eMedicine Specialties > General Surgery > Abdomen

Short-Bowel Syndrome

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, Director, Videoendoscopic Surgical Institute of Oklahoma, Consulting Staff, Department of Surgery, Comanche County Memorial Hospital; Consulting Staff, Great Plains Surgical Clinic, Lawton, Oklahoma
Contributor Information and Disclosures

Updated: Jul 25, 2008

Introduction

The average length of the adult human small intestine is approximately 600 cm, as calculated from studies performed on cadavers. According to Lennard-Jones and to Weser, this figure ranges from 260-800 cm.1 Any disease, traumatic injury, vascular accident, or other pathology that leaves less than 200 cm of viable small bowel or results in a loss of 50% or more of the small intestine places the patient at risk for developing short-bowel syndrome.

Short-bowel syndrome is a disorder clinically defined by malabsorption, diarrhea, steatorrhea, fluid and electrolyte disturbances, and malnutrition. The final common etiologic factor in all causes of short-bowel syndrome is the functional or anatomic loss of extensive segments of small intestine so that absorptive capacity is severely compromised. Although resection of the colon alone typically does not result in short-bowel syndrome, its presence or loss can be a critical factor in the management of patients who lose significant amounts of small intestine.

Massive small intestinal resection compromises digestive and absorptive processes. Adequate digestion and absorption cannot take place, and proper nutritional status cannot be maintained without supportive care. Today, the most common causes of short-bowel syndrome in adults include Crohn disease, radiation enteritis, mesenteric vascular accidents, trauma, and recurrent intestinal obstruction. In the pediatric population, necrotizing enterocolitis, intestinal atresias, and intestinal volvulus are the most common etiologic factors. Other conditions associated with short-bowel syndrome include congenital short small bowel, gastroschisis, and meconium peritonitis.

Not all patients with loss of significant amounts of small intestine develop short-bowel syndrome. Important cofactors that help to determine whether the syndrome will develop or not include the premorbid length of small bowel, the segment of intestine that is lost, the age of the patient at the time of bowel loss, the remaining length of small bowel and colon, and the presence or absence of the ileocecal valve.

History of the Procedure

Several operative or invasive procedures and therapies have been designed and applied to the treatment of short-bowel syndrome. These include the establishment of central venous access for delivery of total parenteral nutrition, intestinal transplantation, and nontransplantation abdominal operations. The history of these various treatment strategies is discussed in this section.

Total parenteral nutrition was developed successfully by Dudrick, Wilmore, Vars, and Rhoads.2 Their landmark paper included laboratory studies in a canine model and clinical results in 30 adult patients with a variety of gastrointestinal maladies ranging from achalasia to traumatic pancreatitis to regional enteritis. The animal model clearly demonstrated efficacy. Beagle puppies fed entirely intravenously surpassed their littermate controls in weight gain and were equal in terms of activity level, skeletal growth, and other developmental landmarks. In the clinical arm of the study, the 30 subjects receiving total parenteral nutrition were able to achieve positive nitrogen balance, maintain weight, heal wounds, and close fistulae. Wilmore and Dudrick reported positive nitrogen balance, growth, and development in an infant born with diffusely atretic small bowel who was fed entirely parenterally.3

After these initial successes, the new technique was introduced into the clinical mainstream, and indications for its use have expanded tremendously. Patients with short-bowel syndrome are now routinely treated with total parenteral nutrition, especially early in their course. New therapeutic strategies that may allow patients to discontinue or curtail the use of total parenteral nutrition are discussed in subsequent sections.

Numerous nontransplant operative approaches have been used in the treatment of patients with short-bowel syndrome. The creation of reversed intestinal segments was popular in the 1960s and 1970s. The aim of this operation was to produce a sort of functional partial small bowel obstruction that would slow intestinal transit time, thereby encouraging greater nutrient absorption and decreasing diarrhea and nutrient loss. Around that time, recirculating small bowel loops were also being created, with the same idea in mind. The results were mixed to questionable, and these procedures are rarely used today. Intestinal lengthening (Bianchi procedure), the creation of artificial enteric valves, strictureplasty, and intestinal tapering procedures continue to be employed at some centers today.

