Nutritional management of short bowel syndrome in adults

Short bowel syndrome (SBS) comprises the sequelae of nutrient, fluid, and weight loss that occurs subsequent to greatly reduced functional surface area of the small intestine. Signs and symptoms of SBS include electrolyte disturbances; deficiencies of calcium, magnesium, zinc, iron, vitamin B12, or fat-soluble vitamin deficiency; malabsorption of carbohydrates, lactose, and protein; metabolic acidosis, gastric acid hypersecretion; formation of cholesterol biliary calculi and renal oxalate calculi; and dehydration, steatorrhea, diarrhea, and weight loss. Thorough nutritional management is the key factor in achieving an optimal outcome in SBS. Total parenteral nutrition is necessary in the early stages, as is replacement of excess fluid and electrolyte losses. Nutritional management of SBS has traditionally been divided into three phases: an acute phase when total parenteral nutrition is usually begun, an adaptation phase, and a maintenance phase. Recommendations regarding the need for parenteral nutrition vary depending on the presence or absence of certain factors: the ileocecal valve, jejunum, and functional colon. Patients with residual small bowel length of 100 cm or less usually require the administration of parenteral nutrition at home with good results. The total parenteral nutrition diet should consist of a majority of calories from fat, followed by protein, and the remaining as carbohydrates. Vitamins, minerals, and trace elements should also be added accordingly. Although total parenteral nutrition is initially necessary, treatment goals should focus on early transition to enteral nutrition followed by oral feeds. Other recent advances in the medical management of SBS include pharmacologic treatment and the use of specific nutrients and growth factors to stimulate intestinal absorption and adaptation. Both animal studies and clinical trials in humans have shown much promise in supplementation with growth factors and hormones. This strategy is likely to play a greater role in the treatment of SBS in the future.     

Nutritional absorption in short bowel syndrome

Eight patients with a short bowel resulting from intestinal resection and clinically stable for at least one year were studied for 10 days. The diet chosen was lactose-free with a low fiber content and contained 22% of total calories as protein, 32% as carbohydrate, and 46% as fat. Total fluid volume was kept constant, and all patients were in positive nitrogen balance. During the 10-day period, blood chemical concentrations, stool, and/or ostomy volume, urine volume, electrolyte excretion, and calorie and divalent cation absorption were measured. In addition it was determined that fluid restriction during meals did not affect these parameters. In these patients the absorptions of fat, carbohydrate, protein, and total calories were 54%, 61%, 81%, and 62%, respectively. Similarly the absorption of the divalent cations, calcium, magnesium, and zinc, were 32%, 34%, and 15%, respectively. We suggest that patients with short bowel syndrome, who have been stable for at least one year and who can tolerate oral diets, do not need to restrict fat or to separate fluids from solids during their meals. Furthermore, they should increase their oral intake to 35–40 kcal/kg ideal body weight in order to counteract their increased losses. The diet should contain 80–100 g protein/day in order to maintain a positive nitrogen balance and a large margin of safety. In addition, these patients may take oral supplementation of calcium, magnesium, and zinc to maintain divalent cation balance.This work was supported by a grant from the Ontario Ministry of Health PR. 228.     

Nutritional support and therapy in the short bowel syndrome

The clinical response of a patient to intestinal resection depends on several factors. With more than 60 to 80 cm of bowel remaining, refeeding usually will be progressive until a full oral diet is reached. The type of diet and vitamin supplements are then prescribed according to the site of resection. In general, the diet should not be restricted in terms of fat. In the case of ileal resection and a preserved colon, a low-oxalate diet should be prescribed along with calcium supplements. These patients may also develop a cholereic diarrhea, depending on the size of the ileal resection. Cholestyramine should then be added. With a very short bowel (less than 60 to 80 cm), parenteral nutrition is started immediately. This type of nutrition may be tapered progressively over a period of time as enteral feeding is gradually increased, according to the amount of residual disease and the rate of adaptation of the intestinal remnant. If patients cannot maintain their nutritional status and also be free of serious diarrhea when on a normal or modified oral or enteral diet, then long-term parenteral nutrition is considered.     

The surgical management of short bowel syndrome

Short bowel syndrome is a clinical entity that results from a diverse group of congenital and acquired conditions in the pediatric population. The pathophysiology of this syndrome is characterized by malabsorption, malnutrition, and metabolic disturbances. The vast majority of children with this condition undergo spontaneous adaptation of the intestinal remnant and achieve enteral nutritional autonomy. However, a small portion of pediatric patients develop intestinal failure and require long-term or permanent dependence on total parenteral nutrition. These children may benefit from surgical interventions that facilitate intestinal adaptation. Such adjunctive procedures facilitate nutrient absorption by improving motility, prolonging intestinal transit, and/or increasing mucosal contact time. In selected patients, this may allow them to be weaned from parenteral nutritional support or to have it discontinued. The purpose of this review is to discuss the various surgical techniques for the management of short bowel syndrome in children, along with their indications, complications, and outcomes.     

