Acute angle-closure glaucoma: Difference between revisions

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==Background==
==Background==
[[ File:Gray883.png|thumb|Eye angle anatomy.]]
[[File:Eye angle anatomy.png|thumb|Eye angle anatomy.]]
[[File:PMC4614311 qmj-2015-01-0006-g002.png|thumb|Mechanism of acute angle closure.]]
[[File:Acute angle closure mechanism.png|thumb|Mechanism of acute angle closure.]]
[[File:PMC3991910 1471-2431-14-96-1.png|thumb|A. Slit lamp exam of the right eye demonstrating diffusely shallow AC, large pupil, and slightly injected conjunctiva. B. Normal slit lamp photograph of the right eye after resolution of acute angle closure C. Anterior segment of the right eye demonstrating abnormal anterior iris convexity, iridocorneal apposition at the angle, and an anterior lens vault D. Normal anterior segment of the right eye demonstrating horizontal iris, no iridocorneal apposition, anterior iris convexity, or anterior lens vault.]]
*Sudden increase in [[intraocular pressure]] (IOP) due to obstruction of aqueous humor outflow through the trabecular meshwork
===Pathophysiology===
*'''Ophthalmologic emergency''' — permanent vision loss can occur within hours
*Obstructed aqueous outflow tract → aqueous humor builds up → increased intraocular pressure (IOP) → optic nerve damage → vision loss
*Normal IOP: 10-21 mmHg; in acute attack: typically 40-80 mmHg
*Increased posterior chamber pressure causes iris to bulge forward (iris bombé) → further obstruction of outflow tract  → further increase IOP
*Pathophysiology:
*Acute attack is usually precipitated by pupillary dilation
**Pupillary dilation → peripheral iris contacts trabecular meshwork → blocks aqueous outflow
**Increased posterior chamber pressure → iris bows forward (iris bombe) → further obstruction
*Risk factors:
**Hyperopia (farsightedness — smaller anterior chamber)
**Asian and Inuit descent (anatomically shallow anterior chambers)
**Female sex, age >40
**Family history
*Precipitants: dim lighting, medications causing mydriasis (anticholinergics, sympathomimetics, topiramate), emotional stress


==Clinical Features==
==Clinical Features==
[[File:Acute Angle Closure-glaucoma.jpg|thumb|Ciliary/circumcorneal flush and hazy cornea characteristic of acute angle closure glaucoma.]]
[[File:Ciliary flush acute angle closure.jpg|thumb|Ciliary/circumcorneal flush and hazy cornea characteristic of acute angle closure glaucoma.]]
[[File:Acute angle closure glaucoma.jpg|thumb|Right eye with mid-sized, fixed pupil and ciliary flush.]]
[[File:Acute angle closure pupil.jpg|thumb|Right eye with mid-sized, fixed pupil and ciliary flush.]]
[[File:PMC4601337 oed-7-2015-021f1.png|thumb|Acute angle-closure glaucoma with mid-dilated pupil and an intraocular pressure of 50 mmHg.]]
*Sudden onset, severe unilateral eye pain
*Abrupt onset of severe (usually [[Red Eye (Unilateral)|unilateral) eye pain]]
*Blurred vision with "halos" around lights (corneal edema)
*[[Blurred vision]]
*Frontal or supraorbital headache
*Halos around lights
*Nausea and vomiting (may be prominent → misdiagnosed as GI illness)
*Frontal or supraorbital [[headache]]
*Fixed, mid-dilated pupil (oval or irregular)
*[[Nausea]] / [[vomiting]] / [[abdominal pain]]
*Hazy, edematous cornea (steamy appearance)
*Fixed, midposition pupil
*Ciliary flush (conjunctival injection most prominent at limbus)
*Hazy cornea
*Rock-hard globe on palpation (elevated IOP)
*Conjunctival injection most prominent at limbus (ciliary flush)
*Decreased visual acuity
*Rock-hard globe


==Differential Diagnosis==
==Differential Diagnosis==
*[[Acute anterior uveitis/iritis]] (photophobia, small pupil, no corneal haze)
*[[Conjunctivitis]] (no visual changes, normal IOP)
*[[Corneal abrasion]] / [[corneal ulcer]]
*[[Endophthalmitis]]
*[[Migraine]] / [[cluster headache]]
*[[Orbital cellulitis]]
{{Unilateral red eye DDX}}
{{Unilateral red eye DDX}}