Intestinal transplantation was first attempted in dogs in 1959. The procedures failed because of the great concentration of immune system cells associated with the gut. The discovery and clinical implementation of powerful immunosuppressive drugs, such as FK506 (tacrolimus) and cyclosporine A, made successful small bowel transplantation possible. The first successful combined transplantation of small intestine and liver in a human was performed in 1990. Since that time, the technique of isolated small intestinal transplantation has been developed and applied. Better graft survival rates are achieved when patients receive their transplant before complications secondary to short gut syndrome occur, especially that of cirrhosis.

Problem

Each year in the United States, many patients undergo resection of long segments of small intestine for various disorders, including inflammatory bowel disease, malignancy, mesenteric ischemia, and others. Juvenile survivors of necrotizing enterocolitis, midgut volvulus, and other abdominal catastrophes are becoming more common. Various nonoperative procedures can leave patients with a functional short-bowel syndrome. An example of this clinical scenario is radiation enteritis.

Those patients who are left with insufficient small bowel absorptive surface area develop malabsorption, malnutrition, diarrhea, and electrolyte abnormalities. The subset of patients with clinically significant malabsorption and malnutrition are said to have developed short-bowel syndrome.

Frequency

Estimates of the incidence and prevalence of short-bowel syndrome are difficult to make and, therefore, are rare. Most estimates are based on data describing patients requiring long-term home parenteral nutrition for short-bowel syndrome.

One report from the United Kingdom was published by Lennard-Jones (1990).4 This report estimated that the incidence of short-bowel syndrome requiring such therapy in the United Kingdom was 2 patients per million in the population.

Byrne and her colleagues (1995) have estimated the frequency in the United States.5 She reported that approximately 10,000-20,000 patients are currently receiving home-delivered total parenteral nutrition for short-bowel syndrome in the United States.

Moreno and coworkers (2005) published data derived form the 2002 registry of patients receiving home-based parenteral nutrition in Spain.6 The program had an enrollment of 74 patients, making the prevalence 1.8 patients per 1 million in the general population.

Etiology

In the first decades of the twentieth century, bowel strangulation and midgut volvulus were the most common etiologies resulting in short-bowel syndrome. By the 1950s and 1960s, mesenteric vascular accidents, including thrombosis and embolism of the superior mesenteric artery, had become the most common causes of short-bowel syndrome.

Jejunoileal bypass procedures once were popular for the treatment of morbid obesity. However, they produced an iatrogenic short gut syndrome and the attendant metabolic and hepatic complications associated with chronic malabsorption. These procedures have since been abandoned.

Studies by Ladefoged and colleagues (1996) and Nightingale and Lennard-Jones (1993) found that Crohn disease has become the most common etiology of short-bowel syndrome in adults, accounting for 50-60% of cases.7,8 Other important causative entities include mesenteric ischemia and radiation enteritis.

In contrast, the Spanish home parenteral nutrition registry data reported by Moreno and colleagues (2005) described mesenteric ischemia as the leading cause of short-bowel syndrome (29.7%), followed by neoplastic diseases (16.2%), radiation enteritis (12.2%), motility disorders (8.1%), and Crohn disease (5.4%).6

Occasionally, trauma that involves one or more of the major mesenteric vessels result in extensive bowel necrosis and short-bowel syndrome.

Leading pediatric and neonatal etiologies of short-bowel syndrome include necrotizing enterocolitis, multi-level small bowel atresia, and midgut volvulus with ischemic bowel infarction.

Pathophysiology

Physiologic derangements in short-bowel syndrome are the result of the loss of large amounts of intestinal absorptive surface area. The sequelae of this loss include malabsorption of water, electrolytes, macronutrients (ie, proteins, carbohydrates, fats), and micronutrients (ie, vitamins, minerals, trace elements).

The gastrointestinal tract is a vital locus for water and electrolyte absorption and transport. In addition to managing exogenously obtained sources of these nutrients, such as daily water intake and the electrolytes found in liquid and solid foods, the gastrointestinal tract must deal with its own considerable daily secretions. The monumental nature and efficiency of this task is illustrated by Sellin (1998).9 He describes that the gastrointestinal tract processes 8000-9000 mL of fluid per day, with the vast majority of this derived from endogenous secretions. Fluid reabsorption by the healthy gastrointestinal tract is efficient (98%), and only 100-200 mL are lost in fecal matter each day. The great majority (80%) of this reabsorption occurs in the small intestine.

