eMedicine Specialties > General Surgery > Abdomen

Short-Bowel Syndrome: Treatment

Author: Burt Cagir, MD, FACS, Assistant Professor of Surgery, State University of New York, Upstate Medical Center; Consulting Staff, Director of Surgical Research, Robert Packer Hospital; Associate Program Director, Department of Surgery, Guthrie Clinic
Coauthor(s): Michael AJ Sawyer, MD, Consulting Staff, Department of Surgery, Southwestern Medical Center; Consulting Staff, Department of Surgery, Comanche County Memorial Hospital; Consulting Staff, Great Plains Surgical Clinic, Inc
Contributor Information and Disclosures

Updated: Sep 8, 2009

Treatment

Medical Therapy

Patients undergoing massive small bowel resections frequently experience large fluid shifts and difficulties with volume and electrolyte homeostasis in the early postoperative period. The first priority is to ensure that the patient is adequately resuscitated and hemodynamically stable. Fluid and electrolyte disorders make up the most important group of complications in the early postoperative period in this group of patients, according to Cosnes and associates.25

Scolapio and Fleming described therapeutic guidelines for the fluid and electrolyte management of these patients.26 These include replacement of fluid and electrolytes lost through nasogastric suctioning and in stool. They recommended that 300-500 mL be added to the total volume administered to replace insensible losses. These replacement volumes are added to the patient's calculated daily maintenance volume. Daily urine output should be at least 1 L.

Parenteral nutrition is an important therapy in the care of the patient with short-bowel syndrome. Parenteral nutrition provides adequate protein, calories, other macronutrients, and micronutrients until the bowel has had time to adapt. The time required for optimal bowel adaptation is a source of controversy. Booth stated that bowel adaptation may not be complete until a year or more after resection.27 Carbonnel and others wrote that little bowel compensation occurs after 3 months.28 Data from animal studies conducted by Wilmore and colleagues suggested that supplementing enteral intake with parenteral nutrition early in the postoperative course results in better overall bowel adaptation.2 This is most likely because it facilitates provision of adequate calorie and nitrogen sources.

According to Nightingale and colleagues, when enteral nutrient absorption falls to below one third of premorbid capacity, some amount of parenteral nutrition is needed.29 Parenteral nutrition can be started with standard formulations and administered over the course of 24 hours daily on an inpatient basis. Make efforts to infuse daily requirements in shorter time periods before the patient is discharged. This is called cycling and it allows liberation from the solution pump for at least some time each day. In addition, laboratory studies, including serum chemistries and mineral and trace element levels, are monitored frequently and provision of these nutrients adjusted accordingly in the parenteral nutrition formula.

Gradually, most patients are able to resume and increase oral food intake. This is begun by providing small frequent feedings and slowly advancing the diet as tolerated. According to Scolapio and Fleming, the process of weaning the patient off parenteral nutrition can begin once oral calorie intake exceeds 1000 kcal/d.26 Further reductions in parenteral nutrition are predicated on increased oral intake. Woolf and associates reported that nutrient absorption is not complete in patients with loss of half or more of the small bowel.30 Therefore, they usually require 30-40 kcal/kg/d to meet daily energy requirements.

A subset of patients who have lost significant amounts of ileum and colon may have massive fluid losses. Stomal outputs may exceed 2.5 L/d. Many of these patients are likely to be dependent on prolonged intravenous fluid therapy. Some may do well with oral sources of water, glucose, and sodium. Wilmore's group reported good success with the use of Gatorade.17 Scolapio and Fleming stated that the solution should contain at least 90 mmol/L of sodium.26 This may require supplementation with salt in some of the commercially available solutions.

Despite bowel adaptation and meticulous nutritional therapy, some patients are unable to be liberated from parenteral nutrition. These patients usually are those with less than 60 cm of small bowel remaining, loss of the ileum and ileocecal valve, and loss of the colon. Wilmore, Byrne, and colleagues have been leaders in the concept of pharmacologic bowel compensation, which includes measures aimed at further enhancing bowel adaptation and increasing the chances that even these patients with difficult cases can be liberated from parenteral nutrition.31 This includes provision of growth hormone 0.03-0.14 mg/kg/d subcutaneously for 4 weeks, parenteral (0.16 g/kg/d) or enteral (30 g/d) glutamine supplementation, and a high-carbohydrate (55-60%) calories from carbohydrate versus 20-25% from fat and 20% from protein) diet.

Somatropin (Zorbtive) is a recombinant human growth hormone that elicits anabolic and anticatabolic influence on various cells, including myocytes, hepatocytes, adipocytes, lymphocytes, and hematopoietic cells. It exerts activity on specific cell receptors, including insulinlike growth factor-1 (IGF-1). Actions on the gut may be direct or mediated via IGF-1. Somatropin is indicated to treat short-bowel syndrome in conjunction with nutritional support. The adult dose is 0.1 mg/kg SC qd for up to 4 weeks (not to exceed 8 mg/d). Pediatric dosing has not been established.