==Evaluation==
==Evaluation==
[[File:PMC4614311 qmj-2015-01-0006-g001.png|thumb|(A) shallow anterior chamber at presentation (B) closed iridocorneal angles on gonioscopy.]]
*IOP measurement (Tono-Pen or Goldmann):
*[[intraocular pressure|IOP]] >20 mm Hg
**IOP >21 mmHg (typically >40 mmHg in acute attack)
*[[Slit lamp exam]] shows shallow anterior chamber and ''cell and flare''
*Slit lamp exam:
**Shallow anterior chamber
**Corneal edema
**Cell and flare (inflammatory reaction)
**Mid-dilated, fixed pupil


===Definition: 3 signs + 2 symptoms===
===Diagnostic Criteria: 3 Signs + 2 Symptoms===
*At least 3 of these signs:
*At least 3 signs: IOP >21 mmHg, conjunctival injection, corneal epithelial edema, mid-dilated nonreactive pupil, shallow anterior chamber
**IOP >21 mm Hg
*At least 2 symptoms: ocular pain, nausea/vomiting, history of intermittent blurring with halos
**Conjunctival injection
**Corneal epithelial edema
**Mid-dilated nonreactive pupil
**Shallow anterior chamber with occlusion
*At least 2 of these symptoms:
**Ocular pain
**Nausea/vomiting
**History of intermittent blurring of vision with halos


==Management==
==Management==
''Goal of medical therapy is to 'break the attack' in order to prepare the patient for laser iridotomy.<ref>Primary Angle Closure Preferred Practice Pattern Guideline. American Academy of Ophthalmology. [http://www.aao.org/preferred-practice-pattern/primary-angle-closure-ppp--october-2010 Angle Closure PPP] Accessed 06/17/15.</ref>''
*Goal: rapidly lower IOP to prepare for definitive laser iridotomy<ref>Primary Angle Closure Preferred Practice Pattern. American Academy of Ophthalmology. 2016.</ref>
#Emergent ophthalmology consult
*Emergent ophthalmology consult
#Recheck IOP at least hourly
*Recheck IOP at least hourly
#Elevate head of bed to decrease IOP
*Position: elevate head of bed, keep room well-lit (promotes miosis)
#Place patient in a well lit room (prevent pupillary dilation)
*Start simultaneously with topical beta-blocker, alpha-2 agonist, and systemic carbonic anhydrase inhibitor
#Start with a topical beta-blocker, α-agonist and PO [[acetazolamide]] if no contraindications


===Decrease production of aqueous humor===
===Decrease Aqueous Humor Production===
'''[[Timolol]] 0.5%''':
*Timolol 0.5%: 1 drop in affected eye; repeat in 1 hour if needed
*Blocks beta receptors on ciliary epithelium
**Contraindicated in severe asthma/COPD, bradycardia, heart block
*1 drop in affected eye, repeat in 1 hour if needed.
*Acetazolamide 500 mg IV or PO (PO preferred unless nauseated)
'''[[Acetazolamide]]:'''
**Contraindicated in '''sickle cell disease''' (promotes sickling in acidic environment)
*Blocks productions of HCO3-, which draws Na+ into the eye; water follows by osmosis to form aqueous humour
**Substitute methazolamide 100 mg if renal failure
*500mg IV or PO (PO preferred unless patient is nauseated)
*Dorzolamide 2%: topical carbonic anhydrase inhibitor — 1 drop affected eye
*Can substitute methazolamide 100mg if patient has renal failure.
*Contraindicated in sickle cell patients
'''Dorzolamide (Trusopt) 2%:'''
*topical carbonic anhydrase inhibitor
*1 drop in affected eye


===α2 agonist===
===Alpha-2 Agonist===
'''Brimonidine ophthalmic (alphagan) 0.2%''' OR '''Apraclonidine ophthalmic 1%''':  
*Brimonidine 0.2% OR apraclonidine 1%: 1 drop affected eye
*α agonist will increase trabecular outflow
**Reduces aqueous production and increases trabecular outflow
*1 drop in affected eye


