Special Senses & Otolaryngology

Acute angle-closure glaucoma: recognition and management

Clinical Overview and When to Suspect Acute Angle-Closure Glaucoma

— Aqueous, secreted by the ciliary body, normally flows from the posterior chamber through the pupil into the anterior chamber and exits via the trabecular meshwork.

— In predisposed eyes with shallow anterior chambers, mid-dilation causes the iris to bow forward against the lens, blocking flow through the pupil → posterior chamber pressure rises → peripheral iris pushed against trabecular meshwork → outflow obstructed.

— Hyperopic (farsighted) eyes (short axial length, crowded anterior segment)

— Age >55, female sex, Asian or Inuit ancestry

— Family history of angle closure

— Mature cataract (intumescent lens pushes iris forward)

— Dim light (movie theater, evening) → mid-dilated pupil

— Anticholinergics (diphenhydramine, scopolamine patch, TCAs, oxybutynin, ipratropium nebulizer mist)

— Sympathomimetics (decongestants, ephedrine, cocaine)

— Topiramate (idiosyncratic ciliary body swelling — bilateral closure even in non-hyperopic eyes)

— Pupillary dilation for fundoscopy

— Emotional stress, prone positioning

Board pearl: Any patient presenting to the ED with acute unilateral red eye, headache, nausea/vomiting, and blurred vision with halos around lights — especially after starting an anticholinergic or being in a dark room — has AACG until proven otherwise. Do not dilate the eye to examine the fundus; check IOP first.

Definition: Acute angle-closure glaucoma (AACG) is a true ophthalmologic emergency caused by sudden obstruction of aqueous humor outflow at the iridocorneal angle, producing a rapid spike in intraocular pressure (IOP), often >40–60 mmHg (normal 10–21).

Core mechanism — pupillary block:

High-risk anatomy/demographics:

Common precipitants tested on Step 3:

Why urgency matters: Sustained IOP elevation causes optic nerve ischemia and irreversible vision loss within hours. Permanent damage can begin in 6–12 hours.

Presentation Patterns and Key History

— Severe unilateral eye pain (deep, boring, periorbital), often described as the worst pain of the patient's life

— Blurred vision with colored halos around lights (corneal edema diffracts light)

— Frontal headache ipsilateral to the eye

— Nausea and vomiting (vagal response to high IOP) — frequently the chief complaint, leading to misdiagnosis as gastroenteritis or migraine

— Red eye with photophobia

— "Were you in a dark room, movie theater, or did you wake from sleep?"

— Medication review: diphenhydramine, scopolamine, TCAs, SSRIs, topiramate, sulfa drugs, anticholinergic inhalers via mask, decongestants, MDMA

— Recent pharmacologic pupil dilation (eye exam, MRI prep)

— Prior similar episodes that resolved spontaneously (subacute angle closure)

— Refractive error: do they wear glasses for distance (myopia) or reading at young age (hyperopia)?

— Family history of glaucoma or "eye attacks"

— Predominant GI symptoms → admitted to medicine for "abdominal pain, nausea"

— Predominant headache → worked up as migraine or SAH

— Bilateral simultaneous closure → think topiramate or other sulfa-related ciliochoroidal effusion

— Postoperative patients (prone positioning, anticholinergic premeds)

Key distinction: Migraine causes photophobia and nausea but does not cause a fixed mid-dilated pupil or a rock-hard globe. SAH causes thunderclap headache but pupils are typically reactive and there is no corneal haze. Always palpate the globe and check visual acuity in any patient with headache plus eye complaints — a 30-second exam prevents permanent blindness.

Classic symptom pentad:

Tempo: Symptoms develop over minutes to a few hours, often in the evening. Patients may report prior intermittent episodes that self-resolved when going to sleep (sleep miosis breaks attack).

Targeted history questions:

Atypical presentations that fool examiners:

Physical Exam Findings

— Conjunctival injection with ciliary flush (perilimbal redness)

— Corneal edema — "steamy" or "hazy" cornea; iris details appear blurred

— Fixed, mid-dilated (4–6 mm), nonreactive pupil — pathognomonic when combined with high IOP

— Shallow anterior chamber — oblique penlight test: shine light from temporal side; if nasal iris is in shadow, chamber is shallow (positive eclipse sign)

— Contralateral eye also typically has a shallow chamber (anatomic predisposition)

— IOP usually 40–80 mmHg (normal 10–21)

— Tono-Pen or iCare in ED; digital palpation of globe through closed lid reveals rock-hard "marble-like" eye compared with soft contralateral globe — a high-yield bedside finding when tonometer unavailable

— Often obscured by corneal edema

— When visible: optic disc may appear hyperemic acutely; cupping develops chronically

— Do NOT dilate the pupil pharmacologically — will worsen block

Step 3 management: In a CCS case, your first orders are: visual acuity both eyes, tonometry (IOP), slit-lamp exam, and STAT ophthalmology consult — placed in parallel with starting pharmacologic IOP reduction. Do not wait for the consultant to arrive before initiating therapy; vision loss is time-dependent.

Board pearl: The triad of red eye + fixed mid-dilated pupil + hard globe = AACG. A reactive pupil essentially rules it out.

General appearance: Patient is acutely uncomfortable, often vomiting, photophobic, holding the affected eye.

