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29 Short Bowel Syndrome
451
Parenteral Nutrition
Key Concept: Despite the multitude of potential complica­tions associated with its use, parenteral nutrition is a life­saving intervention for many patients with SBS, and a signifi cant percentage of patients can eventually be weaned off parenteral nutrition completely.
Total parenteral nutrition (TPN) is often the fi rst form of alimentary support initiated following massive bowel resec­tion, and in most instances it is continued for at least 7–10 days. Parenteral nutrition can be used to provide macronutri­ents and energy required for intestinal adaptation and to pre­vent defi ciencies in vitamins and minerals [ 3 , 5 ]. To replace water and electrolyte losses during the immediate postopera­tive period, usually both parenteral nutrition and supplemen­tal intravenous fl uid are needed. Sodium, potassium, and magnesium are commonly defi cient in this context, and their serum levels should be closely monitored to help guide the composition of parenteral solutions.
In general, patients require approximately 25–35 kcal/kg/ day; parenterally, this is delivered with a combination of dextrose, lipids, and amino acids. Fat should account for 20–30 % of the total energy requirement, and protein should be provided at 1.0–1.5 g/kg/day [ 1 ]. Intravenous lipid emul- sion, traditionally derived from soybean oils, is thought to contribute to parenteral nutrition-associated liver disease (PNALD) [ 58 ]. Several groups have recently suggested the use of fi sh oil-based lipid emulsions to mitigate and reverse cholestasis [ 5961 ]. While these early reports have demon- strated encouraging results with fi sh oil, further studies are required to better defi ne its safety and effi cacy.
Some patients may require parenteral supplementation of certain vitamins, depending on their remnant bowel anatomy and amount of enteral intake. Water-soluble vitamin defi ­ciencies are rare in SBS except in patients with a proximal jejunostomy. To maintain normal thiamine levels, 3 mg of thiamine hydrochloride may be included in TPN solutions
62 ]. Vitamin B 12 defi ciency should be anticipated following
[ resection of more than 60 cm of ileum, and subcutaneous injections of 200 μg monthly may be required [ supplementation of fat-soluble vitamins is often needed after loss of ileum due to impaired absorption of fat and bile acids [ 9 ]. Trace metals can also be replaced parenterally when enteral intake is unable to match gastrointestinal losses. In particular, zinc and selenium defi ciencies may arise in the setting of severe diarrhea [ 63 , 64 ].
Home parenteral nutrition is the mainstay of therapy for the majority of patients with chronic intestinal failure [ 57 ]. Its successful implementation requires a multidisciplinary effort that extends beyond hospital discharge with home care support until patient self-management is achieved. While in hospital, patients and their caregivers should receive educa­tion regarding preparation and administration of parenteral
7 , 8 ]. As well,
solutions, catheter care, and signs and symptoms of potential complications [ 1 ].
Parenteral nutrition is usually tapered as enteral feeding is successfully advanced. Depending on the amount and func­tion of a patient’s residual bowel, complete or partial transi­tion to enteral intake may be possible. Tolerance of enteral and oral nutrition can continue to improve over the fi rst few years after resection, as the remnant intestine’s absorptive function is enhanced through adaptation [ 55 ]. Overall, up to half of patients who initially require home parenteral nutri­tion are able to achieve independence from it [ 65 , 66 ].
Complications Associated with Long-Term Parenteral Nutrition
Key Concept: The long-term use of parenteral nutrition is associated with several potentially life-threatening compli­cations. Their repeated occurrences often curtail continued delivery of parenteral nutrition and account for signifi cant mortality among patients with chronic intestinal failure.
Parenteral nutrition is not without a wide array of morbid­ity and mortality [ 65 , 67 ]. A range of liver pathologies have been associated with chronic parenteral nutrition, including cholestasis, steatosis, steatohepatitis, fi brosis, and cirrhosis [ 68 ]. Cholestatic liver disease is particularly common among SBS patients due to other contributory factors such as lack of enteral intake and recurrent sepsis related to bacterial over­growth or indwelling catheter [ 31 ]. In one study of 90 patients with intestinal failure receiving home parenteral nutrition, chronic cholestasis occurred in 65 % of patients after a median of 6 months, and complicated liver disease (extensive portal fi brosis or cirrhosis) was demonstrated in 50 % of patients at 6 years [ 69 ]. To reduce to the risk of these complications, the study’s authors suggested limiting the intake of ω-6 rich lipid emulsions to less than 1 g/kg/day [ 69 ]. Excessive dextrose feeding should also be avoided [ 70 ]. Other strategies to prevent liver disease include opti- mizing the patient’s enteral intake and preventing sepsis of any etiology [
58 ]. As mentioned previously, the use of fi sh-
oil- based lipid emulsions have also shown some promise in this regard [
5961 ]. The use of ursodeoxycholic acid can
also be considered, as there is limited evidence for its benefi t in treating cholestasis [ 71 , 72 ].
Sepsis related to the indwelling venous feeding catheter is a signifi cant cause of mortality among patients on chronic parenteral nutrition. A French study involving 124 adults with nonmalignant SBS found that 5 of the 32 deaths (16 %) among patients with permanent intestinal failure were directly attributable to catheter-related sepsis [ 39 ]. However, with proper line care technique, the incidence of line sepsis can be as low as 0.26 episodes per patient year [
73 ]. A local
infection at the catheter’s exit site will often respond to intra­venous antibiotic therapy with empiric coverage for S. aureus , though the choice of antimicrobial agents may
452
I. Yang and R.P. Boushey
require subsequent adjustment based on culture and sensitiv­ity results [
1 ]. Lack of response to antibiotic therapy, evi-
dence of infection along the subcutaneous tunnel tract, or septicemia in an unstable patient will mandate removal of the catheter [ 1 , 57 ].
