78 Short Bowel Syndrome

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Yeo: Shackelford's Surgery of the Alimentary Tract, 6th ed.Copyright 2007 Saunders, An Imprint of Elsevier

Chapter 78 Short-Bowel Syndrome Jon S. Thompson Alan N. Langnas Intestinal failure refers to a condition that results in inadequate digestion or absorption of nutrients, or both, so that an individual becomes malnourished and requires specialized medical and nutritional support.[1] Short-bowel syndrome is a type of intestinal failure caused by a shortened remnant after intestinal resection. The pathophysiologic changes that occur in short-bowel syndrome relate primarily to the loss of intestinal absorptive surface and more rapid intestinal transit ( Box 781 ). The consequences of malabsorption of nutrients include malnutrition, diarrhea, steatorrhea, specific nutrient deficiencies, and fluid and electrolyte abnormalities. These patients are at risk for other specific complications, including an increased incidence of nephrolithiasis, cholelithiasis, and gastric hypersecretion. The clinical manifestations of short-bowel syndrome vary greatly among patients and depend on intestinal remnant length, location, and function; the status of the remaining digestive organs; the presence or absence of the ileocecal valve; and the adaptive capacity of the intestinal remnant. Thus, short-bowel syndrome is not entirely dependent on a given length of remaining intestine. Box 78-1 Pathophysiologic Consequences of Massive Resection General Malnutrition and weight loss

Diarrhea and steatorrhea

Vitamin and mineral deficiencies

Fluid and electrolyte abnormalities Specific Cholelithiasis

Gastric hypersecretion

Liver disease

Nephrolithiasis

The prevalence of short-bowel syndrome is 3 to 4 per million, and thousands of patients are now surviving with short-bowel syndrome.[1] This condition occurs in about 15% of adult patients who undergo intestinal resection, with three fourths of these cases resulting from massive intestinal resection and one fourth from multiple sequential resections.[2] Massive intestinal resection continues to be associated with significant morbidity and mortality, primarily related to the underlying diseases necessitating resection. [8] [9] About 70% of patients in whom short-bowel syndrome develops are discharged from the hospital, and a similar percentage are alive 1 year later.[4] This improved survival rate has been achieved primarily by the ability to deliver long-term nutritional support. The long-term outcome of these patients is often determined not only by their age and underlying disease but also by complications related to the management of short-bowel syndrome. FACTORS INFLUENCING OUTCOME Intestinal remnant length is the primary determinant of outcome in patients with short-bowel syndrome. The length of the small intestine in adults varies between 12 and 20 ft (360 to 600 cm), depending on how it is measured and the height and sex of the individual. The duodenum measures 10 to 12 inches (25 to 30 cm). The length of the small intestine from the ligament of Treitz to the ileocecal junction is about 16 ft (480 cm), with the proximal two fifths being jejunum and the distal three fifths being ileum. Resection of up to half of the small intestine is generally well tolerated. Although short-bowel syndrome may develop in patients with less than 180 cm of small intestine, or about a third the normal length, permanent parenteral nutrition (PN) support is likely to be needed in patients with less than 120 cm of intestine remaining without colon in continuity and less than 60 cm remaining with colonic continuity ( Table 78-1 ). [10] [11] Table 78-1 -- Intestinal Length and Nutritional Prognosis Intestinal Anatomy Intestinal Length to Avoid Permanent Parenteral Nutrition End-jejunostomy (type 1) 100 cm

Intestinal Anatomy

Intestinal Length to Avoid Permanent Parenteral Nutrition Jejunocolic anastomosis (type 2) 65 cm

Jejunoileocolic anastomosis 30 cm (type 3) Adapted from Messing B, Crenn P, Beau P, et al: Long term survival and parenteral nutrition dependence in adult patients with the short bowel syndrome. Gastroenterology 117:1043, 1999.

