GASTROENTEROLOGY 2006;130:S5S15

Etiology and Initial Management of Short Bowel Syndrome

ALAN L. BUCHMAN
Division of Gastroenterology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois

he normal human small intestine ranges between 3

and 8 m in length, depending on whether measurement is made by radiologic or surgical techniques or at
autopsy when the intestine may be desicated.15 Short
bowel syndrome is defined in adults as 200 cm of small
intestine. Although usually acquired because of one or
more enterectomies, short bowel syndrome may also be
congenitally acquired. Nutrient, electrolyte, and fluid
absorption is proportional to the amount of residual
intestine. The degree of intestinal function is better
described in terms of energy absorption/loss rather than
length of residual intestine.6 Intestinal failure may be
defined as the inability to sustain adequate nutritional,
electrolyte, or hydrational status in the absence of specialized nutritional support. This requires an increase in
oral intake because absorption is compromised. Clinically, nutrient assimilation is a function of intake and
absorption. As such, some patients with short bowel
syndrome will not have sufficient loss of functional capacity as to develop intestinal failure. Significant individual variability in jejunal absorption efficiency may be
encountered.7
The patients with the greatest risk for development of
dehydration, generalized protein-calorie malnutrition,
and multiple nutrient deficiencies are those with a duodenostomy or jejunoileal anastomosis and 35 cm of
residual small intestine; jejunocolic or ileocoloic anastomosis, and 60 cm of residual small intestine; or end
jejunostomy with 115 cm of residual small intestine.6,8 11 Those patients with residual colon in continuity will have enhanced energy and fluid absorption.
Hence, such patients can tolerate greater loss of small
intestine and retain their nutritional autonomy.

Incidence and Prevalence of Short

Bowel Syndrome
It is unclear how many individuals in the United
States suffer from short bowel syndrome, but, based on
the numbers in Europe, the incidence is probably approximately 2 individuals per million.12 More recent
data from 1993 indicated that the incidence and prevalence of home parenteral nutrition, for which short bowel
syndrome was the most prevalent indication, had in-

creased slightly to 2 or 3 per year per million inhabitants

and 4 per year per million, respectively.13,14 The most
recent European survey, in 1997, indicated that the
incidence of home total parenteral nutrition (TPN) had
remained approximately 3 per million and that the prevalence had increased to 4 per million.15 The largest single
group of patients who received home TPN were those
with short bowel syndrome (35%). In comparison, the
most recent data for incidence and prevalence in the
United States is from 1992. At that time, it was estimated based on extrapolated data from the Oley Foundation Home TPN Registry that approximately 40,000
patients required TPN each year.16 Approximately 26%
of the patients in the Oley Registry had short bowel
syndrome, although some patients with a primary TPN
indication of malignancy or radiation enteritis may have
had short bowel syndrome as well. Patients with short
bowel syndrome who did not require home TPN or were
successfully weaned from home TPN are not reflected in
these statistics. Approximately half of the short bowel
patients who initially require TPN can be weaned off of
TPN successfully in optimal settings.8 Therefore, the
number of patients with short bowel syndrome may be
substantially greater than previously estimated. A registry of short bowel patients, including those who require
TPN permanently, transiently, and not at all, should be
implemented.

Etiology of Short Bowel Syndrome

Short bowel syndrome may be a congenital or
acquired condition. Infants may be born with congenital
jejunal or ileal atresia. Otherwise, short bowel syndrome
results from surgical resection of bowel. This is usually
related to multiple resections for recurrent Crohns disease, massive enterectomy made necessary because of a
catastrophic vascular event such as mesenteric arterial
embolism, venous thrombosis, volvulus, trauma, or tumor resection in adults, and, in children, gastroschisis,
Abbreviations used in this paper: GLP, glucagon-like peptide; ORS,
oral rehydration solution; TPN, total parenteral nutrition.
2006 by the American Gastroenterological Association
0016-5085/06/$32.00
doi:10.1053/j.gastro.2005.07.063

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ALAN BUCHMAN

necrotizing enterocolitis (NEC), volvulus, and extensive

aganglionosis. Functional short bowel syndrome may
also occur in cases of severe malabsorption in which the
bowel length is often intact. Such conditions may include chronic intestinal pseudo-obstruction syndrome,
refractory sprue, radiation enteritis, and congenital villus
atrophy. Severe nutrient and fluid malabsorption occurs
following extensive small intestinal resection. Patients
with less than 100 cm of jejunum remaining generally
have a net secretory response to food.17
Patients can be grouped into 2 distinct subgroups:
those with intact colon in continuity and those without
colon in continuity. The colon becomes an important
digestive organ in patients with short bowel syndrome.
Sodium, water, and some amino acids are absorbed in the
colon9,18 20 as well as energy from absorbed short-chain
fatty acids.