Clinical management of patients with short bowel syndrome

Diarrhoea, malabsorption and malnutrition characterise the short bowel syndrome. The underlying gastrointestinal disorders, the types of intestinal resections performed and the subsequent pathophysiological situations are reviewed. Recommended therapeutic measures in the postoperative period as well as in the rehabilitation of patients with short bowel syndrome are discussed in more detail. In the postoperative period, parenteral nutrition is essential followed by an enteral diet to stimulate bowel adaptation, reduce fluid loss and increase nutrient absorption. The final diet should be based on the anatomy of the retained bowel (presence or absence of a colon and ileum). The importance of the colon as a digestive organ in patients with short bowel and the need of a low-oxalate diet are underlined. The possible benefit of new treatment options (glutamine, growth hormone and glucagon-like peptide 2) is discussed. Both typical complications of the short bowel syndrome and management of these complications are presented.     

Advances in the management of short bowel syndrome

Short bowel syndrome (SBS) is the predominant cause of intestinal failure and is thus associated with a high degree of morbidity and mortality. One of the reasons this occurs is the dramatic reduction in nutrient absorptive capacity. Of the many causes of SBS, the most common cause is extensive surgical resection. The impressive ability of the bowel to adapt functionally and morphologically is critical for decreasing morbidity and mortality in these patients. The degree of adaptation is vital in decreasing the dependence on parenteral nutrition (PN) and for improving patient quality of life and long-term outcome. Provision of appropriate and sufficient nutritional and fluid support is essential for the management of these patients. The primary goal is to prevent or eliminate the need for PN. Recent developments have promoted a greater understanding of the process of intestinal adaptation. Various intestinal trophic factors have been recognized. These efforts have led to the early development of hormonal therapy to stimulate intestinal adaptation and enhance intestinal absorption. Intestinal transplantation remains an option for those who have developed life-threatening complications from PN and cannot be managed using more conservative techniques.     

The management of patients with the short bowel syndrome

The surgeon is invariably the primary specialist involved in managing patients with short bowel syndrome. Because of this they will play an important role in co-ordinating the management of these patients. The principal aims at the initial surgery are to preserve life, then to preserve gut length, and maintain its continuity. In the immediate postoperative period, there needs to be a balance between keeping the patient alive through the use of TPN and antisecretory agents and promoting gut adaptation with the use of oral nutrition. If the gut fails to adapt during this period, then the patient may require therapy with more specific agents to promote gut adaptation such as growth factors and glutamine. If following this, the patient still has a short gut syndrome, then the principal options remain either long term TPN, or intestinal transplantation which remains a difficult and challenging procedure with a high mortality and morbidity due to rejection.     

The short bowel syndrome

The authors demonstrate on case-histories their experience with short-loop syndrome which develops after extensive resections of the small intestine. The clinical picture of the syndrome is characterized by diarrhoea, steatorrhoea, maldigestion and malabsorption with loss of body weight. Non-surgical treatment of the syndrome copies its different stages. The objective of conservative therapy is above all to preserve the nutritional integrity of the organism and gradual adaptation of the gut which will make eventually a change to oral intake possible. This adaptation takes 1 to 2 years. Last not least, treatment should eliminate the diarrhoea. The authors demonstrate on examples that properly conducted treatment prevented the development of malnutrition, contrary to another case where the sequelae of surgery were underestimated and the patient developed cachexia and pernicious anaemia.     

Surgical management and autologous intestinal reconstruction in short bowel syndrome

Short bowel syndrome (SBS) is a serious condition with considerable morbidity and mortality. When treatment with parenteral nutrition fails and life-threatening complications occur, autologous intestinal reconstruction (AIR) should be considered before intestinal transplantation (ITx). Single or combined ITx should be reserved for patients with severe liver disease and as last resort in the treatment of SBS. Longitudinal intestinal lengthening and tailoring (LILT) has proven its value in AIR, but its availability depends on the expertise of the surgeons. Serial transverse enteroplasty (STEP) has similar success rates as LILT and fewer patients progress to ITx. STEP is also applicable at small bowel dilatation in ultra-short bowel syndrome. The scope may be widened when duodenal dilatation can be treated as well. Spiral intestinal lengthening and tailoring (SILT) is a promising alternative. More research is needed to confirm these findings. Therefore we suggest an international data registry for all intestinal lengthening procedures.     

