eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology
Short Bowel Syndrome: Treatment & Medication
Updated: Apr 15, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
The management of short bowel syndrome (SBS) requires an aggressive multidisciplinary approach that is most often tailored to the individual needs of the patient. Nutrition plays an important role in the management of short bowel syndrome. The institution of early and aggressive enteral therapy is the most important stimulus for intestinal adaptation and the eventual discontinuation of parenteral therapy.
Parenteral nutrition
The length and function of the remaining intestine and the presence of normal physiologic mechanisms that regulate intestinal transit time, including the ileocecal valve and colon, determine whether the patient requires a limited course of specialized enteral therapy or prolonged total parenteral nutrition (TPN).
In 1991, Goulet et al studied the relative importance of several clinical factors in predicting the long-term needs for parenteral nutrition.4 In 54 neonates who underwent extensive small-bowel resection, the presence of less than 40 cm of small intestine in children with either colonic resection or an absent ileocecal valve had a strong association with a prolonged need for parenteral nutrition (>48 mo).
Although this has been the experience at most pediatric tertiary care centers that care for children with short bowel syndrome, the authors' collective experience at The Johns Hopkins Children’s Center suggests that, with aggressive introduction of continuous modular enteral feeds and selective weaning of protein and fats from the parenteral nutrition, children with extensive small bowel resection may be salvaged sooner and weaned off of parenteral nutritional support. The ultimate goal is avoiding the need for either liver or multivisceral transplantation.
In addition, the health of the remaining bowel, its absorptive capacity, and its ability to adapt are important. For example, the motility of the existing small bowel may have been affected by the patient's primary illness leading to short bowel syndrome. Indeed, patients who experience severe intestinal ischemia may be left with small-bowel dysmotility, rendering patients susceptible to bacterial overgrowth.5 Another example is patients with Crohn disease who have undergone repeated small-bowel resections for fibrostenotic disease. Postsurgery, these patients may have repeated exacerbations of their disease that may injure the existing small bowel, thereby affecting its absorptive capacity.
Excessive fluid losses
Massive fluid and electrolyte losses are usually observed during the first week after excessive intestinal resection. Patients with short bowel syndrome most often require aggressive resuscitation with fluids or parenteral nutrition, or both. Instituting enteral therapy as soon as possible is very important in order to facilitate the adaptive intestinal response.
In the early postoperative period, monitor serum electrolytes and a comprehensive biochemical pattern daily. When these values have stabilized, monitor them on a biweekly or triweekly basis. The hypersecretion noted within the first 12 months postresection is usually treated with histamine 2 (H2)–receptor antagonists or proton pump inhibitors.
The provision of adequate parenteral fluid replacement needs may be ongoing depending on the amount of stool or ostomy output. Indeed, enteral nutrition can cause significant osmotic diarrhea.
Malabsorption
Extensive jejunal resection leads to carbohydrate malabsorption. The undigested foods produce an osmotic diarrhea typical of most patients with short bowel syndrome. The proximal small bowel is also important in the absorption of proteins, fat, and certain micronutrients, including copper.
Extensive resection of the ileum may lead to severe malabsorption of bile salt and vitamin B-12. Bile salt malabsorption produces a choleretic diarrhea. Furthermore, bile salt depletion affects fat absorption, thereby worsening steatorrhea and fat-soluble vitamin malabsorption. Ileal resection leads to the malabsorption of bile salts and an abnormal bile acid pool that leads to the formation of a lithogenic bile and cholelithiasis.
The ileocecal valve is important in preventing bacterial overgrowth. Problems associated with proximal small-bowel overgrowth include deconjugation of bile salts and depletion of bile salt stores. Bacteria often compete for vitamin B-12, which may facilitate a pernicious anemia. Bacteria overgrowth also leads to carbohydrate malabsorption, worsening of osmotic diarrhea, and increased risk of metabolic acidosis and dehydration. Treatment is generally aimed at lessening the degree of bacterial overgrowth with antibiotic therapy, including administration of metronidazole alternating with either kanamycin or oral gentamicin.
Motility disturbances
Patients with short bowel syndrome have a decrease in intestinal transit time. Patients with extensive proximal small-bowel resection have increased gastric emptying, thereby further decreasing intestinal transit time.
The absence of normal physiologic mechanisms that increase intestinal transit, including the ileocecal valve and colon, also shortens intestinal transit time. However, if the existing small bowel or colon shows signs of dysmotility due to fibrosis or surgical narrowing, stagnant bowel contents may aggravate an existing bacterial overgrowth, thereby worsening malabsorption and diarrhea.