The site of resection is also an important factor. Patients with an ileal remnant generally fare better than those with a jejunal remnant. The ileum has specialized absorptive properties for bile salts and vitamin B12, unique motor properties, a hormone profile different from that of the jejunum, and a greater capacity for intestinal adaptation. [12] [13] The presence of the ileocecal junction improves the functional capacity of the intestinal remnant.[7] Although previously this had been attributed to a barrier function and transit-prolonging property of the ileocecal valve, this advantage may actually be related to the specialized property of the terminal ileum itself. The status of the other digestive organs also contributes to outcome. The stomach influences oral intake, mixing of nutrients, transit time, pancreatic secretion, and protein absorption. Pancreatic enzymes are important in the digestive process and particularly influence fat absorption. The colon absorbs fluid and electrolytes, slows transit, and participates in the absorption of energy from malabsorbed carbohydrates. When compared with an end-jejunostomy (type 1 anatomy), a jejunoileal anastomosis with an intact colon (type 3 anatomy) is equivalent to 60 cm of additional small intestine, and a jejunocolic anastomosis (type 2 anatomy) is equivalent to about 30 cm of small intestine.[5] A variety of conditions requiring intestinal resection lead to short-bowel syndrome ( Table 78-2 ).[8] Patients with underlying inflammatory disease may have impaired intestinal function. The cause of resection will also influence the outcome because of the effect on other digestive organs. Long-term treatment and survival are influenced by the patient's age and other morbid conditions. Underlying disease will also influence these parameters. Table 78-2 -- Causes of Short-Bowel Syndrome Postoperative 52 (25%) Irradiation/cancer 51 (24%)

Mesenteric vascular disease 46 (22%) Crohn's disease Other benign causes 34 (16%) 27 (13%)

Total 210 From Thompson JS, DiBaise JK, Iver KR, et al: Short bowel syndrome as a postoperative complication. J Am Coll Surg 201:85, 2005.

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INTESTINAL ADAPTATION The small intestine is able to adapt to compensate for the reduction in absorptive surface area caused by intestinal resection. [15] [16] [17] This process occurs within the first year or two after resection and improves intestinal absorptive capacity ( Fig. 78-1 ). [11] Whether the adaptive response can be significantly accelerated or augmented is not clear. The overall intestinal adaptive response results from changes in intestinal structure, function, and motility.

Figure 78-1 Schematic presentation of intestinal adaptation. AA, accelerated adaptation; AHA, accelerated hyperadaptation; HA, hyperadaptation; SA, spontaneous adaptation. (From Jeppesen PB: Clinical significance of GLP-2 in short bowel syndrome. J Nutr 133:3721, 2003.)

Structural adaptation after intestinal resection involves all layers of the intestine. [15] [16] Mucosal DNA and protein synthesis and crypt cell proliferation are increased within hours after resection. Both the total number of cells and the proportion of proliferating cells are increased in the crypt. Enterocytes migrate at a faster rate along the villus. Villus lengthening occurs by an overall increased number of cells. Rates of apoptosis, or programmed cell death, increase in both crypt and villus enterocytes after resection. However, the proliferative stimulus dominates, so adaptation occurs. The ratio of crypts to villi may also increase. Microvilli along the epithelial surface increase as well. Overall, mucosal weight increases. The thickness and length of the muscle layers also increase after resection, primarily as a result of hyperplasia rather than hypertrophy of the muscle cells.[9] Muscle adaptation, however, occurs at a later time than mucosal adaptation and only after more extensive resection. These changes in the components of the intestinal wall

