Emergency Medicine
Emergency
High Evidence

Acute Angle-Closure Glaucoma

Acute angle-closure glaucoma (AACG) is a vision-threatening condition caused by sudden blockage of aqueous humor outflow... ACEM Fellowship Written, ACEM Fellow

Updated 24 Jan 2025
46 min read

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Urgent signals

Safety-critical features pulled from the topic metadata.

  • Sudden-onset severe eye pain with headache
  • Mid-dilated non-reactive pupil ('beating steam engine')
  • Intraocular pressure greater than 40-50 mmHg (normal 10-21)
  • Corneal edema with hazy cornea

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  • ACEM Fellowship Written
  • ACEM Fellowship OSCE

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  • Acute Open-Angle Glaucoma
  • Anterior Uveitis

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Quick Answer

One-liner: Acute angle-closure glaucoma is an ophthalmic emergency characterized by sudden-onset eye pain, headache, nausea/vomiting, and elevated intraocular pressure (greater than 21 mmHg) due to pupillary block, requiring immediate IOP reduction and urgent laser peripheral iridotomy.

Acute angle-closure glaucoma (AACG) is a vision-threatening condition caused by sudden blockage of aqueous humor outflow at the anterior chamber angle, leading to rapid elevation of intraocular pressure (IOP). Without prompt treatment, permanent optic nerve damage can occur within hours. Immediate management involves a combination of topical and systemic medications to lower IOP, followed by definitive treatment with laser peripheral iridotomy (LPI). This condition presents more commonly in Asian and Pacific Islander populations, with Aboriginal and Torres Strait Islander peoples at higher risk due to anatomical factors.


ACEM Exam Focus

Primary Exam Relevance

  • Anatomy: Anterior chamber angle anatomy, iris configuration, ciliary body, trabecular meshwork, Schlemm's canal
  • Physiology: Aqueous humor production (ciliary body) and outflow (trabecular meshwork, Schlemm's canal), pupillary block mechanism
  • Pharmacology: Carbonic anhydrase inhibitors, beta-blockers, cholinergic agonists, hyperosmotic agents, alpha-agonists

Fellowship Exam Relevance

  • Written: Pharmacological management protocols, indications for different treatments, contraindications, complications
  • OSCE: Ophthalmologic examination, tonometry, medication administration, communication with ophthalmology, analgesia provision
  • Key domains tested: Medical Expert (diagnosis and management), Collaborator (ophthalmology consultation), Health Advocate (population health disparities)

Key Points

Clinical Pearl

The 5 things you MUST know:

  1. Classic presentation: Sudden unilateral eye pain, headache, nausea/vomiting, blurred vision, halos around lights
  2. Key finding: Mid-dilated (4-6 mm), fixed, non-reactive pupil ("beating steam engine") in the affected eye
  3. IOP threshold: Emergency when greater than 40-50 mmHg (normal 10-21); immediate intervention required to prevent optic nerve damage
  4. First-line medications: Acetazolamide 500 mg PO/IV, timolol 0.5% drops, avoid pilocarpine until IOP lowered (below 40 mmHg)
  5. Definitive treatment: Urgent ophthalmology referral for laser peripheral iridotomy (LPI) once corneal edema improves

Epidemiology

MetricValueSource
Incidence1-2 per 100,000/year (general population)[1] PMID: 27799693
Incidence (Asian)10-15 per 100,000/year[2] PMID: 29358689
Incidence (Indigenous)2-3x general population (ATSI), 2-3x general population (Māori)[8] PMID: 33726720; [9] PMID: 35252342
Female:Male ratio2:1 to 4:1[3] PMID: 28635507
Mean age at presentation55-70 years[4] PMID: 26972622
Bilateral involvement risk40-60% (contralateral eye at risk)[5] PMID: 25834203
Visual loss without treatment50-80%[6] PMID: 27428640
Time to permanent damage24-48 hours untreated[7] PMID: 27741712
Mortalitybelow 1% (visual morbidity significant)[28] PMID: 16488940

Risk Factors

Anatomical risk factors:

  • Shallow anterior chamber (Van Herick grade 1-2)
  • Short axial length (below 22 mm)
  • Thick lens (age-related)
  • Narrow anterior chamber angle
  • Hypermetropia (+2.00 to +5.00 diopters)
  • Plateau iris configuration

Demographic risk factors:

  • Age greater than 55 years (lens thickening, anterior chamber shallowing)
  • Female sex (anterior chamber generally shallower)
  • Asian ethnicity (highest risk group)
  • Aboriginal and Torres Strait Islander (2-3x higher incidence)
  • Māori (2-3x higher incidence)
  • Family history of glaucoma

Precipitating factors:

  • Pupillary dilation (dark environment, emotional stress)
  • Anticholinergic medications (atropine, hyoscine, antihistamines)
  • SSRIs (paroxetine, sertraline)
  • Topiramate (sulfa-derived antiepileptic)
  • Sympathomimetics (adrenaline, phenylephrine)
  • Sudden position changes
  • Reading or prolonged near work
  • General anesthesia

Australian/NZ Specific

  • Aboriginal and Torres Strait Islander: 2-3 times higher incidence due to shallower anterior chambers [8] PMID: 33726720
  • Māori: Similar anatomical predisposition, higher rates in older populations [9] PMID: 35252342
  • Asian-Pacific migrants: Highest risk group in Australia [10] PMID: 29542798
  • Rural/remote: 30-40% delayed presentation (greater than 12 hours from symptom onset) [11] PMID: 29198976
  • Access barriers: Limited local ophthalmology services, geographic isolation, cultural factors
  • Medication access: PBS subsidizes standard IOP-lowering agents, but travel to obtain prescriptions may be difficult

Pathophysiology

Mechanism

Acute angle-closure glaucoma results from pupillary block, where iris lens diaphragm bows anteriorly and makes contact with cornea, occluding trabecular meshwork and preventing aqueous outflow.

Stepwise mechanism:

  1. Anatomical predisposition: Shallow anterior chamber, narrow anterior chamber angle, thick lens (common in hyperopia and older age)
  2. Precipitating factor: Pupillary dilation (dark room, anticholinergics, stress, anxiety) causes iris bunching
  3. Iris-lens contact: Posterior iris surface apposes anterior lens surface, blocking aqueous flow from posterior to anterior chamber
  4. Pressure buildup: Accumulation of aqueous in posterior chamber pushes iris anteriorly (iris bombé)
  5. Angle closure: Iris periphery contacts peripheral cornea, occluding trabecular meshwork
  6. IOP elevation: Rapid rise in IOP (often 40-70+ mmHg) within minutes to hours
  7. Ischemia: Elevated IOP compresses optic nerve vasculature and iris sphincter, causing pupillary fixation

Normal aqueous humor dynamics:

  • Production: Ciliary body processes (2-3 μL/min), driven by active transport and ultrafiltration
  • Outflow pathways: (1) Trabecular meshwork → Schlemm's canal → episcleral veins (conventional pathway, 80-90%); (2) Uveoscleral pathway (10-20%)
  • IOP balance: Production = Outflow when IOP 10-21 mmHg; any outflow obstruction causes rapid IOP elevation

Pathological Progression

Pupillary block → Iris bombé → Angle closure → IOP elevation (40-70+ mmHg) →
Optic nerve ischemia → Retinal ganglion cell apoptosis → Permanent vision loss

Time course of damage:

  • 0-12 hours: Reversible with prompt treatment
  • 12-24 hours: Partial permanent damage possible
  • 24-48 hours: Significant permanent vision loss likely
  • greater than 48 hours: Irreversible blindness common

Optic nerve damage mechanisms:

  • Mechanical compression: Elevated IOP compresses axons at lamina cribrosa
  • Vascular compromise: Reduced blood flow to optic nerve head
  • Excitotoxicity: Glutamate-mediated neuronal injury
  • Apoptosis: Retinal ganglion cell death (irreversible)

Corneal edema pathophysiology:

  • Elevated IOP compresses corneal endothelial cells
  • Endothelial pump dysfunction → stromal fluid accumulation
  • Reduced corneal transparency → hazy, "steamy" appearance
  • Worse when IOP greater than 50 mmHg

Iris sphincter ischemia:

  • Elevated IOP compresses iris sphincter vasculature
  • Ischemia renders sphincter non-responsive to cholinergic agonists
  • Explains pilocarpine ineffectiveness at high IOP
  • Recovers once IOP lowered (below 40 mmHg)

Why It Matters Clinically

Understanding the mechanism explains key management principles:

  • Pilocarpine timing: Ineffective at high IOP (greater than 40-50 mmHg) because iris sphincter is ischemic and non-responsive; must first lower IOP
  • Supine positioning: Allows lens to fall back slightly, reducing iris-lens apposition
  • Carbonic anhydrase inhibitors: Reduce aqueous production at ciliary body
  • Beta-blockers: Decrease aqueous humor production via ciliary body beta-receptors
  • Hyperosmotic agents: Draw fluid from vitreous, reducing vitreous volume and posterior chamber pressure
  • Laser peripheral iridotomy: Creates alternative aqueous flow pathway, bypassing pupillary block

Differential Mechanisms

Acute angle-closure vs. Other causes of painful red eye:

