Esophageal Necrosis Etiology: - Ischemia and Gastric Outlet Obstruction with GERD may be inciting events - Associated with broad spectrum antibiotic use, infections (Candida, CMV, HSV, Klebsiella), Gastric volvulus, Paraesophageal hernia, Hyperglycemia, DKA, Underlying malignancy, Stevens-Johnson syndrome, Prolonged vomiting following alcohol binge, Alcoholic hepatitis and lactic acidosis, and Aortic dissection. Can also occur after caustic ingestion. - "Two hit" Hypothesis: initial event (low flow vascular state) predisposes esophageal mucosa to severe topical injury (by acid reflux and pepsin). Gastroparesis and Gastric outlet obstruction lead to fluid accumulation in stomach and promote esophageal reflux resulting in direct injury with necrosis. Necrosis should resolve rapidly when blood flow is restored to esophagus Clinical Manifestations: - Most patients present with upper GIB with hematemesis and/or melena - Other GI symptoms include dysphagia and epigastric/retrosternal chest pain Diagnosis: - EGD showing circumferential black discoloration with underlying friable hemorrhagic tissue - Usually involves distal third of esophagus Treatment: - Treatment of underlying illness - NPO for at least 24-48 hours - IV PPI - Consider Sucralfate to prevent further esophageal injury - NGT placement should be avoided unless patients are vomiting or have gastric outlet obstruction - Most patients have resolution of necrosis with supportive care Complications: - Esophageal perforation should be suspected in patients with persistent severe retrosternal or back pain and requires prompt surgical intervention - Esophageal stricture formation is the most common long term complication and may require esophageal dilation Sinai Hospital of Baltimore IM Residency @SinaiBmoreIMRe #Esophageal #Necrosis #diagnosis #management #gastroenterology
