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Ophthalmology
Emergency Medicine
EMERGENCY

Acute Angle-Closure Glaucoma

High EvidenceUpdated: 2025-12-22

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Red Flags

  • IOP >50 mmHg
  • Fixed mid-dilated pupil
  • Duration >6 hours
  • Severe vision loss
Overview

Acute Angle-Closure Glaucoma

1. Clinical Overview

Summary

Acute angle-closure glaucoma (AACG) is an ophthalmic emergency with sudden IOP elevation (40-80 mmHg) from iris blocking aqueous drainage. Classic triad: severe eye pain, halos, fixed mid-dilated pupil. Treat with topical timolol + apraclonidine, IV acetazolamide, then pilocarpine. Urgent ophthalmology for laser iridotomy.

Key Facts

  • Definition: Sudden IOP elevation from iris blocking trabecular meshwork
  • IOP: Typically 40-80 mmHg (normal 10-21)
  • Treatment: Multi-drug approach + laser peripheral iridotomy
  • Time-critical: Permanent vision loss within hours if untreated

2. Epidemiology

Acute angle-closure glaucoma (AACG) is an ophthalmic emergency characterized by sudden, marked elevation of intraocular pressure (IOP) due to physical blockage of the trabecular meshwork drainage pathway by the peripheral iris. This results from pupillary block where aqueous humor cannot flow from the posterior to the anterior chamber, causing forward bowing of the iris against the cornea and closing the drainage angle.

Epidemiology

  • Incidence: 0.5-1 per 1,000 population per year
  • Age: Most common in older adults (peak 55-70 years)
  • Sex: More common in women (3-4:1 ratio)
  • Ethnicity: Higher incidence in Asians (especially East Asians), Inuit populations
  • Refractive error: More common in hyperopes (farsighted individuals)

Classification

TypeDescription
Primary AACGPupillary block in anatomically predisposed eye
Secondary AACGUnderlying pathology (lens swelling, tumor, medications)
Chronic angle closureGradual closure without acute episodes
Intermittent angle closureEpisodic attacks that resolve spontaneously

3. Pathophysiology

Anatomical Predisposition

Certain anatomical features predispose to angle closure:

  1. Short axial length (hyperopic eye)
  2. Shallow anterior chamber (<2.5mm central depth)
  3. Thick crystalline lens (increases with age)
  4. Anteriorly positioned lens
  5. Small corneal diameter
  6. Narrow iridocorneal angle

Mechanism of Attack

Pupillary Block Sequence

  1. Mid-dilated pupil creates maximum iris-lens contact
  2. Aqueous humor trapped behind iris
  3. Posterior-to-anterior chamber pressure differential
  4. Iris bows forward (iris bombé)
  5. Peripheral iris apposes trabecular meshwork
  6. Aqueous outflow blocked → IOP rises rapidly

Triggers for Attack

  • Dim lighting (pupil dilation)
  • Emotional stress
  • Medications (anticholinergics, sympathomimetics)
  • Post-operative mydriasis
  • Acute angle closure on instillation of mydriatic drops

Consequences of Elevated IOP

Corneal Effects

  • Epithelial and stromal edema
  • Decreased visual acuity
  • Halos around lights (from light diffraction)

Anterior Segment Effects

  • Iris ischemia (fixed, mid-dilated pupil)
  • Trabecular meshwork damage

Posterior Segment Effects

  • Optic nerve ischemia
  • Retinal ganglion cell death
  • Permanent vision loss if prolonged

Time-Dependent Damage

DurationRisk of Permanent Damage
<2 hoursLow (usually reversible)
2-6 hoursModerate
6-24 hoursHigh
>4 hoursVery high (often irreversible)

4. Clinical Presentation

Classic Presentation

Symptoms

Signs

Atypical Presentations

Intermittent Attacks

Subacute Presentation

Chronic Angle Closure

Associated Findings

History Red Flags


Severe, unilateral eye pain (throbbing, aching)
Common presentation.
Decreased vision (may be profound)
Common presentation.
Halos around lights (from corneal edema)
Common presentation.
Frontal headache (often ipsilateral)
Common presentation.
Nausea and vomiting (vagal response to severe pain/IOP)
Common presentation.
Photophobia
Common presentation.
5. Clinical Examination

(Integrated into Clinical Presentation and Diagnostic sections)

Red Flags (Vision-Threatening)

Vision-Threatening Features

Red FlagSignificanceAction
IOP >0 mmHgSevere attackAggressive IOP lowering, urgent ophthalmology
Duration > hoursHigh damage riskEmergent ophthalmology, consider surgical intervention
No pupil responseIris ischemiaPoor prognostic sign, aggressive treatment
Hand motions visionSevere attackMaximum medical therapy
Corneal opacificationSevere edemaIndicates prolonged elevated IOP
Previous attack to fellow eyeVery high riskProphylactic treatment needed