Small-bowel overgrowth also leads to d-lactic acidosis and may be associated with CNS disturbances. Antibiotics are used to prevent small bowel overgrowth and should be cycled on a weekly or biweekly basis. Numerous potential antibiotic therapies can be used. At the Johns Hopkins Children’s Center, metronidazole, kanamycin, nitazoxanide and rifaximin are the preferred therapies used in managing patients with small bowel bacterial overgrowth.
Short bowel syndrome associated colitis is not an infrequent complication. Patients often present with hematochezia and have histologic signs of colitis on intestinal biopsies.
In patients where the colon is not removed, histological signs of colonic mucosal hypertrophy that serves to increase colonic fluid and electrolyte absorption are noted. Studies have shown that these adaptive responses may actually be hormonally mediated by various growth factors, including glucagonlike polypeptides. Although a functional colon is always preferred in short bowel syndrome, patients who exhibit colonic dysmotility may generally achieve a more rapid advancement with enteral feeds with a diversion proximal colostomy. The authors' experience at The Johns Hopkins Children’s Center has shown that prokinetic agents such as erythromycin and raglan have limited efficacy in improving residual bowel function, especially in patients with significant small and large bowel dysmotility.
Among patients with significant dysmotility issues, the authors' experience has shown that a diverting ileostomy can be used to prevent the stagnation of stool. By establishing a good flow of stool, enteral feeds are allowed to continue and be maximized. Rectal tubes can also be used to facilitate the flow of stool, albeit somewhat problematic in the older child. Among those children that a rectal tube is only partially effective, a diversion ileostomy can be performed.
Patients with ongoing issues of dysmotility should have a small bowel enema performed to rule-out intestinal strictures. Those lesions should be dealt with by surgery. Furthermore, proximal GI issues, including gastroparesis can be medically treated; however, the authors' experience has shown that among the most refractory cases that postpyloric feeding tubes are required.
Gastric acid hypersecretion
Gastric acid hypersecretion is common in patients with short bowel syndrome. The degree of hypersecretion is proportional to the degree of bowel resected. Hypersecretion may contribute to malabsorption by inactivating pancreatic enzymes and, thus, interfering with fat absorption. The usual treatment is with H2 blockers.6
Although the usual treatment is with H2 blockers, the availability of proton pump inhibitors especially in pharmacological forms conducive to the needs of children with enteral feeding tubes has now been the treatment therapy of choice in managing children with short bowel syndrome and gastric acid hypersecretion.
Medical therapies
Codeine and loperamide can be used in pediatric patients to slow intestinal transit time; however, results have been mixed because of concerns for worsening of bacterial overgrowth. Octreotide is rarely used to limit the amount of intestinal losses after bowel resection. Its use in pediatric patients is controversial because of concerns of the effect on growth and worsening cholestatic liver disease. Cholestyramine has been used as a means of binding bile salts in patients with choleretic diarrhea. Antibiotics are sparingly used to prevent small-bowel overgrowth.
Children, especially young infants, also have a greater capacity to adapt than adults in response to massive small bowel resection. Numerous physiological responses to short bowel syndrome are observed. Although the small intestine is unable to extend itself in length, it does have the capacity to hypertrophy by increasing the number and size of intestinal villi, as well as crypt depth. All these adaptive functions are important in increasing intestine’s absorptive surface area by increasing mucosal mass.
Several mechanisms are involved in stimulating mucosal hypertrophy, including hormones secreted by the small bowel on exposure to intraluminal nutrients, as well as intestinal growth factors produced by both the pancreas and biliary system. Intestinal growth factors, including glucagonlike peptide and other proglucagon-derived peptides produced by the epithelium have been shown to stimulate intestinal growth and adaptation. Similarly, nonGI hormones (eg, cortisol, thyroxin) may also be involved. Mucosal hyperplasia also depends on exposure to intraluminal contents. Certain dietary components have a trophic influence on the intestinal mucosa; thus, an aggressive provision of enteral nutrition can be regarded as an important therapeutic tool in allowing for intestinal adaptation.
Glutamine is an important fuel for the intestinal mucosa and has been shown to stimulate mucosal growth. However, most clinical trials have not shown any selective advantage with the supplementation of children with short bowel syndrome with pharmacological doses of glutamine. The same can also be said with the supplementation of pharmacological doses of cholecystokinin.
An uncontrolled clinical trial using intravenous cholecystokinin in patients with short bowel syndrome and cholestasis did not show any added therapeutic benefit. The authors are also in the process of investigating the usefulness of choline therapy. The authors' experience has shown that the best way of managing cholestasis is usually through aggressive weaning of parenteral nutritional therapy because patients with short bowel syndrome show improved tolerance of enteral feeds. If parenteral nutrition cannot be entirely weaned, the authors tend to selectively eliminate amino acid and fat supplementation, assuming that the patient’s nitrogen balance and caloric needs are being met through enteral nutrition.