Wilmore, Byrne, and colleagues published their results on 87 patients treated with this regimen in Current Problems in Surgery in 1997.17 After 4 weeks, 52% were completely off parenteral nutrition and an additional 38% had significantly reduced parenteral nutrition requirements. The same group of investigators published results with this regimen, also in 1997, in 45 patients with a jejunoileal remnant less than 50 cm and with a segment of colon remaining in continuity. After 4 weeks on the regimen, 58% were liberated from parenteral nutrition. After a mean follow-up of 1.8 years, this had fallen to 40%.

Specific drug therapies in short-bowel syndrome are mainly aimed at decreasing gastric hypersecretion or decreasing diarrhea.32,33 Gastric hypersecretion may be treated by proton pump inhibitors or histamine-2 (H2) blockers in the early postoperative period. In most patients, gastric hypersecretion severe enough to cause clinical problems is self-limited.

Diarrhea is a more vexing problem. When the patient is on nothing by mouth (NPO), codeine 60 mg IM q4h may be helpful. When enteral intake is resumed, Imodium (4-5 mg q6h) or Lomotil (2.5-5 mg qid) is useful. In refractory cases, tincture of opium in doses of 5-10 mL q4h may be tried. Cases involving patients who have lost all of their colon and ileum, with less than 100 cm of jejunum and an end jejunostomy, are the most difficult to manage. In these patients, the somatostatin analogue octreotide can be administered in doses of 100 mcg subcutaneously 3 times a day. This can reduce stool output by as much as 50% according to Farthing.34

Surgical Therapy

Operative therapies for short-bowel syndrome can be divided into 2 broad categories: (1) intestinal or combined liver-intestinal transplantation, and (2) nontransplant operations. Nontransplant components of the surgical armamentarium for the treatment of short-bowel syndrome include intestinal lengthening (Bianchi) procedures, intestinal tapering for dilated dysfunctional bowel segments, strictureplasty, and creation of intestinal valves or reversed bowel segments for patients with rapid intestinal transit times.

In 1995, Thompson et al reported their results from various nontransplant and transplant surgical procedures in 160 patients with short-bowel syndrome.35 The study population included 48 adults and 112 children. In this population, the type of operation was selected based on criteria that included the age of the patient; the remaining bowel length; the presence or absence of bowel dilatation; the overall functional status of the bowel remnant, including intestinal transit time; and the presence or absence of complications related to parenteral nutrition.

Fifteen patients had intestinal remnants greater than 120 cm but with dilated dysfunctional bowel, in some cases proximal to a stricture. Patients in this group underwent Heineke-Mikulicz strictureplasties (n = 4) or intestinal tapering procedures (n = 11). Intestinal tapering creates a decrease in the circumference of dilated bowel by imbrications or resections of a portion of the antimesenteric side of the intestine. Approximately 87% of these 15 patients experienced clinical improvement.

Small bowel remnants 90-120 cm associated with rapid intestinal transit times were present in 14 patients. Two of these patients underwent creation of an artificial valve, which is made by intussuscepting a distal small bowel segment and suturing it in place. Both of these patients improved clinically. A reversed segment was placed in one patient but subsequently was taken down because of poor bowel function.

Intestinal lengthening was performed in 14 patients who had short small bowel remnants that were dilated. Intestinal lengthening is performed by transecting the bowel segment along its longitudinal axis between the antimesenteric and mesenteric borders. This converts one dilated loop of intestine into 2 parallel segments that then are anastomosed in series. Clinical improvement was observed in 86% of these patients.

In 1997, Thompson and Langnas reported additional results from nontransplant operations for treatment of short-bowel syndrome.36 Ninety patients were evaluated for possible surgical therapy. Thirty-seven of 43 procedures (86%) resulted in clinical improvement. The best results were achieved with operations designed to increase intestinal surface area, such as restoration of gastrointestinal tract continuity and intestinal lengthening (86%), and those that were intended to correct functional problems, such as strictureplasty, the removal of diseased bowel segments, and closure of fistulae (85%). Clinical improvement rates of only 50% were observed in patients who underwent operations aimed at slowing intestinal transit time, such as creation of valves or reversed segments.

In contrast, Panis reported good results in patients treated with segmental small bowel reversal.37 However, his series was small (n = 8). These patients had very short small bowel remnants (median was 40 cm). The median length of the reversed segment was 12 cm. Median follow-up was 35 months. One patient died of a pulmonary embolism in the seventh postoperative month. Of the remaining 7 patients, 3 were completely liberated from parenteral nutrition, 1 required only intravenous fluid and electrolyte therapy, and 3 received only 3-5 nocturnal cycles of parenteral nutrition per week.