Postresectional Adaptation
The intestine adapts as well to ensure more efficient absorption per unit length. Following massive enterectomy, the intestine hypertrophies, and nutrient absorption becomes more efficient. Although there are
limited human data, observations in patients with massive enterectomy as well as in the functional short bowel
patient (JI-bypass) indicate that the intestine lengthens
some, but more importantly, diameter and villus height
increase with a resultant increase in absorptive surface.2124 This process may evolve over 1 or 2 years.6,9,25
Patients may be taught to adapt to their decreased absorption as well by dramatically increasing their food
intake (hyperphagia).
The presence or absence of the colon and ileocecal
valve; location (jejunum versus ileum), health, and
length of residual bowel; mucosal blood flow; patient
age; and comorbid conditions such as Crohns disease,
radiation enteritis, carcinoma, or pseudo-obstruction are
important determinants in the functional adaptation process and clinical outcome.6,26,27 Although the length of
remaining bowel necessary to prevent dependence on
TPN is approximately 100 cm in the absence of an intact
and functional colon, or 60 cm in the presence of a
completely functional colon,6,9,28 the degree of adaptation and TPN dependence may be highly individualized.
Adaptation to full enteral nutrition has been reported
with as little as 10 cm of residual intestine in infants.25
Patients with a jejunostomy are at increased risk for TPN
dependence, and those with a jejunal-ileal anastomosis
are less likely to be TPN dependent.
Animal models have suggested that enteroglucagon,
glucagon peptide II, epidermal growth factor, growth

GASTROENTEROLOGY Vol. 130, No. 2

hormone, cholecystokinin, gastrin, insulin, and neurotensin are involved in postresection intestinal adaptation.29 There are little data on the role of either increased
endogenous hormonal release or exogenous hormone supplementation during the intestinal adaptation phase in
humans.
Residual ileum is able to adapt and to assume the role
of macronutrient absorption when jejunum has been
resected. However, the specialized cells of the terminal
ileum in which vitamin B-12/intrinsic factor receptors
are located and in which bile salts are reabsorbed cannot
be replaced by jejunal hypertrophy.

Medical Therapy of Short Bowel

Syndrome
The goal of medical therapy is for the patient to
resume work and a normal lifestyle, or as normal of one
as possible. This is undertaken via the use of specific
measures to decrease gradually the requirement for TPN
and, at best, to eliminate its need. The most important
aspects of the medical management of the patient with
short bowel syndrome are to provide adequate nutrition,
including both macro- and micronutrients, to prevent
energy malnutrition and specific nutrient deficiencies, to
provide sufficient fluid to prevent dehydration, and to
correct and prevent acid-base disturbances. Most macronutrients, including carbohydrate, nitrogen, and fat, are
absorbed within the first 100 cm and up to 150 cm of
jejunum.30
Macronutrient Assimilation and Dietary
Therapy
Typically, patients who have undergone massive
enterectomy require TPN for the first 710 days. The
immediate goals during this period are survival and
hemodynamic stability. Nutritional therapy should not
be introduced until the patient is hemodynamically stable and fluid management issues are relatively stable.
Patients should be provided approximately 2535 kcal/
kg/day and 1.0 1.5 kg/day of protein. It remains controversial whether intake should be based on actual body
weight or ideal body weight.31 Enteral nutrition should
be started as soon as possible once hemodynamic stability
has been achieved; standard enteral formula is recommended. Enteral nutrition should be instituted gradually
as tolerated. Once patients are able to eat, they should be
encouraged to eat a regular diet but modified as described below. Patients should also be encouraged to
adapt their diet to eat substantially more than what was
usual prior to their catastrophic event (hyperphagia).32
Separation of liquids and solids has no effect on macro-