Surgical Care
Surgical care is related to venous access (ie, central line placement to provide TPN). The loss of intravenous access through repeated episodes of sepsis and thrombosis can lead to the early need for intestinal transplantation despite good hepatic function. Surgery may be required for gastrostomy tube placement to provide for enteral access.
Intestinal lengthening procedures and transplantation are always avoided if at all possible. Several attempts at increasing bowel length through surgical means have been made over the last decade. The bowel is transected longitudinally to preserve the blood supply. The largest experience comes from the University of Nebraska. In this experience, surgical intervention improved intestinal adaptability and weaning from parenteral nutrition in a dozen patients. However, with repeated surgical interventions, the risk of intestinal stricture formation increases, as well as the risk of small-bowel obstruction secondary to adhesion formation.
Small-bowel transplantation has shown mixed success. The problems associated with transplantation, including the need for immunosuppression and the risk for intestinal rejection and lymphoproliferative disease, has limited this treatment option for most patients with short bowel syndrome unless absolutely necessary in patients with associated severe advanced liver disease and those with major vascular access problems. Isolated orthotopic liver transplantation without small-bowel transplantation has been demonstrated to be effective.
Consultations
The authors' experience has also shown that most catheter infections can be managed on an out-patient basis. With a robust nursing home support mechanism, most infections, including fungal infections can be managed effectively at home. This clinical approach requires a committed family willing to take on this responsibility in administering intravenous antibiotics and a specialized medical support system that sustains an optimized level of communication with the family, especially during the weekends and evenings. When sepsis is present with no identifiable bacterial source, the aid of an infectious disease specialist may be requested.
In addition to consultation with a gastroenterologist, in the setting of fungemia, consulting an infectious disease specialist to guide antifungal therapy is best and, in the setting of liver or intestinal failure, consult a transplant surgeon.
Diet
Enteral therapy
In infants with massive small-bowel resection, enteral nutrition is initiated very quickly by using elemental formulas. The mixture of monosaccharides and polysaccharides is preferred to disaccharides in order to limit osmotic load, in combination with long-chain triglycerides (LCT) and medium-chain triglycerides (MCT). The authors favor starting with formulas that are either one-fourth or one-half strength, depending on the patient's tolerability, and increasing in volume before increasing energy density. Oligopeptide formulas are better absorbed than elemental amino acid formulas because di-tripeptide absorption exceeds that of amino acids.
MCTs are important in the dietary management of patients with short bowel syndrome because they are readily absorbed in the stomach and proximal small bowel, thereby improving fat and total energy absorption. Current recommendations are to use MCTs as the main source of fat and energy needs. Long-chain fatty acids are required to prevent essential fatty acid deficiency and should make up approximately 10% of the patient's energy needs. Long-chain fatty acids may have a trophic effect on the intestinal mucosa.
The question of fat intolerance has always been a point of contention; however, the use of long-chain fats, which have increased energy density, is usually better tolerated than use of carbohydrates. Testing the tolerability of either fats or carbohydrates and adjusting the modular formula accordingly is advisable. In some cases, providing carbohydrates parenterally and providing fats enterally is preferred in order to improve a patient's tolerance. The use of continuous enteral feeds is better tolerated than bolus feeds in patients with small-bowel resection. An increase in stool output with the appearance of fecal-reducing substances is an indication that the patient may have reached the tolerance limit.
Enteral nutrition remains the lone medical therapy that can facilitate intestinal adaptation. The residual bowel must be constantly exposed to nutrients in order to allow the bowel to adapt. Hence, the physician must be able to allow for substantial stool volume and frequency, as long as it does not compromise the child's hydration, acid base balance, and serum electrolyte levels. A common mistake is the tendency to either stop enteral feeds or substantially lower the volume and frequency of feeds in response to changes in stool volume. Most fluid and electrolyte perturbations that result from short bowel syndrome, or in response to modifications in enteral nutritional therapy, can be easily compensated through an adjustment in the parenteral formula. If possible, the physician should avoid altering the rate or the concentration of the enteral formula too aggressively, in order to allow the adaptive process to proceed.
Many animal models have shown that the bowel is very sensitive to starvation. In the absence of enteral nutrition, the crypt cell population decreases and epithelial cell cycle increases, thereby decreasing the proliferation of the intestinal epithelium. In contrast, in response to a continual and large supply of enteral nutrients, crypt cells proliferate, leading to an increase in crypt depth and lengthening of the intestinal villi. An increase in the absorptive area does not always coincide with functional adaptation.
