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Short Bowel Syndrome

Barre Guillen; Nichole S. Atherton.

Author Information and Affiliations

Last Update: July 17, 2023.

Continuing Education Activity

Short bowel syndrome (SBS) in adults is defined as less than 180 to 200 centimeters of
remaining small bowel (normal length 275 to 850 cm) leading to the need for nutritional and
fluid supplements. Patients present with signs and symptoms of malabsorption such as weight
loss, diarrhea, steatorrhea, dehydration, malnutrition, and electrolyte imbalance. Patients are
managed using either lifelong parenteral nutrition or intestinal transplantation. This activity
illustrates the assessment and management of short bowel syndrome and reviews the role of the
interprofessional team in improving outcomes in those with this condition.

Objectives:

Describe the findings expected in short bowel syndrome.

Summarize the expected signs and symptoms of short bowel syndrome.

Outline the treatment of short bowel syndrome.

Review the importance of collaboration and communication among the interprofessional

team to educate the patients on the possible need for lifelong parenteral nutrition, which
will enhance the delivery of care for those with short bowel syndrome.

Access free multiple choice questions on this topic.

Introduction
The normal length of small bowel in an adult, starting from the duodenojejunal flexure, measures
between 275 to 850 centimeters. Around 9 liters of fluid passes through the small bowel daily in
the form of oral fluids, saliva, gastric, biliary, and pancreatic secretions. On average, about
7 liters of those fluids are absorbed in the small bowel and 2 liters in the large bowel. The large,
healthy bowel absorbs roughly 150 kilocalories per day but can absorb up to 1000 kilocalories
per day in those patients with malabsorption.

The absorption of most nutrients occurs in the first 100 centimeters of the jejunum. B12 and bile
salts are absorbed in the last 100 centimeters of the ileum; magnesium is absorbed in the terminal
ileum and proximal colon; water and sodium absorption occur throughout the bowel.

Short bowel syndrome (SBS) in adults is defined as less than 180 to 200 centimeters of
remaining small bowel leading to the need for nutritional and fluid supplements. Although there
is no accepted definition for SBS in children, the need for intravenous supplementation when
having less than 25% of remaining small bowel that is expected for gestational age has been
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 suggested.

About 75% of cases of SBS develop after a single, massive resection of bowel; whereas, the
remaining 25% occur after multiple resections. Around two-thirds of patients who develop SBS
survive their initial hospitalization, and a similar number survive their first year after developing
SBS. Age and underlying disease primarily determine a patient's long-term outcome.[1][2][3]

Etiology
SBS can result from extensive surgical resection or congenital intestinal diseases. The most
common pathologies that lead to SBS in adults are Crohn disease, mesenteric ischemia, radiation
enteritis, post-surgical adhesions, and post-operative complications. In children, the most
common pathologies include volvulus, intestinal malformations, and necrotizing enterocolitis.[1]

Epidemiology
The epidemiology of SBS is not well-delineated as there are no data on the frequency of
intestinal failure secondary to SBS.

Pathophysiology
SBS can be classified by anatomical, pathophysiological, and postoperative criteria.
Anatomically, there are three types of SBS: end-jejunostomy, jejunocolonic anastomosis where
the jejunum is in continuity, most commonly, with the left colon, and jejunoileal anastomosis.
The pathophysiological criteria can also be subdivided into categories where the colon is in
continuity and those where it is not.

The primary pathophysiological mechanism of chronic intestinal failure secondary to SBS is

intestinal malabsorption due to the loss of intestinal absorptive surface and more rapid intestinal
transit. The successful rehabilitation of a patient with SBS depends upon the management of the
three phases of SBS: acute phase, adaptation phase, and maintenance phase.

The acute phase of SBS lasts 3 to 4 weeks and involves metabolic derangement and significant
intestinal losses as well as gastric hypersecretion due to the lack of inhibitory hormones that are
normally released from the terminal ileum. It requires close monitoring in the hospital setting to
avoid sequelae such as dehydration with acute kidney failure, acid-base abnormalities, and
electrolyte deficiencies.