Disturbances in the major determinants of intestinal fluid absorption negatively impact the ability to reabsorb this large fluid load. The major determinants include intestinal mucosal surface area, the health or integrity of the mucosa, the status of small bowel motility, and the osmolarity of solutes in the intestinal lumen. Clinically, these disturbances can manifest as major components of short-bowel syndrome, namely diarrhea, dehydration, and electrolyte imbalance. Thus, short-bowel syndrome can be produced by clinical entities that result in critical loss of mucosal surface area (eg, massive small bowel resection) or degrade mucosal integrity (eg, radiation enteritis).

Macronutrients and micronutrients are absorbed along the length of the small intestine. However, as described by Clarke (1970), the jejunum has taller villi, deeper crypts, and greater enzyme activity compared to the ileum.10 Therefore, under normal conditions, about 90% of digestion and absorption of significant macronutrients and micronutrients are accomplished in the proximal 100-150 cm of the jejunum according to work conducted by Borgstrom and colleagues (1957) and by Johansson (1975).11,12 This includes absorption of proteins; carbohydrates; fats; vitamins B, C, and folic acid; and the fat-soluble vitamins A, D, E, and K.

However, if a significant portion or all of the jejunum is resected, the absorption of proteins, carbohydrates, and most vitamins and minerals can be unaffected because of adaptation in the ileum. Unfortunately, enzymatic digestion suffers because of the irreplaceable loss of enteric hormones produced by the jejunum. Biliary and pancreatic secretions decrease. Gastrin levels rise, causing gastric hypersecretion. The resultant high acid output from the stomach may injure the small bowel mucosa. Additionally, the low intraluminal pH creates unfavorable conditions for optimal activity of the pancreatic enzymes that are present. Diarrhea may then result if a large osmotically active solute load of unabsorbed nutrients is delivered to the ileum and colon.

Ileal resection severely decreases the capacity to absorb water and electrolytes. In addition, the terminal ileum is the site of absorption of bile salts and vitamin B-12. Loss of significant lengths of ileum almost invariably results in diarrhea. Continued loss of bile salts following resection of the terminal ileum leads to fat malabsorption, steatorrhea, and loss of fat-soluble vitamins. Retention of the ileocecal valve plays a pivotal role in massive small bowel resection. If the ileocecal valve can be preserved, intestinal transit is slowed, allowing more time for absorption. If the ileocecal valve is lost, transit time is faster, and loss of fluid and nutrients is greater. Furthermore, colonic bacteria can colonize the small bowel, worsening diarrhea and nutrient loss.

Preservation of the colon has positive and negative attributes. Philips and Giller (1973) demonstrated that colonic water absorption could be increased to as much as 5 times its normal capacity following small bowel resection.13 Also, by virtue of its resident bacteria, the colon has the inherent capacity to metabolize undigested carbohydrates into short-chain fatty acids, such as butyrate, propionate, and acetate. These are a preferred fuel source for the colon. Interestingly, work by Pomare and colleagues (1985) and Halverstad (1980) has demonstrated that the colon can absorb up to 500 kcal daily of these metabolites, which then can be transported via the portal vein to be used as a somatic fuel source.14

In contrast, maintenance of the colon increases the incidence of urinary calcium oxalate stone formation. The oxalate is normally bound by calcium in the small bowel and, thus, is insoluble when it reaches the colon. After massive enterectomy, much of this calcium is bound by free intraluminal fats. Free oxalate is delivered to the colon, where it is absorbed. This can eventually lead to saturation of the urine with calcium oxalate crystals and result in stone formation. As mentioned above, retention of the colon in the absence of a competent ileocecal valve can lead to small intestinal bacterial overgrowth.

