Mucosal lesions in the human small intestine in shock.

Abstract

SUMMARY Characteristic mucosal lesions in resected small intestinal segments from seven patients are reported. Preoperatively, four patients were in shock and general hypotension while the three remaining cases showed signs of local intestinal hypotension. The microscopic appearance of the mucosal lesions was in all patients identical with that previously observed in the feline and canine small intestine after haemorrhage or local intestinal hypotension. It is proposed that an extravascular short-circuiting of oxygen in the mucosal countercurrent exchanger and an intravascular aggregation of blood cells might produce tissue hypoxia which makes the mucosa vulnerable to enzymatic degradation.Haemorrhagic lesions in the small intestinal mucosa have regularly been reported from experimental shock studies on dogs (Wiggers, 1950;Lillehei et al., 1964;Chiu et al., 1970) and cats (Ahren and Haglund, 1973;Haglund, 1973). A characteristic feature is that these lesions appear first at the tips of the villi, and in cases where the entire villus is destroyed the deeper layers of the intestinal wall are still free from inflammatory changes (Chiu et al., 1970;Ahr6n and Haglund, 1973). Similar mucosal lesions have also been reported in patients dying in shock (see, for example, Penner and Bernheim, 1939;Marston, 1962;Bounous, 1969). Most of these studies were, however, 'based on necropsies where postmortem autolysis could not be excluded. There exist in the literature only a few exceptional cases where intestinal mucosal lesions have been reported in patients in shock based on microscopic studies of intestinal segments removed ante-mortem-for example, at operation (Carey et al., 1967;S0rensen and Vetner, 1969;Hugon and Bounous, 1971). This comparatively rare occurrence ofreports on intestinal mucosal lesions in association with clinical shock has led to the suggestion that these lesions may be a peculiarity of the dog and, therefore, it has even been proposed that only primates can be used in experimental studies of shock as it appears in clinical medicine (Brobmann et al., 1970;Swan et al., 1972).This study reports seven patients exhibiting haemorrhagic lesions in the small intestinal mucosa. The microscopic appearance is described and posReceived for publication 24 September 1975. sible pathophysiological mechanisms responsible for the development of such lesions are discussed. Methods CASE HISTORIESThis report is based on seven patients operated upon for different gastrointestinal disorders. During the preoperative period four patients exhibited obvious signs of clinical shock and, in the remaining three, the small intestine had evidently been subjected to a period of local hypotension. The detailed histories are given below.Case 1 A 52 year old man had 14 years earlier had a partial gastrectomy and a gastrojejunal anastomosis for bleeding ulcer. The patient was readmitted with clinical signs of gastric bleeding and signs of shock. Blood transfusions could not restore haemoglobin concentration above 8 g/dl and for two h...

Relative Importance of Heat-Labile Enterotoxin in the Causation of Severe Diarrheal Disease in the Gnotobiotic Piglet Model by a Strain of Enterotoxigenic Escherichia coli That Produces Multiple Enterotoxins

“…In piglets inoculated with either LT ϩ or LT Ϫ strains, hypovolemic shock resulted from severe diarrheagenic water loss. Ischemic bowel necrosis, a lesion consistent with hypovolemic shock (6,22), predisposed the piglets to septicemia. Sloughing of enterocytes from ischemic intestinal villi resulted in villous atrophy, a lesion previously reported to occur in severe ETEC infections of swine (35).…”

“…The increased virulence of these strains in susceptible swine is due in part to their ability to colonize the entire small intestine instead of only the ileum, as occurs with K99 (F5 ϩ ), 987P (F6 ϩ ), and F41 ϩ strains (3,24). The pathogenesis of postdiarrheal septicemia is poorly understood but is related to the development of severe dehydration, hypovolemic shock, and ischemia of the intestinal mucosa, the last presumably a consequence of the shock-induced low-flow state (6,22,40). Histological examination of immunohistochemically stained small intestinal tissue sections of moribund or dead piglets in cases of natural and experimental infection reveal ETEC bacteria adherent to exposed intestinal basement membranes and within juxtaposed villous capillaries (40).…”

A COMPARISON OF THE EFFECTS OF BRADYKININ, 5‐HYDROXYTRYPTAMINE AND HISTAMINE ON THE HEPATIC ARTERIAL AND PORTAL VENOUS VASCULAR BEDS OF THE DOG: HISTAMINE H1 AND H2‐RECEPTOR POPULATIONS

“…These experiments confirm and extend the previous observations of Scholtholt & Shiraishi (1968) Under normal circumstances, bradykinin is unlikely to attain vasoactive levels in the systemic arterial circulation because of its rapid inactivation in the lungs (Vane, 1969) and blood (Douglas, 1975). However, its synthesis and release (Seki, Nakajima & Erd6s, 1972) is suspected to occur in many pathological conditions including gastrointestinal tract disorders such as the carcinoid and dumping syndromes, septic shock, pancreatitis and may explain some of the symptoms following regional hypotension consequent to occlusion of the superior mesenteric artery (Berry, Collier & Vane, 1970;Haglund, Hulten, Ahren & Lundgren, 1975;Lundgren, Hagland, Isaksson & Abe, 1976).…”

Diagnosis and management of splanchnic ischemia

“…This is why countercurrent exchange can take place [15] . The tip of the villus is quite susceptible to ischemia [16] . the portal vein.…”