result in marked thickening of the intestinal wall, as well as increased intestinal circumference and length. Thus, there is an overall increase in mucosal surface area because of both villus hypertrophy and the increases in length and circumference of the remnant. Intestinal motor activity is also altered by intestinal resection.[6] The canine small intestine demonstrates a biphasic motor response to varying degrees of distal resection. There is initial disruption of motor activity, followed by adaptation. In the distal segment of the intestinal remnant after limited resection and more generally after 75% resection, motility recordings are initially dominated by recurring bursts of clustered contractions.[12] With extensive resection, these clusters are prolonged and associated with baseline tonic changes. With limited resection, there is evidence of progressive motor adaptation with eventual slowing of transit and return of migrating motor complex (MMC) cycling. This adaptation is less apparent after massive resection. Motor adaptation is more prominent in the jejunum than in the ileum. These changes are accompanied by modest alterations in smooth muscle contractility. Clinical reports also demonstrate a biphasic adaptive motor response during the first year after resection. There is disrupted motor activity in the first few months after resection, but these changes occur only after extensive resection (remnant shorter than 100 cm). Long-term human studies demonstrate a shorter duration of the MMC cycle and fed pattern after resection.[13] Functional adaptation has been well documented after resection, [7] [11] [20] [21] and structural adaptation increases intestinal absorptive surface area. Both structural adaptation and motor adaptation lead to prolonged transit time. Although the formerly accepted theory of improved absorption by individual enterocytes was discounted, more recent studies suggest that certain transport capabilities do improve. Within months of resection, diarrhea diminishes and nutritional status improves. The mechanism of intestinal adaptation has been studied extensively but is still not entirely understood. The degree of structural adaptation is related to the extent and site of resection. [15] [16] Adaptation is greater with more extensive resection, and the ileum has a greater adaptive capacity than the jejunum does. Subsequent resection elicits a further adaptive response. Luminal nutrients and secretions and growth factors are important for achieving the maximal response but are not essential for adaptation to occur ( Box 78-2 ). [15] [16] The early molecular events associated with this hyperplastic response are being investigated. [22] [23] Intestinal resection results in increased levels of a variety of gene products in enterocytes within hours. There is an immediate increase in genes that encode transcription factors, not only genes that influence cell proliferation but also those that augment nutrient trafficking, as well as heat shock genes, which maintain normal cellular function. Many of these are novel genes not normally present in intestinal epithelium. The specific triggers for these events are not clear, and there are obviously many candidates. Currently, there

is clinical interest in manipulating the adaptive response pharmacologically. Box 78-2 Factors Influencing Intestinal Adaptation

Gastrointestinal regulatory peptides

Luminal contents

Nutrients

Secretions

Systemic factors

Growth factors

Hormones

Cytokines

Tissue Factors

Immune system

Mesenchymal factors

Mesenteric blood flow

Neural influencesCopyright 2007 Elsevier Inc. All rights reserved. - www.mdconsult.comBookmark URL: /das/book/0/view/1430/740.html



MEDICAL MANAGEMENT The early management of a patient with short-bowel syndrome is that of a critically ill surgical patient who has recently undergone intestinal resection and other concomitant procedures. Thus, control of sepsis, maintenance of fluid and electrolyte balance, and initiation of nutritional support are important in the early management of these patients. For patients who have survived this early phase, the primary goals of management are to maintain adequate nutritional status, maximize the absorptive capacity of the remaining intestine, and prevent the development of complications related to both the underlying pathophysiology and the nutritional therapy. Maintain Nutritional Status The most important therapeutic objective in the management of short-bowel syndrome is to maintain the patient's nutritional status. This usually requires PN support in the early period after surgery. Fluid and electrolyte losses from the gastrointestinal tract may be great during the early postoperative period and must be monitored and replaced as soon as possible. Enteral nutritional support should be started as soon as possible when the ileus has resolved. With time, an increasing amount of nutrients are absorbed by the enteral route. This is important for maximizing intestinal adaptation and preventing complications related to PN. As their condition improves and intestinal adaptation occurs, many patients can absorb the necessary nutrients entirely by the enteral route. The length of the intestinal remnant and the status of the colon have important prognostic implications in this regard (see Table 78-1 ). The ability of patients with short-bowel syndrome to maintain adequate caloric intake enterally is determined by a variety of factors, including intestinal remnant length and location, any underlying intestinal disease, and the status of the remaining digestive organs. [21] [24] Whether there is continuity in the intestinal tract or

