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Describe primary angle-closure glaucoma with the management of an acute attack.

Ophthalmology · 3rd Professional

Anatomical Predisposition and Mechanism

Primary angle-closure glaucoma (PACG) is glaucomatous optic neuropathy occurring in an eye in which the angle is occluded by apposition of the peripheral iris to the trabecular meshwork, obstructing aqueous outflow.

PACG is proportionately more important in ASIA than in the West, and accounts for a large share of glaucoma blindness in India, China and South-East Asia — because it blinds faster and more often than open-angle disease
The predisposed eye is a small eye, and every anatomical feature follows from that: a short axial length; hypermetropia; a shallow anterior chamber; a small corneal diameter; a thick and anteriorly positioned lens; and a steep, narrow angle recess

Mechanism	Description
Pupil block — much the commonest	Aqueous passing from the posterior to the anterior chamber must squeeze between the iris and the lens. Where the two are closely apposed, resistance rises — relative pupil block. Pressure then builds behind the iris, bowing the peripheral iris forward (iris bombe) onto the trabecular meshwork. It is worst with a mid-dilated pupil, where the iris is both maximally apposed to the lens and maximally flaccid peripherally — which is why attacks occur in dim light and after mydriatics
Plateau iris	Anteriorly positioned ciliary processes push the peripheral iris forward. Suspected when angle closure persists after iridotomy; confirmed by ultrasound biomicroscopy; and treated by laser iridoplasty
Lens-related	A large or anteriorly positioned lens; and phacomorphic closure from an intumescent cataract
Retrolental and posterior	Aqueous misdirection (malignant glaucoma), tumour, and ciliochoroidal effusion; these produce closure with a uniformly shallow chamber, including centrally — a diagnostic clue
Combined	More than one mechanism operating together, which is common

Acute Angle-closure Attack

Symptoms — severe ocular and periorbital pain; headache; nausea and vomiting, which may be so prominent that the patient is admitted to a medical or surgical ward with a suspected abdominal emergency, migraine or intracranial event — a genuinely common and serious misdiagnosis; coloured haloes around lights from corneal oedema; and rapid, profound loss of vision
Signs — the eye is dramatically abnormal and the diagnosis is made across the room:
Lid oedema and marked ciliary (circumcorneal) congestion

Management of the Acute Attack

1.
Systemic acetazolamide — 500 mg intravenously, followed by 250 mg orally six-hourly.
It reduces aqueous production immediately and is the first drug given → 2.
Intravenous mannitol 20% (1 to 2 g/kg over 30 to 45 minutes) or oral glycerol, to draw fluid osmotically from the vitreous and deepen the chamber.
Avoid glycerol in diabetics (it is metabolised to glucose) and mannitol in cardiac or renal failure → 3.
Topical agents — a beta-blocker, an alpha-2 agonist and a topical carbonic anhydrase inhibitor, given together → 4.
Topical steroid — to reduce the intense inflammation, which itself contributes to synechiae and to a persistently raised pressure → 5.
Pilocarpine 2% — but only once the pressure has fallen below 40 to 50 mmHg.
Above that the iris sphincter is ischaemic and will not respond, so pilocarpine is useless; and by shifting the lens forward it may make matters worse.
Giving pilocarpine first is the classic error → 6.
Corneal indentation with a gonioprism or a squint hook, which mechanically forces aqueous into the angle and may break the attack → 7.
Laser peripheral iridotomy as soon as the cornea is clear enough — this is the definitive treatment, creating an alternative route for aqueous and abolishing the pupil block → 8.
Prophylactic iridotomy to the fellow eye, which is mandatory: the risk of an attack in the untreated fellow eye is of the order of 50% within 5 years

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