Visual acuity: Markedly reduced in affected eye — counting fingers or hand motion is common. Always document baseline VA before any intervention (medicolegal).

External/slit-lamp findings:

Tonometry — the critical measurement:

Fundoscopy:

Systemic vitals: Bradycardia possible from oculocardiac reflex; hypertension from pain. Tachycardia with vomiting suggests volume depletion.

Diagnostic Workup — Initial Assessment

— Tono-Pen, iCare rebound tonometer, or Goldmann applanation all acceptable

— IOP >30 mmHg with symptoms = treat as AACG until ophthalmology arrives

— Document IOP in both eyes at baseline and serially every 30–60 minutes during treatment

— Confirms corneal edema, shallow chamber, mid-dilated pupil, conjunctival injection

— Van Herick technique: peripheral anterior chamber depth <25% of corneal thickness = narrow angle

— Look for glaukomflecken — small anterior subcapsular lens opacities from prior attacks

— Direct visualization of the iridocorneal angle — confirms closure and assesses contralateral eye

— Reveals peripheral anterior synechiae if attack has been prolonged

— Not needed for diagnosis

— Basic chemistry before giving acetazolamide (avoid in severe sulfa allergy, sickle cell, severe COPD/metabolic acidosis, renal failure with eGFR <30)

— Pregnancy test in women of reproductive age (acetazolamide and mannitol have pregnancy implications)

— Glucose, BUN/creatinine before IV mannitol (osmotic load risks in CHF, renal failure)

— Do not pharmacologically dilate the pupil

— Do not patch the eye (dark environment → further dilation)

— Do not delay treatment awaiting imaging or consultant arrival

CCS pearl: Order "tonometry both eyes, ophthalmology consult STAT, IV access, antiemetic" as a clustered initial order set. The clock on optic nerve damage starts the moment IOP exceeds ~40 mmHg.

Key distinction: Unlike open-angle glaucoma (chronic, asymptomatic, diagnosed by screening), AACG is diagnosed by acute symptoms + acute IOP elevation — no visual field testing or OCT needed in the acute setting.

Tonometry is THE diagnostic test. Diagnosis is clinical + IOP measurement; no labs or imaging required to initiate treatment.

Slit-lamp examination:

Gonioscopy (ophthalmology, after IOP reduced and cornea clears):

Laboratory testing:

What NOT to do:

Diagnostic Workup — Advanced and Confirmatory Studies

— Performed by ophthalmology once cornea clears (post-treatment)

— Shaffer grading of the angle: 0 (closed) to 4 (wide open)

— Indentation gonioscopy distinguishes appositional from synechial closure

— Bilateral evaluation — contralateral eye almost always has occludable angle and needs prophylactic iridotomy

— Noncontact imaging of angle anatomy

— Useful when cornea too edematous for gonioscopy

— Identifies plateau iris configuration, lens-induced closure, or ciliary body cysts

— When fundus not visible through hazy cornea

— Rules out posterior segment causes of acute IOP rise: suprachoroidal hemorrhage, posterior scleritis, choroidal effusion, intraocular tumor

— Fundus photography, OCT of retinal nerve fiber layer

— Humphrey visual field testing — baseline for monitoring

— Medication review: topiramate, sulfa drugs, MAOIs, SSRIs/SNRIs → bilateral ciliochoroidal effusion syndrome

— Consider uveitic, neovascular, malignant glaucoma, phacomorphic (intumescent lens), phacolytic

— In neovascular: workup for proliferative diabetic retinopathy or central retinal vein occlusion

— Only if neurologic signs suggest alternative diagnosis (e.g., third nerve palsy with mydriasis, suspected aneurysm)

— Do not delay AACG treatment for head CT

Board pearl: Bilateral simultaneous angle closure = think drug-induced (topiramate is the classic) until proven otherwise. Mechanism is ciliochoroidal effusion with anterior lens-iris displacement, not pupillary block — laser iridotomy will NOT help; stop the drug and use cycloplegics.

Step 3 management: After resolution, definitive prophylactic laser peripheral iridotomy is required in BOTH eyes — the fellow eye has a ~50% risk of attack within 5 years if untreated.

Gonioscopy (gold standard for angle assessment):

Anterior segment OCT (AS-OCT) / Ultrasound biomicroscopy (UBM):

B-scan ultrasound:

Optic nerve assessment (after acute attack resolves):

Workup for secondary angle closure (when bilateral or atypical):

Imaging of brain:

Risk Stratification and First-Line Management Logic

— Decrease aqueous production (β-blockers, α2-agonists, carbonic anhydrase inhibitors)

— Increase aqueous outflow (pilocarpine — miosis pulls iris away from angle; prostaglandin analogs)

— Osmotically draw fluid out of vitreous (mannitol, oral glycerin) to deepen anterior chamber

— Position patient supine — gravity allows lens to fall posteriorly, deepening chamber

— Place IV, give antiemetic (ondansetron); control pain

— Topical drops at 1-minute intervals: timolol → apraclonidine/brimonidine → dorzolamide → prednisolone

— Oral or IV acetazolamide 500 mg (IV preferred if vomiting)

