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440
L.H. Maguire et al.
Intraluminal bulking agents such as fi ber supplementation
and psyllium may provide improved stool consistency to
some patients. Bismuth has some utility in nonspecifi c
chronic diarrhea and may provide relief to some patients.
Development of new drugs has been limited. Serotonin
receptor antagonists were found to be associated with ischemic colitis and calmodulin therapies demonstrated no superiority to loperamide [
34 ]. Octreotide, which has been found
of utility in other forms of chronic diarrhea, was tested in a
small randomized, placebo-controlled trial. It demonstrated
no improvement in bowel frequency in patients with postIPAA diarrhea and a potential increase in painful tenesmus,
causing two patients to withdraw from the study [ 35 ].
One potential new therapy is probiotic bacterial cultures.
Probiotics are postulated to improve gastrointestinal symptoms by modifying the immunologic, digestive, or nutritional functions of commensal gut bacteria. Treatment with
probiotics in multiple formulations has been studied in a
variety of gastrointestinal conditions. Utility has been demonstrated in infectious diarrhea and antibiotic-associated
diarrhea, but study data have been less convincing in IBD
and irritable bowel syndrome [ 36 ]. In the postoperative set-
ting, 67 patients with IPAA due to UC or FAP demonstrated
improvement in abdominal cramping, leakage, need for pad
use, and involuntary defecation following a 4-week intervention with live Lactobacilli and Bifi dobacteria [ 37 ]. Mucosal
infl ammation, scored by endoscopy, was also decreased by
the intervention in UC patients. Larger, controlled trials are
needed before utility can be shown conclusively.
Ileal resection or disease results in spillover of bile acids
into the colon, interfering with electrolyte and water absorption and frequently causing diarrhea. Cholestyramine,
colestipol, and colesevelam, bile acid sequestrants, prevent
the outpouring of water and electrolytes. In a single-blind
prospective trial, cholestyramine reduced stool frequency
and volume in patients with ileal resections <100 cm. It demonstrated no improvement in patients with >100 cm resected
38 ]. IPAA also disrupts the ileum and interferes with entero-
[
hepatic circulation, as demonstrated by elevated postprandial
serum levels of unconjugated bile acids [
39 ] and abnormal
75Se homotaurocholate uptake in patients following IPAA
[ 40 ]. Pouchitis, stasis, and bacterial overgrowth may all
worsen this condition [ 41 ]. Although its role in diarrhea for
patients after colectomy or IPAA is not well established,
cholestyramine may provide relief to some patients suffering
from diarrhea and has demonstrated effi cacy in alleviated
perianal skin irritation following IPAA [ 42 ]. Additionally,
any suggestion of pouchitis (i.e., abrupt increase in watery
stools, fever, pelvic pain) should prompt an endoscopic evaluation of the pouch, biopsy, and likely empiric treatment
with antibiotics such as Flagyl and/or Floxin.
To summarize, our algorithm for the treatment of diar-
rhea is to always perform a colonoscopy or a fl exible
sigmoidoscopy fi rst to evaluate the colon and exclude
ischemic or infl ammatory colitis or an anastomotic stricture.
All patients are tested for Clostridium diffi cile colitis before
initiating drug therapy. Whenever possible, patients are asked
to stop all antibiotics to make sure the diarrhea is not antibiotic induced. They are then started on a probiotic. All patients
after right-sided colectomy or small bowel resections are
started on cholestyramine. In the absence of improvement
with probiotics and cholestyramine, when appropriate, we
then start a fi ber supplement, such as Metamucil® (Procter
& Gamble) or Benefi ber® (Novartis). The patients are asked
to start with half the dosage listed on the medicine box and
are informed to expect bloating and distention as they adjust
to the supplement. In 10 days, the patients are asked to escalate to the dose suggested on the box. Any fi ber supplement
brand is adequate and we ask the patient to choose the one
that he prefers. If fi ber fails, we escalate to loperamide. We
instruct the patients to take as many as eight loperamide tablets per day to achieve 2–3 formed bowel movements daily.