The production of digestive enzymes and nutrient receptors is in direct response to the quality and quantity of intestinal nutrients. The physician must ensure a constant provision of macronutrients, in order to facilitate this adaptive process. The adaptive process may, in large part, also depend on the production of trophic intestinal hormone and secretions that are produced in response to nutritional therapy.
In a healthy individual, other than fluid and calcium absorption, the colon has a limited absorptive capacity; however, in patients with short bowel syndrome, the colon may assume an increased nutritional role. The colonic flora is capable of metabolizing nonabsorbed starch and fiber into the production of short-chain fatty acids. These short-chain fatty acids are regarded as the preferred fuel for the colon and may actually stimulate water absorption. Therefore, the residual colon may provide an opportunity to improve water absorption in patients with short bowel syndrome.
Decreasing the amount of carbohydrates within the enteral feeds and decreasing the volume and concentration of feeds help manage the problems with excessive stool volume and abdominal distension in the setting of significant malabsorption. The addition of fiber can also increase stool frequency. Decreasing either the volume or rate of feeds may treat patients with gastroesophageal reflux and vomiting. The advancement of enteral feeds is based on the patient's tolerance.
Parenteral therapy
Provide parenteral nutrition to patients with massive intestinal resections as soon as possible. Increase parenteral nutrition accordingly, based on the patient's tolerance level. Before the availability of parenteral nutrition, most patients with short bowel syndrome died. The dramatic improvement in patient survival primarily is because of advances in parenteral nutrition. Today, survival has been shown in patients with as little as 11 cm of proximal small bowel and an ileocecal valve to as little as 25 cm of small bowel without an ileocecal valve. Anecdotal reports of children surviving with as little as 12 cm of bowel without an ileocecal valve are also noted. The clinical factors that are associated with prolonged (>2 y) parenteral nutritional requirements include the following:
- Residual bowel
- Limited absorptive function
- Bowel adaptation (ileum has greater adaptability than jejunum)
- Dysmotility
- Bowel length (<40 cm)
- Absent ileocecal valve
- Colon resection
- Bacterial overgrowth
Several strategies have been proven to improve a patient's tolerance of parenteral nutrition in the setting of short bowel syndrome, including limiting the amount of toxic amino acids administered parenterally and providing protein requirements enterally with specialized infant amino acid formulas. Similarly, because enteral feeds are known to facilitate bile flow, the initiation and progression of enteral feeds may actually prevent cholestasis. Choleretic agents, such as phenobarbital and ursodeoxycholic acid, have also been shown to help treat cholestatic liver disease. Patients on long-term parenteral nutrition are at risk for central intravenous catheter infection and sepsis. Patients require aggressive home care nursing and the outpatient execution of investigations, including hematologic, biochemical, and microbiologic testing.
Moreover, these patients are at risk for intestinal bacterial translocation. Approximately 20% of all central venous catheters are removed secondary to recurrent infection. In the author's experience at the Johns Hopkins Hospital, approximately 90% of central venous catheter infections can be cleared with antibiotics alone. The role of prophylactic antibiotic therapy is controversial.
Specific nutrient requirements
Multivitamins and minerals are preferentially administered parenterally in patients with extensive small-bowel resections. In the presence of significant steatorrhea, water-soluble forms of vitamin A, vitamin E, and vitamin D are available commercially. Because calcium supplementation is important in the setting of vitamin D deficiency and malabsorption, provide supplementation enterally in order to allow for bone mineralization and growth. Regularly monitor serum calcium. Dual energy x-ray absorptiometry (DEXA) scanning may be used to monitor bone density. Because enteric bacteria synthesize vitamin K, supplementation is not necessary but can be monitored with the measurement of prothrombin time. The deficiency of water-soluble vitamins is rare.
Vitamin B-12 can be administered parenterally on a monthly basis as needed in patients with extensive ileal resections. It is also available as a nasal gel. Patients with iron deficiency secondary to either bacterial overgrowth or malabsorption should be monitored carefully and can be supplemented with intravenous iron infusions. Zinc supplements are often needed secondary to increased fecal losses. In individuals who are not on parenteral nutrition, zinc supplements can be provided in tablet form. Other micronutrients, including manganese and selenium, can be provided in pharmacologic doses as required. Although copper deficiency is rare, deficiency has been associated with anemia and cardiomyopathy. Periodic measurements of copper and selenium are merited for individuals on long-term parenteral nutrition.
Outcome
The successful nutritional management of patients with short bowel syndrome has increased long-term survival rates. The complex pathophysiology of short bowel syndrome often requires a multidisciplinary approach to patient management. Additional experience with adjunct medical and surgical therapies will potentially expand existing treatment options, thereby improving patient survival and precluding potential complications associated with long-term parenteral nutrition support.
