Abstract
Acute esophageal necrosis is characterized by a full length, circumferential black discoloration of the entire mucosa of the esophagus that ends abruptly at the esophagogastric junction [1]. The clinical presentation of cases is almost universally related to upper gastrointestinal bleeding [2]. Although unclear, the etiology is likely to be multifactorial [1, 2]. Case history: A 61-year-old male, alcoholic with liver cirrhosis was found lying unconscious on a cold bathroom floor. The patient was in a deep coma, hypotensive with accompanying metabolic acidosis, slight hyperglycemia, significantly elevated urea, creatinine, and liver enzymes levels, and had progressing secondary anemia. The patient died approximately 46 h after he was initially found in his house. The autopsy found that the distal third of the esophagus contained blackish necrotic mucosa, which ended abruptly at the esophagogastric junction. The stomach mucosa had numerous red-brownish erosions— Wischnewski spots (Fig. 1). The entire length of the intestine was filled with dark-red blood. Microscopic examination revealed an acute full-thickness necrosis of the esophagus mucosa in which the epithelium was almost completely consumed, and acute inflammatory cells in the submucosa and mucosa. The cause of death was fatal blood loss from the upper gastrointestinal tract. Hypothermia stimulates profound vasoconstriction, especially in the splanchnic region, and alterations in microcirculation, which leads to ischemic organ damage [3]. A somewhat atypical presentation of a black esophagus as seen in this case, where only the lower third of the organ is affected, is most likely related to its segmental vascular supply. The distal esophagus receives its blood flow from branches of the left gastric artery or left inferior phrenic artery, and is the least vascularized section of the esophagus. Therefore, the first signs of an ischemic injury to the esophagus typically appear in the distal section [2]. Although the black esophagus in this case could perhaps be related to acute alcohol intoxication, or liver cirrhosis, the most probable cause has been considered to be the vasoconstriction of the common arteries of the stomach and the distal section of the esophagus due to hypothermia. Wischnewski spots would seem to occur more frequently in the elderly after having been exposed to cold stress for an extended period of time [4, 5]. The presence of them in this case indicates that the cooling of the body was not rapid, that is, the patient had most probably been lying on the cold ceramic floor for some time before being found, loosing body heat via conduction during that time. The microscopic appearance of acute esophagitis with a sharp demarcation of mucosal necrosis by predominantly neutrophilic granulocytes places the noxious mucosal injury within a time frame of approximately 24–72 h prior to death [1]. The microscopic picture of the black esophagus in this case is consistent with this finding, as the patient died approximately 46 h after he was admitted to hospital. The cause of death in this case has been attributed to fatal exsanguination from the upper gastrointestinal tract. All other potential sources of bleeding from the gastrointestinal tract were excluded by autopsy. The fatal blood loss was facilitated by coagulopathy due to the preexisting alcoholic liver cirrhosis, as well as liver failure caused by re-warming [3]. The mucosal necrosis of the distal section of the esophagus may represent a delayed complication of V. Živkovic S. Nikolic (&) Institute of Forensic Medicine, University of Belgrade School of Medicine, 31a Deligradska str., 11000 Belgrade, Serbia e-mail: bobanvladislav@yahoo.com; slobodan.nikolic@mfub.bg.ac.rs
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.