Case studies · Ophthalmology · 7 November 2026

Acute angle‑closure glaucoma case study

The case

Patient: 58‑year‑old female, teacher

Presenting complaint: Sudden, severe pain in the right eye for 6 hours, associated with blurred vision, halos around lights, nausea and one episode of vomiting.

History of present illness:

Past ocular history:

Systemic history:

Medications: Amlodipine 5 mg daily, occasional over‑the‑counter antihistamine for seasonal allergies.

Family history: Mother had cataract surgery at 70 years; no known glaucoma.

Social history: Non‑smoker, occasional wine, works as a school teacher, lives in a city with moderate altitude.

Examination:

Parameter Right eye (OD) Left eye (OS)
Visual acuity (Snellen) 20/200 20/30
Pupil size Mid‑dilated (5 mm), sluggish reaction to light 3 mm, brisk reaction
Intra‑ocular pressure (IOP) (Goldmann applanation) 52 mm Hg 16 mm Hg
Conjunctiva Conjunctival injection (ciliary flush) Normal
Cornea Diffuse corneal edema, “steamy” appearance Clear
Anterior chamber depth Shallow, peripheral iris apposition to trabecular meshwork (Van Herick grade 1) Deep
Gonioscopy (performed after IOP reduction) Closed angle (0–10°) in all quadrants Open angle (30–45°)
Fundus (indirect ophthalmoscopy) Optic disc appears slightly swollen, blurred margins, no hemorrhages Normal disc, cup‑disc ratio 0.3

Vital signs:

Initial investigations (performed after initial IOP‑lowering therapy):

The patient was started emergently with:

After 2 hours, the pain decreased, and IOP fell to 28 mm Hg.


Questions

  1. What is the most likely diagnosis?
  2. Which clinical findings in the history and examination point toward this diagnosis, and why?
  3. List the investigations that confirm the diagnosis and explain the significance of their results.
  4. Outline the acute management steps for this patient, including pharmacologic and laser/surgical options, with current guideline references.
  5. Discuss the possible short‑term and long‑term complications if the condition is not promptly treated.

Answers

1. Diagnosis

The most likely diagnosis is Acute Primary Angle‑Closure Glaucoma (APACG) affecting the right eye.

2. Clinical findings that point toward APACG

Finding Reason it supports APACG
Sudden severe unilateral ocular pain Acute rise in IOP due to sudden blockage of aqueous outflow.
Nausea and vomiting Vagal response to high IOP; common in acute attacks.
Blurred vision with halos Corneal edema (stromal swelling) acts as a diffraction grating, producing halos.
Mid‑dilated, sluggish pupil Iris is stretched by high pressure; sphincter muscle dysfunction.
Conjunctival injection (ciliary flush) Vascular congestion from increased episcleral venous pressure.
Corneal “steamy” appearance Corneal edema secondary to endothelial dysfunction from high IOP.
Shallow anterior chamber (Van Herick grade 1) Indicates a narrow angle predisposing to appositional closure.
IOP 52 mm Hg Far above normal (10–21 mm Hg), diagnostic of an acute attack.
Gonioscopy showing closed angle Direct visualization of angle closure confirms the mechanism.
Absence of secondary causes (normal labs, no trauma) Supports primary angle‑closure rather than secondary.

3. Investigations and their significance

  1. Goldmann Applanation Tonometry – Gold standard for IOP measurement. An IOP >30 mm Hg in the acute setting is diagnostic; the measured 52 mm Hg confirms severe elevation.

  2. Gonioscopy – Direct assessment of the angle. Closed angle (0–10°) in all quadrants confirms that the mechanism is appositional closure of the trabecular meshwork.

  3. Anterior Segment OCT (AS‑OCT) – Non‑contact imaging of the angle. AOD500 of 0.15 mm (normal ≥0.25 mm) quantifies the narrow angle and supports the diagnosis.

  4. Slit‑lamp examination – Shows corneal edema, shallow chamber, and pupil changes; essential for bedside diagnosis.

  5. Fundoscopy – May reveal optic disc swelling; helps to assess for glaucomatous damage and rule out other posterior segment pathology.

  6. B‑scan ultrasonography – Used when media opacity prevents fundus view; confirms normal posterior segment, excluding secondary causes like choroidal effusion.

  7. Systemic labs (electrolytes, renal function) – Baseline before acetazolamide or mannitol; ensures safe administration of carbonic anhydrase inhibitors and osmotic agents.

All these investigations together confirm primary acute angle‑closure glaucoma by demonstrating a narrow angle, elevated IOP, and characteristic anterior segment changes.

4. Acute management

Management aims to lower IOP rapidly, break the pupillary block, and then prevent recurrence. The American Academy of Ophthalmology (AAO) Preferred Practice Pattern (PPP) for Primary Angle‑Closure Glaucoma, 2023, outlines the following steps:

4.1 Immediate IOP‑lowering (first 1–2 hours)

Drug Dose & Route Mechanism Time to peak effect
Topical β‑blocker (timolol 0.5 %) One drop BID Decreases aqueous production 30 min
Topical α2‑agonist (apraclonidine 1 %) One drop QID Reduces aqueous production, increases uveoscleral outflow 15 min
Topical carbonic anhydrase inhibitor (dorzolamide 2 %) One drop TID Decreases aqueous production 1 h
Oral carbonic anhydrase inhibitor (acetazolamide) 500 mg PO loading, then 250 mg q6h Systemic reduction of aqueous production 1–2 h
IV osmotic agent (mannitol 20 % 1 g/kg) Infuse over 45 min Creates osmotic gradient, draws fluid from eye, rapid IOP drop 30 min (peak 1–2 h)
Topical miotic (pilocarpine 2 %) One drop after IOP <40 mm Hg Contracts ciliary muscle, pulls peripheral iris away from trabecular meshwork 15–30 min

Key point: Pilocarpine is ineffective while IOP >40 mm Hg because the sphincter muscle is ischemic; therefore, it is given after initial IOP reduction.

4.2 Definitive angle‑opening procedure (within 24 h)

  1. Laser peripheral iridotomy (LPI) – First‑line definitive treatment.

    • Procedure: Nd:YAG laser (or combined argon‑Nd:YAG) creates a 0.5–1 mm full‑thickness opening in the peripheral iris, allowing aqueous to bypass the pupillary block.
    • Timing: After IOP ≤30 mm Hg and corneal edema cleared enough for visualization (usually within 12–24 h).
    • Success rate: >90 % in preventing recurrence.
  2. If LPI fails or is contraindicated – Consider laser iridoplasty (peripheral iris bombe reduction) or surgical iridectomy (manual removal of a peripheral iris segment).

4.3 Post‑acute phase (preventive)

4.4 Follow‑up schedule (AAO 2023)

5. Complications of delayed or inadequate treatment

Complication Pathophysiology Clinical consequence
Permanent optic nerve damage Sustained IOP >30 mm Hg leads to axonal transport blockade, ischemia, and retinal ganglion cell death. Irreversible visual field loss; may progress to blindness.
Corneal endothelial decompensation Chronic corneal edema damages endothelial cells, reducing pump function. Persistent corneal haze, bullous keratopathy, may require corneal transplant.
Secondary cataract formation Elevated IOP and inflammation accelerate lens opacification. Decreased visual acuity, need for cataract surgery.
Peripheral anterior synechiae (PAS) Iris adheres to trabecular meshwork after prolonged closure. Permanent angle closure, refractory to laser iridotomy, may need trabeculectomy.
Systemic complications from treatment Over‑use of acetazolamide → metabolic acidosis, electrolyte imbalance; mannitol → pulmonary edema in susceptible patients. Requires monitoring of ABG, renal function.
Recurrent angle‑closure attacks Incomplete LPI, residual pupillary block, or plateau iris configuration. Re‑elevation of IOP, repeated acute attacks.

Prompt IOP reduction and definitive iridotomy dramatically reduce the risk of these complications.


Key learning points


Practice MCQs

1. Which of the following is the most appropriate first‑line pharmacologic agent to be given after the IOP has been lowered to <40 mm Hg in an acute angle‑closure attack?
A. Timolol 0.5 % eye drops
B. Pilocarpine 2 % eye drops
C. Brimonidine 0.15 % eye drops
D. Dorzolamide 2 % eye drops

Answer: B — Pilocarpine is a miotic that contracts the sphincter pupillae, pulling the peripheral iris away from the trabecular meshwork and breaking the pupillary block. It is ineffective when IOP is >40 mm Hg because the iris sphincter is ischemic; therefore it is administered after initial IOP reduction.


2. A 62‑year‑old man presents with an acute painful red eye. His IOP is 55 mm Hg, and gonioscopy shows a closed angle. Which laser procedure provides the definitive treatment for this condition?
A. Argon laser trabeculoplasty
B. Nd:YAG laser peripheral iridotomy
C. Selective laser trabeculoplasty
D. Laser cyclophotocoagulation

Answer: B — Nd:YAG laser peripheral iridotomy creates a full‑thickness opening in the peripheral iris, allowing aqueous to bypass the pupillary block and permanently opening the angle. This is the standard definitive treatment for acute primary angle‑closure glaucoma.


3. Which of the following complications is most directly related to prolonged corneal edema during an untreated acute angle‑closure attack?
A. Peripheral anterior synechiae
B. Bullous keratopathy
C. Neovascular glaucoma
D. Retinal detachment

Answer: B — Persistent corneal edema damages the endothelial cell layer, leading to loss of pump function and development of bullous keratopathy. While PAS can also result from prolonged high IOP, the direct sequela of corneal edema is endothelial decompensation.

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