— Recheck IOP at 30 and 60 minutes

— Pilocarpine 1–2% — only AFTER IOP begins to fall (<40 mmHg). At very high IOP, iris sphincter is ischemic and paralyzed → pilocarpine ineffective and may worsen by increasing inflammation

— If IOP not falling after 30–60 min → IV mannitol 1–2 g/kg over 30–45 min

— Corneal indentation ("Anderson technique") by ophthalmology can mechanically break attack

— Laser peripheral iridotomy (LPI) within 24–48 hours of attack resolution

— Prophylactic LPI in the fellow eye during the same admission or shortly after

— In cases refractory to medical therapy: surgical iridectomy, lens extraction (clear lens or cataract extraction), or anterior chamber paracentesis as temporizing maneuvers

CCS pearl: In your CCS case, the correct sequence is (1) position supine, (2) topical timolol + apraclonidine + dorzolamide + prednisolone, (3) IV/PO acetazolamide, (4) pilocarpine once IOP <40, (5) IV mannitol if refractory, (6) ophthalmology to perform LPI. Skipping pilocarpine timing or giving it first is a classic distractor.

Therapeutic goal: Reduce IOP rapidly to <35 mmHg and ideally to baseline (<21), break pupillary block, and clear cornea for definitive laser peripheral iridotomy (LPI).

Three simultaneous mechanisms targeted:

Sequencing (high-yield order):

Definitive therapy:

Pharmacotherapy — First-Line Drug Regimen

— Timolol 0.5% — nonselective β-blocker, decreases aqueous production. Avoid in asthma, severe COPD, bradycardia, decompensated heart failure, heart block.

— Apraclonidine 1% or Brimonidine 0.2% — α2-agonist, decreases aqueous production and increases uveoscleral outflow. Avoid brimonidine in infants (CNS depression, apnea) and in patients on MAOIs.

— Dorzolamide 2% or Brinzolamide 1% — topical carbonic anhydrase inhibitor. Sulfa derivative — caution with severe sulfa allergy.

— Prednisolone acetate 1% — reduces inflammation and trabeculitis; given every 15–30 minutes initially.

— Pilocarpine 1–2% — muscarinic agonist causing miosis that mechanically pulls peripheral iris from angle. Give only after IOP <40 mmHg; ineffective at higher pressures due to iris ischemia. Avoid in phacomorphic or malignant glaucoma.

— Acetazolamide — 500 mg IV or PO, then 250 mg q6h. Decreases aqueous production by ~50%. Contraindications: sulfa hypersensitivity (severe), sickle cell (acidosis precipitates crisis), severe COPD/respiratory acidosis, hepatic cirrhosis (hepatic encephalopathy risk), eGFR <30, hyponatremia/hypokalemia, profound metabolic acidosis.

— Mannitol 20% — 1–2 g/kg IV over 30–45 min. Osmotic agent dehydrates vitreous. Avoid in CHF, pulmonary edema, anuric renal failure, severe dehydration, intracranial bleeding. Monitor electrolytes, urine output, volume status.

— Oral glycerin 50% (1–1.5 g/kg) or isosorbide — alternatives to mannitol; glycerin contraindicated in diabetes (hyperglycemia/ketoacidosis risk).

Board pearl: A patient with AACG plus severe sulfa allergy still typically tolerates acetazolamide (cross-reactivity is low), but if there is a history of Stevens-Johnson syndrome, substitute methazolamide or rely on mannitol + topicals. Document the risk-benefit decision.

Key distinction: Pilocarpine timing is the single most-tested pharmacology point — give it AFTER initial IOP reduction, never first.

Topical agents (administered serially, 1 minute apart):

Systemic agents:

Analgesia/antiemetic: Ondansetron IV; opioids cautiously (some cause miosis, beneficial, but watch for emesis).

Procedures — Definitive and Rescue Interventions

— Nd:YAG laser creates a small (~150–500 μm) full-thickness hole in the peripheral iris, equalizing pressure between posterior and anterior chambers

— Eliminates pupillary block permanently

— Performed once cornea clears (usually within 24–48 hours of medical IOP reduction)

— Bilateral procedure: the fellow eye carries ~50% risk of acute attack within 5 years and requires prophylactic LPI

— Complications: transient IOP spike, bleeding, iritis, corneal burns, late closure of iridotomy, dysphotopsia (visual artifacts)

— Emergent decompression when IOP refractory to maximal medical therapy and LPI not immediately available

— A small-gauge needle removes ~0.1–0.2 mL of aqueous from anterior chamber

— Performed only by ophthalmology — high risk of lens or iris injury

— Open surgical alternative when LPI not possible (very cloudy cornea, uncooperative patient)

— Increasingly first-line in phacomorphic angle closure or when cataract present

— EAGLE trial: clear lens extraction superior to LPI in primary angle closure with IOP >30 or established glaucoma

— For chronic angle closure with extensive peripheral anterior synechiae and persistent IOP elevation

— Used in malignant glaucoma (aqueous misdirection) and drug-induced (topiramate) angle closure — paradoxically tighten the lens-zonule complex and pull the lens posteriorly

— Pilocarpine is contraindicated in these settings

Step 3 management: Plan disposition with ophthalmology: admit or close outpatient follow-up within 24 hours for LPI. Discharge instructions must include the medication list, IOP recheck plan, return precautions (recurrent pain, vision loss, vomiting), and explicit prohibition on anticholinergic OTC medications.