Dietary and medical management of short bowel syndrome in adult patients

Resection of the small bowel can lead to malabsorption of fluid, electrolytes, minerals, and other essential nutrients, resulting in malnutrition and dehydration. Individualized and tailored nutritional management for patients with short bowel syndrome (SBS) helps to optimize intestinal absorption, leading to nutritional independence such that a patient can resume as normal a lifestyle as possible. Parenteral nutrition (PN), used to supply the required nutrients following resection, is associated with a number of complications affecting patient morbidity and mortality. Attempts should be made to wean patients from PN to an oral diet as soon as possible. Dietary management is complex and needs to be individualized for each patient on the basis of his or her specific gastrointestinal anatomy, underlying disease, and lifestyle. In addition to nutrient intake, management of SBS also requires appropriate oral rehydration, vitamin and mineral supplementation, and pharmacotherapy. Several medications provide a useful adjunctive function to dietary intervention, including antidiarrheal agents, H2 antagonists and proton pump inhibitors, pancreatic enzymes, somatostatin analogs, antimicrobials, and trophic factors.     

Enhancing bowel adaptation in short bowel syndrome

Malabsorption of both nonessential and essential nutrients, fluid, and electrolytes will, if not compensated for by increased intake, lead to diminished body stores and to subclinical and eventually clinical deficiencies. By definition, intestinal failure prevails when parenteral support is necessary to maintain nutritional equilibrium. After intestinal resection, adaptation, a progressive recovery from the malabsorptive disorder, may be seen. Research has focused on optimizing remnant intestinal function through dietary or pharmacologic interventions. In this review, factors responsible for the morphologic and functional changes in the adaptive processes are described. Results of clinical trials employing either growth hormone and glutamine or glucagon-like peptide-2 in short bowel patients are presented.     

Nutritional therapy of irritable bowel syndrome

Nutritional factors relative to IBS include diagnostic and therapeutic considerations. Etiologically, foods do not cause IBS. A small percentage of patients with childhood allergic diatheses, usually in association with atopic dermatitis and asthma, may be intolerant to one or more of wheat, corn, dairy products, coffee, tea, or citrus fruits. Diagnostically, many patients labeled as IBS subjects are in fact intolerant to the ingestion of lactose-containing foods, sorbitol, fructose, or combinations of fructose and sorbitol. A precise dietary history will characterize this group. Taken in its broadest context, IBS involves the entire hollow tract inclusive of esophagus, stomach, small bowel, and colon. The symptomatic presentation relative to the hollow organ involved allows the selection of dietary manipulations that may help to reduce symptoms. Gastroesophageal reflux, a consequence of low LES pressure in some IBS patients, may be treated with the elimination of fatty foods, alcohol, chocolate, and peppermint. Delayed gastric emptying may be helped by the elimination of fatty foods and reduction of soluble fiber. Aberrant small bowel motor function may be ameliorated by reduction of lactose, sorbitol, and fructose and the addition of soluble fiber. Gas syndromes may be improved by reduced intake of beans, cabbage, lentils, legumes, apples, grapes, and raisins. Colonic motor dysfunction may be overcome by the gradual addition of combinations of soluble and insoluble fiber-containing foods and supplements. The selective use of activated charcoal and simethicone may be helpful.     

Nutritional management of inflammatory bowel disease

Nutritional deficits commonly occur in patients of all ages suffering from chronic inflammatory bowel diseases. Growth failure represents a common, serious complication unique to the pediatric age group. Although the etiology of nutritional problems and growth failure is multifactorial, malnutrition owing to inadequate nutrient intake is the primary cause. Nutritional supplementation via the enteral or parenteral route restores normal body composition and can reverse linear and ponderal growth failure if administered effectively and prior to bone maturation. Both parenteral and enteral nutrition have been shown to effectively induce remission in acute Crohn's disease, but appear to be less satisfactory for patients with ulcerative or Crohn's colitis. The mechanisms by which such nutritional therapies improve disease activity are unclear but may involve the intestinal adaptive response to "bowel rest," immunologic effects, and nutritional factors.     

