SHORT GUT SYNDROME

The short gut syndrome develops after extensive resection of the small intestine and in functional damage to large sections of the gut. Croh n's disease and mesenteric infarction play a major causal role. The ef fects of the short gut syndrome are attributable to the reduction in t he absorptive surface area with accelerated passage of chyme, the loss of certain absorption sites and removal of the ileocaecal valve. Acce lerated chyme passage diminishes the effects of the digestive enzymes. Most of the bile salts and vitamin B-12 are largely absorbed in the t erminal ileum. The first symptom of absent enteric absorption of bile salts is chologenic diarrhoea. The loss of bile is initially compensat ed by increased synthesis for a long time. Decompensated bile acid los s syndrome with steatorrhoea occurs when hepatic synthesis is no longe r sufficient to sustain the bile acid pool. Extensive gut resection sh ould be followed promptly by enteric nutrition in order to exploit the adaptation capability of the remaining gut. Chologenic diarrhoea can be treated with ion-exchange resins (cholestyramine, colestipol). The gastric hypersecretion frequently encountered with the short gut syndr ome requires treatment with H-2-receptor antagonists.