Medications That Can Precipitate Attack

Anticholinergics

  • Atropine, cyclopentolate (eye drops)
  • Scopolamine, glycopyrrolate (systemic)
  • Antihistamines, antipsychotics
  • Tricyclic antidepressants

Sympathomimetics

  • Phenylephrine (topical, systemic)
  • Epinephrine, norepinephrine
  • Decongestants (pseudoephedrine)
  • Amphetamines

Others

  • Topiramate
  • Sulfas-containing drugs
  • Selective serotonin reuptake inhibitors (SSRIs)
  • Botulinum toxin (facial injections)

6. Investigations

Differential Diagnosis

ConditionKey Distinguishing Features
Acute anterior uveitisMiotic pupil, cells/flare in anterior chamber, normal/low IOP
Corneal ulcer/keratitisFocal corneal defect on fluorescein, discharge
ConjunctivitisNo vision loss, normal pupil, normal IOP, discharge
Cluster headacheIpsilateral autonomic features, normal eye exam
MigraineNeurological symptoms, normal eye exam, normal IOP
Scleritis/episcleritisDeep tenderness, normal or near-normal IOP
Neovascular glaucomaRubeosis iridis, diabetes/CRVO history, elevated IOP
Traumatic iritisHistory of trauma, cells in anterior chamber
Phacolytic glaucomaMature cataract visible, elevated IOP

Key Differentiating Physical Exam Features

FeatureAACGUveitisConjunctivitis
PupilMid-dilated, fixedMioticNormal
IOPVery elevated (40-80)Normal or lowNormal
CorneaCloudy, edematousClear or slight hazeClear
Anterior chamberShallowCells/flare presentNormal
DischargeNoneNonePresent
VisionDecreasedMay be decreasedNormal

Diagnostic Approach

Initial Assessment

History

  1. Onset and duration of symptoms
  2. Precipitating factors (medications, dim light)
  3. Previous similar episodes
  4. Eye history (refractive error, previous surgeries)
  5. Medical history (diabetes, cardiovascular disease)
  6. Current medications

Physical Examination

  1. Visual acuity (each eye separately)
  2. Pupil examination (size, reactivity)
  3. External eye examination (injection pattern)
  4. Corneal clarity
  5. Anterior chamber depth (penlight test)
  6. Globe firmness (through closed lid)

Diagnostic Tests

Essential Tests

TestFindings in AACG
TonometryIOP 40-80 mmHg (markedly elevated)
Visual acuityReduced, may be counting fingers or worse
Pupil examinationMid-dilated (4-6mm), fixed, minimally reactive
Penlight testShallow anterior chamber (see below)
Fluorescein stainingDiffuse punctate staining from corneal edema

Penlight (Van Herick) Test

  • Shine light tangentially from temporal side
  • In normal eye: Anterior chamber depth > ¼ corneal thickness
  • In narrow angle: Anterior chamber depth < ¼ corneal thickness
  • If peripheral iris shadows nasal cornea, angle is likely narrow

Slit-lamp Examination (if available)

  • Corneal epithelial and stromal edema
  • Shallow anterior chamber centrally and peripherally
  • Mid-dilated, fixed pupil
  • Iris may appear atrophic (spiral/sector atrophy if ischemic)
  • May see cellular reaction in anterior chamber

Gonioscopy

  • Definitive test for angle anatomy
  • Performed by ophthalmologist
  • May not be possible if cornea very cloudy

Assessing the Fellow Eye

Critical step: The fellow eye often has similar anatomy and is at high risk for an attack.

  • Check anterior chamber depth
  • Measure IOP
  • Examine pupil response
  • Document findings for ophthalmology

7. Management

Immediate Management Algorithm

Acute Angle-Closure Glaucoma Confirmed
              ↓
Step 1: Position patient supine
        (helps move lens posteriorly)
              ↓
Step 2: Topical therapy (affected eye)
        - Timolol 0.5% x1 drop
        - Apraclonidine 1% x1 drop
        (Do NOT give pilocarpine initially - 
        ischemic iris won't respond)
              ↓
Step 3: Systemic IOP reduction
        - Acetazolamide 500mg IV
        OR
        - Acetazolamide 250-500mg PO if no IV
              ↓
Step 4: Support care
        - IV access and fluids
        - Antiemetics (ondansetron 4mg IV)
        - Analgesia (morphine if needed)
              ↓
Step 5: After 30-60 minutes (when IOP begins to drop)
        - Pilocarpine 2% every 15 min x 3
        (Constricts pupil, opens angle)
              ↓
Step 6: If refractory (IOP still very elevated)
        - IV Mannitol 1-2 g/kg over 45 min
              ↓
Step 7: Urgent ophthalmology consultation
        - Laser peripheral iridotomy (definitive)

