Digestive Diseases and Sciences (2023) 68:29–37

https://doi.org/10.1007/s10620-022-07760-w

MENTORED REVIEWS

Management of Short Bowel Syndrome (SBS) and Intestinal Failure

Mark Radetic1   · Amir Kamel2 · Mark Lahey2 · Michelle Brown3 · Anil Sharma1

Received: 2 April 2022 / Accepted: 2 November 2022 / Published online: 25 November 2022
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022

Abstract
Short bowel syndrome (SBS) is a chronic disease whose natural history requires a changing array of management strategies
over time. Chief amongst these is the chronic use of parenteral nutrition (PN) to ensure adequate nutritional intake. With
time and appropriate management, approximately half of all SBS patients will successfully regain a functional, baseline level
of intrinsic bowel function that will allow for them to achieve PN independence. However, the other half of SBS patients
will progress into chronic intestinal failure which warrants a change in therapy to include more aggressive medical and
potentially surgical measures. This review examines the evolving treatment strategies involved in the management of SBS
as well as intestinal failure.

Keywords  Short bowel syndrome · Short gut syndrome · Intestinal failure · Teduglutide · Gastrointestinal reconstruction
procedures · Intestinal transplantation

Introduction as a profuse, watery diarrhea that results in dehydration,

Short bowel syndrome (SBS) is characterized by the mal-
absorption of fluid, electrolytes, and nutrients that develops
following the loss of a significant quantity of small intes-
tine—typically appearing in patients with less than 180 cm
of small bowel [1, 2]. The spectrum of disease ranges from
compensated intestinal insufficiency to complete intestinal
failure requiring parenteral nutritional support with factors
such as the total length of remnant small bowel, the site of
bowel resection, and the presence or absence of the colon
dictating disease severity [1, 3].
Typically, SBS is a post-surgical disease that arises in the
aftermath of significant small intestinal resection which can
occur in patients with extensive Crohn’s disease, mesenteric
ischemia, malignancy, or abdominal trauma [4]. It presents
* Mark Radetic
mark.radetic@medicine.ufl.edu
1
Division of Gastroenterology, Hepatology, & Nutrition,
University of Florida Health, 1600 SW Archer Rd,
Gainesville, FL 32608, USA
2
Department of Pharmacy, Nutrition Support/Critical
Care Clinical Pharmacy Specialist, University of Florida,
Gainesville, FL, USA
3
Department of Food & Nutrition Services, University
of Florida, Gainesville, FL, USA
electrolyte derangements, and malnutrition. In this article,
we review the pathophysiology of SBS, explore current
management options, and discuss some future directions in
therapeutics.
Pathophysiology
The average adult has 300–800 cm of small intestine consist-
ing of duodenum (25–30 cm), jejunum (200–300 cm), and
ileum (300–400 cm) [5–7]. Short bowel syndrome arises
when total small intestinal length is reduced to less than
180 cm which results in the development of significant intes-
tinal malabsorption with subsequent malnutrition and an
osmotic diarrhea produced by the unabsorbed intra-luminal
solutes [1, 2]. The true prevalence of SBS is unknown but
estimated to affect up to 15% of adults undergoing bowel
resection [8].
Physiologically, SBS is split into an acute phase and an
adaptation phase with therapeutic goals differing somewhat
between the two phases. The acute phase begins immedi-
ately following small bowel resection and lasts approxi-
mately 1 month [9]. It is characterized by the sudden devel-
opment of nutrient malabsorption with high intestinal fluid
losses and metabolic derangements resulting from the abrupt
loss of absorptive intestinal surface area. The primary goals