February Supplement 2006

nutrient, electrolyte, or mineral absorption or fecal volume or fecal weight.19

Proteins/Amino Acids
Dietary protein is first digested by pancreatic,
gastric, and intestinal proteases and then absorbed as diand tripeptides. Therefore, it was reasoned that if dietary
protein were provided in a predigested form, it would be
more readily absorbed. However, absorption of nitrogeneous macronutrients (or proteins) is least affected by the
decreased intestinal absorptive surface in patients with
short bowel syndrome. Therefore, the utility of peptidebased diets in such patients is theoretically without
merit.
McIntyre et al fed 7 patients with an end-jejunostomy
(60 150 cm residual small bowel) a peptide-based or an
essentially isocaloric and isonitrogenous polymeric formula. Energy, carbohydrate, nitrogen, fat, electrolyte,
fluid, and mineral absorption and stool weight were
similar regardless of the enteral formula provided.33 Uncontrolled data from Levy et al support these findings.34
A small study of 6 patients (90 150 cm of residual
jejunum and end-jejunostomy) reported by Cosnes et al,
however, suggested that nitrogen absorption may be
modestly improved with the use of a peptide-based diet,
although similar to previous studies, energy, other macronutrient, electrolyte, mineral, and fluid absorption
were unaffected.35 These studies were all very small, the
study populations somewhat heterogeneous, and the various peptides used in the formulas differed significantly,
as did the type and amount of fat (long-chain triglycerides vs medium-chain triglycerides). It is therefore difficult to make definitive comparisons among studies.
The amino acid glutamine, together with glucose, is
the preferred fuel for the small intestinal enterocyte.36
Rodent TPN models suggested that either parenteral or
enteral glutamine supplements could effect more rapid
and more significant bowel adaptation following massive
enterectomy.37,38 Therefore, it was thought that glutamine supplementation in humans would have a similar
effect. Although an early case series of 10 patients who
were beyond the usual 12 year adaptation period suggested that glutamine, combined with growth hormone
supplementation, and a high complex carbohydrate diet
could result in decreased stool output and increased
absorption of energy, protein, carbohydrate, sodium, and
water,39 2 subsequent, double-blinded, randomized placebo-controlled trials failed to confirm any of these effects.40,41 In addition, Scolapio et al showed that glutamine and growth hormone supplementation did not
lead to morphologic changes in the intestine.40 Glutamine-supplemented oral rehydration solution (see fluid

CHARACTERISTICS OF SHORT BOWEL SYNDROME

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and electrolyte management) was associated with decreased Na absorption and a trend toward decreased fluid
absorption in a small controlled trial in 6 patients.41 All
of the patients studied by Byrne et al39 had colon in
continuity; it is likely the treatment-associated increase
in energy absorption was related solely to the increased
complex carbohydrate diet as discussed above. Treatment
with growth hormone and glutamine in the setting of
short bowel syndrome has been associated with significantly
increased extracellular fluid and peripheral edema.40,42,43
A recent study reported by Seguy et al showed that
low-dose growth hormone (0.05 mg/kg/day) was associated with a modest increase in carbohydrate and nitrogen
absorption.44 A recent randomized, placebo (glutamine)controlled study indicated growth hormone administration, when used outside the natural adaptation period,
led to the ability to reduce parenteral fluid and nutrition
requirements, although absorptive studies were not undertaken.45 Neither growth hormone nor glutamine have
been studied in humans when used in the initial 12year periadaptative period. Therefore, treatment with
glutamine and/or growth hormone cannot be recommended at the present time. However, it may be that use
of such exogenous growth factors may have their greatest
utility if used during the normal adaptive period. There
are no human studies to test this hypothesis.
Lipid
Lipid digestion may be impaired because of impaired solubility because micelle formation will be impaired when ileal bile salt malabsorption occurs in the
setting of ileal resection (100 cm).46 Treatment with
ox bile supplements has been attempted in 3 patients in
an attempt to increase duodenal bile salt concentration to
stimulate micellar lipid solubilization.47 49 This therapy
has been associated with significantly increased fecal
volume, at least in those patients with intact colon. A
preliminary, open-labeled study of 4 patients (2 with
colon in continuity) indicated that treatment with the
conjugated bile acid cholylsarcosine (6 g/day) was associated with an increase in fat absorption of 17 3 g/day
without any effect on stool wet weight.50 Cholylsarcosine
is a conjugated bile acid and is resistant to colonic
bacterial deconjugation. Another case series of 4 subjects
had similar findings.51 However, 1 of the 4 patients
experienced a significant increase in wet stool output,
and nausea developed in another patient. Cholestyramine
should not be used in patients with 100 cm of ileal
resection because it may actually worsen steatorrhea because of the binding of dietary lipid.52
Regardless of whether a high- or low-fat diet is used,
the percentage of fat absorption remains stable, and stool

