Introduction: Acute esophageal necrosis (AEN) is a rare syndrome with incidence of .01 to .28% on endoscopic series and mortality of 32%. Known as “Black Esophagus,” it's characterized endoscopically by circumferential black mucosa ending abruptly at the gastroesophageal junction. It has been postulated that precipitating events include hypoperfused states and gastric outlet obstruction with concurrent esophageal reflux. Case: A 77-year-old Caucasian female with remote history of peptic ulcer disease and progressive multiple sclerosis (MS) presented with diffuse abdominal pain, nausea, and vomiting. Urinalysis was suggestive of a urinary tract infection (UTI) and she was discharged on five-days of cephalexin. She delayed taking cephalexin and returned four days later with fatigue, worsening dysphagia, and melena. She was hypotensive and labs revealed leukocytosis, acute blood loss anemia, and acute kidney injury. Urine culture grew extended-spectrum beta lactamase producing multi-drug resistant proteus mirabilis. She was admitted for septic and hypovolemic shock secondary to multi-drug resistant UTI and suspected upper gastrointestinal bleeding. Ertapenem was started in light of the resistance and sensitivity pattern of the causative organism. Upper endoscopy revealed diffuse mucosal changes characterized by black discoloration throughout the esophagus and obstructive duodenal ulcer with adherent clot (Figure 1). Endoscopic findings and presentation was consistent with AEN. She improved with vasopressor support, fluid resuscitation, and 14-days of ertapenem. Discussion: AEN is a multifactorial syndrome with notable morbidity. Risk factors include alcohol abuse, hypertension, male gender, diabetes, dyslipidemia, malnourishment, and chronic kidney disease. The most common presentation is upper GI hemorrhage but dysphagia, chest and epigastric pain can also occur. Diagnosis is made endoscopically and histologic confirmation of tissue necrosis is recommended but not required. Treatment involves management of inciting insult(s), acid suppression with intravenous proton pump inhibitor therapy and “nil per os.” A video swallow study revealed mild oral and moderate pharyngeal dysphagia that was attributed to MS. Dysphagia and regurgitation of stomach contents from gastric outlet obstruction predisposed patient to hypovolemia. Septic shock and an obstructive duodenal ulcer with blood loss anemia culminated to promote the development of AEN.1793 Figure 1. Black discoloration of mucosa in the upper third of the esophagus (A), and the middle third of the esophagus (B), normal mucosa at the gastroesophageal junction as seen in retroflexion (C), and duodenal bulb ulcer (D).
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