
pmid: 7040159
The association of burns with erosive and necrotic lesions in the gastrointestinal mucosa was first recognized in the early part of the 19th century (l-5). The clinical history of these gastrointestinal complications clearly suggests a common pathogenetic mechanism represented by the state of shock which follows extensive skin burns. Since that time numerous reports have described, in cases of circulatory insufficiency of different etiologies, a syndrome characterized by hemorrhagic, or necrotic lesions of the gastrointestinal mucosa, or both, for which there is ni, apparent anatomic explanation. Efforts to better understand this complex intestinal syndrome are all the more justified in that the intestinal mucosa so affected releases substances to which numerous investigators have attributed an important role in the pathogenesis of shock (6-12). The specific susceptibility of the intestinal mucosa to low flow states is evidenced by the clinical and laboratory observations of localized or diffuse zones of necrosis in this area during severe systemic hypotension or hypoxia. In the present review an attempt will be made to define this clinical entity in terms of etiologies, frequency, clinical Significance, pathogenesis, anatomic distribution, and pathological description. In addition to inadvertent omissions, regrettably numerous reports in which the involved area of intestinal tract was not specified are not included in this study. Naturally the clinical material is obtained from postmortem examination and only very few cases have been described at surgery.
Adult, Colon, Duodenum, Stomach, Infant, Newborn, Syndrome, Rats, Necrosis, Dogs, Gastric Mucosa, Intestine, Small, Animals, Humans, Intestinal Mucosa, Enterocolitis, Pseudomembranous
Adult, Colon, Duodenum, Stomach, Infant, Newborn, Syndrome, Rats, Necrosis, Dogs, Gastric Mucosa, Intestine, Small, Animals, Humans, Intestinal Mucosa, Enterocolitis, Pseudomembranous
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