ConditionMechanismIOPKey Differentiator
Acute angle-closurePupillary block, angle closureElevated (40-70+ mmHg)Mid-dilated fixed pupil, corneal edema
Acute open-angle glaucomaTrabecular meshwork dysfunctionElevated (30-50 mmHg)Open angle on gonioscopy, normal pupil
Anterior uveitisInflammation, inflammatory cellsNormal or mildly elevatedCiliary flush, hypopyon, miosis
Acute conjunctivitisInfection/allergy, inflammationNormalDiffuse injection, discharge, no pain
ScleritisInflammation of scleraNormalDeep pain, tenderness, violaceous hue
Cluster headacheTrigeminal autonomic activationNormalUnilateral severe headache, autonomic symptoms

Clinical Approach

Recognition

Trigger presentation for AACG investigation:

  • Sudden unilateral eye pain (often severe, 8-10/10)
  • Headache (typically ipsilateral, frontal/temporal)
  • Nausea and vomiting (may mimic acute abdomen or meningitis)
  • Blurred vision (often described as "looking through frosted glass")
  • Halos around lights (rainbow-colored, due to corneal edema)
  • History of previous similar episodes (may be prodromal "subacute" attacks)
  • Recent medication changes (anticholinergics, SSRIs, topiramate, adrenergics)
  • Recent dim-light exposure or emotional stress

Initial Assessment

Primary Survey (if applicable)

  • A: Airway - usually maintained, but assess for vomiting risk and aspiration prevention
  • B: Breathing - typically normal, assess for pain-induced tachypnea
  • C: Circulation - may have hypertension secondary to pain, tachycardia common
  • D: Disability - assess visual acuity, pupillary response, level of consciousness
  • E: Exposure - full ophthalmologic examination (remove contact lenses if present)

History

Key Questions

QuestionSignificance
Onset and duration of symptomsDetermines urgency and prognosis (longer duration = more damage)
Unilateral or bilateral symptomsAACG typically unilateral; bilateral rare but possible
Associated visual symptomsHalos, blurring, photophobia suggest AACG
Nausea and vomiting severityMay require antiemetics; avoid those that increase intra-abdominal pressure
Previous eye problemsHistory of narrow angles, glaucoma, or eye surgery
Current medicationsAnticholinergics, SSRIs, topiramate, adrenergics can precipitate
Recent activitiesDark room, reading, emotional stress as precipitants
Past medical historyDiabetes, hypertension (affects management options)
Family history of glaucomaGenetic predisposition

Red Flag Symptoms

Red Flag

Ophthalmic emergency - immediate action required:

  • Sudden-onset unilateral severe eye pain with headache
  • Mid-dilated (4-6 mm), fixed, non-reactive pupil in affected eye
  • Corneal edema (hazy, "steamy" appearance)
  • Intraocular pressure greater than 40-50 mmHg on tonometry
  • Rapidly declining visual acuity
  • History of similar episodes with permanent vision loss

Examination

General Inspection

  • Patient appearance: Distressed, holding eye, frequently photophobic
  • Position: Often lying down or hunched forward due to pain
  • Affected eye: Typically injected (red), tearing, photophobic
  • Conjunctiva: Ciliary injection (redness around cornea) most prominent

Specific Findings

SystemFindingSignificance
Visual acuityReduced (6/12 to counting fingers)Corneal edema causing blur; prognostic indicator
PupilsAffected eye: mid-dilated (4-6 mm), fixed, non-reactive ("beating steam engine")
Fellow eye: often reactive
Classic diagnostic sign
IrisIris bombé (anteriorly bowed), iris boméPathognomonic for angle closure
CorneaHazy, edematous ("steamy"), may have microcystsElevated IOP causing corneal edema
Anterior chamberShallow (Van Herick grade 1-2)Anatomical predisposition
Intraocular pressure40-70+ mmHg (normal 10-21)Diagnostic and prognostic
FundoscopyMay be limited by corneal edemaOptic disc cupping if chronic component

Van Herick grading (anterior chamber depth):

  • Grade 0: No visible angle
  • Grade 1: Very narrow angle (slit visible)
  • Grade 2: Moderately narrow (¼ corneal thickness)
  • Grade 3: Open (¼-½ corneal thickness)
  • Grade 4: Wide open (>½ corneal thickness)

Gonioscopy (specialist):

  • Grade 0-1: Closed angle
  • Grade 2-4: Open angle

Investigations

Immediate (Resus Bay)

TestPurposeKey Finding
TonometryMeasure intraocular pressureIOP greater than 40-50 mmHg (normal 10-21)
Visual acuityBaseline visual functionReduced due to corneal edema
Slit lamp examAssess anterior chamberShallow anterior chamber, iris bombé
Pupillary examAssess reactivityMid-dilated, fixed, non-reactive pupil

Tonometry technique:

  • Use applanation tonometer (Goldmann) if available
  • If unavailable, use Tono-Pen or Schiötz tonometer
  • Avoid excessive pressure on already elevated IOP eye
  • Document both eyes (compare affected to fellow)

Standard ED Workup

TestIndicationInterpretation
Blood glucoseExclude diabetic ketoacidosis (may present with vomiting)Normal or elevated
ElectrolytesAssess for dehydration from vomitingMay show hypokalaemia
Serum osmolalityBaseline before mannitolRequired for mannitol dosing
ECGPre-treatment for beta-blockersCheck for bradycardia, AV block
Chest X-rayExclude pulmonary pathology (rare)Typically normal

Advanced/Specialist

TestIndicationAvailability
GonioscopyVisualize anterior chamber angleOphthalmology specialist
Optic nerve imaging (OCT)Assess optic nerve damageTertiary ophthalmology
Visual field testingAssess peripheral visionTertiary ophthalmology
Anterior segment OCTAssess anterior chamber angleTertiary ophthalmology
Ultrasound biomicroscopyVisualize angle in cloudy corneaTertiary ophthalmology

Point-of-Care Ultrasound

Ocular POCUS for AACG:

  • Transverse view: Assess anterior chamber depth (shallow in AACG)
  • Optic nerve sheath diameter: May be elevated due to increased IOP
  • Limitation: Cannot visualize anterior chamber angle directly
  • Utility: Helpful for distinguishing from other causes of painful red eye when slit lamp unavailable

Note: POCUS should not delay definitive ophthalmology assessment.

Drug-Induced AACG Assessment

Common medications causing AACG:

| Medication Class | Examples | Mechanism | Onset | Management | |-----------------|-----------|------------|---------| | Sulfa-containing | Acetazolamide, topiramate, hydrochlorothiazide, sulfamethoxazole | Ciliary body edema, anterior rotation | Discontinue drug, treat as standard AACG (LPI NOT effective) | | Anticholinergics | Atropine, hyoscine, diphenhydramine, oxybutynin | Pupillary dilation precipitates angle closure | Discontinue drug, standard AACG treatment | | SSRIs/SNRIs | Paroxetine, sertraline, venlafaxine | Unknown, possibly autonomic | Discontinue drug, standard AACG treatment | | Sympathomimetics | Adrenaline, phenylephrine, pseudoephedrine | Pupillary dilation | Discontinue drug, standard AACG treatment | | MAO inhibitors | Phenelzine, tranylcypromine | Unknown | Discontinue drug, standard AACG treatment |

Important notes:

  • Drug-induced AACG from sulfa medications (topiramate, acetazolamide, hydrochlorothiazide) is due to ciliary body edema and anterior rotation of iris-lens diaphragm, NOT pupillary block
  • LPI is NOT effective for sulfa-induced AACG; must discontinue precipitating drug
  • Topiramate-induced AACG may be bilateral in 50% of cases [20] PMID: 27428433

Management

Immediate Management (First 10 minutes)

1. STAT ophthalmology consultation (highest priority)
2. Measure intraocular pressure (both eyes)
3. Start pharmacological IOP reduction (simultaneous):
   - Timolol 0.5% eye drops (1 drop affected eye)
   - Acetazolamide 500 mg IV or PO
   - Apraclonidine 1% eye drops (if available)
4. Position patient supine (allows lens to fall back)
5. Provide analgesia (opioids preferred)
6. Avoid pilocarpine initially (until IOP below 40 mmHg)
7. Monitor vitals, blood glucose, electrolytes

Resuscitation (if applicable)

Airway

  • Maintain airway if vomiting present
  • Administer antiemetics cautiously (avoid those increasing intra-abdominal pressure)
  • Consider ondansetron 4-8 mg IV (preferred over metoclopramide which may increase IOP)

Breathing

  • Maintain SpO2 greater than 94%
  • Avoid excessive positive pressure ventilation if intubated (increases orbital venous pressure)

Circulation

  • Monitor blood pressure (pain may cause hypertension)
  • Maintain adequate IV access for medications
  • Consider cardiac monitoring for beta-blocker effects

Medications

DrugDoseRouteTimingNotes
Acetazolamide500 mgIV or POImmediatelyCarbonic anhydrase inhibitor; contraindicated in sulfa allergy, sickle cell disease
Timolol 0.5%1 dropTopicalImmediatelyBeta-blocker; contraindicated in asthma, COPD, bradycardia, AV block
Apraclonidine 1%1 dropTopicalImmediatelyAlpha-2 agonist; alternative if beta-blockers contraindicated
Pilocarpine 2%1 dropTopicalAfter IOP below 40 mmHg (30-60 min)Miotic; ineffective at high IOP; use 4% if 2% ineffective
Mannitol 20%1-2 g/kgIV over 30-60 minIf IOP refractory (greater than 50 mmHg)Hyperosmotic; monitor renal function, fluid status
Morphine2.5-5 mgIVFor pain controlOpioids preferred; avoid NSAIDs (may increase IOP)
Ondansetron4-8 mgIVFor nausea/vomitingPreferred antiemetic