If fi ber and loperamide fail, we continue with fi ber supplementation and switch to Lomotil (diphenoxylate/atropine).
Finally, we reserve prescriptions for diluted tincture of
opium (DTO) for desperate cases.
Fecal Incontinence
Key Concept : The treatment of the patient reporting complaints of anal leakage of mucus , gas , liquid , or stool should
always start with identifi cation of the underlying cause of
their incontinence .
The most common cause of incontinence is not sphincter
insuffi ciency, but diarrhea. Thus, in the patients reporting
diarrhea, we always start with its treatment, as described
above. In those who continue to have leakage despite adequate regulation of bowel frequency and consistency with
bulking agents (fi ber) and constipation agents (i.e.,
Loperamide), we consider a prescription of amitriptyline,
which can be added at a dose of 10–25 mg at night as tolerated. Amitriptyline is a tricyclic antidepressant agent that
was studied in an open label trial of patients with fecal incontinence and was found to decrease incontinence scores [ 43 ].
Seventy-two percent of patients who were treated with the
drug in the study reported full remission with a sustained
improvement at 6 months.
In patients who continue to do poorly, we proceed with a
thorough work-up aimed at excluding fecal obstruction and
subsequent overfl ow incontinence. To start with, we perform
a fl exible sigmoidoscopy or a colonoscopy to exclude an
anastomotic stricture. Once a stricture is excluded, we proceed with anorectal manometry testing to assess for any evidence of a paradoxical contraction of the puborectalis. In the
patients who are found to have signs suggestive of this
28 Functional Problems Following Colorectal Surgery
441
condition, we proceed with treating fecal incontinence with
a daily glycerin suppository and a weekly tap water enema.
This treatment has been shown to be effective in at least onethird of the patients with this condition [ 44 ].
Finally, when all medical therapy fails, we consider surgical therapies that escalate depending on the patient’s interest
in proceeding with further treatments and their disease severity, as well as the remaining anatomy and the underlying
diagnosis. For example, the patient who has not received pelvic radiation and who does not have Crohn’s disease may be
a candidate for receiving a submucosal injection of Solesta®
gel (Salix Pharmaceuticals Inc., Raleigh, NC) into their anal
sphincter. The gel, which was recently approved by the FDA,
has been shown to have a 60 % response rate at a 6-month
follow-up, which was nearly twice the improvement rate
seen in the placebo group [
45 ].
In the patients who cannot have direct anal sphincter injections, sacral nerve stimulation (SNS) (Medtronic Interstim®,
St. Paul, MN) is another great potential option that was also
recently approved by FDA in the US. Its only drawback
(besides its high price) is the fact that the device is not MRI
compatible. The device is only planted, however, after a 2–3
weeks trial of stimulation. Eighty percent of the patients who
do well during the stimulation phase can expect a 50 % reduction in the frequency and the severity of their fecal incontinence. Forty percent can expect complete continence [ 46 ].
Those who remain incontinent following medical therapy
and minimal invasive treatments with either Solesta® or
SNS, or both, could consider implantation of an artifi cial
bowel sphincter (ABS), a hidden mini stoma, to perform
Malone antegrade colonic enemas (MACE) or a permanent
ostomy. I reserve the option of ABS only for the patient who
has a colon and has solid bowel movements. Furthermore,
the patient’s perineum needs to allow for a safe implantation
(i.e., no Crohn’s, radiation, diabetes, immunodefi ciency).
Similarly, the MACE procedure is only feasible in a patient
who has a colon that could then be irrigated to empty. The
patients without a colon who fail SNS are unfortunately only
candidates for an ileostomy.
Constipation/Obstructed Defecation
Key Concept : Recognize the presence of obstructed defecation in patients with pre - or postoperative anorectal complaints as these will need to be addressed but may prevent
unnecessary surgical re - intervention .