Board pearl: EAGLE trial → in primary angle closure with high IOP or glaucomatous damage, lens extraction beats LPI for long-term IOP control and quality of life.

Laser peripheral iridotomy (LPI) — definitive treatment:

Anterior chamber paracentesis:

Surgical peripheral iridectomy:

Lens extraction (clear lens extraction or cataract surgery):

Goniosynechialysis / trabeculectomy:

Cycloplegics (atropine, cyclopentolate) — special situation:

Special Populations — Elderly and Renal/Hepatic Impairment

— Peak incidence in 6th–7th decade; lens thickens and moves anteriorly with age, narrowing the angle

— Comorbid cataract is common — phacomorphic component favors lens extraction over LPI alone

— Polypharmacy risk: anticholinergics for overactive bladder (oxybutynin, tolterodine), TCAs for neuropathic pain, antihistamines for sleep, ipratropium nebulizers — review and deprescribe when possible

— Falls risk with pilocarpine (induced myopia, dim vision from miosis) and with systemic acetazolamide (paresthesias, fatigue, electrolyte derangement)

— Acetazolamide is renally cleared — avoid if eGFR <30 mL/min/1.73m²; risk of metabolic acidosis, hypokalemia, nephrolithiasis

— Mannitol can precipitate volume overload, pulmonary edema, and hyperkalemia in advanced CKD; contraindicated in anuric renal failure

— Topical CAIs (dorzolamide, brinzolamide) have minimal systemic absorption but still cause measurable acid-base changes in ESRD

— Brimonidine — minor renal adjustment; monitor for hypotension and sedation

— Acetazolamide contraindicated in severe cirrhosis — alkalinization of urine reduces NH4+ excretion → hepatic encephalopathy

— Use topical CAIs cautiously

— Methazolamide is hepatically metabolized — similar caution

— Timolol is systemically absorbed; can cause bradycardia, AV block, bronchospasm, and worsen heart failure → use betaxolol (β1-selective) or avoid

— Apraclonidine/brimonidine can cause hypotension and bradycardia

— Mannitol expands intravascular volume initially — caution in CHF

Step 3 management: In an 82-year-old with CKD stage 4 and AACG, your regimen shifts to timolol (or betaxolol if COPD), brimonidine, topical dorzolamide, topical prednisolone, and early ophthalmology for LPI/lens extraction — avoid systemic acetazolamide and mannitol. Document the contraindications and the modified plan in the chart.

Elderly considerations:

Renal impairment:

Hepatic impairment:

Cardiovascular comorbidity:

Special Populations — Pregnancy, Pediatrics, and Other Subgroups

— AACG is rare in pregnancy but can occur, especially in third trimester

— Acetazolamide: historically category C; small case series show teratogenicity in animals; avoid in first trimester, use cautiously later if benefit justifies risk (potential neonatal metabolic acidosis and electrolyte disturbance if used near term)

— Mannitol: can reduce amniotic fluid volume and cross placenta — generally avoided

— Brimonidine: avoid near term (neonatal CNS depression, apnea); avoid during breastfeeding

— Topical β-blockers: associated with neonatal bradycardia/apnea — use lowest effective dose, perform nasolacrimal occlusion to limit systemic absorption

— Pilocarpine and prostaglandin analogs: limited data; prostaglandins theoretically can induce uterine contraction

— Preferred approach: topical β-blocker + topical CAI, with early LPI as definitive therapy (laser is safe in pregnancy)

— Primary AACG is rare; consider secondary causes: retinopathy of prematurity, persistent fetal vasculature, congenital glaucoma, uveitic (JIA), trauma, lens dislocation (Marfan, homocystinuria, Weill-Marchesani)

— Brimonidine is contraindicated <2 years and used cautiously <6 years — risk of bradycardia, hypotension, apnea, profound CNS depression

— Examination often requires sedation or EUA

— Topiramate is the classic culprit — onset typically within 2 weeks of initiation or dose increase

— Other agents: sulfa antibiotics, hydrochlorothiazide, acetazolamide (paradoxical), SSRIs/SNRIs, MAOIs, MDMA, methamphetamine

— Mechanism: ciliochoroidal effusion → anterior rotation of ciliary body and lens-iris diaphragm

— Management: STOP the offending drug, topical cycloplegics (atropine), topical steroids, IOP-lowering agents. LPI does NOT help because there is no pupillary block.

Board pearl: A 32-year-old woman started on topiramate for migraine 10 days ago presents with bilateral acute angle closure and acute myopia → diagnosis is drug-induced ciliochoroidal effusion. Stop topiramate, give atropine + topical steroid + IOP-lowering drops. Do not order LPI.

