Aetiology
Angle-closure glaucoma (ACG) is primarily caused by mechanical obstruction of the anterior chamber angle, leading to impaired aqueous humour outflow and elevated intra-ocular pressure.[4][10] Anatomical factors such as shallow anterior chambers, thick lenses, and narrow iridocorneal angles contribute.[10][11][12] ACG is associated with an intra-ocular pressure >21 mmHg, age >50 years, female gender, Asian and Inuit ethnicity, hyperopia, and family history.[1][2][4][7][8][9][13][14]
ACG can occur secondary to a thick cataractous lens (phacomorphic glaucoma); ectopic lens (e.g., in settings of trauma, as well as Marfan or Weill-Marchesani syndrome); neovascularisation of the angle secondary to diabetic retinopathy or ocular ischaemia; and tumours.[15]
Sulfa-containing drugs (e.g., sulfonamides), diuretics (e.g., acetazolamide), topical pupil dilators (e.g., cyclopentolate, atropine), and anticonvulsants (e.g., topiramate) can precipitate ACG by inducing supraciliary body effusions.[16] This form of ACG is unresponsive to laser peripheral iridotomy; treatment comprises topical corticosteroids, discontinuation of the causative drug, and topical and systemic intra-ocular pressure lowering drugs.[16][17]
Pathophysiology
Angle closure occurs when the peripheral iris is in contact with the trabecular meshwork (TM), either intermittently (appositional closure) or permanently (synechial closure).
Two discrete mechanisms contribute to angle closure:
Those 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.
Those 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.[14]
Angle closure is usually chronic and progressive, but uncommonly it manifests as an acute attack of complete closure with severe symptoms.[14]
Classification
American Academy of Ophthalmology preferred practice pattern[1]
Classifies primary angle-closure disease as follows:
Primary angle-closure suspect: ≥180 degrees iridotrabecular contact (ITC), normal intra-ocular pressure (IOP) and no peripheral anterior synechiae (PAS), no optic nerve damage.
Primary angle closure: ≥180 degrees ITC, presence of elevated IOP or PAS, no optic nerve damage.
Primary angle-closure glaucoma: ≥180 degrees ITC, presence of IOP and/or PAS, with optic nerve damage.
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