Ver el código de «Acute angle-closure glaucoma»

==Background==
[[File:Eye angle anatomy.png|thumb|Eye angle anatomy.]]
[[File:Acute angle closure mechanism.png|thumb|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|thumb|Ciliary/circumcorneal flush and hazy cornea characteristic of acute angle closure glaucoma.]]
[[File:Acute angle closure pupil.jpg|thumb|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==
*[[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

===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<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

===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<ref>Guluma K, Lee JE. Ophthalmology. In: ''Rosen's Emergency Medicine''. 9th ed. Elsevier; 2018.</ref>

==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==
*[[Eye emergencies]]
*[[Open-angle glaucoma]]
*[[Tono-Pen use]]
*[[Anterior uveitis]]

==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]]