Pregnancy:

Pediatrics:

Drug-induced bilateral angle closure:

Complications and Adverse Outcomes

— Glaucomatous optic neuropathy from sustained IOP-induced ischemia — irreversible nerve fiber loss begins within hours

— Central retinal artery or vein occlusion from prolonged extreme IOP

— Ischemic optic neuropathy

— Visual field defects (arcuate scotomas, nasal step, eventual tunnel vision)

— Iris atrophy and a permanently mid-dilated, poorly reactive pupil ("fixed pupil sign of prior attack")

— Glaukomflecken — small grey-white anterior subcapsular lens opacities pathognomonic of prior AACG

— Posterior synechiae (iris-to-lens adhesions) and peripheral anterior synechiae (iris-to-trabecular meshwork) → chronic angle closure

— Corneal endothelial cell loss → bullous keratopathy, chronic corneal edema

— Cataract formation accelerated

— Persistent IOP elevation despite LPI if synechiae are extensive

— Requires long-term IOP-lowering medications, possibly trabeculectomy or tube shunt

— Without prophylactic LPI, ~40–80% risk of fellow-eye attack over years

— Acetazolamide: metabolic acidosis, hypokalemia, paresthesias, nephrolithiasis, aplastic anemia (rare idiosyncratic), Stevens-Johnson syndrome

— Mannitol: volume overload, pulmonary edema, hyperkalemia, acute renal failure, electrolyte derangement

— Timolol: bronchospasm, bradycardia, depression, fatigue

— Pilocarpine: brow ache, induced myopia, retinal detachment risk in high myopes, GI cramping/diaphoresis if absorbed systemically

— LPI: transient IOP spike, hyphema, iritis, dysphotopsia, late closure

— Rare postoperative complication after LPI or filtration surgery; aqueous misdirects posteriorly into vitreous

— IOP rises with progressive shallowing of central anterior chamber — pilocarpine worsens it; treat with cycloplegics, steroids, IOP-lowering agents, and vitrectomy

Board pearl: Glaukomflecken on slit lamp = the patient had a prior unrecognized AACG attack.

Permanent vision loss:

Anterior segment damage:

Chronic angle-closure glaucoma:

Recurrence and contralateral attack:

Treatment-related complications:

Malignant glaucoma (aqueous misdirection):

When to Escalate Care — Consult and Disposition

— Persistent IOP >30 despite maximal medical therapy

— Inability to obtain LPI within 24 hours as outpatient

— Refractory pain or intractable vomiting precluding oral therapy

— Need for IV mannitol or close serial IOP monitoring

— Patient unable to administer or comply with frequent eye drops at home

— Bilateral attack

— Comorbid conditions complicating treatment (CKD, CHF, COPD on β-blocker concerns)

— Hemodynamic instability from mannitol-induced volume shifts or β-blocker bradycardia

— Severe metabolic acidosis from acetazolamide in renal impairment

— Concurrent acute medical emergency

— IOP reduced to <25 mmHg and stable on serial measurements

— Pain and vomiting controlled

— Reliable patient, can administer drops, has transportation

— Ophthalmology follow-up confirmed within 24 hours for LPI

— Document IOP trend, all medications and times given, contraindications considered, and ophthalmology recommendations

— Provide written instructions and a single point of contact

CCS pearl: On CCS, do not "advance the clock" until you have placed the ophthalmology consult and started topical therapy. Then advance in short intervals (15–30 min) to recheck IOP. Premature large time advances missing the recheck window = lost points.

Step 3 management: Always perform a structured handoff using a tool like I-PASS when transferring care between ED and ophthalmology, or ED and admitting service. Include the medication times, IOP trend, allergy considerations, and pending LPI plan — transition-of-care errors are a tested patient safety domain.

Ophthalmology consult: IMMEDIATE — call before, or simultaneously with, initiating medical therapy. AACG is not a "morning rounds" consult; it is bedside, same-hour.

Criteria for admission:

ICU criteria (uncommon but relevant):

Transfer to facility with ophthalmology coverage if none on site — initiate medical therapy first, then transfer; do not delay topical and systemic drops while arranging transfer.

Outpatient disposition (acceptable when):

Communication and handoff:

Key Differentials — Other Causes of Acute Red, Painful Eye

— Pain, photophobia, redness with ciliary flush

— Pupil small and poorly reactive (not mid-dilated), often irregular from posterior synechiae

— IOP usually normal or low; can be elevated if trabeculitis

— Slit lamp: cells and flare in anterior chamber, keratic precipitates

— Associated with HLA-B27 disease, sarcoidosis, JIA, HSV, syphilis, TB

— Pain, redness, photophobia, focal corneal infiltrate with fluorescein-staining epithelial defect

— Contact lens wearer is the classic stem — Pseudomonas until proven otherwise

— IOP normal; pupil reactive

— Dendritic ulcer on fluorescein staining; decreased corneal sensation

— Treat with topical/oral acyclovir; avoid steroids in epithelial disease

— Severe pain, vision loss, hypopyon (layered pus in anterior chamber)

— Postoperative (especially post-cataract) or post-trauma; emergent vitreous tap and intravitreal antibiotics

— Deep, boring pain that wakes patient from sleep

— Bluish-violet hue of sclera not blanching with phenylephrine

— Associated with rheumatoid arthritis, GPA, relapsing polychondritis

— Neovascular glaucoma: rubeosis iridis on iris from PDR or ischemic CRVO

— Phacomorphic (intumescent cataract pushing iris forward)

— Phacolytic (hypermature lens leaks proteins, clogs trabecular meshwork)

— Uveitic angle closure from synechiae

Key distinction: Pupil findings are the fastest discriminator.