Fecal lactate and short bowel syndrome

In patients with short bowel syndrome (SBS), the carbohydrate overload to the colon may disturb the normal pattern of colonic fermentation with production ofd-lactic acid and subsequent development of a metabolicd-lactic acidosis. We measuredd-lactic acid in blood, urine, and feces, as well as the composition of fecal water and fecal reducing substances from 11 patients with SBS, comparing the results with those from normal subjects. The fecal water from patients with SBS was characterized by low pH, potassium, and volatile fatty acids, high osmotic gap, and high concentration ofl- andd-lactic acid. Five of 11 had abnormal amounts of fecal reducing substances. Fecald-lactic acid was increased in nine of 11 patients. However, none of these patients showedd-lactic acid in urine, and only one had a very low concentration in plasma. These results show thatd-lactic acid was overproduced in the colon of most of the patients with SBS. However, other factors such as absorption or impairedd-lactic acid metabolism may be necessary for a plasmatic increase ofd-lactic acid.Unidad de Terapia Nutricional, Hospital de Niños Sor Maria Ludovica, La Plata, Provincia de Buenos Aires, Argentina.Part of this work was presented at the International Symposium on Short Chain Fatty Acids, Strasbourg, France, September 1993.     

Intestinal microbiota in short bowel syndrome

Short bowel syndrome (SBS) is the main cause of intestinal failure especially in children. The colon is a crucial partner for small intestine adaptation and function in patients who have undergone extensive small bowel resection. However, SBS predisposes the patient to small intestine bacterial overgrowth (SIBO), explaining its high prevalence in patients with this disorder. SIBO may significantly compromise digestive and absorptive functions and may delay or prevent weaning from total parenteral nutrition (TPN). Moreover, SIBO may be one of the causes of intestinal failure-associated liver disease, requiring liver transplantation in some cases. Traditional tests for assessing SIBO may be unreliable in SBS patients. Management of SIBO with antibiotic therapy as a first-line approach remains a matter of debate, while other approaches, including probiotics, offer potential based on experimental evidence, though only few data from human studies are available.     

人小肠移植术后的营养支持

目的探讨肠内外营养在移植肠功能恢复中的意义．方法研究对象为１例小肠移植患者，分别于术后２ｄ和４ｄ开始肠外及肠内营养，术后１００ｄ停止静脉营养，口服饮食维持营养．观察术后营养支持的全过程，通过Ｄ＿木糖吸收试验，氮平衡计算以及钡餐检查监测移植肠功能；通过测定体重及血清白蛋白水平监测营养状况．结果该患者营养维持良好，移植肠结构与功能恢复正常．受体体重及血清白蛋白维持于正常水平．结论合理的肠内外营养支持有利于移植肠功能的恢复．     

Surgical therapy of the short bowel syndrome

Patients with the short bowel syndrome should be managed initially by giving total parenteral nutrition and by maximizing the function of the remaining intestine. Enteral feedings should be instituted as soon as the patient stabilizes, usually after 2 to 4 weeks. The gastric hypersecretion that accompanies the syndrome can usually be controlled with an H2-receptor blocker. In those patients who fail to recover adequate digestion and absorption after 6 months to 1 year, operations to improve absorption should be considered. The reversed intestinal segment and the intestinal lengthening procedures are most often employed, but neither type of operation can be recommended without reservation. Newer procedures, such as growing new intestinal mucosa on serosal patches, intestinal pacing, and intestinal transplantation may play a role in future therapies. At present, long-term parenteral nutrition remains the cornerstone of therapy.     

An open trial of octreotide long-acting release in the management of short bowel syndrome

OBJECTIVES: The aim of this study was to assess the effects of the long-acting release (LAR) depot octreotide preparation Sandostatin LAR Depot on stool water and electrolyte losses, fecal fat excretion, and GI transit in patients with short bowel syndrome. METHODS: We performed a 15-wk, prospective, open-label study of intramuscular (i.m.) Sandostatin LAR Depot, 20 mg, at 0, 3, 7, and 11 wk. Balance studies were performed before and at the end of the 15-wk study. Baseline and posttreatment measurements of body weight, stool fat, sodium and potassium, and gastric and small bowel transit of a radiolabeled egg meal were compared by paired analysis. RESULTS: We studied eight patients with short bowel syndrome (five women and three men; mean age 52 yr, range 37-72 yr) who had been TPN dependent for a mean of 11.8 yr (range 1.5-22 yr). The underlying diagnoses were Crohn's disease (n = 6), intestinal ischemia (n = 1), and resection for carcinoid tumor (n = 1). Treatment with Sandostatin LAR Depot significantly increased small bowel transit time (p = 0.03). Changes in body weight, urine volume, stool weight, fecal fat excretion, stool sodium and potassium excretion, or gastric emptying rate were highly variable, and no overall significance was observed. CONCLUSIONS: Sandostatin LAR Depot for 15 wk significantly prolonged small bowel transit time. Body weight and stool parameters in response to Sandostatin LAR Depot treatment needs to be assessed further in multicenter studies assessing dose, frequency of administration, and a larger sample size.