Case Presentation:

A 63–year–old man with diabetes mellitus, end–stage renal disease on hemodialysis, hypertension, aortic stenosis, remote deep venous thrombosis, and anemia presented with 4 days of severe epigastric abdominal pain radiating into the chest with associated nausea and emesis. He also noted 2 months of dysphagia to solids, dyspepsia, reflux symptoms, and eructation with oral intake. Medications included insulin glargine, calcium acetate, sevelamer, lisinopril, and simvastatin. He denied new medications, caustic ingestion, or alcohol intake, and he recently quit smoking. Physical examination revealed epigastric fullness with tenderness to palpation and normal bowel sounds. Laboratory results included a white blood cell count of 5.5 × 10³/ml, blood urea nitrogen 63 mg/dL, creatinine 5.6 mg/dL, and albumin 2.5 g/dL. Chest radiograph was concerning for a possible right hilar mass or enlarged lymph node. CT of the thorax, abdomen, and pelvis revealed diffuse esophageal dilation and moderate wall thickening, gastric distention, and multiple mildly enlarged mediastinal and retroperitoneal lymph nodes. An esophagogastroduodenoscopy revealed blackened and friable mucosa involving the entire esophagus which ended abruptly at the gastroesophageal junction (Figure 1). Biopsies were consistent with acute necrotizing esophagitis. CT angiogram ruled out ischemia, and a barium esophagram did not demonstrate perforation. He was treated conservatively with bowel rest, IV fluids, and an IV proton pump inhibitor. Oral intake was gradually introduced, and he was discharged in improved condition.

Discussion:

Acute esophageal necrosis or “black esophagus” has an estimated frequency of 1 in 10,000 endoscopic procedures. Its exact pathophysiology is unknown, but likely contributors include ischemic insult, gastric outlet obstruction, chemical injury from gastric contents, and compromised mucosal barriers. Predisposing factors include male sex, advanced age, propensity for thromboembolism, and chronic medical conditions like diabetes, renal disease, malignancy, hypertension, and malnutrition. Clinical presentation often consists of upper GI bleeding, epigastric abdominal pain, and dysphagia. Therapy is supportive and includes treatment of comorbidities, short–term avoidance of oral intake, and acid suppression with or without sucralfate. Antimicrobial agents may be considered in select severe cases. Surgical resection is necessary only if complications such as perforation or mediastinitis develop. Mortality rates are significant at 20–35% of those afflicted. Patients who recover usually do so completely, though a minority can develop benign strictures.

Conclusions:

This case serves to increase general awareness of a very rare entity with a common clinical presentation. Hospitalists should consider acute esophageal necrosis in the differential diagnosis of patients with extensive comorbidities and upper gastrointestinal symptoms.

Figure 1Circumferential black and friable esophageal mucosa consistent with acute esophageal necrosis.