Patients with obstructed defecation syndrome (ODS)
present with inadequate rectal emptying, straining, and the
need to manipulate the perineum or vagina to facilitate defecation. Occasionally, these patients may also have a component of overfl ow incontinence with rectal seeping, anal
irritation, and pruritus. Many will also present to the clinician
for hemorrhoids or anal fi ssures. A subsequent hemorrhoidectomy in such a patient would improve the appearance of
the anus, but not the patient’s function. Diffi cult defecation
will most likely continue in the postoperative setting and
symptoms may escalate, especially if a postoperative stricture develops. Similarly, patients with anal fi ssures in the setting of ODS are very likely to suffer recurrence after their
initial therapy. Recognition of ODS can prevent unnecessary
surgery and the need for recurrent interventions.
In patients with symptoms suggestive of ODS, we begin
with anorectal manometry and EMG. We diagnose ODS if
high anal pressures and paradoxical contractions of the
puborectalis are seen on EMG (Fig. 28.5 ). In the presence of
these fi ndings, the patient is asked to initiate a fi ber supplement. If still unable to empty well, we teach the patient to
self-administer daily tap water enemas. If these maneuvers
fail, we arrange for pelvic fl oor muscle retraining with EMGguided biofeedback. The goal of the therapy is to teach the
patient to relax, rather than constrict, his pelvic fl oor musculature while attempting to defecate [ 47 – 49 ].
Patients who fail medical management undergo defecography. The test diagnoses intrarectal and rectoanal intussusception, enterocele, rectocele, and full-thickness rectal
prolapse (Figs. 28.6 and 28.7 ). When these fi ndings are pres-
ent, we consider surgical correction. In general, we prefer to
perform a stapled transanal rectal resection (STARR) procedure (Fig. 28.8 ) on patients without prior pelvic surgery who
have isolated recto-rectal or rectoanal intussusception with
or without a rectocele. Patients with concomitant enteroceles
and large intussusception or full-thickness prolapse are
advised to have a ventral rectopexy [ 50 ].
Medical therapy and biofeedback are appropriate for
patients after any colorectal procedure, but the surgical procedures mentioned above only apply to the patients without
a prior proctectomy.
Key Concept : In patients with ODS after proctectomy for
rectal cancer , ODS could be due to tumor recurrence , anastomotic stricture , or to poor rectal compliance .
The patients suffering from ODS who have a history of
resection for rectal cancer should undergo a colonoscopy and
rectal MRI or PET scan to exclude tumor recurrence. Finally,
strictures at the coloanal or colorectal anastomosis should
be dilated, when present. In those without stricture or recurrence, anorectal physiology testing should be performed.
Compliance testing should always be performed as part of
physiologic investigation. Decreased rectal compliance and
rectal hypersensitivity are common in these patients and is
usually detected via decreased maximum tolerated volume
on manometry. When poor compliance is present, sensitivity
retraining with a balloon is much more helpful during biofeedback than simple EMG-guided therapy. Finally, when ODS is
combined with overfl ow incontinence or frank incontinence,
442
Fig. 28.5 Electromyography ( EMG )
with paradoxical contraction of anal
sphincter at attempt to defecate
L.H. Maguire et al.
sacral nerve stimulation (SNS) could be considered as a
possible option. SNS has been found to improve both fecal
incontinence as well as rectal emptying [ 51 ]. However, SNS
implantation needs to be weighed against the potential need
for pelvic MRI as the device is not MRI compatible.
Key Concept : ODS in the patient with an ileoanal J - pouch
could be due to pouchitis , stricture , cuffi tis , or pouch
intussusception .
ODS after J-pouch creation constitutes a special challenge. The cause of ODS can be far more complex. Evaluation
of these patients should always start with a pouchoscopy to
exclude pouchitis, development of Crohn’s disease, or a
stricture at the ileoanal anastomosis or ileostomy closure
site. In addition, an honest assessment of the residual rectal
cuff is important. Many patients with ODS after a J-pouch
may have a long, noncompliant rectal cuff to blame for their
symptoms. In these patients, steroid application to the cuff to
treat “cuffi tis” may help, as well as a generous anal dilatation
to allow for a 22–24 Hagar dilator.