The adaptation phase of SBS lasts 1 to 2 years and involves adaptive changes of remaining small
bowel to increase the area of bowel available for nutrient absorption, slow down intestinal transit
to maximize the time available for absorption, and adaptive hyperphagia. These processes are
promoted by the presence of nutrients in the bowel, pancreatic and biliary secretions, and
hormones released by the ileum and colon. Chronic intestinal failure – the condition that exists
when the adaptation phase fails to occur – is more likely to be reversible in the following
situations:

When there are more than 35 centimeters of small bowel along with a jejunoileal
anastomosis and an intact ileocecal valve and colon

When there are more than 60 centimeters of small bowel with a jejunocolonic anastomosis
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 When there is more than 115 centimeters of small bowel with an end jejunostomy

The third and final phase of SBS is the maintenance phase. This phase is managed with special
diets, oral or intramuscular supplementation of nutrients, and pharmacological treatments.[1]

Histopathology
Intestinal failure-associated liver disease is a complication of SBS. Histopathological
findings include cholestasis, steatosis, steatohepatitis, ductopenia, and perivenular and portal
fibrosis.

History and Physical

The primary adverse outcome of SBS is malabsorption secondary to decreased intestinal
absorptive surface area and rapid intestinal transit. The most common signs, symptoms, and
findings include malnutrition, weight loss, diarrhea, steatorrhea, dehydration, vitamin
deficiencies, and electrolyte imbalance. The individual with SBS will likely have undergone
extensive small bowel resection related to one of the underlying pathologies listed above.[1]

Treatment / Management
Initial management of SBS involves maintaining good nutritional status, maximizing the
absorptive surface area of the remaining intestine, and preventing complications. This involves
early postoperative parenteral nutrition as well as enteral nutrition once the patient's ileus has
resolved. This promotes intestinal adaptation which improves absorption of nutrients over time.

Those patients in whom intestinal failure is irreversible will require either lifelong home
parenteral nutrition or intestinal transplantation if a life-threatening complication of either SBS
or home parenteral nutrition arises. Treatment of SBS, therefore, largely consists of managing
and preventing complications that arise as a direct result of SBS or secondarily to home
parenteral nutrition. The management of SBS and the prevention of its complications share many
of the same treatments.

Intestinal failure-associated liver disease and liver cholestasis are treated with maintaining
some oral feeding, promptly treating infection or inflammation, optimizing home
parenteral nutrition, decreasing dependence on soy-based lipid emulsions or switching
them to fish oil-based emulsions and non-transplant surgical procedures.

SBS patients with less than 180 centimeters of small bowel or an absent ileocecal valve
are at increased risk of developing gallstones, frequently composed of calcium
bilirubinate. These gallstones can be prevented or reversed by maintaining enteral feeding
and limiting periods of oral fasting and by limiting the use of narcotic and anticholinergic
medications.

Dehydration, hyponatremia, chronic renal failure, and nephrolithiasis secondary to

SBS are managed with intravenous supplementation of fluids to maintain normal hydration
and urinary flow. More specifically, the treatment of dehydration and hyponatremia in
patients with SBS should maintain normal hydration with a urine output of 800 milliliters
per day and urine sodium greater than 20 millimoles/liter.
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 Hypomagnesemia can be caused by malabsorption of magnesium due to loss of the distal
ileum and right colon as well as chelation with fatty acids. Treatment consists of
appropriate hydration as delineated above and magnesium supplementation to a level
greater than 1.5 milligrams/deciliter.

D-lactic acidosis with an increased anion gap can occur in patients with SBS due to the
fermentation of unabsorbed carbohydrates by colon microbiota. This can lead to a D-
lactate encephalopathy that presents with slurred speech, ataxia, altered mental status,
psychosis, and sometimes coma. D-lactic acidosis is primarily a clinical diagnosis.
Treatment includes cessation of enteral feeds with carbohydrates, administration of an
antibiotic active against D-lactate forming bacteria, appropriate hydration, and thiamine
supplementation. Antibiotics include metronidazole, vancomycin, clindamycin, neomycin,
and tetracyclines.

