Fade to Black: Acute Esophageal Necrosis in a Vasculopathic Man Following Traumatic Hip Fracture 1736

• Published in: The American journal of gastroenterology Vol. 113; no. Supplement; pp. S991 - S992
• Main Authors: Bagley, Patrick, Sadowski, Brett W., Wauters, Robert, Lindholm, Philip, Young, Patrick E.
• Format: Journal Article
• Language: English
• Published: New York Wolters Kluwer Health Medical Research, Lippincott Williams & Wilkins 01.10.2018
• Subjects: Bone surgery; Cardiovascular disease; Endoscopy; Esophagus; Fractures; Gastroenterology; Necrosis
• ISSN: 0002-9270; 1572-0241
• DOI: 10.14309/00000434-201810001-01736

Acute esophageal necrosis (AEN), sometimes known as "black esophagus" due to its dramatic endoscopic appearance, is a rare finding, seen less than 0.02% of endoscopies. Risk factors include alcohol use, vascular disease, and malignancy, and most patients are critically ill. We present a case of AEN that developed shortly after a fall in a chronically, but not critically, ill patient. An 82 year old man with a history of alcohol and tobacco abuse, GERD, and coronary artery disease presented with a left hip fracture from a mechanical fall. Admission blood pressure was 104/59. His left leg was tender without deformities, diminished pulses, or hematoma, and the remainder of his exam was unremarkable. During the first twelve hours of admission, his hemoglobin dropped over 2 g/dL, and he subsequently suffered multiple episodes of hematemesis just before his planned orthopedic surgery. The procedure was cancelled, and he instead underwent upper endoscopy (EGD). The EGD revealed a circumferential black and edematous esophagus spanning 14 cm (between 30 and 44 cm from the incisors to gastroesophageal junction). Black spotting was noted just proximal to the circumferential lesion. The proximal esophagus was normal. The mucosa of the stomach and duodenum were normal. The patient was made nil per os and received intravenous pantoprazole and total parenteral nutrition for several days, though he insisted on eating within 4 days, which after counseling regarding perforation risk and shared decision making, he was permitted to do. Repeat endoscopy 7 days later showed no black or necrotic material, though Los Angeles Class D esophagitis with mild stenosis of the distal esophagus was noted. The patient tolerated a solid diet at 7 days and at 6 week follow up reported no significant dysphagia, though he declined further endoscopic evaluations. AEN typically occurs in the distal third of the esophagus, owing to the fact this segment is relative hypovascular to the others. We hypothesize that transient decreases in blood flow in the acute period after his hip fracture or traumatic alterations to the microvascular integrity resulting from his fall may have been the etiology of this patient's AEN, especially in light his underlying vasculopathy. The fact that the patient tolerated oral intake within a few days may indicate that stable patients with AEN can be fed more quickly than has typically been reported, albeit with appropriate counseling.