Thrombosis of the catheter is a relatively rare event, occurring at an incidence of 0.07 episodes per catheter year in patients receiving home parenteral nutrition [ 74 ]. Venous access occlusion accounts for approximately one quarter of all catheter removals [ 75 ]. Furthermore, catheter-related venous thrombosis may be complicated by SVC syndrome and pulmonary embolus [ 74 , 76 ]. It is not uncommon for catheter-related sepsis to precede thrombosis, and the for­mer’s presence should raise the index of clinical suspicion for the latter and prompt consideration of prophylactic anti­coagulation with either warfarin or heparin [ 57 , 77 ]. Treatment for confi rmed venous thrombosis usually consists of at least 6 months of anticoagulation with low-molecular­weight heparin [ 57 ].
Other complications that have been described in patients requiring chronic parenteral nutrition include renal dysfunc­tion, metabolic bone disease, and cognitive defi cits [ 67 , 78 ].
Enteral Nutrition and Oral Diet
Key Concept: Whenever possible, enteral intake should be provided preferentially over parenteral nutrition as the for­mer has several clear advantages. The composition should be individualized based on the residual anatomy.
There is no question that the enteral route is preferred in this setting, as the advantages are clear. Chief among these is the dependence of intestinal adaption upon exposure of the bowel to luminal nutrients [ 79 ]. As these nutrients come in contact with bowel epithelium, adaptive hyperplasia of the intestinal mucosa is induced [ 80 ]. In addition, enteral nutri- tion increases the secretion of trophic gastrointestinal hor­mones that stimulate adaptation [ plethora of potential complications associated with long­term parenteral nutrition, enteral feeding is relatively safe. As well, the administration of enteral nutrition is signifi ­cantly less labor intensive.
Following massive bowel resection, the introduction of enteral nutrition is usually delayed until the patient is hemo­dynamically stable. Initially, enteral feeding may be continu­ously infused via nasogastric tube, gastrostomy, or jejunostomy; this mode of delivery tends to be better toler­ated than bolus feeds. As the patient’s overall condition improves, gradual transition to oral diet can take place. There is evidence to suggest that continuous tube feeding (exclu­sively or in conjunction with oral feeding) increases absorp­tion of lipids, proteins, and energy compared with oral feeding alone [ 81 ]. Therefore, even patients who are
79 ]. In contrast to the
tolerating an oral diet may benefi t from tube feeding supple­mentation as it can reduce or obviate dependence on paren­teral nutrition.
The composition of enteral and oral feedings should be individualized based on the patient’s remnant intestinal anat­omy, comorbid conditions, and susceptibility to certain com­plications. In general, patients with an intact colon should be given a high-carbohydrate diet to take advantage of SCFA production via fermentation, an additional source of energy [
24 ]. If concerns arise regarding d -lactic acidosis (see
above), mono- and oligosaccharides should be restricted in favor of polysaccharides; in addition, thiamine supplementation and broad-spectrum antibiotics are indi­cated [ 5 ]. While there were early advocates for restricting dietary fat to reduce diarrhea, triglycerides are valuable nutrients as they are relatively energy-dense – 9.0 kcal/g compared to 4.0 kcal/g for carbohydrates – and, in the case of long-chain fatty acids, particularly effective stimulators of intestinal adaptation [ 2 , 82 ]. Therefore, a normal fat content is recommended for patients with retained colon. The diet for these individuals should be low in oxalate content to prevent nephrolithiasis [ 5 ].
Compared to jejunum-colon patients, individuals with a jejunostomy face greater challenges with respect to salt and water depletion. Large amounts of stomal losses are exacer­bated by enteral feeding, and careful attention must be given to the composition of fl uid intake. Patients should drink glucose- saline replacement solutions while limiting their oral intake of hypotonic fl uids – such as water, tea, coffee, or juices – to less than 500 ml daily [ 5 ]. Non-elemental diets tend to be favored over peptide-based diets for macronutrient delivery as the former have lower osmolarity while provid­ing comparable absorption [ 83 ]. The diet of jejunostomy patients should also contain a normal amount of fat. Increased dietary fat leads to proportionately increased fat absorption along the remaining jejunum without signifi cantly higher stomal effl uent volumes [ 84 ].
Transition to oral diet should take place gradually for patients with short bowel syndrome. Small and frequent meals are better tolerated and absorbed. However, in order to compensate for the malabsorbed portion of their dietary intake, patients should be encouraged to eventually consume more food overall than the amount to which they had previ­ously become accustomed [ 85 ].
Pharmacologic Agents
Key Concept: Commonly used drug therapies in short bowel syndrome constitute several different classes but act by either mitigating secretory losses or slowing gut transit.
H2 blockers and proton pump inhibitors reduce gastric acid secretion, and both medication classes have been shown
29 Short Bowel Syndrome
453
to decrease stomal effl uent volumes in SBS patients [ 8688 ]. They also prevent peptic ulceration and esophagitis that may result from transient hypergastrinemia and gastric hyperse­cretion in SBS [ 31 , 89 ]. It should be noted, however, that these drugs neither alter macronutrient absorption nor reduce the need for parenteral support [ 5 ]. Octreotide has similarly been shown to reduce intestinal fl uid losses secondary to diarrhea or high stomal output [
90 , 91 ]. In addition to decreas-
ing gastric and pancreatic secretions, octreotide also delays gastric emptying and intestinal transit [ 92 ]. However, experi- mental models have demonstrated octreotide to exert inhibi­tory effects on intestinal adaptation, a potentially signifi cant downside to its use in short bowel syndrome [ 93 , 94 ].