Almost all patients on long-term home parenteral nutrition have metabolic bone disease
that manifests as osteopenia, osteomalacia, or osteoporosis. Diagnosis and evaluation are
done with mineral bone density, serum and urine mineral levels, vitamin D, PTH, and
markers of bone turnover. Management includes lifestyle and dietary changes, treatment of
underlying disease, optimization of vitamin D status and parenteral nutrition, and
sometimes bisphosphonates.

Surgical management is another important treatment strategy available to patients with SBS.
Patients on parenteral nutrition who suffer from rapid transit may benefit from reversing
intestinal segments or interposing segments of colon into the small bowel. Those with less than
60 centimeters of small bowel and parenteral nutrition-related complications may be candidates
for intestinal transplantation. Patients with dilated bowel secondary to obstruction can sometimes
be treated with intestinal tapering or strictureplasty if they have a bowel remnant greater than
120 centimeters or tapering with lengthening if the remnant is less 90 centimeters in adults or
less than 30 centimeters in children.[1][3][4]

Differential Diagnosis
Antral G Cells Hyperplasia

Atrophic Gastritis

Gastric Outlet Obstruction

Gastrinoma

Previous Vagotomy

Renal Failure

Retained Antrum Syndrome

Short Gut Syndrome

Prognosis
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 Those with greater than 180 cm of small bowel generally require no parenteral nutrition. Those
with greater than 90 cm will usually require it for less than 1 year. And those with less than 60
cm will likely require lifetime parenteral nutrition.

Complications
The primary complications of malabsorption are malnutrition, weight loss, steatorrhea, diarrhea,
electrolyte imbalance, and vitamin deficiencies. Other complications include nephrolithiasis due
to hyperoxaluria, cholelithiasis, transient gastric hypersecretion, bacterial overgrowth,
dehydration, hyponatremia, potassium deficiency, magnesium deficiency, renal failure, calcium
oxalate kidney stones, cholestasis secondary to intestinal failure-associated liver disease,
gallstones, and d-lactic acidosis.

In adults and older children, steatosis is more common, whereas in infants cholestasis and rapid
progression to liver fibrosis is the more common progression. Intestinal failure-associated liver
disease deaths are seen in between 16% and 60% of deaths in infants on home parenteral
nutrition.[1]

Enhancing Healthcare Team Outcomes

Ultimately, management of SBS requires an interprofessional team led by a physician with
gastrointestinal expertise. A gastrointestinal surgeon can provide the appropriate surgical
recommendations and management, and a transplant surgeon can expand the patient's therapeutic
options. Other essential team members include administrative support, a nurse coordinator
to handle the patient's day-to-day management, and a nutritionist. A psychologist and social
worker are important to address the psychosocial challenges of SBS.

Review Questions

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Comment on this article.

References
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L, Holst M, Jeppesen PB, Joly F, Kelly D, Klek S, Irtun Ø, Olde Damink SW, Panisic M,
Rasmussen HH, Staun M, Szczepanek K, Van Gossum A, Wanten G, Schneider SM, Shaffer
J., Home Artificial Nutrition & Chronic Intestinal Failure. Acute Intestinal Failure Special
Interest Groups of ESPEN. ESPEN endorsed recommendations. Definition and classification
of intestinal failure in adults. Clin Nutr. 2015 Apr;34(2):171-80. [PubMed: 25311444]
3. Nightingale J, Woodward JM., Small Bowel and Nutrition Committee of the British Society
of Gastroenterology. Guidelines for management of patients with a short bowel. Gut. 2006
Aug;55 Suppl 4(Suppl 4):iv1-12. [PMC free article: PMC2806687] [PubMed: 16837533]
4. Jeppesen PB, Fuglsang KA. Nutritional Therapy in Adult Short Bowel Syndrome Patients
with Chronic Intestinal Failure. Gastroenterol Clin North Am. 2018 Mar;47(1):61-75.
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 [PubMed: 29413019]

Disclosure: Barre Guillen declares no relevant financial relationships with ineligible companies.

Disclosure: Nichole Atherton declares no relevant financial relationships with ineligible companies.

Copyright © 2023, StatPearls Publishing LLC.

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