The severity of symptoms following resections of large segments of the small bowel relates to the extent of the resection, to the specific level of the resected small bowel and to the reason for which the resection was undertaken. The level of resection is important because absorption of nutrients is most effective in the proximal small bowel (iron, folate and calcium). Resection of up to 40% of the intestine is usually tolerated provided the duodenum and proximal jejunum and distal half of the ileum and ileocecal valve are spared. In contrast, resection of the distal two-thirds of the ileum and ileocecal valve alone may induce severe diarrhea and significant malabsorption even though only 25% of the total small intestine has been resected. Resection of 50% of the small intestine results in significant malabsorption, and resection of 70% or more of the small intestine will result in severe malnutrition sufficient to cause death unless the patient's malnutrition is aggressively treated.

The most common cause of massive resection of the small bowel is small bowel ischemia, due to thrombosis or embolism of the superior mesenteric artery, thrombosis of the superior mesenteric vein, or low flow in the splanchnic vessels. Less commonly, volvulus, strangulated hernias, Crohn's disease, neoplasm and trauma necessitate massive resection.

Two major types of diarrhea can develop after massive ileal resection. One is induced primarily by malabsorbed bile acids, and the other by malabsorbed fat. When the ileal resection is small (less than 100 cm), hepatic synthesis of bile acids is sufficient to compensate for increased fecal losses. The luminal concentrations of bile acids are maintained within the micellar range, and significant steatorrhea does not occur. However, with inadequate absorption in the terminal ileum, bile acids enter the colon, impairing electrolyte and water absorption. Thus the term "bile acid diarrhea" is applied to this circumstance.

When the ileal resection is extensive (greater than 100 cm), hepatic compensation for wastage of bile acids is incomplete and the concentration of bile acids in the lumen is too low for adequate micellar solubilization of fat. Steatorrhea results. Here the malabsorbed fat is primarily responsible for the diarrhea. With excessive amounts of fatty acids now in the colon, electrolyte and water absorption are further impaired.

Consistent with these proposed pathogenic mechanisms are the therapeutic observations that a reduction in the dietary intake of long-chain fats will reduce the severity of diarrhea in the second instance (extensive resection and steatorrhea), whereas a sequestrant of bile acids such as cholestyramine, colestipol or aluminum hydroxide is needed for effective therapy of bile acid diarrhea.

Additional metabolic complications arise from the short bowel syndrome. These include hyperoxaluria and subsequent nephrolithiasis. Normally dietary oxalate is excreted in the feces, bound to calcium as an insoluble complex. However, in a patient with steatorrhea, fatty acids in the intestine preferentially bind to calcium, leaving the oxalate soluble and available for absorption in the colon. The short bowel syndrome may also give rise to cholelithiasis. If bile acid malabsorption is extensive, a lithogenic bile will be produced, predisposing to gallstone formation.