Medication
Antibiotics
These agents are used sparingly to prevent small-bowel bacterial overgrowth. They are used on a biweekly basis to prevent bacterial resistance.
Metronidazole (Flagyl)
Used to prevent intestinal small-bowel bacterial overgrowth.
Adult
250 mg PO tid
Pediatric
15 mg/kg/d PO divided tid
May increase toxicity of anticoagulants, lithium, and phenytoin; cimetidine may increase toxicity of metronidazole; disulfiram reaction may occur with PO-ingested ethanol; phenobarbital and rifampin may increase metabolism of metronidazole
Documented hypersensitivity; renal failure (CrCl <10 mL/min)
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Contraindicated in the first trimester of pregnancy; adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy
Gentamicin (Garamycin, Gentacidin)
Aminoglycoside antibiotic for gram-negative coverage. May be used to prevent bacterial overgrowth in children with SBS.
Consider if penicillins or other less toxic drugs are contraindicated.
Gentamicin works well when administered PO to prevent intestinal overgrowth.
Drug interactions and precautions are likely to be clinically insignificant because PO gentamicin has minimal systemic absorption.
Adult
6-7.5 mg/kg/d PO divided q8h; not to exceed 300 mg/d
Pediatric
2.5 mg/kg/dose PO tid; not to exceed 300 mg/d
Coadministration with other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; aminoglycosides enhance effects of neuromuscular blocking agents, thus prolonged respiratory depression may occur; coadministration with loop diuretics may increase auditory toxicity of aminoglycosides; possible irreversible hearing loss of varying degrees may occur
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Narrow therapeutic index (not intended for long-term therapy); caution in renal failure (patient not on dialysis), myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust dose in renal impairment
H2 blockers
This agent is one of two treatment modalities used for gastric acid hypersecretion.
Ranitidine (Zantac)
Inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which in turn reduces gastric acid secretion, gastric volume, and hydrogen concentrations.
Adult
150 mg PO bid; not to exceed 600 mg/d
50 mg/dose IV/IM q6-8h
Pediatric
4-5 mg/kg/d PO divided bid; not to exceed 300 mg/d
0.75-1.5 mg/kg/dose IV/IM q6-8h; not to exceed 400 mg/d
Inhibits CYP450 3A4 and 2D6; may decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment; may increase risk of necrotizing enterocolitis in premature infants
Proton pump inhibitors
This agent is one of two treatment modalities used for gastric acid hypersecretion.
Omeprazole (Prilosec)
Decreases gastric acid secretion by inhibiting parietal cell H+/K+ -ATP pump.
Adult
20-40 mg PO qd
Pediatric
0.7-3.3 mg/kg/d PO; not to exceed 40 mg/d
May decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Bioavailability may increase in elderly patients
Choleretic agents
These agents improve biliary flow and prevent total parenteral nutrition (TPN)-induced liver disease.
Ursodiol (Actigall, Urso)
Also called ursodeoxycholic acid. Improves bile acid–dependent bile flow.
Adult
250-300 mg PO bid
Pediatric
8-10 mg/kg/d PO divided bid; not to exceed 300 mg/d
Decreased effect with aluminum-containing antacids, cholestyramine, colestipol, clofibrate, and PO contraceptives
Documented hypersensitivity; calcified cholesterol stones; radiopaque stones; bile pigment stones
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Diarrhea is a rare problem
Phenobarbital (Barbita, Luminal, Solfoton)
Improves bile acid–independent flow.
Adult
90-180 mg/d PO qd or as 2-3 divided doses; not to exceed 400 mg/24h
Pediatric
3-8 mg/kg/d PO divided bid-tid
May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol, valproic acid, and MAOIs may increase phenobarbital toxicity; rifampin may decrease phenobarbital effects; induction of microsomal enzymes may result in decreased effects of PO contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy; menstrual irregularities may also occur)
Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritis
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; caution in myasthenia gravis and myxedema
Bile salt binders
These agents decrease choleretic diarrhea.
Cholestyramine (Prevalite, Questran)
Forms a nonabsorbable complex with bile acids in the intestine, which in turn inhibits enterohepatic reuptake of intestinal bile salts. Effective in reducing the choleretic diarrhea in patients with SBS.
Adult
4 g PO qd/bid; not to exceed 24 g/d or 6 doses/d
Pediatric
240 mg/kg/d PO divided tid; mix with 240 mL of water or juice immediately before consuming
Inhibits absorption of numerous drugs, including warfarin, thyroid hormone, amiodarone, NSAIDs, methotrexate, digitalis glycosides, glipizide, phenytoin, imipramine, niacin, methyldopa, tetracyclines, clofibrate, hydrocortisone, and penicillin G
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in constipation and phenylketonuria
Antisecretin agents
These agents decrease intestinal secretions.