Javid and colleagues published their results with serial transverse enteroplasty (STEP) for the treatment of short-bowel syndrome in infants.38 A total of 5 children underwent this intestinal lengthening procedure. No significant perioperative complications were reported. The percentage of protein-energy nutrition that the patients were able to take enterally increased significantly in this group following STEP (p <0.05). One child was able to be completely liberated from parenteral nutrition and another child's severe cholestasis was reversed.

Organ transplantation is a recent addition to the surgical approach to short-bowel syndrome. From the outset, intestinal transplantation faced many hurdles, first and foremost because of the massive amount of lymphoid and immunologic tissue associated with the gastrointestinal tract. Effective immunosuppressant drugs needed to be developed. Techniques and postoperative care needed to be refined, and the actual indications for transplantation needed to be clarified. Worldwide, an estimated 25-30 centers are actively engaged in intestinal or liver-intestinal transplantation procedures for short-bowel syndrome.

In 1995, Todo, Reyes, and colleagues reported their experience with 71 isolated intestinal (n = 22), liver-intestinal (n = 30), and multiorgan (n = 11) transplants in 66 patients performed from 1990-1995 at the University of Pittsburgh Medical Center.39 At the time of the report, just over 50% of the patients were alive. Thirty-five grafts had been lost. Sepsis (n = 19) was the most common cause of graft loss, followed by management errors (n = 10) and rejection (n = 6). The authors performed linear regression analysis to identify factors correlated with graft loss. They identified prolonged operative time, inclusion of colon in the graft, a positive cytomegalovirus (CMV) donor infection status, high tacrolimus (FK506) blood levels, use of OKT3, and steroid recycling as predictors of graft loss. During the course of this study, 4 patients received combined intestinal–bone marrow transplants. They were all doing well at 2-3 months of follow-up.

Langnas et al described their experience at the University of Nebraska with 13 liver-intestinal transplants and 3 isolated intestinal transplants in infants and children.40 Their results were published in 1996. In children who received combined liver-intestinal grafts, the 1-year actuarial patient survival rate was 76% and the 1-year actuarial graft survival rate was 61%. Six of these patients had been liberated from parenteral nutrition. All 3 who received isolated intestinal grafts were alive and free from parenteral nutrition. Most significant complications in this series were related to sepsis and graft rejection.

In 1998, Abu-Elmagd et al updated the University of Pittsburgh experience with liver-intestinal and isolated intestinal transplantation.41 Their results in 59 adults and 39 children were presented. These patients received either liver-intestinal (n = 50), isolated intestinal (n = 37), or multivisceral (n = 17) grafts. Twenty were augmented with donor bone marrow. Tacrolimus was the primary immunosuppressant used in all cases. With a mean follow-up duration of 32 months, 48% of patients were alive with grafts that allowed complete (91%) or partial (9%) liberation from specialized nutritional support. In addition, 12 patients had passed the 5-year milestone. The actuarial patient survival rates at 1 and 5 years were 72% and 48%, respectively. Bone marrow transplantation did not appear to increase graft survival.

In 2007, Sudan et al published their clinical results of intestinal lengthening procedures.42  

An outcome analysis of a longitudinal intestinal lengthening (Bianchi procedure) and a serial transverse enteroplasty (STEP procedure) was done. Fifty pediatric patients and 14 adult patients were included in the study. All patients had dilated small bowel loops greater than 3.9 cm in size and also had poor enteral progression.42 The patients underwent 43 Bianchi procedures and 34 STEP procedures. The average intestinal length increased from 44 cm to 68 cm for the Bianchi procedure and from 45 cm to 65 cm for the STEP procedure. 
 
One year after the lengthening procedures, 69% of the patients were off total parenteral nutrition. The authors of this study concluded that surgical lengthening procedures result in an improvement in enteral nutrition.42

Preoperative Details

Patient selection is paramount to operative success. Tailor nontransplant operative approaches to the patient's remaining length of intestine, the presence or absence of strictures or areas of stasis, bowel dilatation, and the intestinal transit time as described above. Various radiographic techniques, including contrast small bowel follow-through and CT scanning, are helpful in the decision.

Transplant surgery is usually reserved for patients who are dependent on parenteral nutrition, who have run out of venous access, who have had several episodes of central line–related sepsis, or who have begun to manifest progressive parenteral nutrition–associated liver dysfunction. Identify these patients early and perform transplant prior to the development of hepatic cirrhosis. This may obviate the need to perform a combined liver-intestinal transplantation, and results are better in patients who have not yet developed cirrhosis, according to Vanderhoff and Langnas.18

According to Abu-Elmagd and colleagues, grafts in their series were obtained from blood group (ABO) antigen-matched cadaveric donors.43 Although human leukocyte antigen (HLA) matching was performed, it usually was poor, and 13 patients in their series had lymphocytotoxic positive cross-matches.

