A 55-year-old woman presents with an acute primary angle-closure attack, intraocular pressure of 56 mmHg and a steamy cornea. Why is topical pilocarpine unlikely to break the attack if instilled immediately?
- A Pilocarpine is inactivated by the acidic aqueous present during the acute attack
- B The ischaemic iris sphincter cannot respond to cholinergic stimulation until the intraocular pressure is lowered ✓
- C Pilocarpine further shallows the anterior chamber by causing forward lens movement
- D Corneal oedema prevents any topical drug from reaching the anterior chamber
Explanation
At very high pressures the iris sphincter and ciliary body become ischaemic and the muscarinic receptor response fails, so pilocarpine is ineffective at presentation. The correct sequence is to lower pressure first with systemic agents such as oral acetazolamide and intravenous mannitol, then instil pilocarpine once the pressure falls below roughly 40 mmHg. Corneal oedema reduces comfort of instillation but the decisive barrier here is the ischaemic, unresponsive sphincter muscle.
Reference: Parsons' Diseases of the Eye, 23rd ed.
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