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of therapy during the acute phase are to offset the intesti-
nal fluid and electrolyte losses while providing nutritional
support in the form of parenteral nutrition (PN). Following
the acute phase, the residual bowel will begin to undergo a
series of structural and physiological changes which func-
tion to slow intestinal transit and maximize nutrient absorp-
tion in an attempt to compensate for lost intestinal function.
Collectively, this process is referred to as “intestinal adap-
tation” and marks the beginning of the adaptation phase of
SBS—which can last up to 2 years [9]. During this phase,
therapeutic goals center on supporting intestinal adaptation
with the end goal of restoring intestinal function to baseline
“pre-resection” levels.
The clinical course of SBS is influenced by several fac-
tors including: the presence/absence of the colon in conti-
nuity with the small intestine, the total length and health of
remaining small intestine, and which bowel segments were
resected [9, 10]. The presence of a colon in continuity with
the remnant small intestine offers a significant advantage
to SBS patients as the colon is able to absorb much of the
unabsorbed fluid that comes pouring out of the shortened
small intestine. A fully intact colon can absorb up to 6 L
of excess fluid each day, thus limiting diarrheal fluid losses
and mitigating the risk of dehydration [11]. Furthermore, the
colon can contribute in nutrient absorption to an extent—
mostly through the absorption of carbohydrates produced
from intra-colonic bacterial metabolism [9, 12]. As a result,
having an intact and continuous colon is functionally equiva-
lent to having approximately 50 cm of “additional” small
intestine [13]. Total intestinal length is of critical importance
as well, as individuals with less than 120 cm of small bowel
(without a colon in continuity) or those with less than 60 cm
of small bowel (with colon in continuity) usually develop
permanent intestinal failure that will require lifelong PN [2,
14, 15].
The final factor that ultimately dictates the course of
SBS is the success (or lack thereof) of intestinal adapta-
tion in achieving a return of intestinal function to baseline
levels. The success of adaptation depends, in part, on which
bowel segments remain as each intestinal segment possesses
slightly different structural and functional properties as well
as adaptation potential [16]. The changes that occur during
intestinal adaptation include both microscopic changes such
as enterocyte hyperplasia, lengthening of villous surface
area, and increases in brush border enzymes and transport
proteins as well as macroscopic changes that result in dila-
tion and elongation of the residual small bowel [17–19]. Of
all the small intestinal segments, the ileum has the “tight-
est” intercellular junctions which, in combination with its
central role in bile acid re-absorption, make it the most fluid
absorptive intestinal segment [20]. The ileum is also the
most “adaptable” small bowel segment which allows it to
mitigate the losses of other small bowel segments [16, 21,
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Digestive Diseases and Sciences (2023) 68:29–37
22]. This is substantiated by the fact that individuals with an
end jejunostomy have little to no probability of recovery via
intestinal adaptation [19, 23]. Thus, retention of the ileum
confers many advantages in patients with SBS.
Management
The primary goals of therapy in SBS depend, to some extent,
on whether the patient is in the acute or the adaptive phase.
During the acute phase (1st month) of SBS, manage-
ment focuses on repleting the significant fluid and electro-
lyte losses and providing nutritional support. Fluid losses
should be closely monitored during the post-operative period
to determine daily intravenous (IV) fluid requirements and
serum electrolytes should be checked daily and repleted as
necessary [9, 24]. Extensive small bowel resections typi-
cally result in a reduction in the intestinal negative feedback
mechanisms that inhibit gastric acid secretion [25–27]. The
loss of this regulatory function leads to increases in the vol-
ume and acidity of gastric secretions which adds to the total
volume of gastrointestinal fluid losses and causes further
intestinal malabsorption through the inactivation of pancre-
atic enzymes by the increased gastric acidity. This gastric
“hypersecretory state” is particularly common during the
early stages of SBS and can result in erosive esophagitis
and peptic ulcer disease [10]. Thus, all SBS patients should
be started on a proton pump inhibitor (PPI) post-operatively
in order to suppress gastric hypersecretion [28, 29]. PPI
therapy should be continued for 6 months after which dis-
continuation can be considered given their increased risk
for causing small intestinal bacterial overgrowth (SIBO) in
patients who are already prone to developing the condition.
In addition to managing fluid and electrolyte requirements
and starting PPI therapy, the mainstay of management during
the acute phase is nutritional support. SBS patients should
be started on PN which will provide the primary source of
nutrition [9]. Enteral nutrition (usually via a feeding tube
initially) should also be started as soon as possible after
bowel resection [30, 31]. The goal of early enteral feeding,
however, is not to try to avoid PN, but rather to stimulate the
process of intestinal adaptation as the most potent stimulant
of adaptation is the presence of nutrients within the intes-