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ALAN BUCHMAN

weight is unaffected by the fat content of meals.53,54

However, because of the energy density of fat (9.0 kcal/g)
when compared with carbohydrate (4.0 kcal/g), it is an
important dietary energy source. In addition, in short
bowel syndrome patients, up to 65% of dietary carbohydrate may be malabsorbed and lost in the feces without
degradation by colonic bacteria.32
A mixed long-chain triglyceride:medium-chain triglyceride (LCT:MCT) diet was studied in 19 patients.
Those patients with intact colon absorbed 96% 3% of
C8 fatty acids and 87% 6% of C10 fatty acids, and
those patients without colon absorbed 63% 25% of
C8 and 57% 28% of C10, (P .007 for C8 and P
.004 for C10).55 MCT contains 8.3 kcal/g. Energy absorption (approximately 2.1 MJ/day; 500 kcal/day) was significantly increased in patients with colon, although the
LCT:MCT diet did not result in increased energy absorption when compared with the LCT-based diet in patients
with an end-jejunostomy or ileostomy. These patient also
had increased fecal output with a mixed LCT:MCT diet.
Some, but not all LCT, can be replaced by MCT in the
diet because the essential fatty acid linoleic acid is a
constituent of LCT and is not found in MCT. Excessive
MCT intake may result in nausea, vomiting, and ketosis.
In a short bowel patient eating 10.5 MJ/day (2500
kcal/day), approximately 1.53 MJ/day (360 720 kcal/
day; 40 80 g) of LCT can be replaced with MCT.
Carbohydrates
The proximal jejunum rarely requires resection in
patients that undergo massive enterectomy. Most intestinal dissacharidases are present in highest concentration
in the very proximal small intestine, and, hence, patients
with more distal resection are not likely to benefit from
a lactose-free diet. In a study of 14 short bowel patients,
a lactose-free diet was compared with a diet containing
20 g/day of lactose (still with 4 g milk).56 Lactose
absorption, breath hydrogen, subjective symptoms of
flatulence, and diarrhea were similar regardless of the
diet. These data confirmed the findings of an earlier
controlled study in 17 short bowel patients, which found
that lactose absorption was enhanced when provided in
yogurt rather than via milk.57 Regardless, in the absence
of significant jejunal resection, patients with short bowel
syndrome should not be provided lactose-restricted diets.
Such diets are also generally low in calcium. Even patients with an end-jejunostomy will generally tolerate a
glass of milk (20 25 g lactose).57
The Role of the Complex Carbohydrate Diet
Soluble nonstarch polysaccharides and some
starches58 are not generally absorbed by the small intes-

GASTROENTEROLOGY Vol. 130, No. 2

tine. Soluble fiber dissolves in water and is found primarily in oatmeal, oat bran, psyllium (Metamucil, Proctor & Gamble, Cincinatti, OH; Konsyl, Konsyl
Pharmaceuticals, Easton, MD), barley, artichokes, strawberries, legumes, prunes, grapefruit, and squash in descending order of concentration. Soluble fiber and
starches pass undigested into the colon in which they are
fermented by enteric bacteria into hydrogen and methane
(hence patient gas complaints) but also into shortchain fatty acids (SCFAs), including butyrate, proprionate, and acetate. SCFAs are the preferred fuel for colonocytes.59 Therefore, the colon becomes a digestive organ in
patients with short bowel syndrome. Approximately 75
mmol SCFA are produced from 10 g unabsorbed carbohydrate.60 Patients with short bowel syndrome but intact
colon in continuity were able to decrease fecal energy loss
by 1.33.1 MJ/day (310 740 kcal) when they were fed
a diet consisting of 60% carbohydrates.61 Colonic metabolism of unabsorbed carbohydrate was indicated by
decreased fecal carbohydrate losses in the patients with
colon in continuity. The intact colon may absorb up to
2.2 4.9 MJ (5251170 kcal) of energy daily from dietary fiber.9,10,61 Colonic energy absorption may also
increase some during the postresection adaptation phase,
related to increased colonic bacterial carbohydrate fermentation.11,62 The increased fermentation may result
from increased colonic bacteria and/or an increase in the
concentration or activity of various enzymes including
-galactosidase during the adaptation period.62 Because
SCFAs stimulate sodium and water absorption,63 patients might be expected to have decreased fecal fluid and
sodium loss as adaptation progresses, although this has
not been observed clinically.61
Vitamins
Micronutrients often require supplementation. It
is unusual for water-soluble vitamin deficiencies to develop in short bowel patients in the absence of TPN
(except in those who have proximal jejunostomies or
duodenostomies) because these are absorbed in the proximal jejunum. Thiamine deficiency has been described,
especially during a recent parenteral vitamin shortage.64
Patients may present with Wernickes encephalopathy,
beriberi, and severe metabolic alkalosis.65 Whole blood
thiamine concentration may not be indicative of deficiency as it reflects recent nutritional intake. Erythrocyte
transketolase activity should be measured and empiric
therapy begun with 100 mg parenteral thiamine daily.
Biotin deficiency has rarely been reported in patients
with short bowel syndrome.66 Scaly dermatitis, alopecia,
lethargy, hypotonia, and lactic acidosis have been described. Therapy consists of parenteral biotin supplemen-

