Ophthalmology/Eye Institute

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Acute angle closure glaucoma

Normal Intraocular pressure in adults usually ranges between about 10 and 21. Acute angle closure glaucoma can cause pressures to rise very high, as seen in this patient. Angle closure is best observed using a goniolens (or gonioscope) that allows the viewer to see into the angle of the eye that cannot be done with a traditional slit lamp examination.

Acute angle closure glaucoma occurs when there is a relatively sudden blockage of the trabecular meshwork by the anterior bulging of the peripheral iris. This may occur initially with pupillary block (where the lens presses up against the iris, decreasing aqueous humor flow into the anterior chamber) resulting in increased intraocular pressure in the posterior chamber, creating a pressure gradient that subsequently presses the iris anteriorly and causes it to block the angle. Pupillary block is greatest when the iris is in a mid-dilated state. When the pupil dilates the iris bunches up on itself and makes pupillary block more likely. Individuals with a naturally occurring narrow angle are at a higher risk for acute angle closure.

As in this patient, acute angle closure typically presents with severe ocular pain, headache, blurred vision, halos around lights, nausea, and vomiting. Some of the apparent non-ocular manifestations (nausea/vomiting) could be misleading to the inexperienced physician. However, the prompt recognition and subsequent treatment of an acute angle closure crisis is paramount in the preservation of the patient’s vision. Even if the acute episode is diagnosed and treated quickly and appropriately there can still be optic nerve damage and resultant visual loss. Other possible changes include iritic ischemia causing sloughing of iris pigment that can be noted in the anterior chamber and on the corneal endothelium. Permanent iris damage may cause the iris to remain in a permanent dilated position. The intraocular pressure also may rise enough to cause retinal vascular occlusion causing retinal ischemia. Anterior subcapsular lens opacities may also occur as a result of ischemia (this is termed glaukomflecken).

Treatment of acute angle closure glaucoma is either laser or surgical peripheral iridectomy (placing a hole in the peripheral iris). This procedure restores aqueous flow from the posterior to anterior chamber by creating an extra opening in the iris, relieving the pathologic pressure gradient. This ultimately allows the iris to regress and pull away from the trabecular meshwork and then normal aqueous humor drainage is restored. This procedure is often curative of the affected eye. Often times, a prophylactic peripheral iridectomy of the non-affected eye is necessary especially when it also has a chronic narrow angle. Individuals with one episode of acute angle closure glaucoma have a 40-80% chance of having another attack of the other eye over the next 5-10 years.

Even when the intraocular pressure has decreased, subsequent follow up is necessary to be sure that the angle remains open. IOP may decrease due to ciliary body ischemia and decreased aqueous humor production, and not because the angle has reopened.

© 2014 Medical College of Wisconsin
Page Updated 08/11/2014