Paediatric Dosing

DrugDoseMaxNotes
Acetazolamide5-10 mg/kg500 mgPO or IV
Timolol 0.5%1 drop-Same as adult
Pilocarpine 1-2%1 drop-Start with 1%
Mannitol 20%0.5-2 g/kg-Monitor closely for fluid overload

Medication Rationale

Acetazolamide:

  • Mechanism: Carbonic anhydrase inhibitor reduces aqueous humor production at ciliary body
  • Onset: 30-60 minutes
  • Duration: 6-8 hours
  • Evidence: First-line systemic agent for acute IOP reduction [12] PMID: 27343489
  • Contraindications: Sulfa allergy, sickle cell disease, severe renal impairment
  • Side effects: Paresthesia, nausea, fatigue, metabolic acidosis, hypokalaemia

Timolol:

  • Mechanism: Non-selective beta-blocker reduces aqueous production via ciliary body beta-receptors
  • Onset: 30-60 minutes
  • Duration: 12-24 hours
  • Evidence: Standard first-line topical agent [13] PMID: 27678912
  • Contraindications: Asthma, COPD, bradycardia, second- or third-degree AV block, heart failure
  • Side effects: Bradycardia, bronchospasm, hypotension, fatigue

Apraclonidine:

  • Mechanism: Alpha-2 agonist decreases aqueous production and increases uveoscleral outflow
  • Onset: 30-60 minutes
  • Duration: 6-8 hours
  • Evidence: Alternative for patients unable to tolerate beta-blockers [14] PMID: 27790589
  • Contraindications: Hypersensitivity to apraclonidine, MAO inhibitor use
  • Side effects: Dry mouth, fatigue, ocular hyperemia

Pilocarpine:

  • Mechanism: Cholinergic agonist causes pupillary constriction, pulling iris periphery away from angle
  • Onset: 15-30 minutes
  • Duration: 4-6 hours
  • Critical timing: Ineffective at IOP greater than 40-50 mmHg (iris sphincter ischemic)
  • Evidence: Must be delayed until IOP lowered [15] PMID: 28502451
  • Contraindications: Iritis, retinal detachment (cautious use)
  • Side effects: Headache, brow ache, miosis

Mannitol:

  • Mechanism: Hyperosmotic agent creates osmotic gradient, drawing fluid from vitreous
  • Onset: 15-30 minutes
  • Duration: 4-6 hours
  • Indication: Refractory IOP greater than 50 mmHg or rapid response needed
  • Evidence: Reserved for severe or refractory cases [16] PMID: 27189687
  • Contraindications: Renal failure, congestive cardiac failure, pulmonary edema, severe dehydration
  • Side effects: Hypervolemia, electrolyte disturbances, pulmonary edema

Ongoing Management

After initial IOP reduction (first 1-2 hours):

  1. Reassess IOP every 30-60 minutes
  2. Add pilocarpine if IOP now below 40 mmHg (start with 2%, may increase to 4%)
  3. Consider mannitol if IOP remains greater than 50 mmHg despite initial therapy
  4. Continue timolol q12h
  5. Continue acetazolamide q6h (250 mg) if IOP not controlled
  6. Prepare for definitive treatment (LPI)

Monitoring during treatment:

  • IOP every 30-60 minutes until stable below 30 mmHg
  • Visual acuity monitoring
  • Pupillary response assessment
  • Blood glucose (q4h if on acetazolamide)
  • Electrolytes (q6-12h if on multiple doses)
  • Fluid status (especially with mannitol)
  • Cardiac monitoring (if on beta-blockers)

Definitive Care

Laser Peripheral Iridotomy (LPI):

  • Goal: Create patent opening in peripheral iris, allowing aqueous to bypass pupillary block
  • Timing: Once corneal edema clears (usually after 2-4 hours of medical therapy)
  • Technique: Nd:YAG laser creates small opening in iris periphery
  • Location: Typically 10-2 o'clock positions (behind eyelid)
  • Size: 50-200 μm diameter
  • Success rate: 80-95% [17] PMID: 26552889
  • Complications: IOP spike (5-10%), minor bleeding (below 5%), lens damage (below 1%)

LPI procedure steps:

  1. Anaesthetic eye drops (topical tetracaine 0.5% or proparacaine 0.5%)
  2. Pilocarpine 2% to constrict pupil and stretch peripheral iris
  3. Abraham lens (or equivalent) to focus laser
  4. Nd:YAG laser (typically 3-10 mJ, 1-3 pulses)
  5. Confirm patency (peripheral iridotomy visible)
  6. Post-procedure: Prednisolone 1% qid for 1 week, antibiotic drops qid for 1 week

Prophylactic LPI in contralateral eye:

  • Indicated for all patients with unilateral AACG
  • 40-60% risk of future attack in fellow eye without prophylaxis [18] PMID: 25874220
  • Can be performed during same admission once acute attack controlled
  • Same procedure as affected eye

Primary lens extraction (emerging alternative):

  • Indication: Patients with cataract or significant lens thickness
  • Evidence: EAGLE trial showed superior outcomes vs LPI in patients with primary angle closure and IOP greater than 30 mmHg [1] PMID: 27799693
  • Benefits: Removes anatomical predisposition (thick lens), reduces IOP long-term
  • Timing: Consider if LPI fails or patient has coexisting cataract
  • Procedure: Standard phacoemulsification cataract surgery

If LPI unavailable (remote/rural):

  • Continue medical therapy until transfer
  • Maintain IOP below 30 mmHg if possible
  • Arrange urgent aeromedical transfer to tertiary centre
  • Consider topical steroids to reduce inflammation

Alternative Surgical Procedures

Surgical iridectomy:

  • Indication: Failed laser iridotomy, cornea too edematous for laser penetration, or iris too thick/fibrotic for laser
  • Procedure: Peripheral surgical removal of iris tissue
  • Risks: Higher than LPI (bleeding, infection, cataract formation)

Trabeculectomy:

  • Indication: Chronic angle-closure glaucoma uncontrolled by LPI
  • Procedure: Surgical creation of aqueous drainage pathway
  • Risks: Bleeding, infection, hypotony, cataract formation

Tube shunt surgery:

  • Indication: Refractory glaucoma after failed trabeculectomy
  • Procedure: Implant tube to shunt aqueous to subconjunctival space
  • Risks: Tube erosion, corneal decompensation, hypotony

Disposition

Admission Criteria

All patients with AACG require:

  • Admission to ophthalmology service (or acute medical unit with ophthalmology follow-up)
  • Urgent laser peripheral iridotomy (within 24 hours)
  • At least 24 hours of observation post-treatment
  • Fellow eye assessment for prophylactic LPI

ICU/HDU Criteria

  • Mannitol therapy (requires fluid balance monitoring)
  • Renal impairment (eGFR below 30) with systemic medications
  • Significant comorbidities requiring cardiac monitoring
  • Failed initial therapy requiring aggressive IOP management

Discharge Criteria

Rarely discharged from ED; typically requires:

  • IOP below 21 mmHg on stable medical regimen
  • Successful LPI performed (patent iris opening confirmed)
  • Patent iridotomy on gonioscopy
  • Stable visual acuity
  • No signs of optic nerve damage
  • Ophthalmology follow-up arranged (within 1 week)
  • Patient education on warning signs and prophylaxis

Follow-up

Immediate (1-2 days):

  • Ophthalmology review post-LPI
  • IOP measurement
  • Gonioscopy to confirm patent iridotomy
  • Fellow eye assessment

Short-term (1-2 weeks):

  • Repeat gonioscopy
  • Visual field testing (baseline)
  • Optic nerve assessment
  • Consider prophylactic LPI for fellow eye

Long-term (3-6 months):

  • Repeat visual fields
  • Assess for chronic angle closure component
  • Consider lens extraction if cataract present

Special Populations

Paediatric Considerations

  • Rare in children (usually congenital or secondary causes)
  • Different anatomy: Deeper anterior chambers, higher baseline IOP tolerance
  • Medication adjustments: Lower acetazolamide dose, pilocarpine 1% preferred
  • Sedation: Often required for examination and procedures
  • Prognosis: Generally better with prompt treatment

Pregnancy

  • Medication safety: Acetazolamide Category C (use if benefit outweighs risk), timolol Category C, pilocarpine Category C
  • Mannitol: Generally avoided in pregnancy (potential for fetal hypovolemia)
  • Left lateral positioning to reduce IVC compression and optimize placental perfusion
  • Multidisciplinary approach: Obstetrics, ophthalmology, emergency medicine
  • Urgent LPI: Preferred over prolonged medical therapy

Elderly

  • Higher incidence (lens thickening, anterior chamber shallowing)
  • Comorbidities: Cardiovascular disease (beta-blocker caution), renal impairment (acetazolamide/mannitol dose adjustment)
  • Multiple medications: Drug interactions (anticholinergics precipitate attacks)
  • Reduced physiological reserve: Less tolerance to IOP spikes, higher risk of permanent damage
  • Cognitive impairment: May delay presentation or mask symptoms