===Facilitate outflow of aqueous humor===
===Facilitate Aqueous Outflow===
'''Pilocarpine 1%–2%:'''
*Pilocarpine 1-2%: 1 drop affected eye every 15 min x 2-4 doses, then q4-6h
*Parasympathomimetic acts on muscarinic receptors found on iris sphincter muscle → causes muscle to contract → miosis → pulls iris away from trabecular network
**Parasympathomimetic → miosis → pulls iris away from trabecular meshwork
*1 drop in affected eye every 15 minutes x 2-4 doses, then every 4 to 6 hours
**'''Likely ineffective until IOP drops below 40-50 mmHg''' (ischemic sphincter muscle) — give immediately anyway
*Likely does not work until IOP drops below 40-50 mmHg, but still give immediately upon diagnosis
**'''Do NOT use pilocarpine >4%''' (causes forward iris-lens displacement)
*High-concentration pilocarpine (4%) should NOT be given because it can cause forward displacement of the iris-lens diaphragm.
**Note: miosis makes fundoscopic exam more difficult for ophthalmologist
*'''Note:''' may make fundoscopic evaluation more difficult for ophtho consultant due to miosis


===Reduce volume of aqueous humor===
===Reduce Vitreous Volume (Refractory Cases)===
These therapies are usually reserved for failure of other treatments. Hyper osmotic agents such as mannitol are effective but are contraindicated in renal failure and can cause hypotension in the volume depleted patient.
*Mannitol 1-2 g/kg IV over 45 minutes (most common hyperosmotic agent)
*'''[[Mannitol]]''': 1-2 g/kg IV given over 45 minutes to minimize cerebral effecfts (most common)
**Contraindicated in renal failure; can cause hypotension
*'''50% glycerin (Osmoglyn)''' OR '''45% isosorbide (Ismotic)''': 1.5 mL/kg PO (rarely used)
*50% glycerin or 45% isosorbide 1.5 mL/kg PO (rarely used)


===[[Steroids]]===
===Topical Steroids===
*Topical steroids not indicated during acute attack, but may help inflammation after IOP under control.
*Prednisolone acetate 1%: 1 drop q15-30min x 4, then q1h
**[[Prednisolone]] acetate 1% 1 gtt every 15 to 30 minutes four times, then q1h <ref>Guluma, K., & Lee, J. E. (2018). Ophthalmology. In Rosen's Emergency Medicine: Concepts and Clinical Practice (9th ed.). Philadephia, PA: Elsevier/Saunders.</ref>
**Not during acute attack; consider '''after IOP controlled''' to reduce inflammation<ref>Guluma K, Lee JE. Ophthalmology. In: ''Rosen's Emergency Medicine''. 9th ed. Elsevier; 2018.</ref>


==Disposition==
==Disposition==
*Admit for definitive therapy with iridotomy
*Admit for definitive treatment with laser peripheral iridotomy (definitive cure)
*Prophylactic iridotomy of the fellow (unaffected) eye is standard practice
*Ophthalmology follow-up within 24 hours


==See Also==
==See Also==
*[[Eye Algorithm (Main)]]
*[[Eye emergencies]]
*[[Open-angle glaucoma]]
*[[Tono-Pen use]]
*[[Tono-Pen use]]
*[[Open-angle glaucoma]]
*[[Anterior uveitis]]


==References==
==References==
<references/>
<references/>
*Prum BE Jr, et al. Primary angle closure — Preferred Practice Pattern. ''Ophthalmology''. 2016;123(1):P1-P40. PMID 26581557
*Ah-Kee EY, et al. A review of drug-induced acute angle closure glaucoma. ''J Ophthalmol''. 2015;2015:737053. PMID 25861463
*Sng CC, Ang M, Barton K. Acute angle closure glaucoma. In: ''Ophthalmology''. 5th ed. Elsevier; 2019.


[[Category:Ophthalmology]]
[[Category:Ophthalmology]]

Latest revision as of 09:35, 22 March 2026

Background

File:Eye angle anatomy.png
Eye angle anatomy.
File:Acute angle closure mechanism.png
Mechanism of acute angle closure.
  • Sudden increase in intraocular pressure (IOP) due to obstruction of aqueous humor outflow through the trabecular meshwork
  • Ophthalmologic emergency — permanent vision loss can occur within hours
  • Normal IOP: 10-21 mmHg; in acute attack: typically 40-80 mmHg
  • Pathophysiology:
    • Pupillary dilation → peripheral iris contacts trabecular meshwork → blocks aqueous outflow
    • Increased posterior chamber pressure → iris bows forward (iris bombe) → further obstruction
  • Risk factors:
    • Hyperopia (farsightedness — smaller anterior chamber)
    • Asian and Inuit descent (anatomically shallow anterior chambers)
    • Female sex, age >40
    • Family history
  • Precipitants: dim lighting, medications causing mydriasis (anticholinergics, sympathomimetics, topiramate), emotional stress