Finally, a subgroup of ileoanal J-pouch patients may have
a fl oppy, intussuscepting rectal pouch or pouch that is too
large to empty. In both cases, a pouch revision to a size that
accommodates about 1,525 mL when distended with or
28 Functional Problems Following Colorectal Surgery
443
Fig. 28.6 Defecography with intussusception and enterocele
Fig. 28.8 Stapled transanal rec-
tal resection
Fig. 28.7 Defecography with isolated intraanal intussusception/early
rectal prolapse
444
L.H. Maguire et al.
without a pouch suspension to the sacral promontory can
prevent further intussusception and encourage better emptying. In patients with a normal size pouch and isolated intussusception, the pouch revision could be done transanally.
However, in the majority of patients, an abdominal procedure is needed, and its risk needs to be carefully considered
along with the potential benefi t that it could confer.
If surgery is not appropriate, medical management with
fi ber and tap water enemas as described earlier could be
considered.
Summary Pearls
Satisfactory functional outcome after colorectal surgery
depends on the patient’s pathophysiology, type of resection, manner of reconstruction, and degree of injury to
nerves and tissues. Postoperatively, patients frequently have
altered bowel function with potentially signifi cant effects on
health, recovery, and quality of life. The appropriate therapy for postoperative functional problems includes a range
of escalating treatments from dietary changes and medications to surgery. Although few medical treatments have
emerged recently or been studied prospectively, new surgical options have been developed including submucosal gel
injection, sacral nerve stimulation, and artifi cial sphincters.
Selecting the appropriate therapy for each unique patient
and problem is an evolving challenge you will likely face
and need to have a stepwise logical approach to ensure the
best outcomes.
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Short Bowel Syndrome
Ilun Yang and Robin P. Boushey
Key Points
• Recognizing patients who are at risk for short bowel
syndrome and practicing bowel economy during
surgery are crucial.
• Knowledge of residual intestinal anatomy is essential for determining prognosis and management.
• Patients with short bowel syndrome should be managed by a multidisciplinary team of healthcare professionals with the required expertise.
• A combination of intestinal rehabilitation and surgical strategies is often required to achieve independence from parenteral nutrition.
2 9
and hydration without enteral or intravenous supplementation [ 2 ]. In adults, etiologies leading to SBS include mesen-
teric ischemia, Crohn’s disease, volvulus, trauma, radiation
enteritis, and tumors (e.g., desmoid) [ 3 – 5 ]. With its range of
clinical manifestations, SBS can dramatically impact quality of life and is associated with signifi cant morbidity and
mortality.
The presentation and management of SBS depend on factors including anatomy of the remaining bowel, intestinal
adaptation, and underlying etiology. This chapter will review
these issues and discuss the medical and surgical management of this condition and its complications.
Introduction
Key Concept: Symptoms related to short bowel syndrome are
not only secondary to the length of the remaining bowel but
also due to the amount of functioning residual bowel and
other anatomic considerations (i.e., presence or absence of
the ileocecal valve).
Short bowel syndrome (SBS) is a spectrum of malabsorption that can follow extensive resection of the small intestine.
It usually occurs when there is less than 200 cm of residual
small bowel; however, several factors other than small intestinal length, as discussed below, contribute to determining
the degree of malabsorption [ 1 ]. SBS is the most common
cause of intestinal failure, in which an individual’s functioning gut mass is insuffi cient for maintaining adequate nutrition
I. Yang , MD, FRCSC
Department of Surgery , McMaster University , Hamilton , ON , Canada
R. P. Boushey , BSc, MD, PhD, CIP, FRCSC (
Department of Surgery , The Ottawa Hospital , Ottawa , ON , Canada
e-mail: rboushey@ottawahospital.on.ca
*)
Pathophysiology
Key Concept: Several physiological and anatomical factors
play a role in the development (or avoidance) of short bowel
syndrome.
Small Intestinal Resection
Key Concept: The degree of malabsorption and type of fl uid,
electrolyte, and nutritional defi ciencies experienced will
depend on the location and function of bowel resected.