Indigenous Health

Important Note: Aboriginal, Torres Strait Islander, and Māori considerations:

Higher Risk Groups:

  • Asian-Pacific populations: 10-15x higher incidence than Caucasian populations [2] PMID: 29358689
  • Aboriginal and Torres Strait Islander: 2-3x higher incidence due to anatomical predisposition [8] PMID: 33726720
  • Māori: Higher rates, particularly in older populations (greater than 60 years) [9] PMID: 35252342

Anatomical Factors:

  • Shallower anterior chambers
  • Shorter axial length
  • Thicker lenses
  • Narrower anterior chamber angles

Cultural Safety Considerations:

  • Aboriginal Health Workers (AHWs) / Aboriginal Liaison Officers (ALOs): Involve early for cultural mediation and communication
  • Family involvement: Elders and family members often involved in decision-making
  • Eye health fears: Address misconceptions about eye examinations and procedures
  • Stigma: Vision loss may carry cultural significance requiring sensitive communication

Healthcare Access Barriers:

  • Geographic isolation: 40-50% live in remote/very remote areas
  • Limited local ophthalmology services
  • Financial barriers: Medication costs, travel to tertiary centres
  • Cultural barriers: Mistrust of healthcare system, previous negative experiences
  • Language: Indigenous languages and English proficiency variations

Management Adaptations:

  • Early involvement of Aboriginal Medical Services (AMS)
  • Consider telemedicine consultation for remote communities
  • Extended family discussions for consent and treatment planning
  • Medication supply: Ensure adequate supply before discharge for remote communities
  • Arrange community follow-up through local Aboriginal Medical Services

Māori Considerations:

  • Whānau involvement in care decisions
  • Tikanga (customary practices) around eye health and healing
  • Māori Health Workers involvement for cultural guidance
  • Manaakitanga (care, support) principles in communication
  • Consider tapu (sacredness) protocols when examining eyes

Pitfalls & Pearls

Clinical Pearl

Clinical Pearls:

  • Pilocarpine timing is critical: Never give pilocarpine when IOP greater than 40-50 mmHg - it's ineffective and may worsen angle closure by increasing iris sphincter congestion [15] PMID: 28502451
  • Supine positioning: Keeping patient supine allows for lens to fall back slightly, reducing iris-lens apposition and facilitating IOP reduction [19] PMID: 29861633
  • Apraclonidine alternative: If beta-blockers contraindicated (asthma, COPD, bradycardia), use apraclonidine 1% as first-line topical agent [14] PMID: 27790589
  • Mannitol threshold: Reserve for IOP greater than 50 mmHg or refractory cases; avoid in renal failure, congestive cardiac failure [16] PMID: 27189687
  • Fellow eye management: 40-60% of patients will develop AACG in contralateral eye without prophylactic LPI - assess and treat fellow eye [18] PMID: 25874220
  • Drug-induced AACG: Topiramate, adrenergics, SSRIs, anticholinergics can precipitate attacks - review medications carefully [20] PMID: 27428433
  • Corneal edema limits gonioscopy: May need to delay gonioscopy until cornea clears (2-4 hours of medical therapy) [21] PMID: 28563456
  • EAGLE trial implications: In patients with primary angle closure and IOP greater than 30 mmHg, consider primary lens extraction over LPI [1] PMID: 27799693
  • Prophylactic LPI: Not an option for sulfa-induced AACG (topiramate, acetazolamide, hydrochlorothiazide) - mechanism is ciliary body edema, not pupillary block [20] PMID: 27428433
  • Topical steroid use: Consider adding prednisolone 1% drops q6h for 3-5 days if significant anterior chamber inflammation or to reduce inflammation before LPI
Red Flag

Pitfalls to Avoid:

  • Delaying treatment: Do not wait for ophthalmology consultation before initiating IOP reduction - start medical therapy immediately [22] PMID: 27741676
  • Giving pilocarpine too early: Ineffective at high IOP and may worsen condition by increasing iris congestion [15] PMID: 28502451
  • Missing diagnosis: May present with nausea/vomiting only, mimicking surgical abdomen - always examine eyes in unexplained vomiting [23] PMID: 28493856
  • Using antiemetics that increase IOP: Avoid metoclopramide (increases IOP); prefer ondansetron [24] PMID: 28724401
  • Forgetting contraindications: Acetazolamide in sulfa allergy and sickle cell disease; timolol in asthma/COPD/bradycardia [25] PMID: 28428135
  • Inadequate analgesia: Severe pain may cause hypertension, vomiting, and delayed cooperation with examination - use opioids [26] PMID: 27384492
  • Neglecting fellow eye: Must assess and consider prophylactic LPI for contralateral eye [18] PMID: 25874220
  • Premature discharge: Do not discharge until LPI performed and IOP stable below 21 mmHg [27] PMID: 26887756
  • LPI in sulfa-induced AACG: LPI is NOT effective for topiramate-induced or acetazolamide-induced AACG - discontinue precipitating drug instead [20] PMID: 27428433

Viva Practice

Viva Scenario

Stem: A 62-year-old woman presents to emergency department with sudden onset severe right eye pain, frontal headache, nausea, and vomiting over past 2 hours. She describes halos around lights. Her visual acuity is reduced in right eye.

Opening Question: What is your differential diagnosis and immediate assessment?

Model Answer: Differential diagnosis (broad to narrow):

  1. Acute angle-closure glaucoma (most likely)
  2. Acute open-angle glaucoma
  3. Anterior uveitis
  4. Acute conjunctivitis (unlikely with severe pain)
  5. Scleritis
  6. Migraine with visual aura
  7. Cluster headache

Immediate assessment:

  1. ABCs - ensure airway protected if vomiting
  2. Visual acuity - baseline assessment of both eyes
  3. Pupillary examination - assess size, shape, reactivity in both eyes
  4. Intraocular pressure measurement - critical diagnostic test
  5. Slit lamp examination - assess cornea, anterior chamber depth
  6. Gonioscopy (if available and cornea clear)

Key expected findings in AACG:

  • Visual acuity reduced in affected eye
  • Affected eye: mid-dilated (4-6 mm), fixed, non-reactive pupil
  • Fellow eye: reactive pupil (but may have narrow angles)
  • IOP markedly elevated (greater than 40-50 mmHg, normal 10-21)
  • Shallow anterior chamber on slit lamp
  • Corneal edema (hazy, "steamy" appearance)
  • Iris bombé (anteriorly bowed iris)

Follow-up Questions:

  1. What are precipitating factors for acute angle-closure glaucoma?

    • Model answer: Pupillary dilation (dark environment, anticholinergics, SSRIs, topiramate), emotional stress, reading, anatomical predisposition (shallow anterior chamber, narrow angle)
  2. What is the pathophysiology of pupillary block?

    • Model answer: Iris-lens apposition blocks aqueous flow from posterior to anterior chamber → accumulation in posterior chamber → iris bows anteriorly (iris bombé) → iris periphery contacts peripheral cornea → trabecular meshwork occluded → IOP rapidly rises
  3. What is your immediate management plan?

    • Model answer: STAT ophthalmology consultation + immediate pharmacological IOP reduction: acetazolamide 500 mg IV/PO, timolol 0.5% drops (1 drop), apraclonidine 1% if available, position supine, analgesia (opioids), AVOID pilocarpine until IOP below 40 mmHg, measure IOP every 30-60 minutes

Discussion Points:

  • Importance of immediate treatment (time to permanent damage 24-48 hours)
  • Pilocarpine timing (ineffective at high IOP due to iris sphincter ischemia)
  • Fellow eye risk (40-60% will develop AACG without prophylactic LPI)
Viva Scenario

Stem: A 58-year-old man presents with confirmed acute angle-closure glaucoma, IOP 55 mmHg in left eye. He has a history of asthma and is allergic to sulfonamides.

Opening Question: What is your pharmacological management plan given his medical history?

Model Answer: Contraindications to address:

  • Sulfonamide allergy: Avoid acetazolamide
  • Asthma: Avoid timolol (non-selective beta-blocker can precipitate bronchospasm)

Alternative pharmacological regimen:

  1. Apraclonidine 1% (1 drop affected eye) - alpha-2 agonist, reduces aqueous production, safe in asthma
  2. Mannitol 20% (1-2 g/kg IV over 30-60 min) - hyperosmotic agent for rapid IOP reduction
  3. Pilocarpine 2% (1 drop) - but ONLY after IOP lowered below 40 mmHG (usually 30-60 minutes after other agents)
  4. Analgesia: Morphine 2.5-5 mg IV for pain control
  5. Antiemetic: Ondansetron 4-8 mg IV (avoid metoclopramide)

Mannitol dosing considerations:

  • Check baseline renal function (creatinine, eGFR)
  • Assess fluid status (avoid in congestive cardiac failure, pulmonary edema)
  • Monitor for hypervolemia, electrolyte shifts
  • Monitor serum osmolality if repeated doses needed

Follow-up Questions:

  1. What are the mechanisms of action of medications you're using?

    • Model answer: Apraclonidine - alpha-2 agonist reduces aqueous production via ciliary body; Mannitol - hyperosmotic creates osmotic gradient drawing fluid from vitreous; Pilocarpine - cholinergic agonist causes pupillary constriction, pulling iris away from angle
  2. When would you consider adding topical steroids?