Loperamide is an antimotility agent with proven effi cacy in reducing water and sodium losses from an ileostomy [ 95 , 96 ]. Typical doses are 4–16 mg/day, but much higher doses may be required as the drug’s pharmacokinetics depend upon the enterohepatic circulation which is often disrupted fol­lowing massive bowel resection [ 3 , 5 ]. Codeine has similar effects in decreasing diarrhea, but there is evidence to sug­gest that it impairs fat absorption [ 95 , 97 ]. With any medica- tion that is administered orally to patients with short bowel, there needs to be vigilance to ensure that it is being ade­quately absorbed as opposed to emerging undigested in sto­mal output or stool [ 5 ].
Cholestyramine can improve secretory diarrhea following ileal resection by binding unabsorbed bile salts [ 98 ]. It should be given at a dose of 4 g prior to meals, up to three times daily [ 4 ]. However, this drug should not be used in patients who have had more than 100 cm of ileum resected; such extensive resection depletes the bile salt pool and ren­ders cholestyramine ineffective, and the drug may actually worsen steatorrhea and cause fat-soluble vitamin defi ciency [ 1 , 2 , 99 ].
Growth Factors
Key Concept: The use of growth factors is an emerging class of therapy for SBS with still widely variable results. While promising, they are most commonly used in specialized cen­ters or still under investigation.
An increasingly active area of research involves the potential of several growth factors to enhance intestinal adaptation and improve absorption in patients with short bowel syndrome. The current depth of evidence varies among these novel therapies, and some of these medications have been incorporated into intestinal rehabilitation pro­grams at specialized centers.
The application of growth hormone in the treatment of SBS was fi rst suggested by early animal model studies that demonstrated the substance’s positive effect on mucosal hyperplasia after extensive bowel resection [
100 , 101 ].
Similarly, the amino acid glutamine, the primary fuel of enterocytes, was shown to exert trophic effects on bowel and stimulate nutrient absorption [
102 , 103 ]. By instituting regi-
mens that included growth hormone, glutamine, and dietary fi ber, some centers have produced case series data showing enhanced absorptive capacity and weaning from parenteral nutrition [ 104 , 105 ]. However, the combination of growth hormone plus glutamine failed to improve nutrient absorp­tion compared to placebo in two randomized controlled stud­ies [ 106 , 107 ]. The benefi t of growth hormone alone in SBS has also been investigated in two randomized placebo- controlled trials; one of the studies demonstrated modestly increased absorptive capacity with growth hor­mone while the other detected no difference [ 108 , 109 ]. Similarly, glutamine alone has not been found to be benefi ­cial compared to placebo [ 110 ]. Nevertheless, these trials are uniformly small in sample size, and the role and effi cacy of these substances in treating SBS remain controversial.
Glucagon-like peptide-2 (GLP-2) is a naturally occurring polypeptide synthesized by enteroendocrine l -cells located primarily in the terminal ileum and colon [ 67 ]. Secreted in response to enteral nutrition, GLP-2 promotes bowel muco­sal growth, enhances absorptive capacity, and stimulates mesenteric blood fl ow [ 80 , 111 , 112 ]. Accordingly, jejunos- tomy patients without an intact colon, who are known to have relatively little capacity for intestinal adaptation, have been shown to exhibit markedly impaired GLP-2 activity follow­ing meals [ 113 ]. It follows, therefore, that GLP-2 therapy may have a clinically signifi cant impact on bowel adaptation and absorptive function in patients with SBS. In a small, non­placebo-controlled study of SBS patients, GLP-2 treatment reduced fecal wet weight but did not signifi cantly change energy absorption or mucosal morphology [ 114 ]. Teduglutide, a long-acting analogue of GLP-2, was similarly shown in an open-label phase 2 study to increase wet weight absorption [ 115 ]. In this study, the drug’s benefi t was seen even in patients with an intact colon and near-normal endogenous GLP-2 levels, a fi nding which suggests that supraphysiologi­cal doses of teduglutide may be advantageous. In a recent multicenter, randomized, placebo-controlled trial, 83 paren­teral nutrition-dependent SBS patients were assigned to receive one of placebo, 0.05 mg/kg/day teduglutide, or
0.10 mg/kg/day teduglutide [ 116 ]. The study’s primary effi - cacy end point was a graded response score (GRS) that accounted for reduction in parenteral requirements and dura­tion of response. The GRS was signifi cantly better in the
0.05 mg/kg/day teduglutide compared to placebo, while no statistically signifi cant benefi t was seen with the 0.10 mg/kg/ day dose. Ad hoc analysis attributed the latter result to a trend toward higher baseline parenteral volume in the 0.10 mg/kg/ day group. Three teduglutide-treated patients were com­pletely weaned off parenteral support. The study also con­fi rmed teduglutide’s intestinotrophic effect through serum
454
I. Yang and R.P. Boushey
citrulline measurements, which increased with both low- and high-dose treatment, but not with placebo. Interestingly, there is also some literature that suggests teduglutide, which has anti-infl ammatory properties, may induce remission and mucosal healing in patients with Crohn’s disease [ Whether this may translate to demonstrable effi cacy of tedu­glutide in Crohn’s-related SBS is just one of many questions surrounding this therapy that require further study.
Several other growth factors have received attention for their potential role in the treatment of short bowel syndrome. Transforming growth factor-α, a polypeptide found in epi­thelium along the gastrointestinal tract, has been shown to improve intestinal adaptation in animal models of SBS [ 118 , 119 ]. Hepatocyte growth factor, when administered in rats following massive small bowel resection, enhanced intesti­nal epithelial cell function and mucosal mass beyond the normal adaptive response [ tors including interleukin-11, insulin-like growth factor, and keratinocyte growth factor also demonstrated positive effects [
121123 ]. The intestinotrophic effects of these peptides
have yet to be demonstrated in humans.