— AACG → mid-dilated, fixed

— Iritis → small, sluggish, irregular

— Keratitis/conjunctivitis → normal, reactive

— Third nerve palsy → dilated, with ptosis and "down-and-out" eye

Board pearl: Conjunctivitis does not cause pain, photophobia, decreased vision, or pupillary changes. If any of those are present, look elsewhere.

Acute anterior uveitis (iritis):

Bacterial keratitis / corneal ulcer:

Herpes simplex keratitis:

Endophthalmitis:

Scleritis:

Acute angle-closure crisis from secondary causes:

Key Differentials — Systemic and Non-Ocular Mimics

— Throbbing unilateral headache, photophobia, nausea, vomiting, visual aura (scotoma, fortification spectra)

— Pupils reactive, IOP normal, no corneal edema

— Pain typically improves with dark, quiet room (opposite of AACG, where dark precipitates)

— Severe unilateral periorbital pain, lacrimation, conjunctival injection, ptosis, miosis (Horner-like)

— IOP normal; pupil small or normal, not dilated

— Recurrent stereotyped episodes; treat with oxygen, sumatriptan

— Thunderclap headache, neck stiffness, possible vomiting

— Pupils typically reactive (unless aneurysm compressing CN III)

— CT head and LP if needed

— Painful dilated pupil with ptosis and ophthalmoplegia ("down and out" eye)

— IOP normal; emergent CTA/MRA

— Proptosis, chemosis, ocular bruit, dilated conjunctival vessels (corkscrew), elevated IOP

— History of head trauma or spontaneous in elderly women

— Age >50, headache, jaw claudication, scalp tenderness, sudden vision loss (AION)

— ESR/CRP elevated; start high-dose steroids before biopsy

— Misdiagnosis trap when AACG presents primarily with nausea and vomiting

— Look for any eye complaints, photophobia, blurred vision — perform a focused eye exam in every adult with severe headache + vomiting

— Severe BP elevation with headache and visual changes; fundoscopy shows papilledema, flame hemorrhages

— IOP normal

Board pearl: Any older adult presenting to the ED with headache, nausea, and vomiting deserves a visual acuity, pupil exam, and globe palpation — a 60-second screen that catches AACG masquerading as a GI or neuro complaint.

Key distinction: Anisocoria with a dilated unreactive pupil: AACG (red, painful, hard globe, decreased VA) vs CN III palsy (ptosis, ophthalmoplegia, possibly painful from aneurysm) vs pharmacologic (history of contact with mydriatic, painless, white eye, normal motility).

Migraine with aura:

Cluster headache:

Subarachnoid hemorrhage:

Posterior communicating artery aneurysm with CN III palsy:

Carotid-cavernous fistula:

Giant cell arteritis:

Acute gastroenteritis / abdominal emergency:

Hypertensive emergency with papilledema:

Secondary Prevention and Long-Term Plan

— Bilateral LPI: affected eye after attack resolves and prophylactic LPI in fellow eye (high-yield)

— Typically performed within 24–72 hours of acute attack

— In phacomorphic or phacolytic mechanisms, lens extraction may be preferred (EAGLE trial supports clear lens extraction in primary angle closure)

— Anticholinergics: diphenhydramine, dimenhydrinate, scopolamine patches, oxybutynin, tolterodine, TCAs, hyoscyamine

— Sympathomimetics: pseudoephedrine, phenylephrine, ephedrine, amphetamines, cocaine, MDMA

— Topiramate and other sulfa-based drugs (in patients with bilateral drug-induced attacks)

— Caution with anesthetic premedications (atropine, glycopyrrolate) — anesthesiologist should be alerted preoperatively

— Update allergy list as "intolerance — risk of angle closure" so EHR alerts fire

— Some patients still need long-term topical IOP-lowering drops if extensive peripheral anterior synechiae or coexisting open-angle component

— First-line chronic: prostaglandin analog (latanoprost) once nightly

— Second-line: timolol, brimonidine, dorzolamide

— Sleep in well-lit room is NOT necessary after LPI (block is resolved), but reasonable in pre-LPI window

— Avoid prolonged prone positioning if not yet treated

— Educate on warning symptoms: brow ache, halos, intermittent blurred vision — call ophthalmology immediately

— First-degree relatives, especially Asian and hyperopic, should have gonioscopy screening for occludable angles

— Update problem list, allergy/intolerance list, medication-avoidance list

— Share with primary care physician and pharmacy

Step 3 management: At discharge, your medication reconciliation must explicitly discontinue any provoking anticholinergic (e.g., bedtime diphenhydramine for sleep) and provide an alternative (sleep hygiene counseling, trazodone if needed). This is a board-favorite transition-of-care intervention.

