Cushing's ulcer, a stress ulcer seen after severe head injury, is pathophysiologically distinct from Curling's ulcer (burns). The mechanism of Cushing's ulcer formation is:

• A Mucosal ischaemia due to hypoperfusion from systemic hypotension
• B Reflux of bile acids due to lower oesophageal sphincter dysfunction
• C Hyperacidity due to vagal stimulation from raised intracranial pressure via hypothalamic-vagal pathway ✓
• D Corticosteroid-induced suppression of prostaglandin synthesis

Explanation

Cushing's ulcer follows severe head injury or neurosurgical operations due to raised intracranial pressure stimulating the hypothalamus and dorsal vagal nucleus, resulting in excessive vagal outflow that causes gastric hypersecretion of acid. Unlike Curling's ulcer (burns — mucosal ischaemia/hypovolaemia), Cushing's ulcer is specifically hyperacid-driven and therefore more prone to perforation rather than just haemorrhage. Prophylaxis with proton pump inhibitors is indicated in neurocritical care patients.

Reference: Bailey & Love's Short Practice of Surgery, 27th ed.

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Written and medically reviewed by the StethoPrep medical team.