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Acute Esophageal Necrosis Associated With Acute Pancreatitis

Jaiswal, Palashkumar MD1; Araujo, James L. MD2

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doi: 10.14309/crj.0000000000000295
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First described in 1967, acute esophageal necrosis (AEN) or “black esophagus” is characterized by necrosis of the esophageal mucosa.1 This condition usually affects older men with multiple comorbidities, including hypertension, diabetes, chronic kidney disease, and chronic liver disease.2 The most common presenting symptom is upper gastrointestinal hemorrhage (hematemesis or melena) but may also present with nausea, vomiting, epigastric pain, chest pain, and dysphagia. Endoscopy is diagnostic and characterized by circumferential black discoloration of the esophageal mucosa with sharp demarcation at the esophagogastric junction. The distal esophagus is almost universally involved, and the extent of proximal involvement is variable but may involve the entire esophagus.2,3 Importantly, the mucosa distal to the esophagogastric junction is spared. Biopsy may reveal nonviable epithelium, loss of epithelial layer, mucosal necrosis or ulceration, polymorphonuclear-predominant or mixed inflammatory cell populations, visible vascular thrombi, and deranged muscle fibers. Histology may confirm infectious etiologies including viral, fungal, and bacterial pathogens.2


A 77-year-old man with class I obesity (body mass index of 34 kg/m2), atrial fibrillation on anticoagulation, heart failure with decreased ejection fraction, poorly controlled diabetes, and stage 3 chronic kidney disease presented with 3 days of right upper quadrant abdominal pain exacerbated by deep inspiration. The patient was afebrile with normal white blood cell count and total bilirubin of 2.9 mg/dL. Computed tomography identified gallbladder wall thickening suggestive of acute cholecystitis and a calculus in the gallbladder neck for which antibiotics were initiated. A percutaneous cholecystostomy tube was placed within 24 hours of admission. Bile culture revealed the presence of Escherichia coli, Klebsiella pneumoniae, and vancomycin-resistant Enterococcus. By day 5, the total bilirubin had normalized. However, a cholecystogram demonstrated nonobstructing stones at the gallbladder neck and distal common bile duct. On hospital day 13, the patient underwent endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy and 9-mm balloon sweep with debris swept from the duct; the pancreatic duct was cannulated once in the process, and postprocedural rectal indomethacin was not administered; no esophageal abnormalities were noted during this examination. The following day, the patient developed anorexia, vomiting, and abdominal pain with elevated serum lipase of 2,084 units/L, consistent with post-ERCP pancreatitis for which supportive therapy was provided. During the 48 hours immediately after the ERCP, serum creatinine increased from 1.3 to 2.9 mg/dL, and Acute Physiology and Chronic Health Evaluation II score was 9. After 7 days of nil per os and poor tolerance of clear liquids, a nasogastric tube aspirate was noted to contain blood in the setting of an international normalized ratio level of 6.07, which had been elevated for 2 days. Hemoglobin was 7.2 g/dL from a previous baseline of 9 g/dL. In the preceding 24 hours, heart rate ranged between 80 and 90/min and blood pressure ranged consistently between 140 and 150/70–80 with no episodes of hypotension.

Esophagogastroduodenoscopy (EGD) identified severe circumferential esophagitis characterized by necrosis and diffuse oozing, which extended continuously from the esophagogastric junction to the midesophagus, for a total length of 16 cm (Figure 1). There was a distinct demarcation of normal mucosa immediately proximal and distal to the necrotic segment of the esophagus (Figure 2). The stomach (including retroflexion) and duodenum appeared normal. These findings were consistent with AEN, and the patient was managed conservatively with hemodynamic resuscitation, intravenous antibiotics, glycemic control, nil per os restriction, and continuous intravenous proton-pump inhibitor infusion. A repeat EGD performed 9 days later demonstrated erythematous and friable mucosa with ulceration, which appeared to be healing in the previous areas of necrosis; a subsequent EGD 6 weeks later demonstrated normal esophageal mucosa (Figure 3). Despite resolution of the esophageal disease, the patient's clinical course slowly deteriorated with complications including a peripancreatic fluid collection and progressive renal failure requiring dialysis, and he ultimately died 6 months after the initial diagnosis of pancreatitis.

Figure 1.
Figure 1.:
Endoscopic image of the distal esophagus showing continuous, circumferential, necrotic appearing mucosa which was friable with active oozing. This was consistent with acute esophageal necrosis.
Figure 2.
Figure 2.:
Retroflexed view of the esophagogastric junction. Arrows indicate the gastroesophageal junction marking the margin of necrotic esophageal mucosa and viable gastric mucosa.
Figure 3.
Figure 3.:
Endoscopic image of normal-appearing esophagogastric junction 8 weeks after the episode of acute esophageal necrosis.


The pathogenesis of AEN is multifactorial and believed to develop because of a combination of ischemia, impaired mucosal barrier mechanisms, and corrosive injury from gastric contents. The arterial supply of the esophagus is segmental and anatomic variations are common, but esophageal infarction is quite rare. However, the distal segment, commonly supplied by the left gastric and left phrenic arteries, is less densely vascularized with fewer types of collateral, making it more vulnerable to ischemia.4 In low-flow hemodynamic states, vascular compromise predisposes the esophagus to perfusion injury. In addition, critical illness, malnutrition, and deconditioning may contribute to the diminished mucosal buffering and impaired defense mechanisms that predispose the lower third of the esophagus to ischemic and caustic injury from prolonged exposure to refluxed gastric contents.4 We posit that the patient's advanced age and compromising comorbidities (obesity, decreased ejection fraction, acute-on-chronic kidney disease), in combination with moderately severe acute pancreatitis leading to extravasation of intravascular fluid into third spaces, led to systemic hypoperfusion, vascular insult, and the resultant AEN.

The management of AEN is supportive and includes aggressive intravenous fluids, correction of anemia, and hypotension. Initially, intravenous proton-pump inhibitors are recommended. In addition, sucralfate has an ability to bind pepsin and stimulate mucus secretion along with its cytoprotective effects and hence may be beneficial. Antimicrobials should be considered in patients with suspected or histologically confirmed bacterial, viral, or fungal infection. Nourishment of patients with AEN can be challenging because nasogastric tube must be avoided to prevent local trauma. Nil per os status must be maintained until there is clinical or endoscopic evidence of healing. Surgery is usually reserved for patients with perforation or mediastinal disease. A recent comprehensive review suggests a high mortality rate of 28% (30 of 106 patients died) associated with the diagnosis.2 Potential complications are perforation with associated mediastinitis, abscess formation, and empyema. Delayed complications may occur a few weeks after the diagnosis and include stricture and sepsis-related to superinfection.


Author contributions: P. Jaiswal wrote the article. JL Araujo edited and reviewed the article and is the article guarantor.

Financial disclosure: None to report.

Informed consent was obtained for this case report.


1. Grudell ABM, Mueller PS, Viggiano TR. Black esophagus: Report of six cases and review of the literature, 1963–2003. Dis Esoph. 2006;19:105–10.
2. Ullah W, Mehmood A, Micaily I, Khan MS. Comprehensive review of acute oesophageal necrosis. BMJ Case Rep. 2019;12:e227967.
3. Gurvits GE, Cherian K, Shami MN, et al. Black esophagus: New insights and multicenter international experience in 2014. Dig Dis Sci. 2015;60:444–53.
4. Gurvits GE. Black esophagus: Acute esophageal necrosis syndrome. World J Gastroenterol. 2010;16:3219–25.
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