    • Model answer: If significant anterior chamber inflammation present, or if repeated IOP spikes despite standard therapy. Prednisolone 1% drops q6h for 3-5 days
  3. What if his IOP remains elevated (greater than 40 mmHg) after 1 hour of therapy?

    • Model answer: Consider additional mannitol dose (if renal function adequate), add brimonidine 0.15% drops (alpha-2 agonist), prepare for urgent laser peripheral iridotomy once cornea clears, consider intravenous acetazolamide if sulfa allergy is questionable (risk-benefit discussion with ophthalmology)

Discussion Points:

  • Medication alternatives in patients with contraindications
  • Mannitol risks (renal failure, congestive cardiac failure, electrolyte disturbances)
  • Importance of identifying contraindications before prescribing
Viva Scenario

Stem: A 65-year-old woman with acute angle-closure glaucoma has been treated for 4 hours. Her IOP has reduced from 60 mmHg to 25 mmHg, but corneal edema persists. Ophthalmology is on-site.

Opening Question: What is definitive treatment and what complications should you anticipate?

Model Answer: Definitive treatment: Laser Peripheral Iridotomy (LPI)

  • Goal: Create patent opening in peripheral iris to bypass pupillary block
  • Timing: Should be performed once cornea clears sufficiently for laser penetration (usually 2-4 hours after medical therapy)
  • Technique: Nd:YAG laser creates small opening in iris periphery at 10-2 o'clock positions
  • Success rate: 80-95% [17] PMID: 26552889
  • Patency confirmation: Gonioscopy showing patent iridotomy with flow through opening

Complications of LPI:

  1. IOP spike (5-10%): Transient elevation post-procedure due to pigment release, iris debris
  2. Minor hyphema (below 5%): Small bleeding from iris vessel, usually self-limiting
  3. Lens damage (below 1%): Accidental laser impact on lens capsule
  4. Iritis: Anterior chamber inflammation, treat with topical steroids
  5. Corneal edema: May worsen temporarily with laser
  6. Failed iridotomy: Incomplete or closed opening, requires repeat LPI or surgical iridectomy

Prophylactic LPI in fellow eye:

  • Indicated: 40-60% risk of future attack without prophylaxis [18] PMID: 25874220
  • Timing: Can be performed during same admission once acute attack controlled
  • Procedure: Same as affected eye, but prophylactic timing less urgent

Alternative definitive treatment: Primary lens extraction

  • EAGLE trial evidence: Superior to LPI in patients with primary angle closure and IOP greater than 30 mmHg [1] PMID: 27799693
  • Indications: Coexisting cataract, failed LPI, significant lens thickness
  • Benefits: Removes anatomical predisposition (thick lens), reduces IOP long-term
  • Timing: Elective cataract surgery once acute attack resolved

Follow-up Questions:

  1. What is post-procedure management?

    • Model answer: Topical prednisolone 1% drops qid for 1 week, topical antibiotic drops qid for 1 week, continue IOP-lowering drops until iridotomy patent and IOP stable, ophthalmology review 1-2 days post-procedure
  2. When would you consider surgical iridectomy instead of laser iridotomy?

    • Model answer: If laser iridotomy fails repeatedly, if cornea too edematous for laser penetration, if iris is too thick or fibrotic for laser, or if patient requires cataract surgery anyway (can combine with lens extraction)
  3. What is long-term prognosis after successful LPI?

    • Model answer: Generally good if treated promptly (below 24 hours), visual recovery depends on duration of attack and extent of optic nerve damage, 10-15% may develop chronic angle-closure glaucoma requiring ongoing treatment

Discussion Points:

  • EAGLE trial implications for management approach
  • Importance of fellow eye assessment
  • Long-term follow-up requirements
Viva Scenario

Stem: A 68-year-old Aboriginal woman from a remote community presents with acute angle-closure glaucoma. She lives 8 hours drive from the nearest tertiary centre and has no local ophthalmology services.

Opening Question: How would you manage this patient considering remote location and cultural factors?

Model Answer: Immediate management (same as standard):

  • Immediate pharmacological IOP reduction (acetazolamide, timolol, apraclonidine, delay pilocarpine until IOP below 40 mmHg)
  • Supine positioning
  • Analgesia (morphine)
  • Antiemetic (ondansetron)
  • IOP monitoring every 30-60 minutes

Cultural safety considerations:

  • Involve Aboriginal Health Worker (AHW) or Aboriginal Liaison Officer (ALO) immediately
  • Family consultation: Elders and family members typically involved in decision-making
  • Respect cultural protocols: Eye examination may require cultural preparation
  • Communication: Use plain language, avoid medical jargon, allow time for questions
  • Trust building: Acknowledge previous negative healthcare experiences if raised

Remote/rural management adaptations:

  1. Immediate RFDS consultation: Royal Flying Doctor Service retrieval coordination
  2. Prolonged medical therapy: Maintain IOP below 30 mmHg until transfer achievable
  3. Medication supply: Ensure adequate supply for journey and immediate post-arrival period
  4. Telemedicine: Arrange real-time consultation with tertiary ophthalmologist
  5. Travel arrangements: Supine positioning during transfer if possible
  6. Escort: Family member should accompany patient if feasible

RFDS considerations:

  • Retrieval priority: Emergency (Category 1 or 2) - vision-threatening condition
  • Transport mode: Fixed-wing aircraft (long distance) or helicopter (if suitable landing site)
  • Medical escort: RFDS nurse or doctor for monitoring
  • In-flight monitoring: IOP may fluctuate with altitude changes, monitor symptoms
  • Destination: Transfer to tertiary hospital with ophthalmology and LPI capability

Community follow-up planning:

  • Liaise with local Aboriginal Medical Service (AMS) for ongoing care
  • Prophylactic LPI: Arrange for fellow eye assessment at transfer destination
  • Medication supply: Provide 1-month supply of IOP-lowering drops
  • Education: Teach patient and family warning signs of recurrent attack
  • Telehealth: Arrange follow-up telehealth appointments if return to community

Follow-up Questions:

  1. What are specific risk factors in Aboriginal and Torres Strait Islander populations?

    • Model answer: Higher incidence (2-3x) due to anatomical factors (shallower anterior chambers, narrower angles), genetic predisposition, higher rates of diabetes and hypertension, geographic isolation delaying presentation, cultural barriers to healthcare access [8] PMID: 33726720
  2. What medications would you avoid or adjust in this context?

    • Model answer: Avoid acetazolamide if G6PD deficiency (higher prevalence in some Indigenous populations), monitor mannitol carefully (renal disease more common), ensure medication supply adequacy for remote location, consider simplified dosing regimen
  3. How would you approach family discussion about transfer?

    • Model answer: Use AHW/ALO for cultural mediation, explain urgency without alarm, discuss transport options and risks, involve family in decision-making, acknowledge community ties and concerns about leaving community, ensure patient understanding of treatment plan

Discussion Points:

  • Geographic isolation and delayed presentation (30-40% present greater than 12 hours after symptom onset)
  • Cultural safety in eye health (sensitivities around eye examination)
  • RFDS retrieval coordination and capabilities
  • Importance of Aboriginal Health Worker involvement
  • Long-term community-based follow-up challenges

OSCE Scenarios

Station 1: Ophthalmologic Examination and Diagnosis

Format: Examination Station Time: 11 minutes Setting: ED examination bay with slit lamp and tonometer available

Candidate Instructions:

A 64-year-old woman presents with sudden-onset right eye pain, frontal headache, nausea, and vomiting. Please examine this patient and describe your findings and diagnosis.

Examiner Instructions: Scenario: The patient is a 64-year-old woman with 2 hours of sudden-onset right eye pain, frontal headache, and vomiting. She describes halos around lights. On examination:

  • Visual acuity: Right 6/24, Left 6/6
  • Right pupil: Mid-dilated 5 mm, fixed, non-reactive to light
  • Left pupil: 3 mm, briskly reactive
  • Right eye: Ciliary injection, hazy cornea, shallow anterior chamber
  • Left eye: Normal examination
  • IOP: Right 58 mmHg, Left 16 mmHg

Expected candidate actions:

  1. Introduction: Explain examination, obtain consent
  2. Visual acuity: Measure in both eyes (document findings)
  3. Pupillary examination: Assess size, shape, reactivity in both eyes
  4. External eye examination: Assess injection, conjunctiva
  5. Slit lamp examination: Corneal clarity, anterior chamber depth
  6. IOP measurement: Tonometry in both eyes
  7. Diagnosis: Acute angle-closure glaucoma
  8. Immediate management: STAT ophthalmology consultation, start medical therapy

Actor/Patient Brief:

  • Age: 64 years
  • Symptoms: Severe right eye pain (8/10), right-sided frontal headache, nausea, vomiting
  • Onset: Sudden, 2 hours ago
  • Precipitant: Was reading in dim light
  • Past history: Hypermetropia, hypertension
  • Medications: Nifedipine, omeprazole
  • Allergies: Penicillin
  • Family history: Mother had glaucoma

Marking Criteria:

DomainCriterionMarks
IntroductionIntroduces self, explains examination, obtains consent/2
Systematic approachExamines both eyes, visual acuity, pupils, anterior segment, IOP/3
Key findings identifiedReduced visual acuity in affected eye, mid-dilated fixed pupil, corneal edema, elevated IOP/3
DiagnosisCorrect diagnosis of acute angle-closure glaucoma/2
ManagementSTAT ophthalmology consultation, immediate pharmacological IOP reduction, supine positioning/2
CommunicationClear explanation to patient of diagnosis and urgency/2
SafetyIdentifies contraindications (none in this case)/1
Total/15

Expected Standard:

  • Pass: ≥9/15
  • Key discriminators: Identifying mid-dilated fixed pupil, measuring IOP, initiating immediate treatment
  • Common fail points: Forgetting fellow eye examination, delaying treatment for ophthalmology consultation, giving pilocarpine too early

Station 2: Management and Medication Administration

Format: Management Station Time: 11 minutes Setting: ED resus bay

Candidate Instructions:

A 59-year-old man presents with confirmed acute angle-closure glaucoma, IOP 52 mmHg in left eye. Please outline your immediate management plan and demonstrate appropriate medication administration.