120 ]. Studies of other growth fac-
117 ].

Surgical Management

Key Concept: Surgery for SBS aims to improve the patient’s quality of life by increasing residual absorptive function and reducing overall morbidity and complications.
Surgical options for SBS include small bowel transplanta­tion and a variety of non-transplant procedures. The choice and timing of these interventions depend on the patient’s remnant intestinal anatomy, comorbid conditions, and response to medical management.
Restoration of Intestinal Continuity
Key Concept: Never miss out on an opportunity to restore intestinal continuity if enough residual bowel remains.
For patients with an end stoma and residual distal bowel, intestinal continuity should be reestablished when possible. This intervention restores the absorptive functions and hor­monal “braking” mechanisms of the previously diverted bowel and prolongs intestinal transit [ improvement in overall absorption may be suffi cient to allow weaning off parenteral nutrition [ 67 ]. When large bowel is brought back into continuity, one should be cognizant of the corresponding increase in the patient’s susceptibility to complications such as nephrolithiasis and d -lactic acidosis.
With respect to timing, reoperation should be deferred until the patient is hemodynamically stable and medically optimized. Further waiting may be prudent to avoid diffi cult adhesions and minimize surgical morbidity. Any intra­abdominal sepsis should be resolved preoperatively,
124 ]. The resulting
if possible. Many underlying etiologies in SBS predispose to stricture formation, and distal obstruction must be ruled out prior to restoring intestinal continuity.
Procedures to Slow Intestinal Transit
Key Concept: For patients who have failed medical therapy and have maximized adaptation, surgical procedures aimed at slowing intestinal transit can improve absorption as fl uids and nutrients remain in contact with bowel mucosa for lon­ger periods of time.
In general, these slowing procedures should be consid­ered only for patients whose residual bowel is already in continuity and maximally adapted [ 125 ]. Of these individu- als, the subset with relatively ample intestinal length, but with lack of response to medical therapy, is most likely to benefi t from this surgical strategy [ 67 ].
Among this group of procedures, segmental reversal of small bowel has been most extensively evaluated and appears to be the most effective [ 125 ]. The technique involves sepa- rating a segment of small bowel from the adjacent intestine while leaving its blood supply intact and subsequently reanas­tomosing the segment in the opposite direction of normal intestinal fl ow. To avoid complete volvulus of the mesentery, each of the proximal and distal parts of the bowel can be rotated 90° so that the mesentery of the reversed segment only needs to be rotated 180° [ 126 ]. The ideal length of reversed segment appears to be approximately 10–15 cm; if the anti­peristaltic segment is too long, bowel obstruction can result [ 127 ]. The location of the reversed segment should be chosen as distally as possible to decrease the symptoms of obstruc­tion [ 31 ]. While results vary throughout the literature, adult series have generally shown a favorable response to segmen­tal reversal in approximately 70 % of the patients [ 124 ].
Other techniques to slow intestinal transit include colonic interposition, creation of intestinal valves to produce a par­tial obstruction, and implantation of reversed electrical pac­ing devices [ 128130 ]. Published experience is very limited for these procedures, and they should only be employed by highly experienced surgeons in the absence of more proven alternatives.
Procedures to Lengthen Residual Bowel
Key Concept: Intestinal lengthening surgery should be con­sidered for patients with dilated and severely shortened bowel that precludes independence from parenteral nutrition despite optimal adaptation and medical treatment.
These techniques create additional length by exploiting the compensatory dilatation of the residual bowel that nor­mally occurs following extensive bowel resection [ operations also taper the bowel, which results in improved
124 ]. The
29 Short Bowel Syndrome
455
a
underwent the procedure were successfully weaned off par­enteral nutrition [
131 , 134 ].
A more recent addition to the intestinal lengthening arma­mentarium is the serial transverse enteroplasty (STEP) [
135 ].
The technique involves the partial transection of dilated bowel using a linear cutting stapler, which is applied sequen­tially from alternating and opposite directions, in transverse fashion (Fig.
29.2 ). The goal is to produce a zigzag pattern of
lengthened bowel with a diameter of approximately 2 cm. In contrast to the Bianchi procedure, STEP can be employed for recurrent bowel dilatation after previous lengthening [ 133 ]. Published results with this technique have been promising. A multicenter registry of 21 SBS patients undergoing STEP reported that the percentage of total calories tolerated enter­ally increased from 31 to 67 % at a median follow-up of 12.6 months [ 136 ]. A single-institution experience that included
b
34 STEP and 43 Bianchi procedures demonstrated a trend toward a higher rate of weaning from parenteral nutrition in patients who underwent STEP (60 % vs. 55 %) [ 131 ]. Long- term outcomes after STEP were reported in a single-center series of 12 pediatric patients; while 2 patients subsequently received liver-intestinal transplants and 2 others died of liver failure, 7 of the remaining 8 patients were weaned off paren­teral nutrition by 4 years post-STEP [ 137 ].
Fig. 29.1 The Bianchi longitudinal intestinal lengthening procedure (Reprinted from Bianchi [ divided longitudinally to yield two vascularized halves of the bowel wall. ( b ) End-to-end anastomosis of the newly formed bowel loops results in a longer but narrower segment of bowel compared to the orig­inal loop. © Elsevier 2006)
160 ], ( a ) The bowel and its mesentery are
motility and reduced bacterial overgrowth. It should be noted that patients with advanced liver disease are poor candidates for lengthening and should be referred for intestinal trans­plantation instead [ 131 ].