tinal lumen [30–32]. Several nutrients, in particular, have
been shown to play an important role in the stimulation of
intestinal adaptation. These include the amino acid arginine,
citrulline, long-chain triglycerides, and omega-3 fatty acids
among others [33, 34]. Many of these nutrients stimulate the
production and release of intestinotrophic hormones such
as glucagon-like peptide 2 (GLP-2) from neuroendocrine
L-cells residing within the ileum and colon [35]. Continu-
ous tube feeding is usually preferred over bolus feeding as
Digestive Diseases and Sciences (2023) 68:29–37 31
it is generally more easily tolerated and achieves maximal
“around-the-clock” intestinal stimulation [36].
Parenteral nutrition (PN) should be started early in the
post-operative period and optimized during the hospitaliza-
tion in order to allow for a successful transition to home
PN on discharge. In order to minimize its impact on normal
day-to-day living, home PN is typically infused overnight.
It is usually tapered on/off at half its target rate during the
first and last hours of infusion, which is done to help mini-
mize rapid electrolyte shifts and prevent hyperglycemia fol-
lowed by rebound hypoglycemia. Prior to hospital discharge,
patients should be instructed on the basics of proper care and
hygiene of the central line, how to store and administer PN,
basics of pump operation and troubleshooting, and should
be educated on some of the potential complications that
can arise from PN use. Home health nursing visits are typi-
cally arranged in the beginning to ensure appropriate home
management of PN by patients and their families. Routine
outpatient lab monitoring is essential—electrolytes should
be checked 1–2 times per week and repleted as necessary,
whereas micronutrients can be monitored more periodically
(i.e., every 3–4 months).
During the adaptation phase of SBS, the primary focus of
management shifts towards using pharmacological therapy
to maximize intestinal absorption and gradually weaning
PN with the goal of liberating the patient from parenteral
nutrition. The optimization of intestinal absorption involves
a combination of lifestyle changes as well as the introduction
of anti-diarrheal medications to slow gastrointestinal transit
in order to maximize the amount of time the intestines have
to absorb luminal contents. Patients should avoid hypertonic
fluids (fruit juice, soda, etc.) as they will exacerbate diar-
rheal fluid losses—especially in individuals with an end
Table 1  Common medications used in the management of short bowel syndrome
Dosing
Proton pump inhibitors (PPI)
 Pantoprazole 40 mg PO/IV twice daily
 Omeprazole 40 mg PO twice daily
Anti-diarrheal agents
 Loperamide 2–4 mg PO four times daily
 Diphenoxylate-atropine 5 mg PO four times daily
 Tincture of opium 3–10 mg PO four times daily Should be given 30 min before meals and at bedtime
 Codeine 15–60 mg PO four times daily Should be given 30 min before meals and at bedtime
Glucagon-like peptide 2 (GLP-2) analog
 Teduglutide 0.05 mg/kg SQ once daily
PO per os or “by mouth”, IV intravenous, SQ subcutaneous
jejunostomy [9, 23]. Additionally, patients should follow a
diet that is high in complex carbohydrates with moderately
restricted fat intake in order to minimize steatorrhea [23].
A diet high in complex carbohydrates is particularly helpful
in those with a colon in continuity given the colon’s ability
to partake in nutrient breakdown and absorption [37, 38].
However, those with a colon should take care to minimize
dietary oxalate due to an increased risk for developing cal-
cium oxalate nephrolithiasis from excessive oxalate absorp-
tion [10, 23].
The mainstay of pharmacological therapy involves the use
of anti-diarrheal medications to reduce fluid losses and slow
intestinal motility to maximize the available time for nutrient
absorption (Table 1). First-line anti-diarrheal agents include
loperamide and/or diphenoxylate—both of which should be
taken 30 minutes before meals and at bedtime [39, 40]. In
patients with persistent diarrhea despite maximal therapy
on first-line anti-diarrheals, second-line medications such as
codeine and/or tincture of opium can be added as adjuncts
to treatment [39]. Other commonly used anti-diarrheals
such as cholestyramine or octreotide should generally be
avoided in these patients. SBS patients often develop a bile
acid deficiency—particularly those who have undergone
resections of the terminal ileum. The use of cholestyramine
will only further exacerbate this bile acid deficiency and
result in impairments to fat absorption which, paradoxi-
cally, will worsen the diarrhea while increasing oxalate
absorption which places the patients at-risk for developing
calcium oxalate nephrolithiasis [40]. The use of octreotide
as an anti-diarrheal should also be avoided in SBS patients
as it acts to stunt the process of intestinal adaptation due
to decreased splanchnic blood flow [39, 41, 42]. A trial of
octreotide can be considered, however, in patients outside of
Comments
PPI therapy should be continued for the first 6 months after which it
should be discontinued (if able)
As above
Should be given 30 min before meals and at bedtime
The typical daily maximum of loperamide is 16 mg but patients with
SBS may require higher doses of up to 64 mg per day
Should be given 30 min before meals and at bedtime
Daily maximum of 20 mg per day
Comes in liquid form with a morphine concentration of 10 mg/mL
Contraindicated in patients with an active gastrointestinal malignancy
13