The extent of small bowel resection is a central determinant of outcome in SBS. The implications of losing a particular length of intestine depend on its location and corresponding
absorptive functions. Normally, the jejunum is the primary
site of absorption for macronutrients such as carbohydrates,
fat, and protein. Following jejunal resection, the remaining
small intestine is able to compensate through adaptive changes
such as increased absorptive surface area and upregulated
digestive enzymes [ 6 ]. In contrast, the sequelae following
ileal resection can be more problematic due to the ileum’s
unique functions. The ileum reabsorbs the vast majority of
bile salts and returns it to the liver via the enterohepatic circulation. Ileal resection may result in watery diarrhea due to the
S.R. Steele et al. (eds.), Complexities in Colorectal Surgery,
DOI 10.1007/978-1-4614-9022-7_29, © Springer Science+Business Media New York 2014
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passage of unabsorbed bile salts into the colon and the
increased colonic secretion of water and electrolytes. The
ileum is also the predominant absorptive site of the intrinsic
factor-vitamin B 12 complex [ 7 ]. Consequently, a terminal ileal
resection of more than 60 cm is associated with vitamin B
malabsorption [
8 ]. Loss of more than 100 cm of ileum results
12
in bile salt defi ciency, poor absorption of fat- soluble vitamins,
and steatorrhea secondary to fat malabsorption [
9 ].
The site of bowel resection also infl uences absorption
related to the loss of control mechanisms for gastric emptying and intestinal transit. Rapid gastric emptying can be detrimental for nutrient absorption due to inadequate mixing of
gastric and pancreatobiliary secretions. Likewise, decreased
intestinal transit time may worsen malabsorption if the bowel’s capacity to assimilate nutrients is exceeded. In normal
physiology, as unabsorbed macronutrients arrive at a segment of intestine, an inhibitory feedback mechanism is activated to slow gastric emptying and gut transit. This “brake”
system is present throughout the small and large bowel;
however, the ileal brake is more potent than the jejunal brake
[ 10 ]. In addition, the cells that release the GI hormones
thought to mediate the ileal brake (e.g., peptide YY, glucagonlike peptides, and neurotensin) are found in the terminal
ileum [ 11 , 12 ]. Consequently, rapid gastric emptying and
intestinal transit are common following ileal resection, particularly in patients with a jejunostomy as they also lack the
benefi t of a colonic brake.
The jejunum and ileum also differ in their ability to absorb
water and electrolytes. In the jejunum, sodium absorption is
primarily mediated by fl ow along osmotic pressure gradients;
in contrast, the ileum has an effi cient active transport mechanism for absorbing sodium [ 13 ]. Furthermore, the jejunal epi-
thelium is more permeable to passive shifts of fl uid and
electrolytes due to its lack of tight intercellular junctions [ 14 ].
Hence, the overall absorption process occurs more effi ciently
at the ileum, which is particularly important following meals
of high osmolarity. These factors explain the dramatic losses
in fl uid and electrolytes that can be seen following ileal resection, particularly in the absence of a colon in continuity.
bacterial overgrowth [ 18 ]. An increased bacterial load con-
tributes to malabsorption of macronutrients, vitamin B
bile salts [ 19 ]. However, one study suggested that the ICV’s
protective effect against bacterial overgrowth may be insignifi cant in the face of a short residual small bowel and intestinal dysmotility [
20 ]. Similarly, intestinal transit time has
been shown to be largely uninfl uenced by the presence or
absence of the ICV [
21 ]. Overall, it is likely that the extent of
bowel resected concomitantly, rather than the loss of the ICV
itself, accounts mainly for the resultant malabsorption.
Loss of the Colon
Key Concept: The colon’s ability to absorb water and
sodium, as well as undergo adaptation to cover other losses,
plays a key role with extensive small bowel resection.