a stoma is also an important consideration. Diarrhea and perianal complications may markedly diminish oral intake. Patients with stomas are more likely to have a greater percentage of their calories taken enterally. Hyperphagia develops in many patients with short-bowel syndrome to overcome inefficient absorption.[19] Many patients with short-bowel syndrome require long-term PN for survival, and this therapy has considerable expense and morbidity. Patients without malignancy have 1-, 3-, and 5-year survival rates of about 90%, 70%, and 60%, respectively.[4] One third of deaths are related to the underlying disease, 50% to other supervening disease, and 10% to 15% to PN therapy. Sepsis and liver disease related to PN are important factors in long-term survival. The incidence of sepsis varies from 0.1 to 0.3 episodes per patient year of PN. Sepsis may be associated with catheter thrombosis. The need for prolonged therapy makes vascular access a long-term problem, and catheters may eventually need to be placed in the azygos, hepatic, or inferior vena cava veins. End-stage liver disease develops in about 15% of long-term adult PN patients and is associated with a survival time of about 1 year without liver transplantation. [26] [27] Although the etiology of the liver disease is not completely understood, it appears to be a multifactorial process that is initially reversible but ultimately leads to severe steatosis, cholestasis, and cirrhosis. Liver disease occurs more frequently in children than adults. Provision of enteral nutrients may prevent this problem, but overfeeding is a predisposing factor. Control of sepsis and bacterial overgrowth is important to minimize this liver disease. Patients with abnormal liver function test results while receiving PN should undergo abdominal ultrasound for evaluation of the gallbladder and bile ducts and should have a liver biopsy performed as appropriate.Copyright 2007 Elsevier Inc. All rights reserved. - www.mdconsult.comBookmark URL: /das/book/0/view/1430/741.html



Maximize Enteral Nutrient Absorption Because the morbidity associated with nutritional support in patients with shortbowel syndrome is related primarily to PN, maximizing enteral absorption of nutrients is important for long-term survival. Furthermore, diarrhea and stomal fluid losses can also be important clinical problems that affect the patient's quality of life. Thus, it is beneficial to ensure that the patient's intestinal remnant is functioning optimally and absorbing nutrients and fluid. The optimal diet for patients with short-bowel syndrome remains controversial.

Provision of nutrients in their simplest form to minimize digestion has been one strategic approach. Simple sugars and dipeptides and tripeptides are rapidly absorbed from the intestinal tract. However, partially hydrolyzed diets appear to be just as effective and are less expensive. Complex carbohydrates reduce the osmotic load, but concentrated sugars, such as fruit juices, should be avoided because they generate a high osmotic load. Whether the diet should have a high-fat or low-fat content is another issue. There appears to be increasing agreement that patients with colon should have a low-fat (20% to 30% of calories), high-carbohydrate (50% to 60% of calories) diet but that patients with an end-enterostomy do not require fat restriction (30% to 40% of calories). Fat absorption obviously requires more digestion unless the fat is supplied in the form of medium-chain triglycerides. The ability to absorb these nutrients improves with time, so the diet may need to be continually modified. Specific problems such as lactase deficiency are often present, and the diet should be altered appropriately. Ingestion of a glucose-electrolyte oral rehydration solution with a sodium concentration of at least 90 mmol/L will optimize water and sodium absorption in the proximal jejunum and prevent secretion into the lumen. Minimizing gastrointestinal secretions and controlling diarrhea are also important goals for maximizing absorption. Both histamine H2 receptor antagonists and proton pump inhibitors are effective in controlling gastric hypersecretion, correcting malabsorption, and improving nutritional status in patients with short-bowel syndrome. Furthermore, cimetidine may also increase intestinal adaptation. Somatostatin and its long-acting analogue octreotide have been investigated for the management of severe refractory diarrhea in short-bowel syndrome. They improve diarrhea by prolonging small intestinal transit time and reducing salt and water excretion. Part of the beneficial effect may also be related to a reduction in gastric hypersecretion. Although these therapeutic agents are beneficial in the short term, it is not clear whether they continue to be effective after a few months, and they may have some potential deleterious effects. Somatostatin may exacerbate steatorrhea because of impaired pancreatic exocrine function. Other potential adverse effects of octreotide are inhibition of intestinal adaptation and the development of cholelithiasis. Recent evidence supports the use of ox bile and cholylsarcosine, a synthetic conjugated bile acid, as replacement therapy because they improve fat absorption without exacerbating diarrhea. Another important aspect of dietary management is to provide a diet that will maximize the intestinal adaptive response. [15] [16] [24] Provision of fat and dietary fiber may be particularly important in this regard. Long-chain and short-chain fatty acids appear to have a greater trophic effect on the intestine than medium-chain fatty acids do. Although these nutrients directly stimulate intestinal adaptation, nutrients also stimulate intestinal adaptation through endocrine and paracrine effects. Pharmacologic therapy for short-bowel syndrome is a rapidly expanding area of