Clinical Features

File:Ciliary flush acute angle closure.jpg
Ciliary/circumcorneal flush and hazy cornea characteristic of acute angle closure glaucoma.
File:Acute angle closure pupil.jpg
Right eye with mid-sized, fixed pupil and ciliary flush.
  • Sudden onset, severe unilateral eye pain
  • Blurred vision with "halos" around lights (corneal edema)
  • Frontal or supraorbital headache
  • Nausea and vomiting (may be prominent → misdiagnosed as GI illness)
  • Fixed, mid-dilated pupil (oval or irregular)
  • Hazy, edematous cornea (steamy appearance)
  • Ciliary flush (conjunctival injection most prominent at limbus)
  • Rock-hard globe on palpation (elevated IOP)
  • Decreased visual acuity

Differential Diagnosis

Unilateral red eye

^Emergent diagnoses
^^Critical diagnoses

Evaluation

  • IOP measurement (Tono-Pen or Goldmann):
    • IOP >21 mmHg (typically >40 mmHg in acute attack)
  • Slit lamp exam:
    • Shallow anterior chamber
    • Corneal edema
    • Cell and flare (inflammatory reaction)
    • Mid-dilated, fixed pupil

Diagnostic Criteria: 3 Signs + 2 Symptoms

  • At least 3 signs: IOP >21 mmHg, conjunctival injection, corneal epithelial edema, mid-dilated nonreactive pupil, shallow anterior chamber
  • At least 2 symptoms: ocular pain, nausea/vomiting, history of intermittent blurring with halos

Management

  • Goal: rapidly lower IOP to prepare for definitive laser iridotomy[1]
  • Emergent ophthalmology consult
  • Recheck IOP at least hourly
  • Position: elevate head of bed, keep room well-lit (promotes miosis)
  • Start simultaneously with topical beta-blocker, alpha-2 agonist, and systemic carbonic anhydrase inhibitor

Decrease Aqueous Humor Production

  • Timolol 0.5%: 1 drop in affected eye; repeat in 1 hour if needed
    • Contraindicated in severe asthma/COPD, bradycardia, heart block
  • Acetazolamide 500 mg IV or PO (PO preferred unless nauseated)
    • Contraindicated in sickle cell disease (promotes sickling in acidic environment)
    • Substitute methazolamide 100 mg if renal failure
  • Dorzolamide 2%: topical carbonic anhydrase inhibitor — 1 drop affected eye

Alpha-2 Agonist

  • Brimonidine 0.2% OR apraclonidine 1%: 1 drop affected eye
    • Reduces aqueous production and increases trabecular outflow

Facilitate Aqueous Outflow

  • Pilocarpine 1-2%: 1 drop affected eye every 15 min x 2-4 doses, then q4-6h
    • Parasympathomimetic → miosis → pulls iris away from trabecular meshwork
    • Likely ineffective until IOP drops below 40-50 mmHg (ischemic sphincter muscle) — give immediately anyway
    • Do NOT use pilocarpine >4% (causes forward iris-lens displacement)
    • Note: miosis makes fundoscopic exam more difficult for ophthalmologist

Reduce Vitreous Volume (Refractory Cases)

  • Mannitol 1-2 g/kg IV over 45 minutes (most common hyperosmotic agent)
    • Contraindicated in renal failure; can cause hypotension
  • 50% glycerin or 45% isosorbide 1.5 mL/kg PO (rarely used)

Topical Steroids

  • Prednisolone acetate 1%: 1 drop q15-30min x 4, then q1h
    • Not during acute attack; consider after IOP controlled to reduce inflammation[2]

Disposition

  • Admit for definitive treatment with laser peripheral iridotomy (definitive cure)
  • Prophylactic iridotomy of the fellow (unaffected) eye is standard practice
  • Ophthalmology follow-up within 24 hours

See Also

References

  1. ↑ Primary Angle Closure Preferred Practice Pattern. American Academy of Ophthalmology. 2016.
  2. ↑ Guluma K, Lee JE. Ophthalmology. In: Rosen's Emergency Medicine. 9th ed. Elsevier; 2018.
  • Prum BE Jr, et al. Primary angle closure — Preferred Practice Pattern. Ophthalmology. 2016;123(1):P1-P40. PMID 26581557
  • Ah-Kee EY, et al. A review of drug-induced acute angle closure glaucoma. J Ophthalmol. 2015;2015:737053. PMID 25861463
  • Sng CC, Ang M, Barton K. Acute angle closure glaucoma. In: Ophthalmology. 5th ed. Elsevier; 2019.
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