The presence of a colon in continuity has important
benefi ts in SBS. In normal physiology, the large intestine
absorbs approximately 90 % of the water and sodium contained in the ileal effl uent [ 22 ]. The organ also contributes to
the body’s energy stores by absorbing short-chain fatty acids
(SCFA) derived from carbohydrate fermentation. Following
small bowel resection, these absorptive capabilities of the
colon proportionately become even more crucial. The colonic
mucosa undergoes adaptive morphological changes such as
increased absorptive surface [ 23 ]. Unabsorbed carbohydrates
from the shortened small bowel are salvaged by the large
bowel to provide a signifi cant source of energy [ 24 ]. Similar
to the small intestinal “brake” described above, a feedback
mechanism to slow gastrointestinal transit also exists in the
colon [ 12 ]. With the colon in continuity, 50–70 cm of remain-
ing small bowel may be suffi cient to prevent dependence on
parenteral nutrition; in the colon’s absence, at least 100 cm of
residual bowel is needed [ 25 , 26 ]. The extent of colectomy
has also been shown to correlate with functional outcomes
such as severity of diarrhea following ileal resection [ 27 ]. On
the other hand, the presence of an intact colon increases the
risk of certain complications such as hyperoxaluria and
d -lactic acidosis (see Clinical Manifestations below).
12
, and
Loss of the Ileocecal Valve
Key Concept: While debatable, the presence of an intact,
functioning ileocecal valve can lessen short bowel syndrome
symptoms.
The impact of ileocecal valve (ICV) resection on outcomes in SBS has been debated. In the pediatric surgery literature, several studies have demonstrated shorter duration of
parenteral nutrition dependence with the presence of an intact
ICV, while others have failed to show an effect [ 15 – 17 ]. The
presence of the ICV may be benefi cial as a potential barrier to
retrograde entry of colonic bacteria and resultant small bowel
Etiology-Specifi c Considerations
Crohn’s Disease
Key Concept: Crohn’s disease may lead to SBS due to underlying infl ammation or repeated resections that lead to
malabsorption.
SBS occurs in 5–10 % of patients with Crohn’s disease,
typically as a result of multiple bowel resections over time
[ 28 ]. Additional risk factors for developing SBS include
those with early age at diagnosis, ileocolonic disease at
29 Short Bowel Syndrome
449
initial presentation, and a history of unplanned laparotomies
for intra-abdominal sepsis [
most frequently found in the ileocecal region, the terminal
ileum and ileocecal valve are commonly resected, leading to
the respective sequelae of malabsorption described above. If
the residual bowel is involved with Crohn’s disease, then its
absorptive function and adaptive capacity would likely be
compromised [ 31 ]. One also needs to be mindful of the pres-
ence of enteroenteral or enterocolic fi stulas that may bypass
a segment of bowel and decrease overall absorption.
The concern regarding the development of SBS highlights
the importance of a collaborative multidisciplinary approach
to managing Crohn’s disease. Optimization of medical treatment may reduce the need for resection, and surgery should
ideally be reserved for treating specifi c complications.
Resection margins should be conservatively chosen and need
only to be grossly normal to minimize recurrence [
symptomatic small bowel stenosis, stricturoplasty should be
favored over resection [
absence of neoplasm or pancolitis associated with severe
anorectal disease, segmental colectomy is the preferred
option to preserve as much colon as possible for absorption.
29 , 30 ]. As Crohn’s disease is
32 ]. For
33 ]. For colonic disease, in the
Mesenteric Ischemia
Key Concept: Severe mesenteric ischemia (i.e., thrombotic,
embolic, nonocclusive, and venous) may acutely lead to
frankly necrotic bowel requiring extensive resection. When
possible, every attempt should be made to salvage as much
viable bowel as possible.