The Bianchi longitudinal intestinal lengthening proce­dure involves separating the two layers of small bowel mes­entery, each layer containing blood vessels that enter one side of the bowel wall (Fig. 29.1 ) [ 132 ]. The dilated bowel is then divided longitudinally between the mesenteric layers to form two parallel lumens. End-to-end anastomosis of these two newly formed bowel loops creates an intestinal segment that is longer but narrower than the original seg­ment [ 125 ]. Over time, the absorptive surface area may increase as the lengthened segment dilates [
124 ]. The
reported experience with the Bianchi procedure predomi­nantly consists of case series data in the pediatric literature [ 133 ]. In two larger series, the majority of patients who
Other Non-transplant Procedures
Key Concept: Dilation and adaption of the bowel can be helpful but also can lead to complications that may need to be addressed with other surgical procedures.
As alluded to previously, dilatation of the intestinal rem­nant normally occurs as an adaptive response following resection in order to slow intestinal transit and increase mucosal absorptive area [ 124 ]. However, this compensatory process can lead to pathologic consequences such as dys­motility, bacterial overgrowth, and impairment of absorptive function. For such scenarios in patients with moderately shortened bowel, plication of the bowel wall and tapering enteroplasty may be benefi cial [ 67 , 127 ].
Small Bowel Transplantation
Key Concept: Small bowel transplantation is a viable thera­peutic option for intestinal failure as improvements have occurred in immunosuppressive agents. While select patients are typically in the end stage who have failed parenteral nutrition, there is controversy regarding the need to expand this to more patients earlier in their SBS course.
Historically, transplantation of the small intestine was believed to be associated with seemingly insurmountable challenges related to the organ’s immunogenicity and colo­nization with microorganisms [ 138 ]. Earlier efforts were
456
Fig. 29.2 The serial transverse enteroplasty (STEP) procedure (Reprinted from Javid et al. [ © Elsevier 2005)
I. Yang and R.P. Boushey
Antimesenteric border
161 ]
GIA stapler
associated with very high rates of morbidity and mortality related to rejection, graft loss, and bacterial translocation leading to sepsis. More recently, refi nement of surgical technique in addition to enhanced immunosuppressive and other perioperative strategies has signifi cantly improved outcomes [ 138 , 139 ]. Therefore, small bowel transplanta- tion has become fi rmly established as a viable therapeutic option for intestinal failure. Depending on the extent of liver disease and other abdominal pathology, a combined liver-intestine or multivisceral graft may be indicated [ 139 ]. Recent data from high-volume intestinal transplant centers demonstrate 1-year patient and graft survival rates that exceed 80 and 70 %, respectively [ 140142 ]. While long- term survival has also dramatically improved in recent decades, they still fall short of outcomes seen with other abdominal organ transplants [ 143 ]. The Pittsburgh group reported their series of intestinal and multivisceral trans­plants divided into time periods; for the 322 transplants per­formed during the study’s latest era (between 2001 and
2008), 5-year patient and graft survival rates were 68 and 53 %, respectively [
142 ]. There are ongoing efforts to
develop novel strategies to overcome late graft loss and its sequelae [
142 , 144 ].
Traditionally, intestinal transplantation has been reserved for patients with permanent intestinal failure who can no longer be maintained on total parenteral nutrition therapy
[ 145 ]. Specifi cally, patients should be considered for trans- plantation if they have impending or overt liver failure, repeated loss of central venous access due to thrombosis, recurrent episodes of catheter-related sepsis, or frequent dehydration despite intravenous supplementation [ 146 ]. For these patients, prompt referral to a transplant center for evaluation is imperative for optimizing outcome [ 147 , 148 ]. Early transplantation, as defi ned by less than 12 months of prior parenteral nutrition therapy, has been shown to be associated with better survival [ 142 ]. As clinical outcomes of intestinal transplantation continue to improve, some experts have advocated for the restrictive indications to be broadened [ 149 ]. Indeed, there has been increasing debate regarding the role of “preemptive” transplantation in patients who are at high risk of developing parenteral nutri­tion failure; this may apply to patients with ultrashort small intestine (<50 cm), primary motility disorders, chronic obstruction, and radiation injury [ 144 , 149 ]. The poor prog- nosis associated with parenteral nutrition failure supports early consideration of transplantation [ 149 ]. Furthermore, there are multiple studies that demonstrate improved qual­ity of life indicators following transplantation [ 143 , 149 ]. As well, intestinal transplantation has been shown to be cost-effective for managing intestinal failure as long as graft function is maintained for at least 2–3 years after surgery [ 150 ].
29 Short Bowel Syndrome
457

Future Directions

Key Concept: We remain hampered by a widespread lack of effective options for severe SBS, although emerging technol­ogy is in the investigative phase to give patients additional hope.
Despite its recent advances, small intestinal transplanta­tion continues to be limited by issues such as donor avail­ability, graft rejection, and adverse effects related to immunosuppression. As a potential solution to overcome these diffi culties, tissue-engineered small intestine has been studied in animal models [ 151 , 152 ]. The technology makes use of biomaterials such as small intestinal submucosa to generate new tissue and takes advantage of the regenerative ability of intestinal epithelium [ 153 ]. While normal struc- tural components have been successfully generated, peristal­tic motion of the intestine has yet to be recreated [ well, it may be diffi cult to procure the necessary neonatal intestinal organelles in humans and to scale up the size of the tissue-engineered intestine to clinically useful dimensions [
153 ]. Nevertheless, if this technology were to become fea-
sible in the future, it has the potential to dramatically alter the management of short bowel syndrome.
133 ]. As

Outcomes

Key Concept: The prognosis of patients with short bowel syndrome is determined by their remnant intestinal anatomy and underlying disease and modulated by their response to medical and surgical treatments.