32
the “adaptation window” (i.e., 2 years) who have continued,
profuse diarrhea with IV fluid requirements exceeding 3 L
per day while on maximal anti-diarrheal therapy [19].
In the weeks following the initial bowel resection, many
patients are able to gradually transition from enteral intake
via feeding tube to regular oral intake. As intestinal adapta-
tion unfolds and the remnant small intestine increases its
baseline function, parenteral nutritional requirements will
begin to decline in patients who are able to tolerate oral
nutrition. Over time, as enteral nutritional intake rises, it is
appropriate to begin to wean down PN proportionate to the
oral intake in order to keep the daily caloric intake constant.
SBS patients are at the greatest risk for developing nutri-
tional and vitamin deficiencies during the process of PN
weaning so electrolyte and vitamin levels should be closely
monitored during this process. Figure 1 summarizes the
management strategies during the various phases of SBS
(Fig. 1).
Intestinal Failure
After 2 years, approximately 50% of SBS patients will
recover enough intestinal function through adaptation that
they will be able to come off of PN entirely [10, 14]. How-
ever, the other half of patients will progress to permanent
intestinal failure requiring lifelong PN. Several predic-
tive factors can identify which patients are at high-risk for
developing permanent intestinal failure. The most notable of
these is total intestinal length with individuals having less
than 120 cm of small bowel (without a colon in continuity)
or those with less than 60 cm of small bowel (with colon
in continuity) being highly likely to develop permanent
Fig. 1  Summary of the mainstays of management of short bowel syndrome
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Digestive Diseases and Sciences (2023) 68:29–37
intestinal failure [2, 14, 15]. The serum citrulline level has
also been shown to be predictive of long-term PN use with
levels < 15 µmol/L being associated with permanent PN-
dependence [43].
Treatment options for intestinal failure are limited, but
include both medical and surgical options. The mainstay of
medical management is the medication teduglutide which
is an analog of glucagon-like peptide 2 (GLP-2)—an enter-
oendocrine hormone that stimulates the growth and prolif-
eration of enterocytes in the small intestine and colon [44,
45]. Teduglutide is used to “force” intestinal adaptation
to continue with the goal of achieving PN independence
for patients with intestinal failure [46–50]. The intestino-
trophic properties of teduglutide also provide the basis for its
adverse effects—namely an increased risk for polyp forma-
tion and colorectal cancer in those with a residual colon due
to increased stimulation of colonic cellular growth and pro-
liferation. Thus, colorectal cancer screening is of particularly
high importance for those on teduglutide therapy. Patients
should undergo a baseline screening colonoscopy 6 months
prior to the initiation of teduglutide, a repeat colonoscopy
after 1 year of therapy, and then surveillance colonoscopies
every 5 years thereafter (while on teduglutide) for regular
surveillance [51]. Likewise, the main contraindication to
teduglutide use is the presence of an active gastrointestinal
malignancy due to the medication’s potential to stimulate
tumor proliferation in those with an underlying malignancy
[51]. Longer-acting GLP-2 analogs such as glepaglutide and
apraglutide are currently in development as well [52, 53].
Surgical options in the treatment of intestinal failure
include gastrointestinal reconstruction procedures as well
as intestinal transplantation. Reconstructive surgeries aim
to surgically manipulate the remnant intestines in order
Digestive Diseases and Sciences (2023) 68:29–37 33
to maximize absorption potential and minimize diarrheal
fluid losses. These surgeries are technically very challeng-
ing and are only performed in carefully selected patients at
highly specialized academic medical centers with expertise
in gastrointestinal reconstruction. Examples of reconstruc-
tive procedures include intestinal lengthening, serial trans-
verse enteroplasty, and segmental reversal of the small bowel
or colon (Fig. 2) [10, 54]. Intestinal lengthening involves
cutting the small intestine in half longitudinally and then
re-connecting the divided intestines in an end-to-end fash-
ion to increase total small bowel length in order to increase
small bowel transit time. In serial transverse enteroplasty, a
“zig–zag” pattern is cut into the small intestine in order to
increase total absorptive surface area. Segmental reversal of
the small bowel or colon involves removing a bowel segment
and then re-attaching it in the same spot but “backwards”
