Aetiology

Angle closure can be primary, secondary to another eye disease, or drug-induced.

Eye diseases that can cause ACG include a thick cataractous lens (phacomorphic glaucoma); ectopic lens (e.g., in settings of trauma, as well as Marfan’s or Weill-Marchesani syndrome); neovascularisation of the angle secondary to diabetic retinopathy or ocular ischaemia; and tumours.

Sulfa-containing drugs can cause ACG by causing supraciliary body effusions. This form of ACG has a distinctly different aetiology and is not treated in the same fashion as primary angle-closure glaucoma. It is unresponsive to laser peripheral iridotomy and is treated with topical corticosteroids and discontinuation of the causative drug, as well as topical and systemic intraocular pressure lowering drugs.

Pathophysiology

Angle closure occurs when the peripheral iris is in contact with the trabecular meshwork (TM), either intermittently (appositional closure) or permanently (synechial closure).

Specific mechanisms leading to angle closure can be divided into 2 categories:

  • Mechanisms that push the iris from behind including, most commonly, relative pupillary block (where accumulation of aqueous in the posterior chamber forces the peripheral iris anteriorly, causing anterior iris bowing, narrowing of the angle, and acute or chronic angle-closure glaucoma) as well as plateau iris syndrome, enlarged or anteriorly displaced lens, and malignant glaucoma.

  • Mechanisms that pull the iris into contact with the TM (e.g., contraction of inflammatory membrane as in uveitis, fibrovascular tissue as in iris neovascularisation, or corneal endothelium as in iridocorneal endothelial syndrome).

Chronic intermittent friction between the iris and the TM can lead to progressive dysfunction of the TM. With time, adhesions (synechiae) form between the iris and parts of the TM.

Eventually the TM is so dysfunctional and/or obstructed that aqueous outflow from the eye is impaired, and intra-ocular pressure (IOP) rises.[18]

Prolonged elevation of IOP leads anatomically to glaucomatous changes in the optic nerve head and loss of optic nerve axons, and functionally to progressive loss of the visual field. If untreated this process may progress to complete blindness.

Angle closure is usually chronic and progressive, but uncommonly it manifests as an acute attack of complete closure with severe symptoms.

Classification

Clinical classification[1]

Classification of angle closure based on presence or absence of symptoms

  • Acute: abrupt onset of symptomatic elevation of IOP (>21 mmHg) resulting from total closure of the angle, which is not self-limiting

  • Sub-acute (or intermittent): abrupt onset of symptomatic elevation of IOP, resulting from total closure of the angle, which is self-limiting and recurrent

  • Chronic: elevated IOP resulting from angle closure that is asymptomatic.

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