Definitive prevention — laser peripheral iridotomy:

Medications to avoid lifelong (provide written list and update problem list):

Chronic IOP management after LPI:

Lifestyle and counseling:

Family screening:

Documentation:

Follow-Up, Monitoring, and Counseling

— 24-hour ophthalmology recheck post-discharge: IOP, slit-lamp, plan for LPI

— LPI within 24–72 hours of acute attack resolution

— Fellow-eye prophylactic LPI at the same visit or shortly after

— 1-week post-LPI: IOP, patency of iridotomy, anterior segment inflammation

— 1-month and 3-month: IOP, gonioscopy to confirm angle opening

— Every 6–12 months: IOP, optic disc evaluation, OCT retinal nerve fiber layer, Humphrey visual field

— More frequent if residual glaucomatous damage or chronic angle-closure glaucoma develops

— Teach patient/family the warning signs: eye pain, halos around lights, blurred vision, headache, nausea — immediate ophthalmology contact

— Provide written discharge instructions in plain language

— Provide ophthalmology after-hours contact number

— Demonstrate proper eye drop technique: tilt head back, pull lower lid, single drop, close eye and occlude nasolacrimal puncta for 1 minute (reduces systemic absorption — important for timolol/brimonidine)

— Wait 5 minutes between different drops

— Use written schedule or pillbox-style drop chart for elderly

— Pilocarpine causes miosis → poor night vision and induced myopia; counsel against night driving while on it

— Document visual acuity for driver licensing and report per state requirements (varies by state — some require physician reporting of vision below a threshold)

— Continue primary care follow-up — glaucoma patients often have comorbid HTN, diabetes; address overall vascular risk

— Connect to glaucoma patient education resources (American Academy of Ophthalmology, Glaucoma Research Foundation)

Board pearl: Nasolacrimal occlusion after eye drops is a free, high-yield intervention that reduces systemic side effects of topical β-blockers and α-agonists by up to 60%.

CCS pearl: Don't forget to schedule the follow-up appointment and document medication counseling — both score in CCS metrics.

Immediate follow-up timeline:

Long-term monitoring:

Self-monitoring counseling:

Medication adherence:

Driving and occupational counseling:

Vaccinations and general health:

Support:

Ethical, Legal, and Patient Safety Considerations

— Discuss risks: transient IOP spike, hyphema, iritis, dysphotopsia (glare, line, halo — occasionally chronic), late closure, rare endophthalmitis

— Discuss benefits: definitive prevention of recurrence, ~95% efficacy

— Discuss alternatives: surgical iridectomy, lens extraction, observation (NOT recommended)

— Special case: prophylactic LPI in the asymptomatic fellow eye — the patient must understand they are accepting procedural risk for a 50% lifetime risk of attack; document the shared decision

— Severe pain, vomiting, and opioid analgesia may transiently impair capacity; if emergency LPI needed and patient lacks capacity, proceed under emergency exception to consent (immediate threat to vision) or obtain surrogate consent per state law

— Medication reconciliation at discharge: explicitly remove provoking anticholinergics; add eye drops with clear timing

— Communicate with primary care to update problem list and avoid future prescribing of contraindicated drugs (e.g., topiramate, diphenhydramine, oxybutynin)

— Use EHR allergy/intolerance flag: "angle closure — avoid anticholinergics, sympathomimetics, topiramate"

— Confirm ophthalmology follow-up appointment before discharge (closed-loop referral)

— Some states require physician reporting of vision impairment below a defined threshold for driver licensing (e.g., CA, OR, PA, NJ); know your jurisdiction

— Counsel patient about driving limitations while on pilocarpine or until vision recovers

— If a provoking drug was prescribed by another clinician (e.g., topiramate started by neurology), open and honest disclosure with non-blaming language; the patient is owed transparency

— Higher prevalence in Asian and Inuit populations; ensure access to interpreters and culturally tailored education materials

— Cost of glaucoma drops can drive nonadherence — use generics, 90-day supplies, patient assistance programs

Step 3 management: A common tested scenario: a hospitalist orders diphenhydramine for sleep in a patient with known narrow angles → patient develops AACG overnight. Disclose, document, and add a hard stop in the EHR for future anticholinergic orders. This is a sentinel-event-level patient safety issue worthy of root cause analysis.

Informed consent for LPI:

Capacity and surrogate decision-making:

Transitions of care — patient safety priority:

Mandatory reporting and driving:

Disclosure of error:

Health equity:

High-Yield Associations and Rapid-Fire Facts

— Dim light (movie theater, evening)

— Anticholinergics (Benadryl, scopolamine, TCAs, oxybutynin)

— Sympathomimetics (pseudoephedrine, MDMA, cocaine)

— Topiramate → bilateral drug-induced closure with acute myopia

— Pupil dilation for eye exam or MRI

— Prone positioning, emotional stress

— Fixed, mid-dilated pupil + red eye + rock-hard globe + hazy cornea + halos = AACG

— Glaukomflecken = prior attack

— Diagnosis is clinical + tonometry; no labs required to start treatment

— Gonioscopy = gold standard for angle assessment (after cornea clears)

— AS-OCT or UBM when cornea too hazy

— Pilocarpine fails at IOP >40–50 (iris sphincter ischemic) — give after initial drops reduce IOP

— Acetazolamide: avoid in sulfa SJS, sickle cell, severe COPD, CKD <30, cirrhosis

— Mannitol: avoid in CHF, anuria, pulmonary edema

— Timolol: avoid in asthma/COPD, bradycardia, heart block

— Brimonidine: avoid <2 years (apnea)

— Topiramate-induced: stop drug + atropine + steroids; LPI does NOT help

Board pearl: If a question stem mentions topiramate started 1–2 weeks ago + bilateral red painful eyes + acute myopia (sudden need for reading glasses) → drug-induced angle closure, stop drug, use cycloplegics, NOT LPI.