investigation. Recent evidence suggests that provision of the appropriate diet, nutritional supplements such as glutamine, and growth factors such as growth hormone improves intestinal absorption and perhaps modifies the adaptive response in patients with established short-bowel syndrome.[22] However, which of these components is actually responsible for improved absorption is controversial. Growth hormone and glutamine do not have a consistent beneficial effect. [29] [30] Currently, glucagon-like peptide-2 appears to have the most promise for promoting absorption and adaptation.[11] Epidermal growth factor also stimulates intestinal adaptation and may soon be studied in clinical trials.[25] An important clinical issue is whether to establish intestinal continuity in patients who have a colonic remnant. There are both advantages and disadvantages to restoring continuity ( Box 78-3 ). The colon may improve intestinal absorption by increasing the absorptive surface area, deriving energy from short-chain fatty acids, and prolonging transit time, particularly if the ileocecal valve is intact. Avoiding a stoma also improves quality of life. However, the response of the colon to luminal contents is somewhat unpredictable. Bile acids may cause a secretory diarrhea. Perianal problems can be quite disabling and decrease the patient's oral intake. Oxalate is absorbed primarily in the colon, and restoring continuity places the patient at increased risk for the formation of calcium oxalate stones. Serum and intestinal fluid markers have been investigated as a means of predicting the response of the individual patient to restoring continuity, but none is generally available and useful. Distal reinfusion of enteral contents into a mucus fistula to assess the functional outcome has some usefulness, but it is cumbersome. Not all patients who initially have a stoma created eventually have continuity restored with a satisfactory outcome.[26] This decision should be considered on an individual basis and depends on the length of the intestinal remnant, the status of the ileocecal valve and the colon, and the patient's overall condition. Generally, at least 3 ft of small intestine is required to prevent severe diarrhea and perianal complications. Restoring continuity, however, should always be given strong consideration because of possible improvement in absorption. Box 78-3 Restoration of Intestinal Continuity Advantages Absorptive capacity increased

Energy absorbed from short-chain fatty acids

Infectious complications reduced

Transit time prolonged

Stoma avoided Disadvantages Bile acid diarrhea

Dietary restrictions

Nephrolithiasis increased

Perianal complications From Thompson JS: Intestinal resection and the short bowel syndrome. In Quigley EMM, Sorrell MF (eds): Medical Management of the Gastrointestinal Surgery Patient. Baltimore, Williams & Wilkins, 1994, p 327.Copyright 2007 Elsevier Inc. All rights reserved. - www.mdconsult.comBookmark URL: /das/book/0/view/1430/742.html



Prevent Complications Metabolic complications are common in patients with short-bowel syndrome because of their tremendous fluid and electrolyte losses and the need to replace these losses with specialized solutions. Intravascular volume has to be maintained to prevent dehydration and renal dysfunction. Hypocalcemia is a common problem related to poor absorption and binding by intraluminal fat. Maintaining adequate calcium and magnesium levels and vitamin D supplementation are important to minimize bone disease. Hyperglycemia and hypoglycemia are frequent