Overall, patients who are dependent on home parenteral nutrition (HPN) have higher mortality than their age-matched counterparts in the general population [ 154 ]. A French group recently reported their results over a 25-year period including 268 consecutive adult SBS patients who required HPN [ 66 ]. Survival was 94, 70, and 52 % at 1, 5, and 10 years, respec­tively. Complications related to SBS and HPN combined accounted for only 26 % of the mortality. The study also found the probabilities of a patient remaining dependent on HPN were 74, 64, and 48 % at 1, 2, and 5 years, respectively. Factors signifi cantly associated with HPN dependence at 5 years included remnant small intestinal length of less than 75 cm, less than 4/7 of colon remaining, and postoperative citrulline concentration of less than 20 μmol/L. Comparable results have been reported by other centers regarding the prognosis of HPN-dependent patients, including 5-year sur­vival rates ranging between 60 and 78 % [ 65 , 155 , 156 ].
There have been few studies addressing quality of life (QOL) of patients on HPN. Jeppesen et al. used two vali­dated (QOL) questionnaires on 49 HPN-dependent patients and 36 patients who did not receive HPN but had anatomical or functional short bowel [
157 ]. Compared to the latter
group, the former was found to have a poorer quality of life that was comparable to that reported for dialysis-dependent patients with chronic renal failure. Another research demon­strated that lowest QOL scores are more common during the fi rst year on HPN, particularly if the patient was previously well [ 158 ]. Quality of life then gradually improves under its plateaus after 4–5 years on HPN. A US study found low quality of life in patients requiring long-term HPN to be associated with length of time on total parenteral nutrition, lack of family supports, and fi nancial diffi culties [ respect to intestinal transplantation, there is increasing evi­dence that it results in improved quality of life measures [ 144 ]. In a comparison of QOL measures between 79 adult transplant survivors and 79 HPN patients, Abu-Elmagd et al. reported superior results with transplantation across several psychological, emotional, and social domains [ 143 ].
159 ]. With

Summary Pearls

You will be confronted with patients with SBS, and they may be some of the most challenging that you will encounter. It is important to remember that the management of the patient with short bowel syndrome is guided by a thorough under­standing of the remnant intestinal anatomy and physiology as well as the underlying disease (Fig. 29.3 ). These factors will largely determine the patient’s clinical manifestation, which may range from mild malabsorption correctable with dietary modifi cations to intestinal failure requiring complex bowel rehabilitation and surgical strategies. As outcomes in published series consistently correlate with residual length of small intestine, it is worthwhile during the initial resection operation to preserve as much of it as possible. Similarly, an intact colon is valuable as it can compensate for the lost absorptive function, and its presence is associated with inde­pendence from home parenteral nutrition.
A multidisciplinary approach is essential for the optimal care of these complex patients. In particular, individuals who are dependent on home parenteral nutrition should be man­aged by a center with appropriate expertise and resources. This is likely to optimize intestinal rehabilitation, reduce complications associated with long-term parenteral nutri­tion, and facilitate access to specialized medical and surgical therapies. For nutritional support, you should use the enteral route whenever possible; the presence of luminal nutrients is necessary for intestinal adaption, a process which may con­tinue for several years following resection. Antisecretory and antimotility medications may be useful adjuncts for reducing water and salt losses. Among the growth factors, GLP-2 and its analogue, teduglutide, are promising intestinotrophic agents that can augment a bowel rehabilitation regimen.
In the absence of contraindications to surgery, you should attempt to restore intestinal continuity. For patients whose
458
Fig. 29.3 Algorithm for surgical management of short bowel syndrome
I. Yang and R.P. Boushey
Stoma+ residual distal
bowel?
Yes
Re-establish intestinal
continuity
Yes
Consider
transplantation
Dilated bowel?
Yes
Bianchi or STEP Colonic interposition
No
Severely short bowel?
No
Intestinal valve to
dilatation, followed by
Blanchi or STEP
Tapering enteroplasty
induce bowel
Yes
or plication
No
Dilated bowel?
No
Transit-slowing
Procedures
bowel is already in continuity, but cannot wean off parenteral nutrition despite seemingly adequate intestinal length, seg­mental reversal of small bowel should be considered to slow transit. On the other hand, for patients who are clearly limited by a very short bowel that is dilated, either the Bianchi proce­dure or STEP may be appropriate. Of these two bowel- lengthening operations, STEP is likely easier to per­form and can be used as a repeat procedure. Finally, intestinal transplantation has evolved over recent years to offer improved survival and quality of life outcomes. Most importantly, for SBS patients with adverse risk factors for failing parenteral nutrition or if you do not feel comfortable or have the resources to care for these patients, referral for evaluation regarding transplantation should be considered early in their course.

References

1. Buchman A, Scolapio J, Fryer J. AGA technical review on short bowel syndrome and intestinal transplantation. Gastroenterology. 2003;124:1111–34.
2. Jeejeebhoy KN. Management of short bowel syndrome: avoidance of total parenteral nutrition. Gastroenterology. 2006;130(2 Suppl
1):S60–6.
3. Buchman AL. Etiology and initial management of short bowel syn­drome. Gastroenterology. 2006;130(2 Suppl 1):S5–15.
4. Westergaard H. Short bowel syndrome. Semin Gastrointest Dis. 2002;13(4):210–20.
5. Nightingale J, Woodward JM. Guidelines for management of patients with a short bowel. Gut. 2006;55 Suppl 4:iv1–12.
6. Longshore S, Wakeman D, McMellen M, Warner B. Bowel resec­tion induced intestinal adaptation: progress from bench to bedside. Minerva Pediatr. 2009;61(3):239–51.
