Acute glaucoma

Overview

Acute angle-closure glaucoma (AACG) is a true ophthalmic emergency caused by sudden blockage of the iridocorneal drainage angle by the iris, resulting in a dramatic rise in IOP. Without prompt treatment, irreversible optic nerve damage and permanent visual loss occur.

Risk factors

Hypermetropia (short, long-sighted eye)
Shallow anterior chamber
Older age
Female sex
South/East Asian ethnicity
Pupil-dilating medications
Family history of glaucoma
Low-light conditions

Presentation

•Severe sudden-onset unilateral eye pain - aching/pressure, may radiate to forehead
•Coloured halos around lights - corneal oedema scattering light
•Blurred vision / visual loss
•Headache - frontal, may mimic migraine
•Nausea and vomiting - vagal activation; can mislead towards GI/neurological diagnosis
•Red eye - conjunctival injection (ciliary flush)
•Hazy/steamy cornea - oedema from IOP-induced endothelial failure
•Mid-dilated, fixed, non-reactive pupil - hallmark sign; sphincter muscle ischaemic
•Hard, tender globe on palpation - firm compared to contralateral eye
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Patients may present with headache, nausea, and vomiting without volunteering eye symptoms. Always ask about visual symptoms and examine the eyes in any undifferentiated headache with vomiting - missing AACG leads to permanent blindness.

Investigations

•Tonometry - IOP normal 11-21 mmHg; AACG typically >30 mmHg, often 40-70 mmHg; Goldmann applanation tonometry is gold standard
•Slit-lamp examination - corneal oedema, anterior chamber depth
•Gonioscopy - specialist; directly visualises angle closure
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Diagnosis is primarily clinical in an emergency. Do not delay treatment while awaiting formal tonometry - refer to ophthalmology urgently and treat simultaneously.

Management

•Immediate: lie patient supine (flat) - lens falls posteriorly under gravity, partially relieves pupillary block
•Urgent ophthalmology referral - simultaneously with treatment, do not wait
First-line · Medical
  1. 1Pilocarpine eye drops - 2% (blue eyes) or 4% (brown eyes); miotic, constricts pupil, pulls iris away from trabecular meshwork
  2. 2Acetazolamide 500 mg oral (primary care) or IV (secondary care) - carbonic anhydrase inhibitor, reduces aqueous production; contraindicated in sulfonamide allergy, renal failure, sickle cell disease
  3. 3Timolol 0.5% eye drops - beta-blocker, reduces aqueous production; caution in asthma, COPD, heart block
  4. 4Paracetamol/opioid analgesia + metoclopramide antiemetic
Second-line · Add in secondary care
  1. 1Topical apraclonidine or brimonidine (alpha-2 agonists) - reduce aqueous production, increase uveoscleral outflow
  2. 2Topical prednisolone or dexamethasone eye drops - reduce intraocular inflammation
Third-line · Refractory cases
  1. 1IV mannitol 1-2 g/kg - osmotic agent, draws fluid out of eye; reserved for IOP refractory to other measures
Definitive · Surgical
  1. 1Peripheral laser iridotomy (LPI) - laser creates opening in peripheral iris, allows aqueous to bypass pupillary block; eliminates mechanism of angle closure
  2. 2Prophylactic LPI to contralateral eye - same anatomical predisposition; high risk of future attack
  3. 3If corneal oedema obscures view: surgical iridectomy or phacoemulsification (lens extraction)

Complications

•Irreversible optic nerve damage and permanent visual field loss - primary danger of delayed treatment
•Acute attack in contralateral eye - if prophylactic iridotomy not performed
•Chronic angle-closure glaucoma - repeated episodes cause progressive trabecular damage
•Posterior synechiae - iris-lens adhesions obstructing aqueous flow
•Corneal endothelial decompensation, cataract formation - from prolonged ischaemia
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Prognosis is directly related to speed of treatment. Prolonged IOP elevation beyond 24-48 hours significantly increases risk of permanent optic nerve damage.

Pathophysiology (key mechanism)

•Pupillary block - aqueous trapped behind iris causes iris bombe, pushing peripheral iris against trabecular meshwork, halting drainage; IOP rises to 40-70 mmHg
•Mid-dilated pupil is the danger position - greatest iris-lens contact; triggered by low light, or drugs causing dilation
•Precipitating drugs - anticholinergics (oxybutynin, ipratropium, tropicamide eye drops), adrenergic agents, tricyclic antidepressants