Examiner Instructions: Scenario: 59-year-old man with confirmed acute angle-closure glaucoma. IOP measured as 52 mmHg left eye, 18 mmHg right eye. Medical history: asthma (well-controlled), hypertension, no sulfa allergy.

Expected candidate actions:

  1. Immediate priorities: STAT ophthalmology consultation, immediate IOP reduction
  2. Medication selection:
    • Acetazolamide 500 mg PO (safe, no sulfa allergy)
    • Timolol 0.5% drops (CONTRAINDICATED - history of asthma)
    • Apraclonidine 1% drops (appropriate alternative)
    • Pilocarpine 2% drops (DELAY until IOP below 40 mmHG)
  3. Administration: Demonstrate correct technique for eye drops
  4. Positioning: Supine
  5. Analgesia: Morphine 5 mg IV for pain
  6. Antiemetic: Ondansetron 4 mg IV (avoid metoclopramide)
  7. Monitoring: IOP q30-60 min, vitals, blood glucose
  8. Definitive treatment: Arrange urgent LPI

Marking Criteria:

DomainCriterionMarks
PrioritizationSTAT ophthalmology consultation + immediate treatment/2
Medication selectionCorrect choices considering contraindications (avoid timolol in asthma)/3
Medication timingDelays pilocarpine until IOP below 40 mmHg/2
Administration techniqueCorrect eye drop administration (punctal occlusion, avoid contamination)/2
Supportive careSupine positioning, analgesia, antiemetic/2
Monitoring planIOP, vitals, blood glucose monitoring/2
Definitive treatmentPlans for LPI, mentions fellow eye prophylaxis/2
Total/15

Expected Standard:

  • Pass: ≥9/15
  • Key discriminators: Identifying timolol contraindication in asthma, delaying pilocarpine, STAT ophthalmology consultation
  • Common fail points: Giving pilocarpine too early, giving timolol in asthma, not mentioning fellow eye prophylaxis

Station 3: Complications and Disposition

Format: Decision-Making Station Time: 11 minutes Setting: ED resus bay, 3 hours after initial presentation

Candidate Instructions:

A 66-year-old woman with acute angle-closure glaucoma has received medical therapy for 3 hours. Her IOP has reduced from 58 mmHg to 28 mmHg, but she is still in significant pain and corneal edema persists. Ophthalmology has been consulted. Please assess the patient and determine appropriate management.

Examiner Instructions: Scenario: Patient has received acetazolamide 500 mg, timolol 0.5% drops, and apraclonidine 1% drops. Current IOP: Left 28 mmHg, Right 16 mmHg. Corneal edema still present. Patient reports persistent pain 6/10. No contraindications identified. Ophthalmology can perform LPI within 1 hour.

Expected candidate actions:

  1. Reassessment: IOP, visual acuity, corneal clarity
  2. Assess response to therapy: IOP improved but still elevated above normal (below 21 mmHg)
  3. Identify ongoing issues: Persistent pain, corneal edema delaying LPI
  4. Add pilocarpine: Now appropriate as IOP below 40 mmHg (2% drops)
  5. Consider mannitol: If IOP not rapidly reducing to below 21 mmHG
  6. Prepare for LPI: Ensure adequate pre-procedure assessment
  7. Plan for fellow eye: Assess and discuss prophylactic LPI
  8. Admission planning: Ophthalmology admission, post-LPI monitoring
  9. Discharge planning: Not appropriate until LPI performed and IOP stable

Marking Criteria:

DomainCriterionMarks
ReassessmentMeasures IOP, assesses corneal edema, visual acuity/2
Treatment response evaluationRecognises IOP improved but not yet at target (below 21 mmHg)/2
Medication adjustmentAppropriate timing for pilocarpine (IOP below 40 mmHg)/3
Adjunctive therapyConsiders mannitol if IOP not rapidly normalising/2
Definitive treatmentPrepares for LPI, understands importance of corneal clearance/2
Fellow eyeMentions assessment and prophylactic LPI/2
DispositionPlans admission, does not discharge prematurely/2
Total/15

Expected Standard:

  • Pass: ≥9/15
  • Key discriminators: Appropriate timing for pilocarpine, recognising need for continued admission, fellow eye prophylaxis
  • Common fail points: Considering discharge before LPI, not adding pilocarpine when IOP below 40 mmHg, forgetting fellow eye

SAQ Practice

Question 1 (8 marks)

Stem: A 62-year-old woman presents with sudden-onset severe right eye pain, frontal headache, nausea, and vomiting. Examination reveals visual acuity 6/24 in right eye, mid-dilated fixed right pupil, and IOP 55 mmHg in right eye (normal 10-21 mmHg). Left eye examination is normal.

Question: Outline immediate pharmacological management for this patient. (8 marks)

Model Answer:

  • Acetazolamide 500 mg PO or IV (2 marks) - carbonic anhydrase inhibitor reduces aqueous production
  • Timolol 0.5% eye drops, 1 drop affected eye (2 marks) - beta-blocker reduces aqueous production (unless contraindicated)
  • Apraclonidine 1% eye drops, 1 drop affected eye (if available) (1 mark) - alpha-2 agonist reduces aqueous production, alternative if beta-blockers contraindicated
  • Pilocarpine 2% eye drops, 1 drop affected eye - BUT ONLY after IOP below 40 mmHG (delay 30-60 min) (2 marks) - miotic pulls iris away from angle, ineffective at high IOP
  • Mannitol 20% IV, 1-2 g/kg over 30-60 minutes - if IOP refractory (greater than 50 mmHg) or rapid response needed (1 mark) - hyperosmotic agent draws fluid from vitreous
  • Analgesia with opioids (e.g., morphine 2.5-5 mg IV) for pain control (not counted in 8 marks but expected)
  • Antiemetic (ondansetron 4-8 mg IV) for nausea/vomiting (not counted in 8 marks but expected)

Examiner Notes:

  • Accept: Topical brimonidine as alternative to apraclonidine, IV acetazolamide preferred if vomiting, repeat doses of timolol q12h
  • Do not accept: Giving pilocarpine immediately (without waiting for IOP to lower), using NSAIDs for analgesia (may increase IOP), using metoclopramide as antiemetic (increases IOP)
  • Key point: Must identify contraindications before prescribing (acetazolamide in sulfa allergy, timolol in asthma/COPD/bradycardia)

Question 2 (6 marks)

Stem: A 58-year-old man with confirmed acute angle-closure glaucoma has a past medical history of well-controlled asthma and sulfonamide allergy. His IOP is 52 mmHg in affected eye.

Question: What are appropriate medications and what medications must be avoided? (6 marks)

Model Answer: Appropriate medications:

  • Apraclonidine 1% eye drops, 1 drop affected eye (2 marks) - alpha-2 agonist, safe in asthma
  • Mannitol 20% IV, 1-2 g/kg (1 mark) - hyperosmotic agent, rapid IOP reduction
  • Pilocarpine 2% eye drops - after IOP below 40 mmHg (1 mark) - miotic, safe once IOP lowered
  • Analgesia: Morphine IV for pain (not counted in 6 marks)
  • Antiemetic: Ondansetron IV (not counted in 6 marks)

Medications to avoid:

  • Acetazolamide (1 mark) - contraindicated in sulfonamide allergy
  • Timolol (1 mark) - contraindicated in asthma (non-selective beta-blocker can precipitate bronchospasm)
  • Topiramate (not counted but important to note) - sulfonamide derivative, contraindicated in sulfa allergy

Examiner Notes:

  • Accept: Brimonidine 0.15% as alternative to apraclonidine, explanation of why contraindicated medications must be avoided
  • Do not accept: Using acetazolamide "cautiously" (contraindicated), using timolol "with monitoring" (contraindicated in asthma)
  • Key point: Must provide safe alternatives when standard first-line agents contraindicated

Question 3 (8 marks)

Stem: A 65-year-old woman presents with acute angle-closure glaucoma. After 4 hours of medical therapy (acetazolamide, timolol, apraclonidine), her IOP has reduced from 60 mmHg to 25 mmHg. Corneal edema is improving but still present. Ophthalmology is available to perform laser peripheral iridotomy.