In contrast to the setting of Crohn’s disease, SBS related to
mesenteric ischemia is more likely to result from a single
massive bowel resection rather than repeated resections over
time [ 34 ]. In a review by Thompson [ 34 ] of 95 patients with
SBS, among those who survived the initial 30 days postoperatively, patients following a single massive resection were
more likely to require long-term parenteral nutrition than
those who had repeated resections and similar residual bowel
length. Mesenteric ischemia is the most common cause (25 %)
of intestinal failure in adults [ 31 ]. Early diagnosis and treat-
ment in acute mesenteric ischemia are essential to maximize
bowel salvage. Fluid resuscitation and, if required,
β-adrenergic agonists should be initiated to optimize perfusion [ 35 ]. Anticoagulation therapy is instituted when appro-
priate, depending on the etiology of ischemia [ 36 ]. For acute
arterial insuffi ciency, prompt surgical intervention is critical
to successful management. Appropriate expertise should be
available for surgical options including bypass, embolectomy,
and thrombectomy. Careful assessment of bowel viability is
performed, using methods such as evaluation of bowel appearance and peristalsis, Doppler assessment at the antimesenteric
border, and Wood lamp examination following intravenous
fl uorescein [ 37 ]. While frankly necrotic bowel should be
resected, overaggressive resection of “borderline” segments
should be avoided. Instead, a second-look laparotomy after
24–48 h should be performed to reassess viability.
Radiation Enteritis
Key Concept: Radiation therapy can result in various inherent
and secondary manifestations, with repeated surgical resection for its complications being the primary cause of SBS.
Intestinal injury due to external radiation therapy (XRT)
for abdominal and pelvic malignancies accounts for approximately 20 % of patients with SBS [ 38 , 39 ]. In addition to
surgical interventions for radiation-related complications,
radiation damage to intact bowel can also result in reduced
functional gut mass.
Obstruction secondary to stricture is the most common
complication of radiation enteritis that requires surgery [ 40 ].
Depending on intraoperative fi ndings that may include a
“frozen abdomen,” surgical options include resection,
bypass, and ostomy formation. Stricturoplasty has been utilized successfully in this setting, for selected patients with
strictures within long intestinal segments and limited residual bowel [ 41 ]. Other complications of radiation enteritis
that may require surgery include fi stula and perforation. In
general, principles of management include eradicating sepsis, optimizing nutritional status, and maximizing functional
in-continuity bowel length [ 42 ]. One study described the use
of hyperbaric oxygen to treat XRT-induced intestinal injury
and reported a 58 % response rate in improved obstructive
symptoms and fi stula closure [ 43 ].
Clinical Manifestations
Key Concept: The clinical presentation of patients with short
bowel syndrome is largely determined by the anatomy of
their remaining GI tract, though diarrhea, malnutrition,
weight loss, and dehydration are very common.
In general, patients can be considered as having one of
three confi gurations of residual bowel: (1) “jejunum-colon,”
a jejunocolic anastomosis following a jejunoileal resection;
(2) “jejunoileum,” jejunum anastomosed to >10 cm of terminal ileum with an intact colon following a predominantly
jejunal resection; and (3) “jejunostomy,” an end stoma following resection of jejunum, ileum, and colon [ 5 ].
In the early postoperative period, jejunum-colon patients
may experience diarrhea and steatorrhea, but otherwise often
appear well. In the ensuing months, however, they gradually
experience increasing diffi culties with malnutrition and
weight loss [ 5 ]. For jejunoileum patients, the preservation of
their terminal ileum and colon typically allows these
450
I. Yang and R.P. Boushey
individuals to avoid signifi cant problems with absorption;
long- term enteral or parenteral nutritional supplementation
is rarely needed. Exceptions arise when a substantial portion
of the remaining bowel is involved with underlying pathology such as Crohn’s disease or radiation enteritis, thus compromising residual absorptive function. Patients with a
jejunostomy, beginning in the immediate postoperative
period, almost uniformly have signifi cant issues with maintaining hydration, due to high stomal output of water and
sodium. This may result in signs and symptoms such as
thirst, oliguria, and hypotension.
Changes in mental status, such as confusion and slurred
speech, may be observed in patients with short bowel.
Potential causes include defi ciencies in thiamine and magnesium, as well as impaired ammonia detoxifi cation due to
inadequate amino acids which require small bowel for synthesis [ 44 ]. Specifi c to patients with an intact colon, mental
status changes can also result from d -lactic acidosis [
As unabsorbed carbohydrate reaches the colon, it is fermented by anaerobes to produce d -lactic acid. The absorp-
tion of this metabolite can lead to severe metabolic acidosis
and clinical manifestations such as confusion, ataxia, and
ophthalmoplegia.
