Acute Esophageal Necrosis

Image of the Month Acute Esophageal Necrosis CARLO CALABRESE and GIUSEPPINA LIGUORI Department of Clinical Medicine, University of Bologna, Bologna, Italy

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72-year-old man was admitted to the emergency room with a history of hematemesis for 2 days. His medical history included hypertension, diabetes mellitus, an old cerebral vascular accident, and benign prostatic hypertrophy. Ten days earlier he had undergone amputation of the lower left leg for diabetic gangrene. There was no history of gastroesophageal reflux, gastroduodenal ulcers, or intake of corrosive substances. On admission, he was afebrile, with regular pulse of 110 bpm, blood pressure of 145/85 mm Hg, and respiratory rate of 21 breaths/minute. A digital rectal examination was negative for blood. Test irrigation with normal saline via a nasogastric tube was conducted, and a brown liquid was drained. Laboratory results were as follows: white blood cell count, 18,590/␮L (neutrophils, 81.2%); hemoglobin, 10.5 g/dL; hematocrit, 42.5%; blood urea nitrogen, 10.1 mg/dL; creatinine, 2.1 mg/dL; sodium, 131 mmol/L; potassium, 3.1 mmol/L; serum glucose, 416 mg/dL; glycosylated hemoglobin, 10.1%; prothrombin time, 12.5 seconds; international normalized ratio, 1.1. Upper gastrointestinal endoscopy revealed edematous mucosa with tiny whitish exudates in the proximal esophagus and blackcolored mucosa in the mild to distal esophagus (Figure A). The endoscopic features combined with the histopathologic findings from biopsies (Figure B) indicated the diagnosis of acute esophageal necrosis (AEN). Specific stains and immunostaining were negative for mycotic infections, cytomegalovirus, and herpes simplex virus. He was treated conservatively with a proton pump inhibitor, total parenteral nutrition, and intensive glycemic control. On day 10, follow-up upper gastrointestinal endoscopy was performed and showed complete resolution of the black-colored mucosa of the mild to distal esophagus. The reported incidence of black esophagus is very low, ranging from 0.0125%–0.2%.1 Malignant melanoma, acanthosis nigricans, pseudomelanosis, melanosis, coal dust deposition, and corrosive ingestion can mimic the endoscopic appearance of AEN. Several theories have been proposed to explain the pathogenesis of AEN. An

ischemic phenomenon is viewed by some as the major factor in rapid development of esophageal lesions. Associated duodenal lesions might also suggest vascular compromise as the inciting event. Lowflow states or shock, atherosclerosis, thromboembolic disease, cardiac arrhythmias, and hypoperfusion as a result of severe lactic acidosis have been implied as possible etiologies.2 The blood supply to the proximal esophagus is derived from the superior and inferior thyroid arteries, whereas the rest of the organ receives blood flow from the esophageal branches of the descending aorta and splenic and left gastric arteries. An association between AEN and malnutrition, debilitated state, and malignancy suggests an overall reduction in the mucosal defense mechanism. Blood supply is an important component of the postepithelial defense as well as maintenance of the intrinsic repair mechanism. In combination with atherosclerosis, lowflow states, and thromboembolic phenomena, this can directly cause mucosal necrosis. The treatment of AEN is supportive care in most cases. Adequate hydration and use of proton pump inhibitors are recommended. The prognosis is typically poor, and mortality depends on the underlying illness. References 1. Ben Soussan E, Savoye G, Hochain P, et al. Acute esophageal necrosis: 1-year prospective study. Gastrointest Endosc 2002;56:213–217. 2. Gurvits GE, Shapsis A, Lau N, et al. Acute esophageal necrosis: a rare syndrome. J Gastroenterol 2007;42:29 –38.

Conflicts of interest The authors disclose no conflicts. © 2011 by the AGA Institute 1542-3565/$36.00 doi:10.1016/j.cgh.2011.02.012 CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2011;xx:xxx