Anatomic risk factors: Hyperopia, short axial length, shallow anterior chamber, thick lens, plateau iris, Asian or Inuit ancestry, female sex, age >55, family history.

Classic precipitants:

Pathognomonic findings:

Lab/imaging pearls:

Pharmacology one-liners:

Definitive treatment: Laser peripheral iridotomy bilaterally — affected eye and prophylactically the fellow eye.

Trial to know: EAGLE trial — clear lens extraction beats LPI for primary angle closure with IOP >30 or glaucomatous damage.

Fellow eye risk: ~50% acute attack within 5 years without prophylactic LPI.

Differential triad: AACG (red, painful, mid-dilated) vs uveitis (red, painful, small/irregular pupil) vs conjunctivitis (red, painless, reactive pupil).

Pediatric red flag: AACG in a child → think lens dislocation (Marfan, homocystinuria) or congenital glaucoma.

Board Question Stem Patterns

— 65-year-old hyperopic woman comes from a movie theater with severe right eye pain, nausea, vomiting, blurred vision, halos around lights. Exam: right pupil mid-dilated nonreactive, cornea hazy, globe firm.

— Answer: Acute angle-closure glaucoma → IOP measurement, topical timolol + apraclonidine + dorzolamide + prednisolone, oral or IV acetazolamide, ophthalmology consult, pilocarpine once IOP falls, mannitol if refractory, definitive LPI bilateral.

— 32-year-old woman with migraine started on topiramate 10 days ago; bilateral eye pain, headache, blurred vision, new myopia.

— Answer: Stop topiramate, topical atropine (cycloplegic), topical steroid, topical β-blocker. Avoid pilocarpine and LPI.

— 70-year-old man takes diphenhydramine for insomnia and wakes with severe eye pain.

— Answer: AACG; treat acutely, discontinue diphenhydramine permanently, document allergy/intolerance, schedule LPI.

— Elderly woman with nausea and vomiting; brought to ED, given metoclopramide; persists. Eventually exam reveals red eye and hard globe.

— Answer: Eye exam in any older adult with unexplained vomiting → AACG.

— Post-op patient given scopolamine for nausea develops unilateral red painful eye; answer is AACG.

— AACG in patient with asthma → avoid timolol, use betaxolol or skip β-blocker.

— AACG in patient with CKD 4 → avoid acetazolamide and mannitol, rely on topicals + early LPI.

— AACG in cirrhosis → avoid acetazolamide (encephalopathy).

— AACG in sickle cell → avoid acetazolamide (acidosis → sickling).

— Order set: tonometry, slit-lamp, ophthalmology consult, IV access, ondansetron, supine positioning, topical drops in sequence, acetazolamide, pilocarpine after IOP drops, mannitol if refractory, admit or 24-hr LPI follow-up.

— Hospitalist orders Benadryl for sleep in narrow-angle patient → AACG; disclose error, RCA, EHR hard stop.

Step 3 management: Recognize the mechanism in the stem (pupillary block vs ciliochoroidal effusion) — this dictates whether LPI or drug discontinuation + cycloplegic is the answer.

Stem 1 — Classic presentation:

Stem 2 — Drug-induced bilateral:

Stem 3 — Anticholinergic precipitation:

Stem 4 — Differential trap (GI):

Stem 5 — Postoperative:

Stem 6 — Comorbidity choice:

Stem 7 — CCS management:

Stem 8 — Patient safety:

One-Line Recap

Acute angle-closure glaucoma is an ophthalmologic emergency presenting with a red painful eye, fixed mid-dilated pupil, hazy cornea, rock-hard globe, halos, and nausea — diagnosed by tonometry, treated immediately with topical β-blocker + α2-agonist + carbonic anhydrase inhibitor + steroid plus systemic acetazolamide (and mannitol if refractory), with pilocarpine added only after IOP falls below ~40 mmHg, and definitively cured by bilateral laser peripheral iridotomy (or lens extraction in selected cases).

Board pearl: Three numbers to remember — IOP >40 mmHg is the emergency threshold, 24–72 hours is the window for LPI after acute attack resolves, and ~50% is the fellow-eye attack risk without prophylactic LPI. Master those, the classic pupil findings, the pilocarpine timing rule, and the topiramate exception, and you will get every AACG question on Step 3 right.

Recognize: Red eye + mid-dilated nonreactive pupil + hard globe + halos + vomiting → check IOP immediately. Don't pharmacologically dilate.

Treat: Supine position; topical timolol, apraclonidine/brimonidine, dorzolamide, prednisolone in sequence; oral/IV acetazolamide; pilocarpine only AFTER initial IOP reduction; IV mannitol if refractory; STAT ophthalmology consult.

Special mechanism: Topiramate or sulfa-induced bilateral angle closure is from ciliochoroidal effusion, NOT pupillary block — stop the drug, use cycloplegics, LPI does not help.

Definitive and prevent: Bilateral laser peripheral iridotomy (affected eye and prophylactically the fellow eye, ~50% lifetime attack risk untreated); consider lens extraction per EAGLE trial; permanently avoid anticholinergics/sympathomimetics; document EHR intolerance flag; close-loop ophthalmology follow-up within 24 hours.