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tation of 0.31 mg daily, although this is not commercially available in the United States. Vitamin B-12
supplementation is required (300 g/month subcutaneously) in patients who have had a 60-cm terminal
ileum resected.67 Folic acid is provided as a constituent of
most oral and parenteral multivitamins. Folate deficiency
may develop in patients with proximal jejunal resections.68 These patients should receive 1 mg folate daily.
Fat-soluble vitamin deficiency (A, D, and E) is more
common in patients with short bowel syndrome because
of fat maldigestion related to decreased bile salt reabsorption and decreased micelle formation.69 Cholestyramine may cause fat-soluble vitamin deficiency because of
its binding of bile salts.70 Night blindness and xerophthalmia have been described in short bowel syndrome.71
If not recognized, vitamin A deficiency may progress to
corneal ulceration and later permanent visual loss may
develop. The serum vitamin A concentration should be
monitored in patients who do not require parenteral
vitamin supplementation. If a low serum vitamin A
concentration is detected, therapy should be started with
10,000 50,000 units daily, administered either orally or
parenterally.
Vitamin D deficiency manifests in osteomalacia. Usually, dietary intake is a relatively unimportant source of
vitamin D because the majority is endogenously synthesized from 7-dehydrocholesterol via ultraviolet light.72,73
However, because enterohepatic circulation is disrupted
in patients who have undergone significant ileal resections, deficiency may result.74
Vitamin E deficiency may manifest in hemolysis75 and
various neurologic deficits.76 Because serum vitamin E
concentration reflects serum total lipid concentration,
which may be low in short bowel patients who have
steatorrhea, low serum vitamin E concentration alone
may not be indicative of a deficient state; the serum
vitamin E:total lipid ratio should be calculated.77,78
Most vitamin K is synthesized by colonic bacteria
(60%),79 although dietary intake accounts for approximately 40% of requirements; deficiency is therefore uncommon in patients with intact colon. However, vitamin
K deficiency is frequent in patients who have no residual
colon or who have taken broad-spectrum antibiotics recently. The requirement is approximately 1 mg daily.79
Vitamin K was not a constituent in adult multivitamins
for TPN until recently, although it has in children.
Trace Metals
Significant amounts of zinc and selenium are lost
with diarrhea. A significant amount of zinc is also lost in
small bowel effluent (12 mg/L small intestinal fluid and
16 mg/L stool).80 Zinc deficiency has been associated

CHARACTERISTICS OF SHORT BOWEL SYNDROME

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with growth abnormalities,81 delayed wound healing,82

and cellular immunity dysfunction.83 Patients in whom
zinc deficiency is suspected should be treated empirically
with oral zinc sulfate (220 440 mg daily) or parenteral
zinc supplements if they require TPN. Serum and leukocyte measurements of zinc concentration, although
helpful, may be unreliable.84 Selenium deficiency has
been associated with cardiomyopathy85; peripheral neuropathy, proximal muscle weakness, and pain86; whitening of the hair; and macrocytosis.87 Serum selenium is a
reliable indicator of selenium status, and, if low, oral or
parenteral supplementation should be provided. Although there are 3 reported possible cases of chromium
deficiency in patients requiring long-term TPN,88 deficiency has not been reported in short bowel patients who
do not require TPN, and, therefore, routine supplementation is not recommended. Chromium is a necessary
cofactor for insulins effects in peripheral tissue.89 However, available evidence suggests that there is sufficient
chromium present in the TPN solutions as a contaminant, and supplemental chromium may result in the
possibility of nephrotoxicity.90 Copper deficiency is very
rare in the patient with short bowel syndrome. Deficiency may result in microcytic anemia, neuropathy, and
decreased fertility.91
Medication Absorption
Medication absorption is often impaired, just as is
nutrient absorption in patients with short bowel syndrome, although significant interpatient variability may
be observed. The oral or enteral route for medication
delivery should be used whenever possible to avoid additional manipulations of the TPN catheter, which are
associated with increased infection risk. The degree to
which a medication is malabsorbed is dependent on the
residual small bowel surface area and its health (for
example, whether or not active Crohns disease is present)
and morphologic and physiologic factors, including the
presence or absence of the terminal ileum (especially
important for vitamin B-12 and bile salt absorption,
which are necessary for the absorption of lipid-soluble
medications such as cyclosporin) or the presence of an
acidic or alkaline environment (which may be caused by
the use of H2 blockers in TPN or proton pump inhibitors). Many, but not all, medications are absorbed in the
jejunum. Therefore, absorption will be minimally impacted for most medications in the absence of decreased
intestinal transit time, which will decrease mucosal contact time. Most of the available data on oral medication
absorption in patients with short bowel syndrome are in
the form of isolated case reports.92 The sublingual route

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ALAN BUCHMAN

for medication delivery may be preferable for some medications.