The physiologic changes and adaptation of patients with short-bowel syndrome can be viewed in 3 phases.15   
 
The acute phase occurs immediately after massive bowel resection and may last up to 3-4 months. The acute phase is associated with malnutrition and fluid and electrolyte loss through the gastrointestinal tract.  Fluid and electrolyte loss through the gastrointestinal tract may be as high as 6-8 L/d. Patients will have abnormal liver function test results and transient hyperbilirubinemia.  Enteral feedings may also be initiated, but it should be relatively slow.  Patients with less than 100 cm of small intestine will require total parenteral nutrition.  The presence of ileocecal valve or colon may play a significant role in the outcome of these patients.15
 
The adaptation phase generally begins 2-4 days after bowel resection and may last up to 12-18 months.15  During this second phase, up to 90% of the bowel adaptation may occur.  Villous hyperplasia, increased crypt depth, and intestinal dilatation occur.  Early continuous feedings with a high viscosity elemental diet may reduce the duration of total parenteral nutrition.15
 
In the maintenance phase, the absorptive capacity of the gastrointestinal tract is at its maximum.15  Some patients may still require total parenteral nutrition. In other patients, nutritional and metabolic homeostasis can be achieved by small meals and supplemental nutritional support for life. These patients will also require vitamins and mineral supplements, including vitamins A, B-12, and D, magnesium, and zinc.15
 
A summary of the 3 phases is outlined below. 
  • Acute phase 
    • Starts immediately after bowel resection and lasts 1-3 months
    • Ostomy output of greater than 5 L/d
    • Life-threatening dehydration and electrolyte imbalances
    • Extremely poor absorption of all nutrients
    • Development of hypergastrinemia and hyperbilirubinemia
  • Adaptation phase
    • Begins within 48 hours of resection and lasts up to 1-2 years
    • Approximately 90% of the bowel adaptation takes place during this phase.
    • Enterocyte hyperplasia and villous hyperplasia and increased crypt depth occur, resulting in increased surface area. Intestinal dilatation and lengthening also occur.
    • Luminal nutrition is essential for adaptation and should be initiated as early as possible. Parenteral nutrition is also essential throughout this period.
  • Maintenance phase
    • The absorptive capacity of the intestine is at its maximum.
    • Nutritional and metabolic homeostasis can be achieved by oral feeding, or patients are committed to receiving supplemental or complete nutritional support for life.

Presentation

Patients with short-bowel syndrome invariably present with a history of several intestinal resections, as occurs with Crohn disease, or with a history of a major abdominal catastrophe or vascular accident, such as midgut volvulus or embolus to the superior mesenteric vessels. Pursuant to the resultant malabsorption, diarrhea (with or without steatorrhea) is an almost constant clinical finding.

Patients with short-bowel syndrome may describe significant weight loss, fatigue, malaise, and lethargy. These symptoms are protean but consistent with the diarrheic diathesis and resultant dehydration, electrolyte imbalance, protein-calorie malnutrition, and loss of critical vitamins and minerals.

Vitamin and mineral deficiencies can lead to some specific symptoms. Patients with vitamin A deficiencies may report night blindness and xerophthalmia. Vitamin D depletion can be associated with paresthesias and tetany. Loss of vitamin E can cause paresthesias, ataxic gait, and visual disturbances because of retinopathy. A history of easy bruisability or prolonged bleeding might suggest vitamin K depletion. Patients reporting dyspnea on exertion or lethargy may be anemic from vitamin B-12, folic acid, or iron deficiency. Calcium and magnesium losses can cause paresthesias and tetany. Patients with critically low zinc levels may describe anorexia and diarrhea.

Physical examination of the patient with short-bowel syndrome can reveal many clues to the diagnosis, depending on the duration and severity of the malabsorption.

  • Patients who are severely protein and energy malnourished may present with temporal wasting, loss of digital muscle mass, and peripheral edema. The skin may be dry and flaky. The nails can feature prominent ridges, and the lingual papillae are blunted or atrophic. In children, poor growth performance is a telling feature.
  • The essential fatty acids are linoleic and linolenic acids. Patients with essential fatty acid deficiency experience growth retardation, dermatitis, and alopecia.
  • The physical features of vitamin A deficiency include corneal ulcerations and growth delays.
  • Patients with low levels of the B complex vitamins in general can present with stomatitis, cheilosis, and glossitis. Vitamin B-1 deficiency is associated with edema, tachycardia, ophthalmoplegia, and depressed deep tendon reflexes. Vitamin B-6 deficiency can cause peripheral neuropathies and seizures. Peripheral neuropathy can be a feature of B-12 deficiency also.
  • Vitamin D depletion is associated with poor growth and bowed extremities.
  • Severe vitamin E deficiencies can result in ataxia, edema, and depressed deep tendon reflexes.
  • The physical hallmarks of vitamin K deficiency are related to derangements in hemostasis. These include petechiae, ecchymoses, purpura, or outright bleeding diatheses.
  • Physical clues to the presence of iron deficiency include pallor, spooned nails, and glossitis.
  • Zinc deficiency causes angular stomatitis, poor wound healing, and alopecia. Also, a scaly erythematous rash can erupt around the mouth, eyes, nose, and perineum.