complications of patients receiving a large amount of their calories parenterally. Both metabolic acidosis and metabolic alkalosis can occur. A specific problem is dlactic acidosis, which results from bacterial fermentation of unabsorbed nutrients, particularly simple sugars. Lactate reduces colon pH, thereby permitting the growth of acid-resistant anaerobes capable of producing d-lactate. Impaired metabolism of d-lactic acid may also contribute to elevated serum d-lactic acid levels. This diagnosis is suggested by an unexplained metabolic acidosis and associated neurologic symptoms, such as confusion and somnolence. d-Lactic acid is not measured by standard laboratory techniques for lactic acid determination. Thus, an increased anion gap but normal lactate level in the appropriate clinical setting mandates measurement of d-lactic acid. d-Lactic acidosis is treated by minimizing overall caloric intake or by instituting a low-carbohydrate diet. Administration of intestinal antibiotics may be appropriate, but the optimal duration of such treatment is unclear, and recurrence rates are significant. Specific nutrient deficiencies need to be prevented and monitored closely, including iron and vitamin deficiencies, as well as deficiencies in micronutrients such as selenium, zinc, and copper. Because fat is poorly absorbed, fatty acid deficiency can also occur. Although medium-chain fatty acids can supplement the diet enterally, parenteral lipids are required in patients who depend primarily on that route. Serum free fatty acid levels and triene-to-tetraene ratios may need to be monitored periodically to determine the need for supplementation and response to treatment. In general, enteral intake must greatly exceed the absorptive needs to ensure that these needs are being met. Catheter-related sepsis is an important problem that often necessitates rehospitalization and replacement of catheters. Attention to technique and meticulous patient education are important to prevent this complication. Most infections are due to Staphylococcus species, but gram-negative bacteria and fungi are also associated with line sepsis. An attempt at line sterilization before removal is appropriate when infections are caused by coagulase-negative staphylococci and gram-negative bacteria. Repeated placement of catheters can lead to catheter thrombosis, which is the other common problem. In patients who require PN permanently, this may become an important factor in the patient's survival because vascular access may not be achievable indefinitely. PN-induced liver disease is another potential long-term problem. [26] [27] It can be minimized by providing as large a portion of the calories as possible enterally, avoiding overfeeding, using mixed fuels (less than 30% fat), and preventing specific nutrient deficiencies. Treating bacterial growth and preventing recurrent sepsis are also important. Ursodeoxycholic acid administration may likewise be beneficial. Bacterial overgrowth is another long-term complication associated with both intestinal disease and resection. It may result from impaired motility or stasis caused

by obstructive lesions ( Fig. 78-2 ). Achlorhydria is also a contributing factor. Bacterial deconjugation of luminal bile salts impairs bile salt reabsorption. Bacteria also metabolize intraluminal vitamin B12. Depending on the bacterial species present, secretory diarrhea may occur as well. Bacterial overgrowth requires a high degree of suspicion to make the diagnosis. This complication should be suspected when a patient's absorptive capacity and stool habits change acutely. It may result from a mechanical obstruction or a blind loop, which can be relieved by surgery. However, it is often a primary motor abnormality and requires intermittent therapy with antibiotics. Colonization of the lumen with acidophilus or other nonpathogenic organisms is another potential therapy.[27]

Figure 78-2 Contrast study of a patient with short-bowel syndrome. The shortened remnant lies primarily in the

left side of the abdomen with a large dilated segment in the pelvis. Contrast has passed into the right colon beyond this area.