Intraoperative Details

Although a full dissertation on the operative technique is beyond the scope of this discussion, the authors outline the procedures of combined liver–small bowel transplantation and isolated small bowel transplantation (see Relevant Anatomy and Indications). Some details that bear discussion here were published by Abu-Elmagd and colleagues.43,41 The University of Wisconsin solution was used for graft preservation. These investigators have preserved the donor enteric and celiac ganglia as a measure to decrease postoperative graft dysmotility.

Nontransplant operations require meticulous technique as well. The bowel must be handled gently and the blood supply guarded jealously.

Abdominal visceral organ procurement may begin with an attempt at gastrointestinal tract sterilization by intragastric administration of a nonabsorbable antibiotic suspended in a cathartic solution. Proximal and distal abdominal aortic control is achieved at the aortic hiatus and caudal to the inferior mesenteric artery. The proximal aorta is clamped, and the distal aorta is cannulated. Cold preservation solution is used to perfuse the abdominal viscera to be excised and transplanted. Drainage is provided by the creation of a venotomy in the suprahepatic inferior vena cava. The bowel is stapled proximally and distally. Other visceral vascular connections are divided and the graft specimen removed.

If the patient is to receive a transplant consisting of the liver and intestine, gastrointestinal tract continuity is restored by proximal and distal anastomosis. Some authors have advised creation of proximal and distal stomas via limbs of intestine because prolonged intestinal decompression may be necessary in the early postoperative period. Arterial blood supply is reestablished by anastomosis of a Carrel patch of the celiac axis and superior mesenteric artery to the aorta, or, if donor aorta is included, an aorto-aortic anastomosis is possible. Venous drainage of the intestine is intact to the liver in a combined hepatic-intestinal transplant.

Hepatic venous drainage can be accomplished by harvesting donor retrohepatic inferior vena cava with preservation of the donor hepatic veins distally. This is anastomosed to the recipient inferior vena cava circumferentially. Alternately, the donor inferior vena cava can be anastomosed to the recipient vena cava via an anterior venotomy. This anastomosis "piggybacks" the hepatic venous outflow onto the anterior surface of the recipient vena cava. This requires ligation of the caudal aspect of the donor inferior vena cava. Venous outflow for the recipient's retained organs, such as the stomach, pancreas, and duodenum, can be established by anastomosis of the recipient portal vein to the donor vena cava or the donor portal vein.

When isolated intestinal grafts are used, a Carrel patch of the donor superior mesenteric artery is anastomosed to the recipient aorta. A long segment of donor superior mesenteric and portal vein is preserved for anastomosis to the recipient portal vein. Gastrointestinal tract continuity is reestablished as described above.

Postoperative Details

Postoperatively, fluid and electrolyte balance must be assured. Some of these guidelines have been discussed under the Medical Therapy section above. Calculated maintenance fluids are administered, and nasogastric, stool, stoma, and fistula outputs are recorded. These are replaced with fluids of similar makeup. Most frequently, this involves lactated Ringer solution. If large amounts of gastric secretions are lost, isotonic sodium chloride solution might be a more appropriate choice.

Most patients are maintained on parenteral nutrition initially. Enteral intake should be started as soon as possible, beginning with small amounts and gradually increasing. Several smaller feedings per day are usually advisable.

Transplant recipients are begun on immunosuppressive drug therapy. Standard immunosuppression regimens are based on tacrolimus and prednisone. Investigators at the University of Pittsburgh have used adjunctive drugs, such as cyclophosphamide, mycophenolate mofetil, and azathioprine, early in the postoperative period as well.

Follow-up

Patients with short-bowel syndrome require lifetime follow-up. Those on parenteral nutrition require frequent monitoring of serum chemistries; liver function tests; and vitamin, mineral, and trace element levels.44 Patients should be weighed regularly following resolution of postoperative fluid flux to assure that they are not losing weight on the nutritional regimen they are receiving. Nitrogen balance studies can be performed but are cumbersome because of the need for 12- to 24-hour urine collection. Patients receiving specialized enteral nutrition can be monitored with similar measures.

Patients who have had nontransplant operations are monitored to assure that proper wound healing and bowel function are occurring. In addition, several of the measures described above can be applied to their postoperative care. Ascertaining that they can ingest and absorb adequate amounts of protein and calories is important.

Patients who receive single or multiple organ transplants are monitored, and their cases are followed closely. The most dreaded postoperative complications that must be identified early include organ rejection, opportunistic infection, and development of immunosuppression-related malignancies. These patients may be monitored by all the measures mentioned above. In addition, immunosuppressant drug levels can be monitored.

The physician usually diagnoses acute rejection by endoscopically guided mucosal biopsies, and chronic rejection is diagnosed definitively by complete examination of resected grafts.

