A 93‐year‐old man presented following acute onset of substemal and epigastric pain that progressed to crushing pressure over the course of 4 hours. He described a sensation of fullness in his throat, dysphagia, and mild diaphoresis. He had no similar problems before and noted no additional symptoms, including no dyspnea, cough, fever, vomiting, or diarrhea. He denied abdominal pain, dysphagia, and weight loss. His vital signs were normal, with good oxygenation; he was afebrile. He had a 2/6 holosystolic murmur, heard best at the apex. His PMI was not displaced, and his JVP was not elevated. He had no hepatosplenomegaly. However, he did have dark stools, and his fecal occult blood test was positive. A CT scan of his neck without contrast revealed soft‐tissue swelling and thickening of the esophagus throughout its thoracic course, extending to the GE junction. He was reflexively treated with the acute coronary syndrome protocol, including beta‐blockers, enoxaparin, nitrates, and aspirin. Soon after its initiation, he began vomiting bright red blood. This continue over the course of 1 hour and eventually cleared after a gastric lavage. On further questioning, he revealed that he had been taking aspirin daily and drank a glass of whiskey everyday for many years, having quit drinking approximately 10 years ago. An EGD was emergently performed, which showed a necrotic, friable distal esophagus with no evidence of gastritis.
Chest pain is a common complaint encountered by the hospitalist. A methodical approach to determining the etiology, using an organ‐by‐organ method, is critical in determining less common but still life‐threatening etiologies. The reflexive use of protocols without first sequentially considering the diagnosis may lead to a life‐threatening condition. The cause of our patient's chest pain was a distal esophageal ulcer with acute esophageal necrosis. Known as black esophagus or necrotizing esophagus, it entails circumferential involvement of the distal esophagus, ending sharply at the GE junction. The pathogenesis of AEN remains unknown. Certain underlying conditions are believed to predispose patients to necrotizing esophagitis, such as coronary or peripheral vascular diseases, low flow states (e.g., shock), gastric volvulus, and gastric‐outlet obstruction. AEN has also been associated with herpes infections, broad‐spectrum antibiotics, and hyperglycemia. It is highly unlikely that a single etiologic factor is responsible for AEN. The presumed overall understanding is that of a 2‐hit phenomenon. There is an initial event, typically a low‐flow vascular state, which then predisposes the esophageal mucosa to severe topical injury, such as reflux of acid and pepsin. Although a rare occurrence, necrotizing esophagitis is a condition that physicians should be aware of because of the gravity of the disease and the high risk of perforation. A methodical approach to chest pain is central in identifying this disease when it is present.
S. Patel, none.
To cite this abstract:Patel S. A Punch in the Gut. Abstract published at Hospital Medicine 2009, May 14-17, Chicago, Ill. Abstract 186. Journal of Hospital Medicine. 2009; 4 (suppl 1). https://www.shmabstracts.com/abstract/a-punch-in-the-gut/. Accessed May 26, 2019.