so that the reversed segment undergoes peristalsis in the
“wrong” direction (upstream rather than downstream) in
order to help slow intestinal motility [55, 56].
The final treatment option for patients with persistent
intestinal failure is intestinal transplantation which is typi-
cally only indicated in patients on lifelong PN who develop
irreversible complications of chronic PN use such as fre-
quent central line complications (infection, thrombosis),
chronic liver disease, or persistent malnutrition despite being
on PN (Table 2) [57–60].
Complications
The intestinal malabsorption, diarrhea, and need for par-
enteral nutrition places SBS patients at-risk for develop-
ing several complications—the most obvious of which
involve sequelae of nutritional and vitamin deficiencies.
Early PN use can circumvent many of these deficiencies,
but they can resurface later on in the disease course as PN
is being weaned. For this reason, electrolyte and vitamin
levels should be closely monitored (i.e., every 3–6 months)
to ensure adequate levels.
The most common deficiencies are in fat-soluble vitamins
(ADEK), essential amino acids, and vitamin B12 which
develops in patients who have lost more than 60 cm of ter-
minal ileum [61]. Impaired vitamin D absorption places
patients at-risk for developing osteopenia/osteoporosis, so
yearly screening with a bone mineral density scan is rec-
ommended [62]. In the rare patients with duodenal resec-
tions, there will also be decreased absorption of calcium,
iron, and folate which can result in metabolic bone disease
and anemia, respectively. Bile acid deficiency can occur in
those who have lost more than 100 cm of terminal ileum
which results in a disruption in enterohepatic circulation
with bile acid losses exceeding bile acid production by the
liver [63]. In turn, insufficient bile acids from continual fecal
losses will worsen fat malabsorption and cause steatorrhea.
In those with a colon, unabsorbed fatty acids will bind to
luminal calcium which leaves oxalate free to be absorbed
into the bloodstream, get filtered in the kidney, and then
precipitate out of solution to form calcium oxalate stones
resulting in nephrolithiasis [61]. Thus, a low-oxalate diet is
recommended in patients with a residual colon in continuity.
The gastric hypersecretory state that develops after exten-
sive small bowel resection predisposes patients to develop-
ing esophagitis and peptic ulcer disease in addition to further
exacerbating diarrheal fluid losses. Thus, twice daily PPI
therapy is recommended during the first 6 months of SBS
to mitigate gastric hypersecretion [62]. SBS patients are also
at-risk for developing small intestinal bacterial overgrowth
(SIBO) which presents with bloating, flatulence, and an
acute worsening of diarrhea. Risk factors for SIBO include
loss of the ileocecal valve (which normally acts to prevent
bacterial reflux from the colon into the small intestine) and
long-term usage of PPIs and anti-motility agents which are
staples of medical management in SBS.
Finally, chronic PN use places patients at-risk for experi-
encing catheter-related complications such as line-associated
infections or thrombosis. Moreover, long-term PN predis-
poses patients to the development of a fatty liver as well
as cholestasis from diminished gallbladder activity due to
decreased utilization of the gastrointestinal tract. The risk
of cholestasis is even higher in those with resections of the
terminal ileum as diminished bile acid re-absorption changes
the composition of bile in the gallbladder—causing it to
become supersaturated with cholesterol which increases the
risk for forming cholesterol gallstones.64
Conclusion
SBS is a chronic disease that requires long-term manage-
ment strategies that evolve over time. Initial management
during the acute phase involves aggressive repletion of
IV fluids and electrolytes to replace diarrheal losses, PPI
therapy to blunt gastric hypersecretion, initiation of PN for
nutritional support, and early enteral nutrition to stimulate
the process of intestinal adaptation. As patients stabilize and
transition into the adaptation phase, therapeutic goals shift
towards maximizing residual intestinal function with the
aim of achieving PN independence. This is accomplished
through dietary modifications and the use of anti-diarrheal
medications to minimize fluid losses, slow gastrointestinal
motility, and maximize intestinal absorption.
After 2 years of intestinal adaptation, approximately 50%
of SBS patients will achieve PN independence. For those
with persistent intestinal failure, the use of GLP-2 analogs
such as teduglutide can induce further intestinal growth,
improve intestinal function, and lead to PN independence
13