7. Jeejeebhoy KN. Short bowel syndrome: a nutritional and medical approach. CMAJ. 2002;166(10):1297–302.
8. Thompson W, Wrathell E. The relation between ileal resec­tion and vitamin B12 absorption. Can J Surg. 1977;20(5):
461.
9. Hofmann AF. Bile acid malabsorption caused by ileal resection. Arch Intern Med. 1972;130(4):597–605.
10. Lin H, Zhao X, Wang L. Intestinal transit is more potently inhibited by fat in the distal (ileal brake) than in the proximal (jejunal brake) gut. Dig Dis Sci. 1997;42(1):19–25.
11. Stanley S, Wynne K, Bloom S. Gastrointestinal satiety signals III. Glucagon-like peptide 1, oxyntomodulin, peptide YY, and pancre­atic polypeptide. Am J Physiol Gastrointest Liver Physiol. 2004;286:G693–7.
29 Short Bowel Syndrome
459
12. Nightingale J, Kamm M, van der Sijp J, Ghatei M, Bloom S, Lennard-Jones J. Gastrointestinal hormones in short bowel syn­drome. Peptide YY may be the “colonic brake” to gastric emptying. Gut. 1996;39:267–72.
13. Fordtran J, Rector F, Carter N. The mechanisms of sodium absorp­tion in the human small intestine. J Clin Invest. 1968;47(4): 884–900.
14. Davis G, Santa Ana C, Morawski S, Fordtran J. Permeability char­acteristics of human jejunum, ileum, proximal colon and distal colon: results of potential difference measurements and unidirec­tional fl uxes. Gastroenterology. 1982;83(4):844–50.
15. Chaet M, Farrell M, Ziegler M, Warner B. Intensive nutritional sup­port and remedial surgical intervention for extreme short bowel syndrome. J Pediatr Gastroenterol Nutr. 1994;19(3):295–8.
16. Sondheimer J, Cadnapaphornchai M, Sontag M, Zerbe G. Predicting the duration of dependence on parenteral nutrition after neonatal intestinal resection. J Pediatr. 1998;132:80–4.
17. Andorsky D, Lund D, Lillehei C, Jaksic T, DiCanzio J, Richardson D, et al. Nutritional and other postoperative management of neo­nates with short bowel syndrome correlates with clinical outcomes. J Pediatr. 2001;139:27–33.
18. Dibaise JK, Young RJ, Vanderhoof JA. Enteric microbial fl ora, bac­terial overgrowth, and short-bowel syndrome. Clin Gastroenterol Hepatology. 2006;4(1):11–20.
19. Vanderhoof J, Young R, Murray N, Kaufman S. Treatment strate­gies for small bowel bacterial overgrowth in short bowel syndrome. J Pediatr Gastroenterol Nutr. 1998;27(2):155–60.
20. Kaufman S, Loseke C, Lupo J, Young R, Murray N, Pinch L, et al. Infl uence of bacterial overgrowth and intestinal infl ammation on duration of parenteral nutrition in children with short bowel syn­drome. J Pediatr. 1997;131:356–61.
21. Fich A, Steadman C, Phillips S, Camilleri M, Brown M, Haddad A, et al. Ileocolonic transit does not change after right hemicolectomy. Gastroenterology. 1992;103(3):794–9.
22. Fry R, Mahmoud N, Maron D, Ross H, Rombeau J. Colon and rec­tum. In: Townsend C, Beauchamp R, Evers B, Mattox K, editors. Sabiston textbook of surgery. 18th ed. Philadelphia: Saunders, Elsevier; 2007.
23. Joly F, Mayeur C, Messing B, Lavergne-Slove A, Cazals-Hatem D, Noordine M-L, et al. Morphological adaptation with preserved pro­liferation/transporter content in the colon of patients with short bowel syndrome. Am J Physiol Gastrointest Liver Physiol. 2009;297(1):G116–23.
24. Royall D, Wolever T, Jeejeebhoy K. Evidence for colonic conserva­tion of malabsorbed carbohydrate in short bowel syndrome. Am J Gastroenterol. 1992;87(6):751–6.
25. Gouttebel MC, Saint-Aubert B, Astre C, Joyeux H. Total parenteral nutrition needs in different types of short bowel syndrome. Dig Dis Sci. 1986;31(7):718–23.
26. Nightingale JM, Lennard-Jones JE, Gertner DJ, Wood SR, Bartram CI. Colonic preservation reduces need for parenteral therapy, increases incidence of renal stones, but does not change high preva­lence of gall stones in patients with a short bowel. Gut. 1992;33(11):1493–7.
27. Mitchell JE, Breuer RI, Zuckerman L, Berlin J, Schilli R, Dunn JK. The colon infl uences ileal resection diarrhea. Dig Dis Sci. 1980; 25(1):33–41.
28. Thompson J. Short bowel syndrome and Crohn’s disease. J Gastrointest Surg. 2003;7(8):1069–72.
29. Polito J, Childs B, Mellits E, Tokayer A, Harris M, Bayless T. Crohn’s disease: infl uence of age at diagnosis and site and clinical type of disease. Gastroenterology. 1996;111(3):580–6.
30. Agwunobi A, Carlson G, Anderson I, Irving M, Scott N. Mechanisms of intestinal failure in Crohn’s disease. Dis Colon Rectum. 2001;44(12):1834–7.
31. Donohoe CL, Reynolds JV. Short bowel syndrome. Surgeon. 2010;8(5):270–9. Elsevier Ltd.
32. Kotanagi H, Kramer K, Fazio VW, Petras RE. Do microscopic abnormalities at resection margins correlate with increased anasto­motic recurrence in Crohn’s disease? Retrospective analysis of 100 cases. Dis Colon Rectum. 1991;34(10):909–16.
