Acute angle-closure glaucoma: Difference between revisions
(Strip excess bold)
 
(68 intermediate revisions by 21 users not shown)
Line 1: Line 1:
= Background =
==Background==
Pathophysiology
[[File:Eye angle anatomy.png|thumb|Eye angle anatomy.]]
*Obstructed aqueous outflow tract ==> aqueous humor builds ==> increased intraocular pressure (IOP) ==> optic nerve damage ==> vision loss
[[File:Acute angle closure mechanism.png|thumb|Mechanism of acute angle closure.]]
*Increased posterior chamber pressure causes iris to bulge forward (iris bombé) ==> further obstruction of outflow tract  ==> further increase IOP
*Sudden increase in [[intraocular pressure]] (IOP) due to obstruction of aqueous humor outflow through the trabecular meshwork
*Acute attack is usually precipitated by pupillary dilation
*'''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


=Definition: 3 signs + 2 symptoms=
==Clinical Features==
*At least 3 of these signs
[[File:Ciliary flush acute angle closure.jpg|thumb|Ciliary/circumcorneal flush and hazy cornea characteristic of acute angle closure glaucoma.]]
**IOP >21 mm Hg
[[File:Acute angle closure pupil.jpg|thumb|Right eye with mid-sized, fixed pupil and ciliary flush.]]
**Conjunctival injection
*Sudden onset, severe unilateral eye pain
**Corneal epithelial edema
*Blurred vision with "halos" around lights (corneal edema)
**Mid-dilated nonreactive pupil
*Frontal or supraorbital headache
**Shallow anterior chamber with occlusion
*Nausea and vomiting (may be prominent → misdiagnosed as GI illness)
*At least 2 of these symptoms
*Fixed, mid-dilated pupil (oval or irregular)
**Ocular pain
*Hazy, edematous cornea (steamy appearance)
**Nausea/vomiting
*Ciliary flush (conjunctival injection most prominent at limbus)
**History of intermittent blurring of vision with halos
*Rock-hard globe on palpation (elevated IOP)
*Decreased visual acuity
 
==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}}
 
==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


= Clinical Features =
===Diagnostic Criteria: 3 Signs + 2 Symptoms===
*Abrupt onset of severe eye pain
*At least 3 signs: IOP >21 mmHg, conjunctival injection, corneal epithelial edema, mid-dilated nonreactive pupil, shallow anterior chamber
*Blurred vision
*At least 2 symptoms: ocular pain, nausea/vomiting, history of intermittent blurring with halos
*Frontal or supraorbital headache
 
*Nausea / vomiting / abdominal pain
==Management==
*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
*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


=Diagnosis=
===Decrease Aqueous Humor Production===
*Fixed, midposition pupil
*Timolol 0.5%: 1 drop in affected eye; repeat in 1 hour if needed
*Hazy cornea
**Contraindicated in severe asthma/COPD, bradycardia, heart block
*Conjunctival injection most prominent at limbus (ciliary flush)
*Acetazolamide 500 mg IV or PO (PO preferred unless nauseated)
*Rock-hard globe
**Contraindicated in '''sickle cell disease''' (promotes sickling in acidic environment)
*IOP >20 mm Hg
**Substitute methazolamide 100 mg if renal failure
*Dorzolamide 2%: topical carbonic anhydrase inhibitor — 1 drop affected eye


= Treatment =
===Alpha-2 Agonist===
Emergent opthalmology consult
*Brimonidine 0.2% OR apraclonidine 1%: 1 drop affected eye
**Reduces aqueous production and increases trabecular outflow


To ''decrease production'' of aqueous humor, give:
===Facilitate Aqueous Outflow===
#'''timolol 0.5% drop''': blocks beta receptors on ciliary epithelium
*Pilocarpine 1-2%: 1 drop affected eye every 15 min x 2-4 doses, then q4-6h
#'''apraclonidine 1% drop''': blocks alpha-2 adrenergic receptors
**Parasympathomimetic → miosis → pulls iris away from trabecular meshwork
#'''acetazolamide 500mg IV or PO''': blocks productions of HCO3-, which draws Na+ into the eye; water follows by osmosis to form aqueous humour
**'''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


To ''reduce volume'' of aqueous humor, give:
===Reduce Vitreous Volume (Refractory Cases)===
#'''mannitol 1–2gm/kg IV''': if no contraindications
*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)


To facilitate outflow of aqueous humor, give:
===Topical Steroids===
#'''pilocarpine 1%–2% drop''': parasympatholytic alkaloid acts on muscarinic receptors found on iris sphincter muscle ==> causes muscle to contract ==> miosis
*Prednisolone acetate 1%: 1 drop q15-30min x 4, then q1h
##In USA - green top
**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>
##Use one drop every 15 minutes x 2 doses, then every 4 to 6 hours
##Only effective when IOP <40 mm Hg


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


==Source==
==References==
Tintinalli
<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:Ophtho]]
[[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.
Retrieved from "https://www.wikem.org/w/index.php?title=Acute_angle-closure_glaucoma&oldid=389370"