TextbookOphthalmologyAcute Angle-Closure Glaucoma

Acute Angle-Closure Glaucoma

Acute angle-closure glaucoma is an ophthalmological emergency caused by sudden obstruction of aqueous outflow, presenting with severe eye pain, reduced vision, haloes, and a semi-dilated fixed pupil, requiring immediate IOP reduction.

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Key Facts

Acute angle-closure glaucoma (AACG) is an ophthalmological emergency requiring immediate treatment to prevent permanent vision loss Presentation: severe unilateral eye pain, reduced vision, haloes around lights, nausea/vomiting, semi-dilated fixed pupil, injected eye, hazy cornea IOP is markedly elevated (often 40-80mmHg); eye feels "rock-hard" on palpation through closed lids Risk factors: hypermetropia (short eye), increasing age, female sex, East Asian ethnicity, shallow anterior chamber, family history Precipitants: pupil dilation (dim lighting, mydriatic drops, anticholinergics, sympathomimetics), prone position Emergency treatment: pilocarpine 2% drops (constricts pupil) + timolol 0.5% + IV acetazolamide 500mg + analgesia/antiemetic Definitive treatment: YAG laser peripheral iridotomy (creates alternative drainage pathway); treat BOTH eyes (prophylactic for fellow eye) Misdiagnosis: often misdiagnosed as migraine, acute abdomen, or stroke due to nausea/vomiting and headache

Overview

Key Facts

AACG causes rapid, irreversible optic nerve damage if not treated promptly. It should be considered in any patient presenting with a painful red eye and reduced vision.

Epidemiology

  • Incidence: 12-15 per 100,000 per year (UK)
  • Female:male ratio 3:1
  • Peak age: >60
  • East Asian ethnicity: significantly higher risk (smaller eyes, shallower anterior chambers)
  • Hypermetropic (long-sighted) patients at higher risk

Aetiology

  • Anatomically predisposed eye (short axial length, shallow anterior chamber, thick lens, narrow angle)
  • Pupillary block: mid-dilated pupil causes iris to bow forward → blocks trabecular meshwork
  • Precipitants: dim lighting, mydriatic drugs (tropicamide), anticholinergics (oxybutynin, TCAs, ipratropium), sympathomimetics

Pathophysiology

  • Pupillary block → iris bows forward → peripheral iris occludes trabecular meshwork → sudden cessation of aqueous outflow → rapid IOP rise (40-80mmHg) → corneal oedema (haze) → optic nerve ischaemia → retinal ganglion cell death

Clinical Presentation

Symptoms

  • Severe unilateral eye pain (often frontal/periorbital)
  • Reduced/blurred vision
  • Haloes around lights (corneal oedema causes light diffraction)
  • Nausea and vomiting (vagal response to pain; can mimic acute abdomen)
  • Headache (can mimic migraine or stroke)
  • Profuse lacrimation

Signs

  • Red eye (mixed conjunctival and ciliary injection)
  • Hazy/oedematous cornea (steamy)
  • Semi-dilated, fixed (non-reactive) pupil — oval shaped
  • Rock-hard eye (elevated IOP palpable through closed lids)
  • Shallow anterior chamber (by slit lamp or pen torch — narrow shadow sign)
  • IOP markedly elevated (often 40-80mmHg)

Red Flags

  • This IS a red flag — any presentation matching above requires emergency management
  • Fellow eye may have narrow angles (at risk of same episode)
  • Misdiagnosis risk: nausea/vomiting → "acute abdomen"; headache → "migraine"

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Anterior uveitisMiosis, ciliary flush, cells/flare, normal IOPSlit lamp
KeratitisCorneal opacity, fluorescein uptake, normal IOPSlit lamp
MigraineHeadache, visual aura, normal eye examinationClinical
Cluster headachePeriorbital pain, lacrimation, conjunctival injectionClinical
Phacomorphic glaucomaMature cataract, shallow ACSlit lamp, B-scan

Diagnosis / Investigation

Bedside

  • Visual acuity (usually significantly reduced)
  • IOP measurement (Goldmann tonometry): markedly elevated; if not available, palpation through closed lids (very firm)
  • Pen torch: semi-dilated, oval, fixed pupil; shallow AC (narrow shadow sign)
  • Slit lamp: corneal oedema, shallow AC, closed angle (gonioscopy when acute phase resolved)

Bloods

  • Not needed for diagnosis
  • U&Es if acetazolamide being used (electrolyte disturbance)

Imaging

  • Anterior segment OCT/ultrasound biomicroscopy: angle assessment (specialist)
  • B-scan ultrasound: if no view of posterior segment

Special Tests

  • Gonioscopy: gold standard for angle assessment (performed after acute phase resolved)
  • Fellow eye gonioscopy: assess for narrow angles (prophylactic iridotomy needed)

Management

Emergency Treatment (Reduce IOP)

  1. Lie patient supine (iris falls back, may partially open angle)
  2. Pilocarpine 2% drops to affected eye: every 5 minutes × 3 then 4× daily (constricts pupil → opens angle)
    • Pilocarpine to fellow eye also (prophylactic)
  3. Timolol 0.5% drops to affected eye: single dose (reduces aqueous production)
  4. IV acetazolamide 500mg STAT (reduces aqueous production; oral 250mg QDS maintenance)
  5. Topical steroid (dexamethasone 0.1%): reduces inflammation from acute episode
  6. Analgesia: paracetamol ± opioid
  7. Antiemetic: cyclizine 50mg IM/IV
  8. If IOP not responding: IV mannitol 20% (1g/kg over 20 minutes) — osmotic diuretic
  9. Pilocarpine may not work if IOP >50mmHg (sphincter ischaemia); must reduce IOP first with systemic agents

Definitive Treatment

  • YAG laser peripheral iridotomy (PI): creates small hole in peripheral iris → bypasses pupillary block → allows aqueous flow to trabecular meshwork
    • Performed once cornea has cleared (usually within 24-48 hours)
    • Both eyes treated (fellow eye prophylactic iridotomy — essential)
  • Lens extraction (cataract surgery): removes the thick lens contributing to crowding; increasingly used as primary or early treatment

Surgical/Interventional

  • Surgical peripheral iridectomy: if laser not possible
  • Lens extraction: if angle-closure recurs despite PI or coexisting cataract
  • Goniosynechialysis: to break peripheral anterior synechiae (specialist)

Referral Criteria

  • AACG: immediate ophthalmology referral (same day/emergency)
  • Fellow eye: prophylactic iridotomy arranged urgently
  • Post-acute: ongoing glaucoma monitoring

Prognosis

  • Prompt treatment (within hours): good visual prognosis; IOP reduces within hours of treatment
  • Delayed treatment: permanent optic nerve damage; visual field loss; blindness
  • After laser PI: recurrence is rare; fellow eye protected
  • Chronic angle-closure may develop if repeated/prolonged episodes with synechiae formation
  • Risk of further episodes in fellow eye is 40-80% without prophylactic treatment

Other Relevant Information

Emergency AACG Treatment Summary

StepTreatment
1Lie supine
2Pilocarpine 2% drops (both eyes)
3Timolol 0.5% drops
4IV acetazolamide 500mg
5Topical steroid
6Analgesia + antiemetic
7If refractory: IV mannitol
8Definitive: YAG laser PI (both eyes)

Risk Factors for Angle-Closure

FactorMechanism
HypermetropiaShort eye, shallow AC
Female sexSmaller eyes
Age >60Lens thickens with age
East Asian ethnicityAnatomically narrow angles
Family historyAnatomical predisposition
Anticholinergic drugsPupil dilation