34 Digestive Diseases and Sciences (2023) 68:29–37

Fig. 2  Gastrointestinal
reconstruction procedures. A
Intestinal lengthening. B Serial
transverse enteroplasty (STEP).
C Segmental reversal of the
small intestine or colon

13
Digestive Diseases and Sciences (2023) 68:29–37 35

Table 2  Indications for intestinal transplantation

Conditions related to parenteral nutrition failure or associated complications

 Development of chronic liver disease (cirrhosis) secondary to chronic cholestasis from long-term parenteral nutrition use
 Thrombosis of at least 3 of the 4 upper torso central veins (internal jugular and subclavian veins) OR either brachiocephalic vein—making
these sites inaccessible for central line placement that is required for long-term parenteral nutrition use
 Two or more yearly episodes of cardio-pulmonary failure requiring an ICU admission and level of care (mechanical ventilation, pressor sup-
port) attributable to the underlying bowel disease or central line-associated complications (line-associated septic shock, dehydration with
hypovolemic shock, severe metabolic derangements)
Conditions NOT related to parenteral nutrition
 Invasive intra-abdominal desmoid tumors
 Acute mesenteric ischemia with diffuse intestinal infarction AND liver failure when initial attempts at revascularization are unsuccessful
 Failure of first intestinal transplant

in some patients. Alternative options include gastrointesti- Declarations 

nal reconstruction procedures as well as intestinal transplan-
tation—both of which should only be offered to carefully Conflict of interest  The authors do not have any financial disclosures
or conflicts of interest.
selected patients.
Ethical approval  Ethical approval was not necessary as this is a review
article that does not directly involve experimentation with human or
animal subjects.
Key Messages

• Short bowel syndrome (SBS) is defined by the malab- References

sorption of fluid, electrolytes, and nutrients that devel-
ops following the loss of a significant quantity of small
bowel (typically in patients with less than 180 cm of
small bowel) and presents as a profuse, watery diarrhea.
• The disease severity of SBS depends on several factors
including the total length of remnant small bowel, the
site of bowel resection, and the presence or absence of
the colon in continuity with the remnant small bowel.
• The management of SBS during the acute phase (first
month) involves IV repletion of fluids and electrolytes to
replace diarrheal losses, PPI therapy, initiation of paren-
teral nutrition, and early enteral feeding to help stimulate
intestinal adaptation.
• The management of SBS during the adaptation phase
(months 2–24) involves dietary modifications, anti-diar-
rheal medications, and gradual weaning of parenteral
nutrition.
• Following a 2-year period of intestinal adaptation,
approximately 50% of SBS patients will achieve inde-
pendence from parenteral nutrition.
• The management of chronic intestinal failure involves the
use of the GLP-2 analog teduglutide to support further
intestinal adaptation. Surgical treatment options include
gastrointestinal reconstruction procedures and intestinal
transplantation.
Acknowledgments None
Funding None.
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