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Curling ulcer

Gastroenterology / Surgery (Critical Care)GastrointestinalIntegumentary (burns)Critical care

Summary

Curling ulcer is an acute stress-related gastric or duodenal mucosal ulcer occurring after severe burns (classically >30-50% TBSA). It results from mucosal ischemia and hypoperfusion from hypovolemia. It is classically located in the stomach (or proximal duodenum) and can cause life-threatening upper GI bleeding or perforation.

Detail

**Definition:** A type of acute stress ulcer (stress-related mucosal disease) associated with severe burns. Compare with Cushing ulcer (associated with traumatic brain injury, CNS tumors, or increased ICP).

**Pathophysiology:** - Severe burns cause massive fluid shifts and hypovolemia, which lead to splanchnic vasoconstriction and decreased gastric mucosal blood flow (ischemia). - Ischemia causes loss of mucosal protective barriers: reduced mucus and bicarbonate secretion, decreased prostaglandin synthesis, and impaired mucosal cell turnover. Acid back-diffusion then causes injury. - Reperfusion injury and oxygen free radicals add to the damage. - Gastric acid is necessary but not necessarily increased. This differs from Cushing ulcer, in which vagal stimulation causes acid hypersecretion. - H. pylori is not the primary cause.

**Location and morphology:** Multiple shallow erosions or ulcers, usually in the gastric fundus and body (stomach). The proximal duodenum can also be affected. Lesions may be superficial, but they can erode into vessels.

**Clinical presentation:** - Often painless and asymptomatic until complications occur. - Upper GI bleeding (hematemesis, coffee-ground emesis, melena, drop in hemoglobin) is the most common presentation, typically days after injury (about 3-10 days). - Perforation can cause peritonitis and free air under the diaphragm.

**Risk factors:** Burns >30-50% TBSA, mechanical ventilation >48 hours, coagulopathy, sepsis, shock, ICU stay, and major trauma.

**Diagnosis:** Upper endoscopy shows multiple superficial erosions or ulcers.

**Management and prevention:** - Prevention is key: early enteral feeding, adequate resuscitation to restore perfusion, and stress ulcer prophylaxis with PPIs or H2 blockers in high-risk patients. Sucralfate is another option. - Active bleeding: resuscitation, IV PPI, endoscopic hemostasis, angiographic embolization, and surgery if refractory. - Perforation requires surgical repair.

**Boards pearls:** - Curling = Burns (think "Curling iron" burns). Cushing = brain (high ICP, vagal stimulation, increased acid, higher perforation risk). - Curling ulcers are caused by ischemia and decreased mucosal protection, not acid hypersecretion. - Other acute gastric ulcer causes: NSAIDs, alcohol, and steroids combined with NSAIDs. - Do not confuse them with Marjolin ulcer (squamous cell carcinoma arising in chronic wounds or burn scars).

Sources

  • First Aid for the USMLE Step 1 (Gastrointestinal: Peptic ulcer disease)
  • Robbins & Cotran Pathologic Basis of Disease (Gastritis and gastric ulcers: acute stress ulcers)
  • Sabiston Textbook of Surgery (Stomach, Burns)
  • Harrison's Principles of Internal Medicine (Peptic ulcer disease and related disorders)
  • Cook D, et al. N Engl J Med 1994 (Risk factors for GI bleeding in critically ill patients)

Reviewed by Medusa editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.