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[The blind-loop syndrome after side-to-side anastomoses of the gut (author's transl)].

The postoperative blind-loop syndrome can occur after side-to-side, end-to side or by-pass anastomoses of the gut and presents clinically as malabsorption syndrome. Pathogenetically, stasis or slowing of the bowel movements will cause a rapid increase of pathogenic bacteria in the small intestine. Malabsorption is characterized by 3 symptoms: Loss of weight, anemia, steatorrhoea. The method of choice for therapy is to perform a new, end-to-end, anastomosis of the intestine in order to re-establish a physiological situation. During the last 6 years 14 patients with malabsorption syndromes of varying degrees were operated upon: 6 had pure small intestinal anastomoses, 7 anastomoses between the small and large intestine and 1 patient had a side-to-side sigmoidal anastomosis. In all patients the side-to-side or by-pass anastomoses could be reversed.

Adolescent↗

Glycoprotein degradation in the blind loop syndrome: identification of glycosidases in jejunal contents.

Contents obtained from jejunum of normal controls, self-emptying and self-filling blind loop rats were analyzed for the presence of glycoprotein-degrading glycosidases. The blind loop syndrome was documented by the increased fat excretion and slower growth rate of self-filling blind loop rats 6 wk after surgery. With p-nitrophenylglycosides as substrate, the specific activity of alpha-N-acetylgalactosaminidase, a potential blood group A destroying glycosidase, was 0.90+/-0.40 mU/mg of protein. This level was 23-fold higher than the specific activity of normal controls. In partially purified self-filling blind loop contents, the activity of alpha-N-acetylgalactosaminidase was 9- to 70-fold higher than activities of self-emptying and normal controls. Antibiotic treatment with chloromycetin and polymyxin decreased 24-fold the glycosidase levels in self-filling blind loops. In experiments with natural substrate, the blood group A titer of a20,000g supernate from normal jejunal homogenates decreased 128-fold after 24-h incubation with blind loop contents. Normal contents failed to diminish the blood group reactivity of the natural substrate. Furthermore, blind loop contents markedly decreased the blood group A titer of isolated brush borders. Incubation between blind loop bacteria and mucosal homogenates or isolated brush borders labeled with d-[U-(14)C]glucosamine revealed increased production of labeled ether extractable organic acids. Likewise, intraperitoneal injection of d-[U-(14)C]glucosamine into self-filling blind loop rats resulted in incorporation of the label into luminal short chain fatty acids. These results suggest that glycosidases may provide a mechanism by which blind loop bacteria obtain sugars from intestinal glycoproteins. The released sugars are used and converted by bacteria into energy and organic acids. This use of the host's glycoproteins would allow blind loop bacteria to grow and survive within the lumen independent of exogenous sources.

Animals↗

The blind loop syndrome in children.

Anatomical abnormalities of the small bowel that cause intestinal stagnation result in bacterial overgrowth and a blind loop syndrome (BLS). Bacterial breakdown of bile salts and deamination of protein lead to malabsorption, steatorrhea, and fat-soluble vitamin deficiencies. Four children developed BLS as a complication of necrotizing enterocolitis, jejunal atresia, gastroschisis, and biliary atresia. BLS was suggested by abdominal pain, feculent vomiting, steatorrhea, and hypoalbuminemia. Dilated, stagnant bowel loops were demonstrated in each instance by upper gastrointestinal contrast study. Positive intestinal bacterial aspirates were confirmatory. Antibiotic treatment in two patients improved symptomatology but all children ultimately required surgery. Surgical procedures consisted of blind loop resection, intestinal plication, and catheterization of the bilioenteric conduit. All patients are now asymptomatic but one child suffers from parenteral nutrition-related cirrhosis and another requires chronic antibiotic therapy.

Bacterial Infections↗

Adaptation of the jejunal mucosa in the experimental blind loop syndrome: changes in paracellular conductance and tight junction structure.

Self-filling blind loops of rat jejunum exhibit hyperregenerative transformation of the mucosa. We used this experimental model to characterise mechanisms, which may occur under similar conditions in man (stagnant loop syndrome). Epithelial and subepithelial resistance were measured in the Ussing-chamber by voltage divider ratio measurements after positioning a microelectrode between epithelium and subepithelial tissue layers. In the blind loop, epithelial resistance increased from 8 +/- 1 to 23 +/- 1 omega cm2 and subepithelial resistance from 39 +/- 4 to 86 +/- 8 omega cm2 as compared with control jejunum. The increase in the subepithelial resistance was paralleled anatomically by an increase in the thickness of the subepithelial tissue layers from 63 +/- 4 microns to 177 +/- 19 microns. Ultrastructural analysis of the tight junction area by freeze fracture electron microscopy revealed an increase in the total junctional 'depth' in the crypts from 243 +/- 9 nm in control jejunum to 396 +/- 17 nm in the blind loop, while the number of horizontally oriented 'strands' remained unchanged. Villus tight junctions did not differ between blind loop and control. We interpret the alterations in the self-filling blind loop as an adaptive response of the epithelium which reduces backleakage of already absorbed electrolytes across the tight junction into the intestinal lumen. This mechanism is suitable to support the intestine in maintaining body electrolyte and water contents during cellular electrolyte malabsorption.

Adaptation, Physiological↗

Ischemic jejunal stenosis and blind loop syndrome after blunt abdominal trauma.

One month after suffering blunt abdominal trauma a patient developed severe steatorrhea and profound weight loss in association with an ischemic distal jejunal stricture and blind loop syndrome. Evidence for a partial mesenteric tear was found at resection of the stricture, which resulted in complete cure.

Blind Loop Syndrome↗

[Significance of deficient bacterial colonization in the pathogenesis of mucosal lesions in experimental blind loop syndrome].

A complete evaluation of the bacterial flora in jejunal self-filling blind loops was performed. The results show a significant increase in bacteria of the genera E. coli, Streptococcus and Bacteroides. In further experiments, jejunal self-filling blind loops were created in germ-free animals. In spite of the germ-free state the mucosa displayed marked hyperplasia. The same was true when the blind loops had been contaminated with aerobic bacteria. These results demonstrate that other factors in addition to bacterial overgrowth contribute to the mucosal damage observed in self-filling blind loops.

Animals↗