Octreotide (Sandostatin)
Acts primarily on somatostatin receptor subtypes II and V. Inhibits GH secretion and has multitude of other endocrine and nonendocrine effects, including inhibition of glucagon, VIP, and GI peptides.
Adult
50 mcg SC tid initially; may increase dose to 500 mcg tid
Doses of 300-600 mcg/d or higher seldom result in additional biochemical benefit
Pediatric
1-10 mcg/kg/d IV/SC; not to exceed 1500 mcg/d
May reduce effects of cyclosporine; patients on insulin, PO hypoglycemics, beta-blockers, and calcium channel blockers may need dosage adjustments
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Adverse effects are primarily related to altered GI motility and include nausea, abdominal pain, diarrhea, and increased incidence of gallstones and biliary sludge; because of alteration in counterregulatory hormones (ie, insulin, glucagon, GH), hypoglycemia or hyperglycemia may be observed; bradycardia, cardiac conduction abnormalities, and arrhythmias have been reported; because of inhibition of TSH secretion, hypothyroidism may also occur; exercise caution in patients with renal impairment; cholelithiasis may occur
Hypomotility agents
These agents increase intestinal transit time.
Loperamide (Imodium, Kaopectate)
Acts on intestinal muscles to inhibit peristalsis and slow intestinal motility. Prolongs movement of electrolytes and fluid through bowel and increases viscosity and loss of fluids and electrolytes.
Adult
4 mg PO initially, then 2 mg after each loose stool up to 16 mg/d
Pediatric
Initial doses:
2-5 years: 1 mg PO tid
6-8 years: 2 mg PO bid
9-12 years: 2 mg PO tid
In addition to the initial doses, 0.1 mg/kg PO may be given after each loose stool; not to exceed initial dose
Chronic diarrhea: 0.08-0.24 mg/kg/d PO divided bid/tid; not to exceed 2 mg/dose
Phenothiazines, tricyclic antidepressants, and CNS depressants may increase loperamide toxicity
Documented hypersensitivity; diarrhea resulting from infections; pseudomembranous colitis
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Discontinue use if no clinical improvement occurs in 48 h; because loperamide is primarily metabolized in liver, monitor for CNS toxicity in patients with hepatic insufficiency; do not use medication if high fever or blood in stool coincides with diarrhea
Fat-soluble vitamins
These agents supplement fat-soluble vitamins A, D, E, and K.
Vitamins A, D, E, K (ADEKs Pediatric Drops, Sunkist Multi-Vitamins, Centrum)
Vitamin supplementation in patients with malabsorption. Available in various formulations in multivitamins. Check label for precise ingredients.
Adult
2 tab PO qd
Pediatric
0-1 year: 1 mL PO qd
1-3 years: 2 mL PO qd
4-10 years: 1 tab PO qd
Colestipol, cholestyramine, or mineral oil may decrease absorption; vitamin E delays absorption of iron and increases effects of anticoagulants; thiazide diuretics may increase effects of vitamin D; PO anticoagulants effect antagonized by vitamin K
Documented hypersensitivity
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Pregnancy category C if dose exceeds RDA; vitamin E may induce vitamin K deficiency; necrotizing enterocolitis may occur when large doses of vitamin E are given; caution with large doses of vitamin A in patients with renal or hepatic impairment, large doses may cause toxicity; vitamin A may cause orange stools and cause diarrhea or loose stools at onset of therapy
More on Short Bowel Syndrome |
| Overview: Short Bowel Syndrome |
| Differential Diagnoses & Workup: Short Bowel Syndrome |
 Treatment & Medication: Short Bowel Syndrome |
| Follow-up: Short Bowel Syndrome |
| Multimedia: Short Bowel Syndrome |
| References |
| « Previous Page | Next Page » |
References
Goday PS. Short bowel syndrome: how short is too short?. Clin Perinatol. Mar 2009;36(1):101-10. [Medline].
Cole CR, Hansen NI, Higgins RD, Ziegler TR, Stoll BJ. Very low birth weight preterm infants with surgical short bowel syndrome: incidence, morbidity and mortality, and growth outcomes at 18 to 22 months. Pediatrics. Sep 2008;122(3):e573-82. [Medline].
Seres D, Sacks GS, Pedersen CA, et al. Parenteral nutrition safe practices: results of the 2003 American Society for Parenteral and Enteral Nutrition survey. JPEN J Parenter Enteral Nutr. May-Jun 2006;30(3):259-65. [Medline].
Goulet OJ, Revillon Y, Jan D, et al. Neonatal short bowel syndrome. J Pediatr. Jul 1991;119(1 ( Pt 1)):18-23. [Medline].