Transplant patients must also be monitored for evidence of graft versus host disease. Typically affected areas include the skin, gastrointestinal tract, liver, and lungs.

Complications

Both nontransplant and transplant patients can experience the typical postoperative complications of surgical patients in general. These include hemorrhage, wound complications, postoperative pulmonary dysfunction, renal failure, and pulmonary embolism, to name a few.

In nontransplant patients, the following postoperative complications may occur:

  • Bowel obstruction
  • Bowel necrosis
  • Bowel dysmotility and dysfunction
  • Anastomotic disruption
  • Stasis of intestinal contents with or without bacterial overgrowth

Transplant recipients are subject to all the complications mentioned above. In addition, they may develop serious and sometimes lethal complications specifically related to transplantation and immunosuppression, such as the following:

  • Acute rejection
  • Chronic rejection
  • Hepatic, portal, or mesenteric vein thrombosis
  • Systemic sepsis with ordinary pathogens or opportunistic organisms (eg, CMV)
  • Lymphoproliferative disorders or malignancies

More on Short-Bowel Syndrome

Overview: Short-Bowel Syndrome
Workup: Short-Bowel Syndrome
Treatment: Short-Bowel Syndrome
Follow-up: Short-Bowel Syndrome
References
Further Reading
[ CLOSE WINDOW ]

References

  1. Weser E. Nutritional aspects of malabsorption: short gut adaptation. Clin Gastroenterol. May 1983;12(2):443-61. [Medline].

  2. Wilmore DW, Dudrick SJ, Daly JM, et al. The role of nutrition in the adaptation of the small intestine after massive resection. Surg Gynecol Obstet. Apr 1971;132(4):673-80. [Medline].

  3. Wilmore DW, Dudrick SJ. Growth and development of an infant receiving all nutrients exclusively by vein. JAMA. Mar 4 1968;203(10):860-4. [Medline].

  4. Lennard-Jones JE. Indications and need for long-term parenteral nutrition: implications for intestinal transplantation. Transplant Proc. Dec 1990;22(6):2427-9. [Medline].

  5. 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].

  6. Moreno JM, Planas M, Lecha M, et al. [The year 2002 national register on home-based parenteral nutrition]. Nutr Hosp. Jul-Aug 2005;20(4):249-53. [Medline].

  7. Ladefoged K, Hessov I, Jarnum S. Nutrition in short-bowel syndrome. Scand J Gastroenterol Suppl. 1996;216:122-31. [Medline].

  8. Nightingale JM, Lennard-Jones JE. The short bowel syndrome: what's new and old?. Dig Dis. 1993;11(1):12-31. [Medline].

  9. Stollman TH, de Blaauw I, Wijnen MH, et al. Decreased mortality but increased morbidity in neonates with jejunoileal atresia; a study of 114 cases over a 34-year period. J Pediatr Surg. Jan 2009;44(1):217-21. [Medline].

  10. Sellin JH. Intestinal electrolyte absorption and secretion. In: Feldman M, Scharschmidt BF, Sleisinger MH. Sleisinger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. 6th ed. Philadelphia, Pa: WB Saunders Co; 1998:1451-1471.

  11. Clarke RM. Mucosal architecture and epithelial cell production rate in the small intestine of the albino rat. J Anat. Nov 1970;107:519-29. [Medline].

  12. Borgstrom B, Dahlquist A, Lundh G, et al. Studies of intestinal digestion and absorption in the human. J Clin Invest. 1957;36:1521-1536.

  13. Johansson C. Studies of gastrointestinal interactions. VII. Characteristics of the absorption pattern of sugar, fat and protein from composite meals in man. A quantitative study. Scand J Gastroenterol. 1975;10(1):33-42. [Medline].

  14. Phillips SF, Giller J. The contribution of the colon to electrolyte and water conservation in man. J Lab Clin Med. May 1973;81(5):733-46. [Medline].

  15. Pomare EW, Branch WJ, Cummings JH. Carbohydrate fermentation in the human colon and its relation to acetate concentrations in venous blood. J Clin Invest. May 1985;75(5):1448-54. [Medline].

  16. Sundaram A, Koutkia P, Apovian CM. Nutritional management of short bowel syndrome in adults. J Clin Gastroenterol. Mar 2002;34(3):207-20. [Medline].

  17. Wilmore DW, Byrne TA, Persinger RL. Short bowel syndrome: new therapeutic approaches. Curr Probl Surg. May 1997;34(5):389-444. [Medline].

  18. Vanderhoof JA, Langnas AN. Short-bowel syndrome in children and adults. Gastroenterology. Nov 1997;113(5):1767-78. [Medline].

  19. Cavicchi M, Beau P, Crenn P, et al. Prevalence of liver disease and contributing factors in patients receiving home parenteral nutrition for permanent intestinal failure. Ann Intern Med. Apr 4 2000;132(7):525-32. [Medline].

