Massive fluid and electrolyte losses often occur frequently during the first week or two following a massive small bowel resection, but may improve over the ensuing months. During this postoperative period, patients will usually require parenteral fluids and nutrition. Regardless, it is still important to institute enteral nutrition as soon as possible to hasten the intestinal adaptive response. Transient gastric hypersecretion also occurs for the first 6 to 12 months following a massive intestinal resection. Although the etiology for this process is unknown, it appears related to hypergastinemia. High dose H2 antagonists and proton pump inhibitors are useful for decreasing jejunal fluid and potassium losses during this time. These medications are all absorbed in the proximal jejunum, but are compatible with TPN if IV delivery is necessary. Medications such as loperamide, diphenoxylate, codeine, or tincture of opium (listed in order of increasing need) may be important to slow motility and increase nutrient contact time. Loperamide hydrochloride or diphenoxylate may require doses up to 16 mg daily. If these medications are less than successful in controlling fluid losses, codeine sulfate (30 to 60 mg 3 times daily) or deodorized tincture of opium (10 drops 2 or 3 times daily) may be necessary. High doses of calcium (2.4 to 3.6 g/d of elemental calcium) may also be useful for decreasing diarrhea, prob ably because of increased binding of fatty acids. Octreotide (100 |g subcutaneously 3 times daily 30 min before meals) is rarely necessary, except for in some patients with high output jejunostomies. Its use should be avoided if possible because of an association with decreased pancreatic function, malabsorption, decreased intestinal adaptation, and cholelithiasis.
Malabsorption develops in patients with short bowel syndrome not only because of decreased intestinal surface area, but also related to bacterial colonization of the small intestine. Normally, the ileocecal valve helps prevent the movement of bacteria from the colon into the distal ileum, but in its absence bacteria will enter the small intestine and compete for the available nutrients, such as vitamin B12. Bacterial overgrowth may be difficult to diagnose in patients with short bowel syndrome because the rapid intestinal transit time renders breath tests difficult to interpret; enteroscopy with jejunal aspiration and culture may be necessary.
D-lactic acidosis is a rare complication of bacterial overgrowth, but may result in serious sequalae including ataxia, dysarthria, opthalmoplegia, nystagmus, stupor, and coma. It may develop when simple carbohydrates, such as glucose and lactose, are malabsorbed, leaving the anerobic flora to ferment them. Diagnosis requires the availability of a serum d-lactic acid measurement; the standard lactic acid laboratory test will not detect d-lactic acid.
Bacteria also deconjugate bile salts, which leads to decreased bile salt reabsorption; therefore, fewer bile salts are available for micelle formation and fat maldigestion occurs. Diarrhea may worsen in patients who have had > 100 cm of ileum resected and in whom part or all of their colon remains, in part because bile salts stimulate cyclic adenosine monophosphate and calcium-mediated chloride secretion. Unabsorbed long chain fatty acids may also stimulate colonic electrogenic anion secretion. A low fat intake (20 to 40 g) may lessen diarrhea but removes a source of calories.
Treatment of bacterial overgrowth or d-lactic acidosis may be undertaken with either metronidazole or tetracycline. Unfortunately, the use of broad spectrum antibiotics may also contribute to the worsening of diarrhea because of either Clostridium difficile or non-C.diffcile-associated diarrhea. Antibiotic use may also be associated with vitamin K deficiency because normal gastrointestinal flora synthesize at least half of the body's daily requirement.
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