Cole CR, Ziegler TR. Small bowel bacterial overgrowth: a negative factor in gut adaptation in pediatric SBS. Curr Gastroenterol Rep. Dec 2007;9(6):456-62. [Medline].
Jeppesen PB, Staun M, Tjellesen L, Mortensen PB. Effect of intravenous ranitidine and omeprazole on intestinal absorption of water, sodium, and macronutrients in patients with intestinal resection. Gut. Dec 1998;43(6):763-9. [Medline].
Ascher DP, Shoupe BA, Maybee D, Fischer GW. Persistent catheter-related bacteremia: clearance with antibiotics and urokinase. J Pediatr Surg. Apr 1993;28(4):627-9. [Medline].
Bernard DK, Shaw MJ. Principles of nutrition therapy for short-bowel syndrome. Nutr Clin Pract. Aug 1993;8(4):153-62. [Medline].
Bloom SR. Gut hormones in adaptation. Gut. 1987;28 Suppl:31-5. [Medline].
Buchman AL. The clinical management of short bowel syndrome: steps to avoid parenteral nutrition. Nutrition. Oct 1997;13(10):907-13. [Medline].
Byrne TA, Persinger RL, Young LS, et al. A new treatment for patients with short-bowel syndrome. Growth hormone, glutamine, and a modified diet. Ann Surg. Sep 1995;222(3):243-54; discussion 254-5. [Medline].
Capron JP, Gineston JL, Herve MA, Braillon A. Metronidazole in prevention of cholestasis associated with total parenteral nutrition. Lancet. Feb 26 1983;1(8322):446-7. [Medline].
Cosnes L, Carbonnel F, Beaugerie L. Functional adaptation after extensive small bowel resection in humans. Eur J Gastroenterol Hepatol. 1994;6:197.
Cummings JH. Colonic absorption: the importance of short chain fatty acids in man. Scand J Gastroenterol Suppl. 1984;93:89-99. [Medline].
Dudrick SJ, Latifi R, Fosnocht DE. Management of the short-bowel syndrome. Surg Clin North Am. Jun 1991;71(3):625-43. [Medline].
Fine H, Levine GM, Shiau YF. Effects of cholecystokinin and secretin on intestinal structure and function. Am J Physiol. Sep 1983;245(3):G358-63. [Medline].
Fordtran JS, Dietschy JM. Water and electrolyte movement in the intestine. Gastroenterology. Feb 1966;50(2):263-85. [Medline].
Gazet JC, Kopp J. The surgical significance of the ileocecal junction. Surgery. 1964;56:565-73.
Grant D. Current results of intestinal transplantation. The International Intestinal Transplant Registry. Lancet. Jun 29 1996;347(9018):1801-3. [Medline].
Grosfeld JL, Rescorla FJ, West KW. Short bowel syndrome in infancy and childhood. Analysis of survival in 60 patients. Am J Surg. Jan 1986;151(1):41-6. [Medline].
Hays TL, Saavedra JM, Mattis LE. The use of high-fat low-carbohydrate diets for advancement of enteral feedings in children with short bowel syndrome. Top Clin Nutr. 1995;10(4):35-41.
Hofmann AF, Poley JR. Role of bile acid malabsorption in pathogenesis of diarrhea and steatorrhea in patients with ileal resection. I. Response to cholestyramine or replacement of dietary long chain triglyceride by medium chain triglyceride. Gastroenterology. May 1972;62(5):918-34. [Medline].
Hwang TL, O'Dwyer ST, Smith RJ. Preservation of small bowel mucosa using glutamine enriched parenteral nutrition. Surg Forum. 1986;37:56-8.
Hylander E, Ladefoged K, Jarnum S. Calcium absorption after intestinal resection. The importance of a preserved colon. Scand J Gastroenterol. Jul 1990;25(7):705-10. [Medline].
Hyman PE, Everett SL, Harada T. Gastric acid hypersecretion in short bowel syndrome in infants: association with extent of resection and enteral feeding. J Pediatr Gastroenterol Nutr. Mar-Apr 1986;5(2):191-7. [Medline].
Jeejeebhoy KN. Therapy of the short-gut syndrome. Lancet. Jun 25 1983;1(8339):1427-30. [Medline].
Klish WJ, Putnam TC. The short gut. Am J Dis Child. Nov 1981;135(11):1056-61. [Medline].
Langnas AN, Shaw BW Jr, Antonson DL, et al. Preliminary experience with intestinal transplantation in infants and children. Pediatrics. Apr 1996;97(4):443-8. [Medline].