  20. Klein S, Nealon WH. Hepatobiliary abnormalities associated with total parenteral nutrition. Semin Liver Dis. Aug 1988;8(3):237-46. [Medline].

  21. Quigley EM, Marsh MN, Shaffer JL, et al. Hepatobiliary complications of total parenteral nutrition. Gastroenterology. Jan 1993;104(1):286-301. [Medline].

  22. Puder M, Valim C, Meisel JA, et al. Parenteral fish oil improves outcomes in patients with parenteral nutrition-associated liver injury. Ann Surg. Aug 5 2009;[Medline].

  23. Pansky B. Duodenum-jejunum-ileum, duodenal fossae, and superior mesenteric artery. In: Review of Gross Anatomy. 4th ed. New York, NY: Macmillan Publishing Co; 1979:334-335.

  24. Starzl TE, Todo S, Tzakis A, et al. The many faces of multivisceral transplantation. Surg Gynecol Obstet. May 1991;172(5):335-44. [Medline].

  25. Cosnes J, Gendre JP, Evard D, et al. Compensatory enteral hyperalimentation for management of patients with severe short bowel syndrome. Am J Clin Nutr. May 1985;41(5):1002-9. [Medline].

  26. Scolapio JS, Fleming CR. Short bowel syndrome. Gastroenterol Clin North Am. Jun 1998;27(2):467-79, viii. [Medline].

  27. Booth IW. Enteral nutrition as primary therapy in short bowel syndrome. Gut. Jan 1994;35(1 Suppl):S69-72. [Medline].

  28. Carbonnel F, Cosnes J, Chevret S, et al. The role of anatomic factors in nutritional autonomy after extensive small bowel resection. JPEN J Parenter Enteral Nutr. Jul-Aug 1996;20(4):275-80. [Medline].

  29. Nightingale JM, Lennard-Jones JE, Walker ER, et al. Jejunal efflux in short bowel syndrome. Lancet. Sep 29 1990;336(8718):765-8. [Medline].

  30. Woolf GM, Miller C, Kurian R, et al. Nutritional absorption in short bowel syndrome. Evaluation of fluid, calorie, and divalent cation requirements. Dig Dis Sci. Jan 1987;32(1):8-15. [Medline].

  31. Wilmore DW, Lacey JM, Soultanakis RP, et al. Factors predicting a successful outcome after pharmacologic bowel compensation. Ann Surg. Sep 1997;226(3):288-92; discussion 292-3. [Medline].

  32. Van Gossum A, Cabre E, Hebuterne X, et al. ESPEN Guidelines on Parenteral Nutrition: gastroenterology. Clin Nutr. Aug 2009;28(4):415-27. [Medline].

  33. Wallis K, Walters JR, Gabe S. Short bowel syndrome: the role of GLP-2 on improving outcome. Curr Opin Clin Nutr Metab Care. Sep 2009;12(5):526-32. [Medline].

  34. Farthing MJ. Octreotide in dumping and short bowel syndromes. Digestion. 1993;54 Suppl 1:47-52. [Medline].

  35. Thompson JS, Langnas AN, Pinch LW, et al. Surgical approach to short-bowel syndrome. Experience in a population of 160 patients. Ann Surg. Oct 1995;222(4):600-5; discussion 605-7. [Medline].

  36. Thompson JS, Langnas AN. Surgical approaches to improving intestinal function in the short-bowel syndrome. Arch Surg. Jul 1999;134(7):706-9; discussion 709-11. [Medline].

  37. Panis Y, Messing B, Rivet P, et al. Segmental reversal of the small bowel as an alternative to intestinal transplantation in patients with short bowel syndrome. Ann Surg. Apr 1997;225(4):401-7. [Medline].

  38. Javid PJ, Kim HB, Duggan CP, et al. Serial transverse enteroplasty is associated with successful short-term outcomes in infants with short bowel syndrome. J Pediatr Surg. Jun 2005;40(6):1019-23; discussion 1023-4. [Medline].

  39. Todo S, Reyes J, Furukawa H, et al. Outcome analysis of 71 clinical intestinal transplantations. Ann Surg. Sep 1995;222(3):270-80; discussion 280-2. [Medline].

  40. 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].

  41. Abu-Elmagd K, Reyes J, Todo S, et al. Clinical intestinal transplantation: new perspectives and immunologic considerations. J Am Coll Surg. May 1998;186(5):512-25; discussion 525-7. [Medline].

  42. Sudan D, Thompson J, Botha J, et al. Comparison of intestinal lengthening procedures for patients with short bowel syndrome. Ann Surg. Oct 2007;246(4):593-601; discussion 601-4. [Medline].

  43. Abu-Elmagd K, Fung J, Bueno J, et al. Logistics and technique for procurement of intestinal, pancreatic, and hepatic grafts from the same donor. Ann Surg. Nov 2000;232(5):680-7. [Medline].

