Angle closure glaucoma

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"angle closure glaucoma"[MeSH Terms] AND management

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I now have comprehensive information from Kanski's Clinical Ophthalmology, Goldman-Cecil Medicine, and Tintinalli's Emergency Medicine. Let me compile a thorough, well-structured answer.

Angle Closure Glaucoma

Definition & Overview

Angle closure glaucoma refers to obstruction of the trabecular meshwork by the peripheral iris (iridotrabecular contact — ITC), blocking aqueous outflow and raising intraocular pressure (IOP). It can be:

Primary — occurs in anatomically predisposed eyes
Secondary — caused by another ocular or systemic factor

Primary angle-closure glaucoma (PACG) accounts for up to half of all glaucoma cases globally and is disproportionately common in Asia. It progresses more rapidly and causes more visual loss than primary open-angle glaucoma (POAG). — Kanski's Clinical Ophthalmology, 10e

Classification (Spectrum)

Stage	Definition
Primary angle-closure suspect (PACS)	Occludable angle on gonioscopy, no ITC, no raised IOP, no optic nerve damage
Primary angle closure (PAC)	ITC in ≥3 quadrants ± raised IOP, but no glaucomatous optic neuropathy
Primary angle-closure glaucoma (PACG)	ITC + raised IOP + glaucomatous optic neuropathy
Acute primary angle closure (APAC)	Sudden complete closure causing acute crisis

Pathophysiology

The dominant mechanism is relative pupillary block:

Aqueous flow anatomy — normal (A) vs angle closure with pupillary block (B)

Normal aqueous flow (A) vs angle closure with pupillary block and iris bombé (B) — Tintinalli's Emergency Medicine

Aqueous is produced by the ciliary body and normally flows from the posterior chamber → through the pupil → into the anterior chamber → exits via the trabecular meshwork into Schlemm's canal.
When the posterior iris surface contacts the anterior lens surface, a pressure differential builds between the posterior and anterior chambers.
This bows the peripheral iris forward (iris bombé), narrowing and eventually closing the trabecular meshwork angle.
IOP rises rapidly — from a normal 10–20 mmHg to 50–80+ mmHg.
When IOP exceeds the corneal pump's capacity, corneal epithelial oedema develops → blurred vision and halos.

The mid-dilated pupil state is the most dangerous: the iris is thickest peripherally while still partially covering the lens, maximising pupillary block. Dilation to a widely dilated or miotic state actually reduces risk.

Additional mechanisms (especially in Asians):

Plateau iris configuration — anteriorly rotated ciliary processes hold the peripheral iris in a forward position; not relieved by iridotomy alone
Phacomorphic closure — swollen or anteriorly subluxated lens

Risk Factors

Factor	Detail
Hypermetropia (farsightedness)	Short axial length, shallow anterior chamber, narrow angle; up to 1 in 6 hyperopes ≥1 D are PACS
Age	Lens thickens with age, pushing iris forward
Female sex	More commonly affected than males
Asian ethnicity	Far Eastern and Indian Asians particularly at risk
Family history	Genetic factors, increased prevalence in first-degree relatives
Short axial length / nanophthalmos	Axial length <20 mm = very high risk
Cataracts	Increase lens vault

Precipitating Factors for Acute Attack

Pharmacological mydriasis (atropine, antihistamines, TCAs, cold/flu remedies, motion sickness patches)
Sympathomimetics (epinephrine, pseudoephedrine, intranasal cocaine)
Nebulized bronchodilators (albuterol + ipratropium) in ICU patients
Topiramate and other sulfa derivatives (cause ciliary body effusion)
Dim illumination / watching TV in a dark room
Semi-prone position (e.g. reading)
Acute emotional stress

Clinical Features

Symptoms

Acute: sudden severe periocular/orbital pain, markedly decreased vision, nausea and vomiting (may simulate acute abdomen), headache
Subacute/intermittent: blurring ("smoke-filled room") and haloes around lights from transient corneal oedema

Signs

Acute angle closure — cloudy cornea, conjunctival injection, mid-dilated fixed pupil

Acute angle closure: corneal cloudiness with circumcorneal injection — Tintinalli's Emergency Medicine

Visual acuity typically 6/60 to hand movements
IOP 50–80 mmHg (rock-hard globe)
Hazy/steamy cornea (corneal epithelial oedema)
Circumcorneal (ciliary) injection with violaceous hue
Fixed, mid-dilated, vertically oval pupil — classic and pathognomonic
Shallow anterior chamber with aqueous flare
Fellow eye typically shows an occludable angle