33. Yamamoto T, Fazio VW, Tekkis PP. Safety and effi cacy of strictureplasty for Crohn’s disease: a systematic review and meta­analysis. Dis Colon Rectum. 2007;50(11):1968–86.
34. Thompson JS. Comparison of massive vs. repeated resection lead­ing to short bowel syndrome. J Gastrointest Surg. 2000;4(1): 101–4.
35. Falkensammer J, Oldenburg WA. Surgical and medical manage­ment of mesenteric ischemia. Curr Treat Options Cardiovasc Med. 2006;8:137–43.
36. Sise MJ. Mesenteric ischemia: the whole spectrum. Scand J Surg. 2010;99(2):106–10.
37. Ballard JL, Stone WM, Hallett JW, Pairolero PC, Cherry KJ. A critical analysis of adjuvant techniques used to assess bowel viability in acute mesenteric ischemia. Am Surg. 1993; 59(5):309–11.
38. Thompson JS. Infl ammatory disease and outcome of short bowel syndrome. Am J Surg. 2000;180(6):551–5.
39. Messing B, Crenn P, Beau P, Christine M, Ruault B, Rambaud JC, et al. Long-term survival and parenteral nutrition dependence in adult patients with the short bowel syndrome. Gastroenterology. 1999;117:1043–50.
40. Boland E, Thompson J, Rochling F, Sudan D. A 25-year experience with postresection short-bowel syndrome secondary to radiation therapy. Am J Surg. 2010;200:690–3. Elsevier Inc.
41. Dietz D, Remzi F, Fazio V. Strictureplasty for obstructing small- bowel lesions in diffuse radiation enteritis-successful outcome in fi 1772–7.
42. Girvent M, Carlson GL, Shaffer J, Irving M, Scott NA. Intestinal failure after surgery for complicated radiation enteritis. Ann R Coll Surg Engl. 2000;82:198–201.
43. Marshall GT, Thirlby RC, Bredfeldt JE, Hampson NB. Treatment of gastrointestinal radiation injury with hyperbaric oxygen. Undersea Hyperb Med. 2007;34:35–42.
44. Yokoyama K, Ogura Y, Kawabata M, Hinoshita F, Suzuki Y, Hara S, et al. Hyperammonemia in a patient with short bowel syndrome and chronic renal failure. Nephron. 1996;72:693–5.
45. Mayne A, Handy D, Preece M, George R, Booth I. Dietary manage­ment of D-lactic acidosis in short bowel syndrome. Arch Dis Child. 1990;65:229–31.
46. Dray X, Joly F, Reijasse D, Attar A, Alves A, Panis Y, et al. Incidence, risk factors, and complications of cholelithiasis in patients with home parenteral nutrition. J Am Coll Surg. 2007; 204(1):13–21.
47. Dobbins J, Binder H. Effect of bile salts and fatty acids on the colonic absorption of oxalate. Gastroenterology. 1976;70: 1096–100.
48. Backman L, Hallberg D. Small intestinal length. An intraoperative study in obesity. Acta Chir Scand. 1974;140:57–63.
49. Slater G, Aufses A. Small bowel length in Crohn’s disease. Am J Gastroenterol. 1991;8:1037–40.
50. Nightingale J, Bartram C, Lennard-Jones J. Length of residual small bowel after partial resection: correlation between radiographic and surgical measurements. Gastrointest Radiol. 1991;16:305–6.
51. Crenn P, Messing B, Cynober L. Citrulline as a biomarker of intes­tinal failure due to enterocyte mass reduction. Clin Nutr. 2008; 27(3):328–39.
52. Crenn P, Coudray-Lucas C, Thuillier F, Cynober L, Messing B. Postabsorptive plasma citrulline concentration is a marker of absorptive enterocyte mass and intestinal failure in humans. Gastroenterology. 2000;119:1496–505.
53. Jianfeng G, Weiming Z, Ning L, Fangnan L, Li T, Nan L, et al. Serum citrulline is a simple quantitative marker for small intestinal
ve patients. Dis Colon Rectum. 2001;44(12):
460
I. Yang and R.P. Boushey
enterocytes mass and absorption function in short bowel patients. J Surg Res. 2005;127(2):177–82.
54. Luo M, Fernandez-Estivariz C, Manatunga A, Bazargan N, Gu L, Jones D, et al. Are plasma citrulline and glutamine biomarkers of intestinal absorptive function in patients with short bowel syn­drome? J Parenter Enteral Nutr. 2007;31:1–7.
55. Ziegler T, Leader L. Parenteral nutrition: transient or permanent therapy in intestinal failure? Gastroenterology. 2006;130:S37–42.
56. Sigalet D, Boctor D, Brindle M, Lam V, Robertson M. Elements of successful intestinal rehabilitation. J Pediatr Surg [Internet]. 2011;46(1):150–6. Available from:
pubmed/21238657
57. Messing B, Joly F. Guidelines for management of home parenteral support in adult chronic intestinal failure patients. Gastroenterology. 2006;130(2 Suppl 1):S43–51.
58. Goulet O, Joly F, Corriol O, Colomb-Jung V. Some new insights in intestinal failure-associated liver disease. Curr Opin Organ Transplant. 2009;14(3):256–61.
59. Ekema G, Falchetti D, Boroni G, Tanca AR, Altana C, Righetti L, et al. Reversal of severe parenteral nutrition-associated liver disease in an infant with short bowel syndrome using parenteral fi sh oil (omega-3 fatty acids). J Pediatr Surg. 2008;43(6):1191–5.
60. Gura KM, Lee S, Valim C, Zhou J, Kim S, Modi BP, et al. Safety and effi cacy of a fi sh-oil-based fat emulsion in the treatment of par­enteral nutrition-associated liver disease. