In a burn patient, the doctor was looking for curling ulcer. Which part should be examined?

Ans. a. 1st part of duodenum (Ref: Sabiston 19/e p1167-1168: Schwartz 9/e p925; Bailey 25/e p1053; Schackelford 7/e p728)Stress Gastritis: Characterized by multiple, superficial (nonulcerating) erosions that begin in the proximal or acid- secreting portion of the stomach and progress distallyQCushing ulcer: Stress gastritis due to intracranial injury/increased ICPQCurling ulcer: After burn injury (>35%); in the body and fundusQ; rare in antrum and duodenumCameron ulcers or riding ulcers: Linear gastric erosions in hiatal herniasQStress gastritis (Stress ulcerations/ Stress erosive gastritis/ Hemorrhagic gastritis)Characterized by multiple, superficial (nonulcerating) erosions that begin in the proximal or acid-secreting portion of the stomach and progress distallyQ.Almost always seen in the fundusQ and rarely in the distal stomach.Cushing's ulcer: Occur in the setting of central nervous system disease (Head trauma) QCurling's ulcer: as a result of thermal burn injury involving >30% of BSAQIncreased acid secretion in Cushing's ulcer but not in Curling's ulcerQCushing's ulcers are more prone to perforate than other stress ulcersStress gastritis lesions may be detected within hours after injury and are considered early if they appear within the first 24 hours.Early lesions are typically multiple and shallow , with discrete areas of erythema along with focal hemorrhage or an adherent dot.Pathophysiology:Multi factorial etiologyImpaired mucosal defense mechanisms against luminal acid such as a reduction in blood flow, mucus, and bicarbonate secretion by mucosal cells, or a reduction in endogenous prostaglandinsQ.Stress is considered present when occurs.In stress (hypoxia, sepsis, or organ failure), mucosal ischemia is the main factor responsible for the breakdown of these normal defense mechanismsQ.Risk factors or Predisposing clinical conditions* ARDSQ* Multiple traumaQ* Major burn >35% of BSAQ* Oliguric renal failureQ* Large transfusionQ requirements* Hepatic dysfunctionQ* HypotensionQ* Prolonged surgical proceduresQ* SepsisQClinical Features:More than 50% of patients develop their stress gastritis within 1-2 days after a traumatic event.The only clinical sign may be painless upper Gl bleeding that may be delayed at onset.The bleeding is usually slow and intermittentQDiagnosis:Endoscopy is required to confirm the diagnosisQ and to differentiate stress gastritis from other sources of GI hemorrhage.Treatment:Definitive fluid resuscitation with correction of any coagulation abnormalities and treatment of the underlying sepsisQMore than 80% of patients stop bleeding using this approachQ.Intraluminal gastric pH should be maintained >5.0 with antisecretory agents.Bleeding that recurs or persists requiring >6 units of blood (3(X)0 mL) is an indication for operationQBecause most of the lesions are in the proximal stomach or fundus, a long anterior gastrotomy should be made in this area.All bleeding areas are oversewn with figure-of-eight stitches taken deep within the gastric wall.Most of the superficial erosions are not actively bleeding and therefore do not require ligature unless a blood vessel is seen at its baseQ.The operation is completed by closing the anterior gastrotomy and performing a truncal vagotomy and pyloroplastyQ to reduce acid secretion.Prophylaxis:Complete neutralization of luminal acid or antisecretory therapy precludes the development of experimental stress gastritisQ.Sepsis control, ventilatory support, adequate nutrition and correction of dyselectrolytemiaQDrugs used are: Antacids, H2-receptor antagonists and sucralfate