Indications

Most survivors of massive bowel resections who develop short-bowel syndrome are initially fed with total parenteral nutrition. In these patients, total parenteral nutrition prevents the development of malnutrition and has been shown to benefit patient outcomes. Total parenteral nutrition may be administered concurrently with enteral nutrition early in the clinical course of short-bowel syndrome because the ultimate goal in many of these patients is to enhance intestinal adaptation and render patients free of total parenteral nutrition as described by Wilmore and colleagues (1971) in animal models.16 In many patients, intestinal adaptation, alone or in combination with modified and supplemented diets (eg, growth hormone, glutamine, high carbohydrate, low fat) as described by Byrne and colleagues (1995), eventually allows liberation from total parenteral nutrition.5

Unfortunately, some patients are extremely difficult or impossible to wean from parenteral nutrition. Common characteristics of these patients include very short remaining small bowel segments (<60 cm), loss of the colon, loss of the ileocecal valve, or small bowel strictures with stasis and bacterial overgrowth.

Total parenteral nutrition is not a panacea. Access sites become infected or the cannulated vein thromboses, necessitating replacement. Eventually, the patient may run out of usable veins for access to deliver total parenteral nutrition.

Other than these mechanical and infectious complications, many serious metabolic complications are associated with long-term use of total parenteral nutrition. The most clinically important of these are hepatic and biliary derangements. In fact, according to Vanderhoof (1997), advanced liver disease currently is the most common cause of death of patients with short-bowel syndrome.17

Early in the course of therapy with total parenteral nutrition, nonspecific elevations in hepatic transaminases can be found. Frequently, these biochemical abnormalities are self-limited and require no specific alteration or curtailment of therapy.

The most frequent manifestation of hepatobiliary disease in patients with short-bowel syndrome who are on total parenteral nutrition is cholestasis, as described by Cavicchi and coworkers (2000), Klein and Nealon (1988), and Quigley and colleagues (1993).18,19,20 Biliary sludge or gallstones are found in approximately 50% of patients receiving total parenteral nutrition with no oral intake for 3 months.

Progressive hepatic parenchymal damage is the most feared hepatobiliary complication of prolonged delivery of total parenteral nutrition. Fatty liver is observed frequently in adults. Nonalcoholic steatohepatitis has features of fatty change but is associated with inflammatory cell infiltration and fibrosis. Progressive cholestasis and liver injury can lead to outright portal fibrosis or cirrhosis. This portends progression to liver failure and a poor outcome. Patients with persistent liver function abnormalities should be identified before progression to cirrhosis to assess their candidacy for intestinal transplantation.

Moreno and coauthors (2005) reported complication rates and survival data for their cohort of 74 patients maintained on long-term home parenteral nutrition for the short-bowel syndrome.6 There were 94 significant complications in the group, with the majority being infectious in nature. At the end of the year, 74.3% of the patients remained on total parenteral nutrition. The most common cause for termination of support in the other 23.6% of the group was death (52.9%). Others either were switched to enteral nutritional support (11.8%) or were able to be liberated from specialized nutritional support to return to an oral diet (23.5%).

Relevant Anatomy

The gross anatomy of the small and large bowel and their arterial blood supplies are discussed in this section. The anatomic features peculiar to the small bowel and multivisceral transplantation are briefly described.