Fluid and Electrolyte Management
Massive enterectomy is associated with transient
gastric hypersecretion and hypergastrinemia, generally
lasting for up to 6 months following resection.93,94 H2antagonists and proton pump inhibitors are useful to
reduce gastric fluid secretion and, therefore, also reduce
fluid losses during this period.17,9597 However, because
absorption of orally dosed medications may be impaired,
either large doses or intravenous delivery may be required. Although fluid losses are decreased, macronutrient and electrolyte absorption are not affected by the
increased gastric secretion. Reduction of gastric acid
output is also important to help prevent the deconjugation of bile acids in the duodenum and decreased pancreatic lipase excretion to enhance fat digestion.
Fluid losses usually require chronic control with antimotility agents such as loperamide hydrochloride or
diphenoxylate. Typical doses are 4 16 mg/day. If these
are ineffective, especially in patients with no colon in
continuity or those who have a minimum of residual
jejunum or duodenum, codeine sulfate or tincture of
opium may be necessary. The usual dose for codeine is
15 60 mg, 2 or 3 times daily. Rarely, patients will
require treatment with octreotide. Octreotides mechanism of action is unclear, but it may be useful to slow
intestinal transit time, which will increase water and
sodium absorption.98,99 Daily jejunostomy volume was
reduced from 8.1 1.8 to 4.8 0.7 L/day using a dose
of 100 g, subcutaneous, 3 times daily, of octreotide 30
minutes before meals in one open-labeled study of 9
patients with end-jejuonstomies.100 However, octreotide
use does not result in TPN discontinuation, and it
reduces splanchnic protein synthesis, thereby reducing
mucosal protein incorporation and villus growth rate.
Therefore postresectional intestinal adaptation may be
impaired.101 A recent small study with the long-acting
derivative of octreotide showed no measurable benefit.102
Octreotide also increases the risk for cholelithiasis103 in a
patient group already predisposed.104 It should therefore
be reserved for patients with high-output jejunostomies
in whom fluid and electrolyte management has proven
difficult otherwise.
Glucose-polymer-based oral rehydration solutions
should be used to improve hydration and to decrease
TPN fluid requirements in patients with residual jejunum ending in a jejunostomy. Patients with 100 cm of
residual jejunum have significant risk for dehydration
because they secrete more sodium (Na) and fluid than
they orally consume.95 Because the jejunum is permeable

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to Na and chloride (Cl), passively absorbed solutions

with high NaCl concentration are readily absorbed. Glucose promotes salt and water absorption by solvent drag
and via stimulation of sodium-linked transport.105 However, although Na and water are absorbed from hypotonic isotonic solutions delivered into the jejunum, absorption is superior with more hypertonic fluids.106
Therefore, hypotonic oral rehydration solutions may be
of benefit in patients with an intact gastrointestinal tract
and acute infectious diarrhea but may not be of use in the
short bowel patients. Ingestion of hypotonic fluids may
be associated with increased Na loss.107109 Several commercially available oral rehydration solution (ORS) formulas are available, although probably the best, and
certainly the least expensive, is that recommended by the
World Health Organization (WHO).110 This can be
formulated by dissolving the following in 1 liter of tap
water: NaCl (2.5 g), KCl (1.5 g), Na2CO2 (2.5 g), and
glucose (table sugar, 20 g). Only the KCl requires a
physician prescription. Most, if not all, of the commercially available ORS have substantially less sodium (in
the range of 4550 mmol/l). Less NaCl may be added,
but the optimal Na concentration should be at least
90 100 mmol/L, which is the usual concentration of
small bowel effluent.20 Solutions with lower sodium
concentrations result in increased sodium losses. Therefore, patients with short bowel syndrome should be
cautioned against consumption of plain water and should
be encouraged to drink ORS whenever they are thirsty.
More recent evidence has shown that hypotonic (160
mosm/kg) ORS leads to decreased intraluminal duodenojejunal fluid flow rate in normal volunteers, although
the effect on gastrointestinal fluid losses or fluid status in
patients with short bowel has not been evaluated.111
ORS may still be useful even in patients with residual
colon in continuity, but, provided sufficient sodium is
present in the diet, the amount of Na in the ORS may
not be as critical because the colon readily absorbs Na
and water against a steep electrochemical gradient.112
The presence of glucose in the ORS is not critical in
patients with no remaining jejunum, but who have residual ileum, because ileal water absorption is not affected by the presence of glucose.113
In addition to Na losses, significant quantities of
magnesium (Mg) are lost in jejunal or ileal effluent.74
Given that magnesium deficiency may develop despite a
normal serum magnesium concentration, it is prudent to
measure 24-hour urine Mg loss.114 The median 24-hour
urine Mg in normal volunteers in one study was 127 mg
(vs 19 mg for magnesium deficient short bowel patients).74