Pharmacotherapy Details

Topical Medications

MedicationMechanismDoseNotes
Timolol 0.5%Decreases aqueous production1 dropCaution in asthma, bradycardia
Apraclonidine 1%Decreases aqueous production1 dropAlternative: Brimonidine 0.2%
Pilocarpine 2%Constricts pupil, opens angle1 drop q15min x3Only after IOP starts to decrease
Dorzolamide 2%Carbonic anhydrase inhibitor1 dropAdditional topical option

Systemic Medications

MedicationMechanismDoseNotes
AcetazolamideCarbonic anhydrase inhibitor500mg IV or POAvoid in sulfa allergy, renal disease
Mannitol 20%Osmotic agent1-2 g/kg IV over 45 minRefractory cases; avoid in CHF, renal failure
GlycerolOral osmotic agent1-1.5 g/kg POAlternative if no IV; avoid in diabetics
IsosorbideOral osmotic agent1-1.5 g/kg PODoes not affect blood glucose

Definitive Treatment

Laser Peripheral Iridotomy (LPI)

  • Definitive treatment for pupillary block
  • Creates alternate pathway for aqueous flow
  • Usually performed once IOP controlled
  • Also performed prophylactically on fellow eye

Surgical Options

  • Surgical iridectomy if laser not possible
  • Lens extraction (lensectomy) may be considered
  • Trabeculectomy for persistent IOP elevation

Special Considerations

When Pilocarpine Won't Work

  • Ischemic iris (IOP very high for prolonged period)
  • Lens-induced angle closure (needs lens extraction)
  • Plateau iris configuration (different mechanism)
  • Neovascular glaucoma (treat underlying cause)

Contraindications to Medications

MedicationContraindications
TimololBradycardia, heart block, asthma, COPD
AcetazolamideSulfa allergy, renal failure, severe hypokalemia
MannitolCHF, anuria, pulmonary edema
PilocarpineUveitis, neovascular glaucoma

8. Complications

Disposition

Ophthalmology Consultation

Emergent Consultation (same day)

  • All confirmed cases of AACG
  • Refractory to medical management
  • IOP not decreasing after 1-2 hours of treatment
  • Severe vision impairment

Timing of Definitive Treatment

  • Laser iridotomy typically within 24-48 hours
  • May be same day if IOP controlled and ophthalmologist available
  • Fellow eye should receive prophylactic iridotomy

Admission Criteria

Indications for Admission

  • Refractory IOP elevation despite maximum medical therapy
  • Need for IV mannitol (monitor fluid status)
  • Significant comorbidities (cardiac, renal)
  • Unable to arrange urgent ophthalmology follow-up
  • Complications (persistent corneal edema, uncertain diagnosis)

Discharge Criteria

Safe for Discharge

  • IOP <30 mmHg and stable
  • Pain controlled
  • Ophthalmology follow-up within 24 hours guaranteed
  • Reliable patient/family
  • Clear understanding of medications and warning signs

Discharge Medications

  • Continue prescribed topical medications
  • Oral acetazolamide 250mg every 6-8 hours if prescribed
  • Analgesics as needed
  • Antiemetics as needed

Follow-up Requirements

PriorityTimelinePurpose
OphthalmologyWithin 24 hoursLaser iridotomy, IOP check
Emergency departmentIf worsening symptomsTreatment failure
Post-iridotomy1-2 weeksAssess angle, IOP
Long-termEvery 3-6 monthsMonitor for chronic glaucoma

11. Patient/Layperson Explanation

Understanding the Condition

  • Acute angle-closure glaucoma is an eye emergency
  • Fluid in your eye cannot drain properly, causing dangerous pressure
  • Without treatment, permanent vision loss can occur
  • Treatment aims to lower the pressure and prevent recurrence

Medication Instructions

  • Apply eye drops exactly as prescribed
  • Wait 5 minutes between different drops
  • Gentle pressure at the inner corner of eye after drops
  • Do not stop medications without ophthalmologist approval
  • Take oral medications with food if stomach upset

Prevention of Recurrence

Avoid triggers:

  • Dim lighting for prolonged periods
  • Over-the-counter cold medications with anticholinergics
  • Medications that dilate pupils (check with doctor first)

After iridotomy:

  • Risk of recurrence is very low
  • Still need regular eye exams
  • Fellow eye should also be treated

Warning Signs to Return

  • Return immediately if:
    • Eye pain returns or worsens
    • Vision decreases
    • Halos around lights return
    • Nausea/vomiting returns
    • Headache worsens

Long-term Outlook

  • With prompt treatment, vision can usually be preserved
  • Laser iridotomy is usually curative for this type of glaucoma
  • Regular follow-up is essential
  • Some patients may develop chronic glaucoma requiring ongoing treatment

9. Prognosis & Outcomes

Special Populations

Elderly Patients

  • Higher risk due to larger lens, shallower anterior chamber
  • May present with atypical symptoms (confusion, systemic illness)
  • Consider comorbidities when prescribing (β-blockers, carbonic anhydrase inhibitors)
  • Higher risk of complications from osmotic agents

Pediatric Considerations

  • AACG rare in children
  • Secondary causes more common (lens dislocation, uveitis, tumors)
  • Involves different anatomical considerations
  • Requires pediatric ophthalmology consultation

Pregnant Patients

Medication Safety

MedicationPregnancy Considerations
TimololCategory C; use if benefit > risk
BrimonidineCategory B; preferred topical
PilocarpineCategory C
AcetazolamideCategory C; avoid in first trimester
MannitolCategory C; use cautiously
  • Coordinate care with obstetrics
  • Use minimum effective medications
  • Definitive treatment (laser iridotomy) can proceed

Patients of Asian Descent

  • Higher prevalence of AACG
  • May have different angle anatomy (plateau iris more common)
  • Lower threshold for screening and prophylaxis
  • Consider cultural/language considerations in education

Quality Metrics

Performance Indicators

MetricTarget
Time to IOP measurement<15 minutes of presentation
Time to initial treatment<30 minutes of diagnosis
Ophthalmology consultation100% of confirmed cases
Documentation of IOP100%
Fellow eye examination100%
Appropriate medication selection>5%

Documentation Requirements

  • Pre-treatment visual acuity (both eyes)
  • Pupil size and reactivity (both eyes)
  • IOP measurement (both eyes)
  • Medications administered (timing and response)
  • Post-treatment IOP
  • Ophthalmology consultation documentation
  • Disposition plan and follow-up instructions

10. Evidence & Guidelines

Key Clinical Pearls

Diagnostic Pearls

  1. Triad: Eye pain + halos + mid-dilated fixed pupil = AACG until proven otherwise
  2. Penlight test can quickly screen for shallow anterior chamber
  3. Firm globe on palpation (through closed lid) suggests high IOP
  4. Check both eyes - fellow eye usually has similar anatomy
  5. Consider in patients presenting with headache/vomiting - examine the eyes!

Treatment Pearls

  1. Position supine - allows lens to fall back, may help open angle
  2. Pilocarpine won't work initially - ischemic iris sphincter cannot constrict
  3. Multi-drug approach is necessary - different mechanisms
  4. Acetazolamide IV works faster than oral
  5. Mannitol reserved for refractory cases - monitor fluid status

Disposition Pearls

  1. All patients need ophthalmology - either emergent or within 24 hours
  2. Laser iridotomy is definitive - usually done once IOP controlled
  3. Treat the fellow eye prophylactically - high risk of attack
  4. Education on trigger avoidance is essential
  5. Document pre- and post-treatment IOP for ophthalmology

12. References
  1. Prum BE, et al. Primary Angle Closure Preferred Practice Pattern Guidelines. Ophthalmology. 2016;123(1):P1-P40.
  2. Wright C, et al. Primary angle-closure glaucoma: an update. Acta Ophthalmol. 2016;94(3):217-225.
  3. Sun X, et al. Primary angle closure glaucoma: What we know and what we don't know. Prog Retin Eye Res. 2017;57:26-45.
  4. Weinreb RN, et al. Primary open-angle glaucoma. Lancet. 2014;383(9925):1402-1412.
  5. Ramesh S, et al. Emergency management of acute primary angle closure. J Curr Glaucoma Pract. 2015;9(3):68-72.
  6. AAO Preferred Practice Pattern Committee. Primary Angle Closure PPP. American Academy of Ophthalmology. 2020.

Version History
VersionDateChanges
1.02025-01-15Initial comprehensive version with 14-section template

Last updated: 2025-12-22

At a Glance

EvidenceHigh
Last Updated2025-12-22
Emergency Protocol

Red Flags

  • IOP &gt;50 mmHg
  • Fixed mid-dilated pupil
  • Duration &gt;6 hours
  • Severe vision loss

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines