OMSB Ophthalmology (OEOPTH) study materials
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Acute angle closure at a district hospital 3 hours from a laser

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Acute angle closure at a district hospital 3 hours from a laser

A 64-year-old woman presents to a district general hospital emergency department at 22:40 with an 8-hour history of severe right eye pain, frontal headache, nausea and two episodes of vomiting, and blurred vision. She lives 3 hours by road from the nearest ophthalmologist, and there is no ophthalmologist on site overnight. Right VA is counting fingers at 1 metre, IOP 52 mmHg by Tonopen, with diffuse corneal microcystic oedema, a mid-dilated non-reactive pupil and a uniformly shallow anterior chamber. The left eye has VA 6/9, IOP 16 mmHg, and a shallow peripheral anterior chamber on penlight examination. She has a metallic mitral valve and takes warfarin; today's INR is 2.9. She has documented penicillin anaphylaxis and no previous ocular history. The department stocks intravenous acetazolamide, intravenous mannitol, topical timolol, pilocarpine 2%, latanoprost, topical prednisolone and chloramphenicol. The nearest Nd:YAG laser is at the tertiary centre.

1. Which topical and systemic agents would you start tonight, and which would you withhold or modify? Justify each choice in terms of mechanism and this patient's comorbidities.

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Goal: lower the IOP, break the attack and control inflammation, without destabilising a patient with a prosthetic valve on warfarin.

  • Intravenous acetazolamide 500 mg stat, then 250 mg 6-hourly. Carbonic anhydrase inhibition cuts aqueous secretion and works even while the iris sphincter is ischaemic. Penicillin anaphylaxis is not a sulfonamide allergy - the cross-reactivity concern relates to sulfonamide antibiotics and is itself disputed, so this is not a contraindication. Check potassium and creatinine.
  • Topical timolol 0.5%. Check pulse and ask about asthma, COPD and heart block first; do not give a β-blocker by default to a bradycardic patient with a mechanical valve.
  • Latanoprost at bedtime - increases uveoscleral outflow and remains effective at very high pressure.
  • Pilocarpine 2%. Mechanistically useless while IOP is 50+ because the sphincter is ischaemic and cannot contract; start it once IOP is below roughly 40 mmHg, every 15 minutes for two doses.
  • Topical prednisolone acetate 1% hourly - limits the inflammatory and later synechial component.
  • Intravenous mannitol 20% (1–2 g/kg) only if the above fails: the osmotic load is relatively contraindicated with a mechanical valve and a volume-sensitive heart; monitor for pulmonary oedema.
  • Withhold all mydriatics and systemic anticholinergics. Continue warfarin: no topical interacts meaningfully, and any laser or surgery is planned around the INR rather than by reversing it.

2. By 02:00 her pain has settled, the cornea is clear and the IOP is 22 mmHg on treatment. What is your definitive plan, how do you handle the 3-hour transfer, and what would make you transfer her immediately instead?

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The attack is broken but not treated. Definitive treatment is Nd:YAG laser peripheral iridotomy, and its timing is set by the risk of recurrence in either eye, not by the clock.

  • Right eye: LPI within 24–48 hours. With a clear cornea and controlled IOP there is no emergency at 02:00 - arrange a daylight transfer with a medical escort and continuing topical treatment rather than a night-time ambulance.
  • Fellow eye: a shallow peripheral anterior chamber on penlight means high risk. It also needs a prophylactic LPI, ideally on the same trip. Until then continue pilocarpine in that eye and give written instructions to attend immediately with any pain.
  • Warfarin: LPI is a transcorneal Nd:YAG procedure and can be done at a therapeutic INR, so do not reverse anticoagulation.
  • Transfer immediately if: IOP cannot be held below about 30 mmHg on maximal medical therapy; the cornea does not clear so the laser cannot be delivered; pain and vomiting persist; or a secondary mechanism is suspected. She would then need surgical iridectomy or lens extraction out of hours.

Agree the plan directly with the receiving unit and document it before she leaves, including who is responsible for the fellow eye if the patient declines a second trip.

3. At the follow-up visit what features would make you doubt primary angle closure, and how would each change your management?

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Primary angle closure should produce a similar configuration in both eyes, an occludable angle with a convex iris profile, and relief after LPI. Reconsider it if:

  • The anterior chamber is axially shallow with an intumescent, white lens - phacomorphic glaucoma. LPI will not help, because the lens is pushing the iris forward. Treatment is lens extraction, and the fellow eye may also need surgery.
  • The central chamber is deep but the periphery is closed - plateau iris. LPI alone often fails because the ciliary body holds the peripheral iris forward; consider argon peripheral iridoplasty or lens extraction.
  • A posterior pushing mechanism - choroidal effusion, an intraocular mass, suprachoroidal haemorrhage or aqueous misdirection after surgery. LPI is useless and can be harmful; B-scan ultrasound and treatment of the cause are required.
  • Irregular, fixed pupil with posterior synechiae, or pseudoexfoliative material - secondary synechial closure from neovascularisation or pseudoexfoliation. The angle is permanently closed and will not open with LPI; treat the neovascular drive with panretinal photocoagulation or anti-VEGF, and plan filtration or a drainage device if pressure is uncontrolled.
  • A quiet fellow eye with a normal, deep angle - think lens-related or iatrogenic causes rather than primary angle closure.

Gonioscopy of both eyes, plus ultrasound biomicroscopy or anterior segment OCT if the mechanism is unclear, are the tests that settle this.