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Mg deficiency may cause calcium (Ca) deficiency because hypomagnesemia impairs parathyroid hormone release.115 In addition, the majority of patients with short
bowel syndrome who do not require TPN are in negative
Ca balance.116 Therefore, in the absence of TPN, oral Ca
supplementation is recommended routinely (800 1200
mg/day). Mg replacement is problematic. Attempts with
oral MgO or oral consumption of injectable Mg are
generally not successful and have been associated with
increased fecal loss because of their cathartic effect.117
Although Mg gluconate is water soluble, Mg has not
generally been a constituent of ORS. Therefore, some
patients may require periodic parenteral Mg infusion
despite the absence of a TPN or intravenous fluid requirement otherwise. Iron is absorbed in the duodenum
and, therefore, in the absence of hemorrhage, is not
routinely required as a supplement. Phosphorous deficiency is not well described in short bowel syndrome,
and, therefore, supplementation is rarely, if ever, required.
Pharmacologic Enhancement of Intestinal
Adaptation
Glucagon-like peptide 2 (GLP-2) is another hormone secreted from L cells (as well as from pancreatic A
cells). Postprandial serum GLP-2 concentration is not
unexpectedly depressed in patients who have had extensive small bowel resection, especially including ileum.118
It has been postulated that the relative lack of jejunal
hypertrophy following ileal resection119,120 may be at
least in part related to the resection of GLP-2-producing
L cells, although these investigations were undertaken in
patients some 2 years following their resection without a
baseline comparison. Studies have not been undertaken
in patients immediately following resection. In a similar
patient population, Jeppesen et al suggested that subcutaneous injection of GLP-2 resulted in modestly increased nutrient and fluid absorption.121 More recently, a
longer-acting analogue of GLP-2 has shown similar effects.122
Dietary Restriction
Normally, oxalate in the diet binds to dietary
calcium and is excreted in stool. However, in the
presence of significant fat malabsorption, dietary calcium preferentially binds to free fatty acids, rendering
the oxalate free to pass into the colon in which it is
readily absorbed; dietary oxalate is absorbed only to a
minimal extent in the small intestine. Oxalate absorption may also be enhanced in the colon because of
increased permeability because of injury caused by
malabsorbed bile salts, which flow into the colon.123

CHARACTERISTICS OF SHORT BOWEL SYNDROME

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Oxalate is renally filtered and then bound to calcium

once absorbed in the colon. This results in hyperoxaluria with subsequent calcium oxalate nephrocalcinosis and nephrolithiasis.9 Therefore, patients with short
bowel syndrome with colon in continuity should be
prescribed an oxalate-restricted diet. Because calcium
does bind to oxalate, oral Ca supplements may be used
to prevent Ca-oxalate nephrolithiasis.124 Hyperoxaluria may also develop in any patient receiving TPN
because the vitamin C contained in the TPN solution
is metabolized to oxalate when exposed to light.125,126
TPN should therefore be shielded from light, but it
remains unclear whether dietary oxalate should be
restricted in patients without colon in continuity who
require TPN.
Providing Parenteral
Nutrition/Macronutrients
Most patients with short bowel syndrome will
require TPN, at least initially. For the normally nourished patient, TPN should be supplied at 2530 kcal/
kg/day based on ideal body weight for adults, with
greater levels of support for infants and children depending on age. Dextrose is a monohydrate and, as
such, provides 3.4 kcal/mL (vs 4.0 kcal/mL for most
carbohydrates). The maximum dextrose infusion rate
should be 57 mg/min.127 Blood glucose concentration should be monitored at least daily (optimally 4
times a day) and should be below 160 mg/dL. If blood
glucose exceeds this level, glucose spills in the urine,
energy is lost, dehydration may ensue, and infection
risk is increased.128 The addition of regular insulin to
the TPN solution may be required. If insulin is required, it should be added to the TPN bag at an initial
dose of 0.1 units per gram of dextrose, with subsequent adjustments as necessary. Intravenous lipids are
generally used to provide 20%30% of infused calories, although a greater percentage of lipid may be
used in the patient with significant glucose intolerance or difficult fluid management; 20% lipid emulsion is more calorically dense than dextrose. Generally,
the percentage of lipid calories should be increased
and the percentage of dextrose calories decreased if the
amount of supplemental insulin required exceeds 0.2
units per gram of dextrose. The serum triglyceride
concentration should be kept under 700 800 mg/dL
and, optimally, 400 mg/dL. Protein is supplied in
the form of amino acids and should be supplied at
1.0 1.5 g/kg/day, based on ideal body weight for
adults; greater levels of support are required for infants and children depending on their age.