Levine GM, Deren JJ, Yezdimir E. Small-bowel resection. Oral intake is the stimulus for hyperplasia. Am J Dig Dis. Jul 1976;21(7):542-6. [Medline].
Lowry SF, Brennan MF. Abnormal liver function during parenteral nutrition: Relation to infusion excess. J Surg Res. 1979;26:300-7.
Marotta RB, Floch MH. Dietary therapy of steatorrhea. Gastroenterol Clin North Am. Sep 1989;18(3):485-512. [Medline].
Messing B, Pigot F, Rongier M, et al. Intestinal absorption of free oral hyperalimentation in the very short bowel syndrome. Gastroenterology. Jun 1991;100(6):1502-8. [Medline].
Nightingale JM, Kamm MA, van der Sijp JR, et al. Disturbed gastric emptying in the short bowel syndrome. Evidence for a 'colonic brake'. Gut. Sep 1993;34(9):1171-6. [Medline].
Nordgaard I, Hansen BS, Mortensen PB. Importance of colonic support for energy absorption as small-bowel failure proceeds. Am J Clin Nutr. Aug 1996;64(2):222-31. [Medline].
Parker P, Stroop S, Greene H. A controlled comparison of continuous versus intermittent feeding in the treatment of infants with intestinal disease. J Pediatr. Sep 1981;99(3):360-4. [Medline].
Purdum PP 3d, Kirby DF. Short-bowel syndrome: a review of the role of nutrition support. JPEN J Parenter Enteral Nutr. Jan-Feb 1991;15(1):93-101. [Medline].
Reyes J, Todo S, Bueno J, et al. Intestinal transplantation in children: five-year experience. Transplant Proc. Oct 1996;28(5):2755-6. [Medline].
Scolapio JS, Camilleri M, Fleming CR, et al. Effect of growth hormone, glutamine, and diet on adaptation in short-bowel syndrome: a randomized, controlled study. Gastroenterology. Oct 1997;113(4):1074-81. [Medline].
Sheldon GF, Peterson SR, Sanders R. Hepatic dysfunction during hyperalimentation. Arch Surg. Apr 1978;113(4):504-8. [Medline].
Sial S, Koussayer T, Klein S. Nutritional management of a patient with short-bowel syndrome and large-volume jejunostomy output. Nutrition. Jan-Feb 1994;10(1):37-40; discussion 40-1. [Medline].
Spagnuolo MI, Iorio R, Vegnente A, Guarino A. Ursodeoxycholic acid for treatment of cholestasis in children on long-term total parenteral nutrition: a pilot study. Gastroenterology. Sep 1996;111(3):716-9. [Medline].
Thompson JS. Surgical management of short bowel syndrome. Surgery. Jan 1993;113(1):4-7. [Medline].
Thompson JS, Rikkers LF. Surgical alternatives for the short bowel syndrome. Am J Gastroenterol. Feb 1987;82(2):97-106. [Medline].
Todo S, Tzakis AG, Abu-Elmagd K, et al. Cadaveric small bowel and small bowel-liver transplantation in humans. Transplantation. Feb 1992;53(2):369-76. [Medline].
Treem WR. Short bowel syndrome. In: Wyllie R, Hyams JS, eds. Pediatric Gastrointestinal Disease: Pathophysiology, Diagnosis, Management. Philadelphia, PA: WB Saunders; 1993:573-603.
Vileisis RA, Inwood RJ, Hunt CE. Prospective controlled study of parenteral nutrition-associated cholestatic jaundice: effect of protein intake. J Pediatr. May 1980;96(5):893-7. [Medline].
Woolf GM, Miller C, Kurian R, Jeejeebhoy KN. Diet for patients with a short bowel: high fat or high carbohydrate?. Gastroenterology. Apr 1983;84(4):823-8. [Medline].
Zahavi I, Shaffer EA, Gall DG. Total parenteral nutrition-associated cholestasis: acute studies in infant and adult rabbits. J Pediatr Gastroenterol Nutr. Aug 1985;4(4):622-7. [Medline].
Zurier RB, Campbell RG, Hashim SA, Van Itallie TB. Use of medium-chain triglyceride in management of patients with massive resection of the small intestine. N Engl J Med. Mar 3 1966;274(9):490-3. [Medline].
Further Reading
Keywords
short bowel syndrome, SBS, short-bowel syndrome, total parenteral nutrition, TPN, malabsorption, omphalocele, gastroschisis, intestinal atresia, necrotizing enterocolitis, malrotation, volvulus, cloacal exstrophy, intestinal failure, pancreatitis, treatment, diagnosis, malabsorptive diarrhea, dehydration, gastroesophageal reflux, failure to thrive, midgut volvulus, Crohn disease, inflammatory bowel disease