  44. Fitzgibbons S, Ching YA, Valim C, et al. Relationship between serum citrulline levels and progression to parenteral nutrition independence in children with short bowel syndrome. J Pediatr Surg. May 2009;44(5):928-32. [Medline].

  45. Howard L, Ament M, Fleming CR, et al. Current use and clinical outcome of home parenteral and enteral nutrition therapies in the United States. Gastroenterology. Aug 1995;109(2):355-65. [Medline].

  46. Gorczynski RM. Immunosuppression induced by hepatic portal venous immunization spares reactivity in IL-4 producing T lymphocytes. Immunol Lett. Jun 1992;33(1):67-77. [Medline].

  47. Andorsky DJ, Lund DP, Lillehei CW, et al. Nutritional and other postoperative management of neonates with short bowel syndrome correlates with clinical outcomes. J Pediatr. Jul 2001;139(1):27-33. [Medline].

  48. Baldwin-Price HK, Copp D, Singleton AO Jr. Reversed intestinal segments in the management of anenteric malabsorption syndrome. Ann Surg. Feb 1965;161:225-30. [Medline].

  49. Benedetti E, Baum C, Cicalese L, et al. Progressive functional adaptation of segmental bowel graft from living related donor. Transplantation. Feb 27 2001;71(4):569-71. [Medline].

  50. Chen MK, Badylak SF. Small bowel tissue engineering using small intestinal submucosa as a scaffold. J Surg Res. Aug 2001;99(2):352-8. [Medline].

  51. Cicalese L, Baum C, Brown M, et al. Segmental small bowel transplant from adult living-related donors. Transplant Proc. Feb-Mar 2001;33(1-2):1553. [Medline].

  52. Cicalese L, Rastellini C, Sileri P, et al. Segmental living related small bowel transplantation in adults. J Gastrointest Surg. Mar-Apr 2001;5(2):168-72; discussion 173. [Medline].

  53. Dudrick SJ, Wilmore DW, Vars HM, et al. Long-term total parenteral nutrition with growth, development, and positive nitrogen balance. Surgery. Jul 1968;64(1):134-42. [Medline].

  54. Ellegard L, Bosaeus I, Nordgren S, et al. Low-dose recombinant human growth hormone increases body weight and lean body mass in patients with short bowel syndrome. Ann Surg. Jan 1997;225(1):88-96. [Medline].

  55. Gerwig WH, Ghaphery A. Experimental attempt to delay alimentary transit after small bowel exclusion. Arch Surg. 1963;87:50-57.

  56. Greenberger NJ. State of the art: the management of the patient with short bowel syndrome. Am J Gastroenterol. Nov 1978;70(5):528-40. [Medline].

  57. Howard L, Heaphey L, Fleming CR, et al. Four years of North American registry home parenteral nutrition outcome data and their implications for patient management. JPEN J Parenter Enteral Nutr. Jul-Aug 1991;15(4):384-93. [Medline].

  58. Høverstad T. Studies of short-chain fatty acid absorption in man. Scand J Gastroenterol. Apr 1986;21(3):257-60. [Medline].

  59. Kocoshis S. Evolving concepts and improving prospects for neonates with short bowel syndrome. J Pediatr. Jul 2001;139(1):5-7. [Medline].

  60. Kono K, Sekikawa T, Iizuka H, et al. Interposed colon between remnants of the small intestine exhibits small bowel features in a patient with short bowel syndrome. Dig Surg. 2001;18(3):237-41. [Medline].

  61. Lennard-Jones JE. Review article: practical management of the short bowel. Aliment Pharmacol Ther. Dec 1994;8(6):563-77. [Medline].

  62. Lennard-Jones JE, Wood S. Coping with the short bowel syndrome. Hosp Update. 1991;27:797-807.

  63. Li-Ling, Irving M. The effectiveness of growth hormone, glutamine and a low-fat diet containing high-carbohydrate on the enhancement of the function of remnant intestine among patients with short bowel syndrome: a review of published trials. Clin Nutr. Jun 2001;20(3):199-204. [Medline].

  64. Lord LM, Schaffner R, DeCross AJ, et al. Management of the patient with short bowel syndrome. AACN Clin Issues. Nov 2000;11(4):604-18. [Medline].

  65. Meyer D, Thorwarth WM, Otto C, et al. Orthotopic liver/small bowel transplantation in rats: a microsurgical model inducing tolerance. Microsurgery. 2001;21(4):156-62. [Medline].

  66. Nehra V, Camilleri M, Burton D, et al. An open trial of octreotide long-acting release in the management of short bowel syndrome. Am J Gastroenterol. May 2001;96(5):1494-8. [Medline].

  67. Pansky B. Blood supply of the colon and appendix. In: Review of Gross Anatomy. 4th ed. New York, NY: Macmillan Publishing Co; 1979:340-341.