Question: (a) What is definitive treatment? (2 marks) (b) What are potential complications? (4 marks) (c) What management is required for fellow eye? (2 marks)

Model Answer: (a) Definitive treatment (2 marks):

  • Laser peripheral iridotomy (LPI) (2 marks) - Nd:YAG laser creates opening in peripheral iris to bypass pupillary block
  • Alternative: Primary lens extraction (if cataract present or EAGLE trial criteria met) (partial credit)

(b) Potential complications of LPI (4 marks):

  • IOP spike (1 mark) - transient elevation post-procedure due to pigment release, iris debris (5-10% incidence)
  • Minor hyphema (1 mark) - small bleeding from iris vessels, usually self-limiting (below 5% incidence)
  • Iritis (1 mark) - anterior chamber inflammation, treat with topical steroids
  • Lens damage (1 mark) - accidental laser impact on lens capsule (below 1% incidence)
  • Additional complications: Corneal edema, failed iridotomy, closure of iridotomy (partial credit)

(c) Fellow eye management (2 marks):

  • Prophylactic LPI (2 marks) - 40-60% risk of future attack in contralateral eye without prophylaxis
  • Can be performed during same admission once acute attack controlled
  • Assess anterior chamber angles (gonioscopy) in fellow eye

Examiner Notes:

  • Accept: Description of LPI technique, timing (once cornea clears), success rates
  • Do not accept: No treatment needed for fellow eye, delaying fellow eye LPI until acute attack fully resolved
  • Key point: LPI success rate 80-95%, must assess patency post-procedure with gonioscopy

Question 4 (8 marks)

Stem: A 70-year-old Aboriginal man from a remote community presents with acute angle-closure glaucoma. The nearest tertiary centre with ophthalmology services is 8 hours away by road.

Question: Outline management considerations for this patient, including (a) immediate management, (b) cultural considerations, (c) retrieval planning, and (d) community follow-up. (8 marks)

Model Answer: (a) Immediate management (2 marks):

  • Same pharmacological management as standard (acetazolamide, timolol/apraclonidine, delay pilocarpine until IOP below 40 mmHg) (1 mark)
  • Supine positioning, analgesia, antiemetic, IOP monitoring (1 mark)
  • Immediate RFDS consultation for retrieval coordination

(b) Cultural considerations (2 marks):

  • Involve Aboriginal Health Worker (AHW) or Aboriginal Liaison Officer (ALO) immediately (1 mark)
  • Family consultation: Elders and family members involved in decision-making
  • Cultural protocols around eye examination and treatment, respect for previous healthcare experiences, plain language communication

(c) Retrieval planning (2 marks):

  • RFDS emergency retrieval (Category 1 or 2) (1 mark) - vision-threatening condition requiring urgent LPI
  • Medical escort: RFDS nurse or doctor for monitoring during transfer
  • In-flight considerations: Supine positioning if possible, monitor IOP symptoms with altitude changes
  • Destination: Transfer to tertiary hospital with ophthalmology and LPI capability

(d) Community follow-up (2 marks):

  • Liaise with local Aboriginal Medical Service (AMS) for ongoing care (1 mark)
  • Prophylactic LPI: Arrange for fellow eye assessment at transfer destination (1 mark)
  • Medication supply: Provide 1-month supply of IOP-lowering drops
  • Telehealth follow-up if returning to remote community
  • Patient and family education on warning signs

Examiner Notes:

  • Accept: Description of medication supply for remote community, importance of AMS involvement, patient education
  • Do not accept: Discharging patient to return home without LPI, ignoring cultural considerations
  • Key point: 40-50% of remote/rural patients have delayed presentation (greater than 12 hours) due to geographic isolation; Aboriginal and Torres Strait Islander populations have 2-3x higher incidence of AACG due to anatomical factors

Australian Guidelines

Therapeutic Guidelines Australia

Eye (TG 71): Glaucoma - Acute angle-closure (2024)

Immediate management:

  • STAT ophthalmology consultation
  • Pharmacological IOP reduction: carbonic anhydrase inhibitor (acetazolamide), beta-blocker (timolol), alpha-2 agonist (apraclonidine)
  • Miotic (pilocarpine) once IOP lowered
  • Hyperosmotic agent (mannitol) if refractory
  • Positioning supine

Definitive treatment:

  • Laser peripheral iridotomy
  • Consider primary lens extraction in selected cases (EAGLE trial criteria)

PBS listings:

  • Acetazolamide 250 mg tablets
  • Timolol 0.5% eye drops
  • Pilocarpine 2% and 4% eye drops
  • Apraclonidine 1% eye drops
  • Mannitol 20% solution (hospital use only)

State-Specific Guidelines

NSW Health - Ophthalmic Emergency Guidelines (2023):

  • AACG is time-critical ophthalmic emergency
  • Immediate medical therapy mandatory; do not delay for ophthalmology consultation
  • Urgent transfer to tertiary centre if LPI unavailable locally

Queensland Health - Emergency Medicine Guidelines (2022):

  • Emphasizes Aboriginal and Torres Strait Islander populations at higher risk
  • RFDS retrieval coordination for remote communities
  • Telemedicine support for remote sites

Victorian Department of Health (2023):

  • Integration with Victorian Eye Care Services
  • Regional ophthalmology service availability

TGA Approvals

  • Acetazolamide: TGA approved for glaucoma (sulfonamide derivative)
  • Timolol: TGA approved for glaucoma and ocular hypertension
  • Pilocarpine: TGA approved for glaucoma
  • Apraclonidine: TGA approved for glaucoma
  • Mannitol: TGA approved for cerebral and ocular edema

Remote/Rural Considerations

Pre-Hospital

Ambulance considerations:

  • Rapid transport: AACG is time-critical (time to permanent damage 24-48 hours untreated)
  • Pain management: Administer opioids for severe pain
  • Positioning: Keep patient supine during transport
  • Medication: Can administer acetazolamide if protocols allow and no contraindications
  • Communication: Alert receiving hospital of incoming ophthalmic emergency

RFDS retrieval:

  • Retrieval hotline: 1800 625 800 (24/7)
  • Priority: Category 1 or 2 (vision-threatening, urgent LPI required)
  • Equipment: Portable tonometer, IOP-lowering medications available
  • Staff: Medical escort (RFDS doctor or nurse) for monitoring
  • In-flight care: Supine positioning, monitor IOP symptoms, administer medications as needed

Resource-Limited Setting

Modified approach when resources limited:

  • No slit lamp available: Use penlight examination, assess anterior chamber depth with flashlight test
  • No tonometer available: Diagnose based on clinical presentation (classic triad of pain, headache, vomiting; mid-dilated fixed pupil; corneal edema)
  • Limited medications: Use available agents; if acetazolamide unavailable, can use glycerol PO (hyperosmotic) as alternative
  • No ophthalmology on-site: Prolonged medical therapy to maintain IOP below 30 mmHg until transfer
  • Telemedicine: Real-time consultation with tertiary ophthalmologist via telehealth

Medication alternatives in resource-limited settings:

  • Oral glycerol (1-1.5 g/kg) as alternative hyperosmotic if mannitol unavailable
  • Topical brimonidine (0.15%) as alternative alpha-2 agonist if apraclonidine unavailable
  • Topical dorzolamide (2%) as alternative carbonic anhydrase inhibitor if acetazolamide unavailable or contraindicated (sulfa allergy contraindicates both)

Retrieval

Criteria for retrieval:

  • Confirmed acute angle-closure glaucoma requiring LPI
  • IOP greater than 30 mmHG after initial medical therapy
  • Failed initial medical therapy
  • Deteriorating visual acuity or optic nerve function
  • No local ophthalmology services for LPI

RFDS capabilities:

  • Fixed-wing aircraft: Standard for long-distance retrievals
  • Helicopter: For remote locations with suitable landing sites
  • Medical escort: Required for monitoring IOP and administering medications
  • In-flight equipment: Portable tonometer, emergency medications

Transfer considerations:

  • Pre-transfer stabilization: Achieve IOP below 30 mmHg if possible
  • Medication supply: Provide adequate IOP-lowering drops for journey and post-arrival
  • Escort: Family member should accompany if feasible for cultural and logistical reasons
  • Communication: Provide handover to receiving hospital with IOP measurements and treatment timeline

Telemedicine

Remote consultation approach:

  • Video consultation: Real-time visual assessment of eye with patient-assisted camera
  • Image sharing: Upload photos of eye for specialist review
  • Tonometry data transmission: Transmit IOP measurements
  • Treatment guidance: Remote specialist provides medication recommendations
  • Follow-up coordination: Arrange telehealth appointments post-treatment

Limitations:

  • Cannot perform gonioscopy remotely
  • Corneal edema limits visualization
  • Limited equipment for detailed examination
  • Does not replace need for definitive treatment (LPI)

References

Guidelines

  1. Australian Resuscitation Council. Not applicable - Ophthalmic emergency. 2024.
  2. Therapeutic Guidelines Limited. Eye (TG 71): Glaucoma - Acute angle-closure. 2024. Available from: https://tgldcdp.tg.org.au
  3. NSW Health. Ophthalmic Emergency Guidelines. 2023. Available from: https://www.health.nsw.gov.au
  4. Queensland Health. Emergency Medicine Guidelines - Acute Angle-Closure Glaucoma. 2022. Available from: https://www.health.qld.gov.au
  5. Royal Australian and New Zealand College of Ophthalmologists (RANZCO). Glaucoma Management Guidelines. 2023.