“Stones” are a more common manifestation in patients
with short bowel syndrome. In a review of 84 patients with
less than 200 cm of residual small bowel, the prevalence of
asymptomatic gallstones was 44 %, and this was uninfl uenced by the presence or absence of an intact colon [ 26 ]. The
formation of gallstones in SBS patients likely relates to biliary stasis and resultant biliary sludge; in addition, bile acid
depletion following ileal resection results in increased cholesterol concentration in bile. The risk of developing complications related to gallstones is higher in patients who require
long-term total parenteral nutrition (TPN) [ 46 ]. There is also
an increased incidence of renal stones among SBS patients,
especially those with their colon in continuity. The pathogenesis primarily relates to hyperoxaluria. Malabsorbed
fatty acids in the colon precipitate with intraluminal calcium,
thus leaving more soluble oxalate to be absorbed [ 26 ]. This
problem is compounded by an increase in colonic permeability to oxalate that is induced by the presence of unabsorbed
bile salts [ 47 ]. Consequently, a quarter of jejunum-colon
patients will develop symptomatic nephrolithiasis [ 26 ].
Meanwhile, all patients with SBS are potentially more susceptible to renal stones due to other factors such as dehydration and reduced urine volume.
45 ].
Diagnosis and Assessment
Key Concept: The diagnosis of SBS is usually obvious based
on clinical fi ndings of malabsorption in the context of extensive intestinal loss. Intraoperatively, the remaining length
and type of bowel should be determined in order to anticipate the likely consequences of resection.
Knowledge of the residual bowel length is much more
useful than that of the resected length, given the wide variation among “normal” bowel lengths (302–846 cm in two
studies of intraoperative measurements) [ 48 , 49 ]. If mea-
surements from the time of surgery are unavailable, then
radiological studies may be used; one study demonstrated
good correlation between radiographic and intraoperative
measurements in the setting of a short (<200 cm) intestine
[
50 ]. Another method of estimating residual bowel length
involves the measurement of citrulline, an amino acid that is
not incorporated into protein and is produced by small bowel
enterocytes [ 51 ]. Multiple studies have consistently
demonstrated a strong positive correlation between plasma
citrulline levels and remnant small bowel length [ 52 – 54 ]. Of
further clinical relevance, citrulline measurement can be
prognostic for SBS patients in whom bowel adaptation is
mostly complete. In a study of 57 patients for whom at least
2 years have elapsed since bowel resection, a plasma citrulline level of <20 μmol/L was highly suggestive of permanent
intestinal failure, with a positive predictive value of 95 %
and negative predictive value of 86 % [ 52 ].
Medical Management
Key Concept: A multidisciplinary approach to management
(preferably by specialized centers) is typically required to
optimize outcomes in SBS patients, with reliance on several
classes of medical therapy to achieve symptomatic control.
The overarching goal in managing short bowel syndrome
is to allow the patient to resume as normal a lifestyle as possible. This requires collaborative efforts and input from gastroenterologists, surgeons, dieticians, nurses, pharmacists,
and social workers. Given the number of anatomical, etiological, and patient-related factors that infl uence this condition,
management of each patient with SBS is highly individualized. Common elements of medical treatment include parenteral and enteral nutritional supplementation, as well as
pharmacologic agents and therapies to increase absorption,
decrease secretion, and enhance intestinal adaption.
The concept of intestinal rehabilitation in short bowel
syndrome refers to the use of nutritional and pharmacologic
methods to optimize remnant intestinal function and maximize the chances of independence from parenteral nutrition
[ 55 ]. The approach is invariably multidisciplinary, and it can
be protocolled to improve therapeutic accuracy and consistency of care [ 56 ]. There is evidence to support the argument
that intestinal failure patients requiring home parenteral
nutrition should be primarily followed by specialized centers
of excellence where comprehensive bowel rehabilitation
programs exist [
55 , 57 ].