  68. Pansky B. Pancreas. In: Review of Gross Anatomy. 4th ed. New York, NY: Macmillan Publishing Co; 1979:332-333.

  69. Pansky B. The large intestine. In: Review of Gross Anatomy. 4th ed. New York, NY: Macmillan Publishing Co; 1979:338-339.

  70. Pansky B. Duodenum. In: Review of Gross Anatomy. 4th ed. New York, NY: Macmillan Publishing Co; 1979:330-331.

  71. Pearson PY, O'Connor DM, Schwartz MZ. Novel effect of leptin on small intestine adaptation. J Surg Res. May 15 2001;97(2):192-5. [Medline].

  72. Pertsemlidis D, Kark AE. Antiperistaltic segments for the treatment of short bowel syndrome. Am J Gastroenterol. Dec 1974;62(6):526-30. [Medline].

  73. Ploeg RJ, D'Alessandro AM. Intestinal transplantation: a clinical update. Scand J Gastroenterol Suppl. 1995;212:79-89. [Medline].

  74. Scolapio JS, McGreevy K, Tennyson GS, et al. Effect of glutamine in short-bowel syndrome. Clin Nutr. Aug 2001;20(4):319-23. [Medline].

  75. Sedgwick CE, Viglotti J. Hyperalimentation. Surg Clin North Am. Jun 1971;51(3):681-6. [Medline].

  76. Stern LE, Erwin CR, O'Brien DP, et al. Epidermal growth factor is critical for intestinal adaptation following small bowel resection. Microsc Res Tech. Oct 15 2000;51(2):138-48. [Medline].

  77. Tatsumi Y, Matis LA, Iramajiri K, et al. The molecular mechanism of the functional development of the TcR-gamma delta cells and the effects of cytokines. 9th Congr Immunology. 1995;1499.

  78. Terra RM, Plopper C, Waitzberg DL, et al. Remaining small bowel length: association with catheter sepsis in patients receiving home total parenteral nutrition: evidence of bacterial translocation. World J Surg. Dec 2000;24(12):1537-41. [Medline].

  79. Thompson JS, Pinch LW, Young R, et al. Long-term outcome of intestinal lengthening. Transplant Proc. Sep 2000;32(6):1242-3. [Medline].

  80. Vanderhoof JA. Short bowel syndrome in children and small intestinal transplantation. Pediatr Clin North Am. Apr 1996;43(2):533-50. [Medline].

  81. Vernon AH, Georgeson KE. Surgical options for short bowel syndrome. Semin Pediatr Surg. May 2001;10(2):91-8. [Medline].

  82. Whang EE, Shen KR. Intestinal adaptation: a new era. JPEN J Parenter Enteral Nutr. Mar-Apr 2001;25(2):100. [Medline].

  83. Wilmore DW, Robinson MK. Short bowel syndrome. World J Surg. Dec 2000;24(12):1486-92. [Medline].

  84. Zhou X, Li YX, Li N, et al. Glutamine enhances the gut-trophic effect of growth hormone in rat after massive small bowel resection. J Surg Res. Jul 2001;99(1):47-52. [Medline].

[ CLOSE WINDOW ]

Keywords

short-bowel syndrome, short bowel syndrome, Crohn's disease, total parenteral nutrition, bowel transplant, intestinal atresia, atresia intestinal, jejunal atresia, intestinal transplant, short gut syndrome, anenteric malabsorption syndrome

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Burt Cagir, MD, FACS, Assistant Professor of Surgery, State University of New York, Upstate Medical Center; Consulting Staff, Director of Surgical Research, Robert Packer Hospital; Associate Program Director, Department of Surgery, Guthrie Clinic
Burt Cagir, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, and Society for Surgery of the Alimentary Tract
Disclosure: Nothing to disclose.

Coauthor(s)

Michael AJ Sawyer, MD, Consulting Staff, Department of Surgery, Southwestern Medical Center; Consulting Staff, Department of Surgery, Comanche County Memorial Hospital; Consulting Staff, Great Plains Surgical Clinic, Inc
Michael AJ Sawyer, MD is a member of the following medical societies: American College of Surgeons, Society for Surgery of the Alimentary Tract, Society of American Gastrointestinal and Endoscopic Surgeons, and Society of Laparoendoscopic Surgeons
Disclosure: Nothing to disclose.

Medical Editor

Juan B Ochoa, MD, Assistant Professor, Department of Surgery, University of Pittsburgh
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

David L Morris, MD, PhD, Professor, Department of Surgery, St George Hospital, University of New South Wales, Australia
Disclosure: RFA Medical None Director; MRC Biotec None Director

CME Editor

Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences
Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MA, Vice Chairman, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital
John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract
Disclosure: AMGEN Royalty Other

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.