1997;36:16-18.

2. Spalton DJ, Hitchings RA, Hunter PA. Atlas of Clinical Ophthalmology, 2nd ed. London: Times Mirror International Publishers Ltd., 1995.

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