Black esophagus, also referred to as acute esophageal necrosis (AEN) or necrotizing esophagitis, is an uncommon, but life-threatening cause of GI bleeding.1 First described by Brennan2 during a patient autopsy in 1967, black esophagus remained a postmortem finding until its first description on endoscopy by Goldenberg et al3 in 1990.With the increased use of endoscopy, black esophagus has been more commonly described in case reports and case series but remains an extremely rare diagnosis, with an incidence of 0.008% to 0.2%.4-7 A single study by Yasuda et al8 demonstrated a surprising incidence of AEN in 6% of patients undergoing upper endoscopy for upper GI hemorrhage.
Patients with black esophagus typically present for evaluation as a result of GI bleeding, which occurs in 65% to 90% of cases.9,10 This condition is more common in elderly patients with a disproportionately higher incidence in men, who represent approximately 80% of cases. A variety of comorbidities are associated with AEN, most commonly diabetes mellitus, malignancy, hypertension, renal insufficiency, heart disease, and duodenal ulcer.5,10 In a recent case series by Gurvits et al,11 tachycardia or hypotension was observed in 90% of cases.
Black esophagus is defined by diffuse, circumferential necrosis of the esophagus with preferential involvement of the distal third of the esophagus that abruptly stops at the gastroesophageal junction, and in the absence of caustic ingestion.12 The predilection toward involvement of the distal esophagus is thought to be due to its relatively poor perfusion. Blood flow to the distal esophagus is highly variable, but typically occurs through the left gastric and left inferior phrenic arteries. This is believed to result in a “watershed region” that creates a susceptibility to insult.7,13 Histologically, there is necrosis of the mucosa and submucosa, inflammation of the muscle fibers, and occasional thrombosis of blood vessels.4 However, gross findings alone are sufficient for diagnosis, and biopsy is not mandatory.1,14
The etiology of acute esophageal necrosis is not well understood. The prevailing theory is that the combination of an ischemic insult and reflux of gastric contents leads to mucosal destruction. The watershed distribution of blood flow to the distal esophagus is thought to predispose patients to ischemia or thrombosis.5,7,10 As previously mentioned, a recent series by Gurvits et al11 demonstrated that 90% of patients with black esophagus also develop tachycardia or hypotension. Further, many of the comorbid conditions noted in cases of AEN are characterized by a tendency toward malperfusion or thrombosis.
The mainstay of managing black esophagus in the ED is aggressive fluid resuscitation, bowel rest, and treatment with IV PPIs. Antibiotics are not indicated unless the patient has an infection, is immunocompromised, continues to decompensate despite adequate IV fluid resuscitation, or has an esophageal perforation.7,11 In practice, the necessity of early antibiotic therapy may be unclear in the ED due to other considerations in the differential diagnosis; therefore, it is prudent to treat the patient empirically until these etiologies can be ruled out. Some clinicians recommend sucralfate due to its ability to bind pepsin and stimulate mucus secretion which theoretically prevents further esophageal injury.4 The initiation of sucralfate should be deferred until after endoscopy.