The Medical and Surgical Management of Short Bowel Syndrome

Alan L. Buchman, MD, MSPH

Disclosures
In This Article

Medical Management of Short Bowel Syndrome

Fluid and Electrolyte Management

Fluid and electrolyte management is the most critical part of medical management for the patient with short bowel syndrome. Virtually no patient with this disorder requires macronutrient supplementation alone, but patients may often be weaned successfully from TPN, yet still require fluid and electrolyte support.

During the initial 6 months after massive enterectomy, gastric hypersecretion develops.[6] Basal acid secretion as well as gastrin secretion significantly increase. These increases are associated with an increased risk for peptic ulcer disease as well as with increased fluid losses. In addition, at an acidic pH, pancreatic lipase is deactivated and fat maldigestion worsens. Therefore, high-dose intravenous H2 receptor antagonists or oral proton-pump inhibitors should be prescribed during this period. Just as nutrient malabsorption occurs, so does medication malabsorption, and therefore, increased doses of orally administered medication may be required.

Fluid losses can be controlled with antimotility agents, such as loperamide hydrochloride or diphenoxylate (4-16 mg/day). Patients whose fluid losses are not controlled and who develop dehydration may require codeine (15-60 mg, 2-4 times daily) or a tincture of opium. Rarely, patients with proximal jejunostomy and several liters of daily stomal output will require octreotide (50-100 mcg subcutaneous, 2-4 times daily).[3] Its use should be discouraged because animal studies have suggested that octreotide inhibits intestinal adaptation and increases the risk for cholelithiasis.

Oral rehydration solutions (ORS) are important in the maintenance of adequate fluid balance and help decrease the need for parenteral fluids -- this is especially critical in patients with proximal jejunostomies who are net fluid and sodium excretors. The jejunum is permeable to sodium and chloride; therefore, solutions with a high NaCl content are readily and passively absorbed. Neither sodium nor water is absorbed from hypo- or isotonic solutions in the jejunum. In addition, glucose promotes both salt and water absorption via "solvent drag." Sodium and glucose absorption are mediated by a cotransporter. Although ORS do not decrease fluid losses, their use increases intracellular hydration. Several commercial formulas are available, although the least costly option is for the patient to formulate the solution recommended by the World Health Organization at home. The patient is instructed to mix 2.5 g of NaCl (table salt), 20 g of glucose (table sugar), 1.5 g of KCl (requires prescription), and 2.5 g of Na2CO2 in 1 L of tap water.[7] The critical aspect of ORS is that the optimal sodium concentration should be in the range of 90-120 mEq/L.[8] Most commercially available solutions have substantially less sodium. The use of solutions with less sodium may result in increased sodium loss. Therefore, patients should be strongly encouraged to avoid "plain" water consumption when they are thirsty and to substitute ORS. The need for ORS is not as critical for patients with colon in continuity as long as there is sufficient sodium in the diet because the colon readily absorbs the ion, even against a strong electrochemical gradient.[9] In addition, because ileal water absorption is unaffected by glucose, the glucose concentration of the ORS in patients whose jejunum has been resected has less importance.[10]

Significant quantities of magnesium are lost in jejunal and ileal effluent -- thus, magnesium deficiency may occur. This deficiency often develops despite a normal serum concentration; therefore, a 24-hour urine magnesium measurement is often required.[11] Supplementation may be problematic because magnesium is a cathartic; parenteral supplementation may be required. Magnesium deficiency may also result in calcium deficiency because of impaired parathyroid hormone release. Patients with short bowel syndrome who do not receive TPN are generally in negative calcium balance,[12] and a supplement (800-1500 mg/day) should be prescribed.

Macronutrients and Dietary Therapy

Most patients will require TPN for the first 7-10 days following massive enterectomy. However, this therapy should not be introduced until the patient is hemodynamically stable and in appropriate fluid and electrolyte balance. Energy requirements are generally 25-35 kcal/kg/day, and protein (amino acid) requirements are 1.0-1.5 g/kg/day.[3] Neonates and young children have increased energy and protein requirements. Enteral nutrition therapy with polymeric formulas should be introduced gradually. There is limited, if any benefit, from the use of elemental or free amino acid-based formulas,[13,14,15] and animal investigations have suggested that use of such formulas may be associated with ileal atrophy.[16] Once the patient is able to eat, a regular diet should be prescribed, although patients with colon in continuity should be provided an oxalate-restricted diet to decrease the risk for development of calcium-oxalate nephrolithiasis.[17] Lactose should not be restricted except in the case of proximal jejunal resection.[18,19] Lactose-containing foods are a significant source for dietary calcium. There is no benefit derived from the separation of solid and liquid dietary contents.[20]

Double-blind, randomized, placebo-controlled studies have shown no role for glutamine supplementation in the enhancement of intestinal adaptation and improvement of fluid and/or nutrient absorption.[21,22,23] Glutamine, either with or without growth hormone, has not been shown to increase intestinal villus height or to improve energy, nitrogen, carbohydrate, fat, fluid, or electrolyte absorption.

Soluble, nonstarch polysaccharides and some starches are not normally digested in the intestine. As much as 65% of dietary carbohydrate will be malabsorbed in the patient with short bowel syndrome.[24] This unabsorbed carbohydrate and soluble fiber are fermented by colonic bacteria. Energy can be absorbed in the form of short-chain fatty acids (butyrate, acetate, and propionate), which are the preferred fuel of the colonocyte.[25] As such, the colon becomes an important organ for energy assimilation in patients with short bowel syndrome. An intact colon may absorb up to nearly 1200 kcal/day.[2,17,26] Patients should be encouraged to ingest diets rich in complex carbohydrate and soluble fiber if they have colon in continuity. However, it must be recognized that these diets may also provoke some degree of early satiety and may ultimately reduce overall food intake. It is important for patients to adjust to eating 2-3 times their caloric intake preenterectomy and to eat throughout the day rather than primarily in 3 distinct meals.

Patients with short bowel syndrome will have significant fat malabsorption because of decreased surface area as well as bile salt malabsorption. The latter is associated with decreased micelle formation and deficient fat digestion. However, cholestyramine should not be used in patients who have had > 100 cm of ileum resected because steatorrhea will worsen because of the binding of dietary lipid (as well as binding of fat-soluble vitamins).[27] Dietary fat restriction will decrease steatorrhea, but this must be weighed against the fact that lipid is an energy-dense substrate (9 kcal/g), and dietary fat restriction would thereby significantly reduce energy intake. Medium-chain triglycerides (MCTs) may be added to the diet for additional energy. Their use, however, is limited by their poor taste, induced nausea, and ketosis with excessive intake as well as by a low smoking point (ie, they cannot be used in cooking). Recipes are available from MCT manufacturers. MCTs do not require micelles for absorption and are absorbed directly into the portal circulation. In addition, there is some colonic absorption.[28] MCTs, however, do not provide the essential fatty acid, linoleic acid.

Micronutrient and Trace Metal Supplementation

Patients with short bowel syndrome will have decreased fat-soluble vitamin absorption and will often require relatively large doses of replacement therapy.[3,29] Vitamin A, D, and E status should be determined at regular intervals. In addition, vitamin K deficiency may occur in patients who do not have a colon because colonic bacteria synthesize 60% of daily vitamin K requirements.[30] Water-soluble vitamin deficiency is uncommon. Trace metals, such as zinc and selenium, are lost in fecal effluent; thus, deficiencies may develop.[31] Vitamin and trace metal status should be monitored at regular intervals, especially in patients who do not require TPN.

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