Cholelithiasis occurs in 30% to 40% of patients with intestinal insufficiency. [34] [35] Factors that predispose these patients to gallstone formation include altered hepatic bile metabolism and secretion, gallbladder stasis, and malabsorption of bile acids. Depending on the dominant mechanism, either mixed pigment stones or cholesterol stones may occur. Long-term PN is an important contributing factor causing altered hepatic bile metabolism and gallbladder stasis. Patients receiving PN are susceptible to the development of cholelithiasis and hepatocellular dysfunction and thus require careful clinical evaluation. [34] [35] Biliary sludge forms within a few weeks of initiating PN if there is no enteral intake, but it rapidly disappears when enteral nutrition is resumed. Intestinal mucosal disease and resection, particularly of the ileum, cause bile acid malabsorption, which leads to lithogenic bile and the formation of cholesterol stones. The risk for cholelithiasis is significantly increased if less than 120 cm of intestine remains after resection, the terminal ileum has been resected, and PN is required. The incidence of cholelithiasis can be minimized by providing nutrients enterally whenever possible. Patients totally dependent on PN may be treated with intermittent cholecystokinin injections to prevent stasis and the formation of sludge. Administration of intravenous lipids also stimulates gallbladder emptying. Cholelithiasis may lead to complications in a higher number of patients with short-bowel syndrome than in the general population and also requires more complicated surgical treatment. Thus, several authors now recommend prophylactic cholecystectomy in these patients when laparotomy is being undertaken for other reasons.[29] Nephrolithiasis also occurs with some frequency. Calcium oxalate stones form as a result of increased oxalate absorption from the colon.[29] Oxalate is normally bound to calcium in the intestinal lumen and is not absorbed. Decreased availability of calcium secondary to reduced intake or binding by intraluminal fat leaves free oxalate in the lumen. Thus, the oxalate is absorbed in the colon and forms calcium oxalate in the urine. Nephrolithiasis is unusual in patients after intestinal resection and jejunostomy but occurred in a fourth of such patients with an intact colon within 2 years of resection. Nephrolithiasis can be prevented by maintaining a diet low in oxalate, minimizing intraluminal fat, supplementing the diet with calcium orally, and maintaining a high urinary volume. Foods with high oxalate content include chocolate, tea, cola, spinach, celery, carrots, and other fruits and vegetables. Cholestyramine, which binds oxalic acid in the colon, is another potential treatment. Gastric hypersecretion is a potential problem in patients with short-bowel syndrome. Massive intestinal resection can cause gastric hypersecretion as a result of parietal cell hyperplasia and hypergastrinemia. This phenomenon is usually transient and

lasts several months. The etiology has not been elucidated but may involve loss of an inhibitor from the resected intestine. The associated hyperacidity exacerbates malabsorption and diarrhea. Clinical development of peptic ulcer disease may also occur and is seen in about a fourth of patients undergoing massive resection.[26] Treatment of gastric acid secretion may improve absorption but also prevents peptic ulcer disease. Control of acid secretion by H2 receptor antagonists or proton pump inhibitors should be initiated in the perioperative period after resection and maintained until the increased acid production resolves. Some patients, however, continue to have symptoms of peptic ulcer disease that eventually require surgical intervention. Gastric resection therapy should be avoided when possible. A highly selective vagotomy may be the most desirable procedure if feasible.Copyright 2007 Elsevier Inc. All rights reserved. - www.mdconsult.comBookmark URL: /das/book/0/view/1430/743.html



SURGICAL MANAGEMENT The primary goal of surgical therapy for short-bowel syndrome is to increase intestinal absorptive capacity, which can be achieved either by improving absorption by existing intestine or by increasing the area of absorption ( Box 78-4 ). Recruiting additional intestine into continuity, relieving obstruction, or slowing intestinal transit will often improve absorption. The intestinal lengthening procedure is feasible in selected patients. The most significant increase in length, however, is potentially achieved by intestinal transplantation. The choice of surgical therapy for shortbowel syndrome is influenced by intestinal remnant length and caliber and the clinical condition of the patient ( Table 78-3 ).[3] Box 78-4 Surgical Strategies for Short-Bowel Syndrome

Preserve and maximize remnant

Avoid resection

Restore continuity

Recruit additional intestine

Improve intestinal function

Relieve obstruction

Taper dilated bowel

Slow intestinal transit

Increase absorptive area

Intestinal lengthening

Intestinal transplantation

Table 78-3 -- Surgical Approach to Short-Bowel Syndrome Intestinal Remnant Clinical Condition Surgical Options Adequate length with Enteral nutrition (remnant Optimize intestinal function, normal diameter >120 cm in adults, >60 recruit additional length cm in children) Adequate length with dilated bowel Bacterial overgrowth, stasis Treat obstruction, intestinal tapering Recruit additional length, reversed intestinal segment, artificial valve, colon interposition Optimize intestinal function

Marginal length with normal Rapid transit, need for diameter (remnant 60-120 parenteral nutrition cm in adults, 30-60 cm in children) Short length with normal diameter (remnant

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78 Short Bowel Syndrome