After Resolution (Resolved APAC)

Early: folds in Descemet's membrane, low IOP (ciliary body shutdown)
Late: glaukomflecken (white foci of anterior lens necrosis), iris atrophy with spiral pattern, posterior synechiae, irregular pupil

Diagnosis

Gonioscopy is the definitive tool — it directly visualises the angle and grades closure. Key systems:

Grade	Angle width	Structures visible
4 (35–45°)	Wide open	Ciliary body visible
3 (25–35°)	Open	Scleral spur visible
2 (20°)	Narrow	Trabeculum visible, no scleral spur
1 (10°)	Very narrow	Schwalbe line ± top of trabeculum
0	Closed	Iridocorneal contact

Van Herick slit-lamp method screens angle width by comparing peripheral anterior chamber depth to corneal thickness — a ratio <1/4 warrants urgent gonioscopy.

Additional investigations: UBM (ultrasound biomicroscopy) to diagnose plateau iris; AS-OCT (anterior segment OCT) for angle imaging.

Differential Diagnosis of Acute IOP Elevation

Acute APAC
Lens-induced angle closure (swollen/subluxated lens)
Malignant glaucoma (aqueous misdirection) — especially post-operatively
Secondary angle closure (neovascular, inflammatory)
Hypertensive uveitis / herpetic trabeculitis / Posner-Schlossman syndrome
Scleritis with angle involvement

Treatment

Immediate (Acute Attack)

Position: Lay patient supine — gravity shifts the lens posteriorly, reducing pupillary block.

Medical IOP reduction (combine multiple agents):

Agent Class	Drug & Dose
Carbonic anhydrase inhibitor	Acetazolamide 500 mg IV or PO, then 250 mg q4h (max 1 g/day); or topical dorzolamide/brinzolamide
Topical β-blocker	Timolol 0.5% — 1 drop to affected eye
Topical α₂-agonist	Apraclonidine 1% or brimonidine 0.2% — 1 drop
Hyperosmotic agent (if no IOP response at 1 hour)	IV mannitol 1.5–2 g/kg over 30 min; or oral glycerine

⚠️ Pilocarpine is no longer recommended acutely — at very high IOP, the ischaemic iris sphincter is unresponsive; cholinergic agents can paradoxically shallow the anterior chamber and worsen closure. — Tintinalli's, 10e

Analgesia/antiemetics: Fentanyl is preferred (lowers IOP); ondansetron is safe (no IOP effect). Vomiting increases IOP and should be controlled.

Definitive Treatment

Peripheral laser iridotomy (PI) — creates a full-thickness hole in the peripheral iris to equalize anterior and posterior chamber pressures, bypassing the pupillary block. Performed once the cornea is clear and IOP is controlled.

Bilateral PI is standard (the fellow eye has an occludable angle)
Does not help plateau iris — laser peripheral iridoplasty or lens extraction needed in those cases

Clear lens extraction / phacoemulsification with IOL — the EAGLE trial demonstrated that early lens extraction is more effective and cost-effective than laser PI for PAC and PACG with elevated IOP. Achieves IOP control in ~80% preoperatively elevated eyes and corrects hypermetropia.

Trabeculectomy (with mitomycin C) — reserved for persistent IOP elevation despite an open angle, though carries a risk of malignant glaucoma.

Prophylaxis for PACS

The ZAP trial showed laser PI has only a small protective benefit over 6 years; selective prophylactic PI is appropriate for higher-risk patients (symptoms of intermittent closure, need for frequent dilation, atropine-like medications, limited access to eye care).

Summary Flowchart

Acute red eye + severe pain + fixed mid-dilated pupil + cloudy cornea
                        ↓
           Measure IOP (≥40–50 mmHg) → APAC
                        ↓
    Supine position + Acetazolamide + Timolol + Apraclonidine
                        ↓
         If IOP not ↓ in 1 hr → IV Mannitol
                        ↓
   Urgent ophthalmology consult → Peripheral laser iridotomy
                        ↓
     Prophylactic PI to fellow eye

Key references: Kanski's Clinical Ophthalmology: A Systematic Approach, 10e | Tintinalli's Emergency Medicine, 10e | Goldman-Cecil Medicine, 26e

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