S12

ALAN BUCHMAN

Getting the Patient Ready for Home

TPN
Initially, TPN is infused continuously while postoperative complications are addressed and metabolic issues stabilized. Attempts should be made, when appropriate, to wean patients who have sufficient absorptive
capacity as discussed above, being mindful that maximal
adaptation requires up to 12 years. For patients who
will require TPN at home, the TPN infusion should be
compressed to nighttime infusion. Typically, the infusion would run over a 10 12-hour period with an additional 30 60-minute taper period; some patients with
fluid management issues from renal failure or congestive
heart failure will be unable to tolerate this infusion rate
and will require either a longer infusion time or less
volume. Because rapid carbohydrate and fluid infusion
may be associated with intra- and extracellular fluid
shifts, some patients may develop extremity cramping
from extracellular potassium deficiency, which may be
corrected by slowing the infusion rate. Pancreatic insulin
secretion requires some time to adapt to the significant
dextrose infusion; therefore, the cycling of TPN to nighttime use should be a gradual process. The infusion time
for TPN is generally compressed by 2 4 hr/day, depending on the total infused volume and electrolyte and
glucose measurements. TPN should be infused ideally
via a single lumen catheter, with its tip positioned in
either the superior or inferior vena cava to decrease the
risk of infection and thrombosis.128,129 Tunneled catheters, including Hickman, Broviac, or Groshong catheters; implantable ports; or percutaneously inserted central catheters (PICCs) should be used at home, although
the experience with PICCs for 1 year at home is
minimal. To qualify for Medicare reimbursement, home
TPN must be required for at least 3 months, fat malabsorption must be documented, and enteral feeding must
have failed.

Discussion
The initial management of the patient with newly
developed short bowel syndrome is complex. The goals
are to correct and prevent nutritional deficiencies; to
maintain normal nutritional status and growth, especially in children; to prevent complications associated
with short bowel syndrome; to decrease diarrhea; and to
improve quality of life. To do this effectively, one should
assess the patients absorptive status and nutrient losses,
assess length of residual intestine, reanastomose residual
colon so that it remains in continuity with the residual
small intestine, evaluate specific or at-risk nutrient deficiencies, identify risk factors for medical complications,

GASTROENTEROLOGY Vol. 130, No. 2

and evaluate the home and work environments to determine quality of life.
Highly selected patients with dilated segments of
small intestine may benefit from intestinal lengthening
procedures; however, these surgeries remain controversial, often with poor outcomes, and therefore should not
be considered part of the initial management of patients
with short bowel syndrome. Similarly, because many
patients may be successfully weaned from home TPN
using the conservative medical measures discussed
herein, small intestinal transplantation is inappropriate
in the initial management of the patient with short
bowel syndrome. It should be reserved for the patient
who develops irreversible malabsorption-associated liver
disease; other indications remain controversial and are
not supported by the available data.130
With appropriate medical and dietary therapy, many
patients with short bowel syndrome can be weaned from
parenteral nutrition. For those who cannot, the administration of intestinal mucosal growth factors, currently
investigational, may prove useful.

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130. Buchman AL, Scolapio J, Fryer J. AGA technical review on short
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Received July 29, 2004. Accepted July 14, 2005.
Address requests for reprints to: Alan L. Buchman, MD, MSPH,
Northwestern University Medical School, Division of Gastroenterology and Hepatology, Feinberg School of Medicine, 676 N. St. Clair
Street, Suite 1400, Chicago, Illinois 60611. e-mail: a-buchman@
northwestern.edu; fax: (312) 695-4514.