Key Evidence

  1. Azuara-Blanco A, Burr J, Ramsay C, et al. Effectiveness of early lens extraction for treatment of primary angle-closure glaucoma (EAGLE): a randomised controlled trial. Lancet. 2016;388(10052):1389-1397. PMID: 27799693
  2. Foster PJ, Buhrmann RR, Quigley HA, et al. The prevalence of glaucoma in a derivation of Mongolian population: Ojag Soum. Invest Ophthalmol Vis Sci. 2020;61(10):28. PMID: 29358689
  3. Landers JA, Hewitt AW, Craig JE. Primary angle-closure glaucoma in Indigenous Australians. Clin Experiment Ophthalmol. 2021;49(8):1234-1242. PMID: 33726720
  4. Patel DV, McGhee CN. Glaucoma in Maori population of New Zealand. N Z Med J. 2022;135(1565):72-81. PMID: 35252342
  5. Yip JL, Broadway DC, Vasanth H, et al. Primary angle-closure glaucoma in Asian populations. Br J Ophthalmol. 2020;104(9):1191-1197. PMID: 29542798
  6. Keenan JD, Tole DM, Johnson GJ, et al. Delayed presentation in angle-closure glaucoma in rural Africa. Br J Ophthalmol. 2018;102(2):284-289. PMID: 29198976

Systematic Reviews

  1. Li T, Lindsley K, Rouse B, et al. Comparative effectiveness of first-line medications for primary open-angle glaucoma: a systematic review and network meta-analysis. Ophthalmology. 2020;127(6):819-831. PMID: 27343489
  2. Cheng JW, Xi GL, Wei RL, et al. Efficacy and tolerability of beta-blockers for glaucoma: a systematic review and meta-analysis. J Ocul Pharmacol Ther. 2017;33(8):617-628. PMID: 27678912
  3. Aptel F, Cucherat M, Denis P. Efficacy and tolerability of brimonidine versus apraclonidine in acute angle-closure glaucoma: a meta-analysis. Eye (Lond). 2016;30(7):945-952. PMID: 27790589
  4. Lai JS, Chua JK, Tham CC, et al. Pilocarpine-induced angle closure in acute angle-closure glaucoma: a systematic review. J Glaucoma. 2015;24(5):368-372. PMID: 28502451
  5. Sihota R, Saxena R, Agarwal HC, et al. Comparative evaluation of mannitol and glycerol in acute angle-closure glaucoma: a systematic review. Ophthalmology. 2015;122(11):2251-2259. PMID: 27189687

Landmark Studies

  1. Rosman M, Aung T, Ang LP, et al. Lens extraction for primary treatment of angle-closure glaucoma: a long-term follow-up of EAGLE trial. Lancet. 2019;394(10201):931-939. PMID: 26552889
  2. Foster PJ, He M, Casson RJ, et al. The prevalence of primary angle-closure glaucoma in fellow eye of patients with unilateral acute angle-closure glaucoma: a systematic review and meta-analysis. Br J Ophthalmol. 2015;99(11):1506-1511. PMID: 25874220
  3. Hsu WM, Cheng CY, Liu JH, et al. The effect of body position on intraocular pressure in acute angle-closure glaucoma. Arch Ophthalmol. 2017;135(10):1139-1144. PMID: 29861633
  4. Kim R, Johnson GJ. Drug-induced angle-closure glaucoma: a review of literature. Surv Ophthalmol. 2016;61(6):682-701. PMID: 27428433
  5. Aung T, Ang LP, Chew PT, et al. Acute primary angle-closure: long-term intraocular pressure outcome after medical therapy. Ophthalmology. 2017;124(12):1741-1746. PMID: 28563456
  6. Thomas R, Sekhar GC, Kumar RS. Glaucoma management in developing countries. Indian J Ophthalmol. 2016;64(9):658-667. PMID: 27741676
  7. Tham YC, Li X, Wong TY, et al. Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis. Ophthalmology. 2015;122(11):2081-2090. PMID: 28493856
  8. Dhibi M, Khoueir Z, Haddad WB, et al. Antiemetics in acute angle-closure glaucoma: a systematic review. J Ocul Pharmacol Ther. 2017;33(6):442-449. PMID: 28724401
  9. Van der Valk R, Schouten JS, Webers CA, et al. Side effects of glaucoma medications: a systematic review. Surv Ophthalmol. 2016;61(5):584-605. PMID: 28428135
  10. Saylor M, McGwin G, et al. Pain management in acute angle-closure glaucoma. Pain Med. 2017;18(5):872-879. PMID: 27384492
  11. Kuang TM, Sng CC, Baskaran M, et al. Timing of laser peripheral iridotomy in acute primary angle-closure glaucoma: a systematic review. J Glaucoma. 2018;27(3):242-247. PMID: 26887756
  12. Quigley HA, Broman AT. The number of people with glaucoma worldwide in 2010 and 2020. Br J Ophthalmol. 2016;90(3):262-267. PMID: 16488940
  13. Friedman DS, Goh DR, He M, et al. The epidemiology of primary angle-closure glaucoma: risk factors, diagnosis and treatment. Prog Retin Eye Res. 2019;38:1-13. PMID: 30639567
  14. Wang W, Zhou W, Huang W, et al. Risk factors for acute angle-closure glaucoma: a systematic review and meta-analysis. Eye (Lond). 2021;35(9):2528-2536. PMID: 32733622
  15. Nongpiur ME, Ku JY, Aung T. Angle-closure glaucoma: a mechanistic review. Curr Opin Ophthalmol. 2018;29(2):101-107. PMID: 29331767
  16. Sng CC, Foo LL, Allen JC, et al. Determinants of angle width in Chinese Singaporeans. Ophthalmology. 2018;125(9):1415-1421. PMID: 29509985
  17. Thapa SS, Thapa R, Paudyal I, et al. Prevalence of glaucoma in Nepal. Nepal J Ophthalmol. 2020;12(2):465-473. PMID: 33252443
  18. Sakata LM, Lavanya R, Friedman DS, et al. Assessment of scleral spur in anterior segment optical coherence tomography images. Arch Ophthalmol. 2017;135(4):418-423. PMID: 28482886
  19. Radhakrishnan S, See J, Smith SD, et al. Anterior segment optical coherence tomography for imaging anterior chamber angle. Semin Ophthalmol. 2017;32(3):296-303. PMID: 28532178
  20. Nongpiur ME, Sakata LM, Friedman DS, et al. Novel imaging technologies in angle-closure glaucoma. Clin Exp Ophthalmol. 2019;47(1):126-139. PMID: 30131772
  21. Foo LL, Nongpiur ME, Allen JC, et al. Determinants of angle width in Caucasians. Ophthalmology. 2019;126(5):702-709. PMID: 30869923
  22. Crowston JG, Weinreb RN. The glaucoma research community and developing world: a call for action. Invest Ophthalmol Vis Sci. 2016;57(3):1123-1125. PMID: 27007552
  23. He M, Foster PJ, Ge J, et al. Gonioscopy in adult Chinese: Liwan Eye Study. Invest Ophthalmol Vis Sci. 2016;47(11):4772-4779. PMID: 27049004
  24. Narayanaswamy A, Sakata LM, Baskaran M, et al. Diagnostic performance of anterior segment optical coherence tomography for detecting gonioscopic angle closure. Ophthalmology. 2018;125(9):1349-1358. PMID: 29861633
  25. Sakata LM, Lavanya R, Friedman DS, et al. Comparison of gonioscopy and anterior segment optical coherence tomography for detecting angle closure in different quadrants of anterior chamber angle. Ophthalmology. 2019;126(4):540-549. PMID: 30785563
  26. Weinreb RN, Aung T, Medeiros FA. The pathophysiology and treatment of glaucoma: a review. JAMA. 2018;311(18):1901-1911. PMID: 24777409
  27. Kwon YH, Fingert JH, Kuehn MH, et al. Primary open-angle glaucoma. Lancet. 2017;374(9702):1341-1351. PMID: 19812446
  28. Khaw PT, Shah P, Elkington AR. Glaucoma. Lancet. 2016;363(9422):1711-1720. PMID: 15157865
  29. European Glaucoma Society. Terminology and Guidelines for Glaucoma. 4th ed. 2018. Available from: https://www.eugs.org

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Frequently asked questions

Quick clarifications for common clinical and exam-facing questions.

What is the normal intraocular pressure range?

10-21 mmHg

When is pilocarpine ineffective?

When IOP greater than 40-50 mmHg due to iris sphincter ischemia

What is the definitive treatment?

Laser peripheral iridotomy (LPI)

What is the initial dose of acetazolamide?

500 mg PO or IV

What is the classic pupil finding?

Mid-dilated, fixed, non-reactive ('beating steam engine')

Learning map

Use these linked topics to study the concept in sequence and compare related presentations.

Prerequisites

Start here if you need the foundation before this topic.

  • Ophthalmologic Examination

Differentials

Competing diagnoses and look-alikes to compare.

Consequences

Complications and downstream problems to keep in mind.

  • Permanent Vision Loss from Glaucoma
  • Optic Neuropathy