Pansky (1979) states that the duodenum extends form the pylorus to the duodenojejunal flexure and is about 25 cm in overall length.21 At the upper left border of the second lumbar vertebra is the duodenojejunal flexure. Here the duodenum turns anteriorly and caudally to become the jejunum just distal to the ligament of Treitz. The small bowel is divided relatively arbitrarily into the jejunum (proximal two fifths) and ileum (distal three fifths), although grossly the jejunum may appear to be of greater caliber, with a slightly thicker wall. It is fixed to the retroperitoneum by the root of the mesentery, which extends from the left upper quadrant of the abdomen to the right lower quadrant.

The terminal ileum is located in the right lower quadrant. The ileocecal valve marks the transition from small intestine to large intestine. The first portion of the colon is called the cecum. The ascending colon climbs along the right paracolic gutter and bends toward the midline at the hepatic flexure. Here the transverse colon begins and makes its way to the splenic flexure where the colon angles slightly medially and also inferiorly to become the descending colon. As the descending colon crosses the pelvic brim, it becomes the sinuous sigmoid colon. This portion of the colon heads toward the midline and then proceeds inferiorly. Below the pelvic peritoneal reflection, the sigmoid colon becomes the rectum.

The blood supply to the duodenum is extensive and is derived from branches of both the celiac axis and the superior mesenteric artery. These include, but are not limited to, the gastroduodenal artery, the superior and inferior pancreaticoduodenal arteries, the right gastroepiploic artery, and the supraduodenal and retroduodenal arteries. This dual blood supply helps to preserve the duodenum in the event of sudden occlusion of the superior mesenteric artery. While their blood supply is rich, the jejunum, with the exception of its proximal few centimeters, and ileum depend solely on branches of the superior mesenteric artery. These are termed the jejunal and ileal, or intestinal, arteries. The ileocolic artery, a branch of the superior mesenteric artery, also supplies the terminal ileum.

The ileocolic artery and the right colic artery supply the cecum and the ascending colon. The dominant blood supply of the proximal two thirds of the transverse colon is the middle colic artery. All of these colic arteries are branches of the superior mesenteric artery. Thus, the entire midgut, from jejunum to mid transverse colon, is dependent on the superior mesenteric artery.

Branches of the left colic artery, which is derived from the inferior mesenteric artery, supply the distal transverse colon and the descending colon. The sigmoid arteries and the superior rectal artery are derived from the inferior mesenteric artery as well.

For an exhaustive exegesis on the anatomy and the techniques of multivisceral abdominal organ transplantation, see The Many Faces of Multivisceral Transplantation by Starzl and colleagues.22

Contraindications

No firm absolute contraindications to surgery exist in patients with short-bowel syndrome. The only exception to this might be the creation of a small intestinal valve, designed to increase transit time, in a patient who already has stasis or bacterial overgrowth.

Patients who are severely malnourished with very low albumin or prealbumin levels and those with systemic sepsis or with severe coagulopathy because of advanced liver disease should have these conditions corrected before undergoing surgery.

The decision to operate on a patient with short-bowel syndrome requires great judgment. Surgery is undertaken in these patients usually only after all other therapeutic options, such as parenteral and enteral nutrition or pharmacologic bowel compensation, have been exhausted. Others may require operation because of the complications of prolonged parenteral nutrition or stasis of enteric contents and bacterial overgrowth.

More on Short-Bowel Syndrome

Overview: Short-Bowel Syndrome
Workup: Short-Bowel Syndrome
Treatment: Short-Bowel Syndrome
Follow-up: Short-Bowel Syndrome
References
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References

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Further Reading

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Keywords

short-bowel syndrome, short bowel syndrome, SBS, short gut syndrome, small intestine, small bowel, anenteric malabsorption syndrome, malabsorption, maldigestion, malnutrition, diarrhea, steatorrhea, fluid disturbances, electrolyte disturbances

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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, Director, Videoendoscopic Surgical Institute of Oklahoma, Consulting Staff, Department of Surgery, Comanche County Memorial Hospital; Consulting Staff, Great Plains Surgical Clinic, Lawton, Oklahoma
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: Nothing to disclose.

Managing Editor

David L Morris, MD, PhD, Professor, Department of Surgery, St George Hospital, University of New South Wales, Australia
Disclosure: Nothing to disclose.

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; AstraZeneca Grant/research funds Other

 
 
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