Black Duodenum and Black Esophagus

Abstract

Purpose: Acute esophageal necrosis (AEN) or ‘black esophagus' is characteristically described as diffuse, circumferential, black appearance of the esophagus that stops abruptly at the gastroesophageal junction (GEJ). AEN commonly presents with symptoms of hematemesis, melena or coffee-ground emesis in about 90% of the cases. We describe the first case in the literature of AEN associated with duodenal necrosis (black duodenum) in a patient who presented with a pulmonary embolism without these classic characteristic symptoms. An 80-year-old male ex-smoker with a past medical history of hypertension was admitted to our hospital with symptoms of worsening shortness of breath, left sided back pain, nausea and non-bloody, non-bilious vomiting. He denied abdominal pain, chest pain, fever, chills, dysphagia, odynophagia, or history of caustic ingestion. The patient was tachycardiac, mildly hypoxic on room air and had normal abdominal and rectal examination. Pertinent laboratory results included a white blood cell count of 17.8/μl with 82% neutrophils and hemoglobin of 14.4 g/dl. Computed Tomography angiogram revealed bilateral pulmonary emboli, diffuse esophageal and proximal duodenal thickening. Esophagogastroduodenoscopy (EGD) revealed black discoloration with underlying friable hemorrhagic tissue from the mid-esophagus up to the distal esophagus and a normal appearing GEJ and stomach. The duodenal bulb and the proximal aspect of the second portion of duodenum had a black discoloration similar in appearance to the involved segment of the esophagus. Biopsies of the black mucosa from the esophagus and the duodenum revealed necrosis. The patient was discharged home on warfarin and proton pump inhibitor (PPI). A follow-up EGD one week later revealed a normal esophagus and a normal duodenum. Conclusion: This is the only case of AEN described in the literature associated with a pulmonary embolism (PE) and duodenal necrosis. AEN and duodenal necrosis may have been secondary to hypoxia from the PE, explaining the complete rapid improvement with anticoagulation therapy. Given our case, we suggest that a lower threshold for a diagnosis of pulmonary embolism should be considered in a patient with AEN in an appropriate clinical setting.Figure: [1331] Figure 1. Black esophagus and black duodenum.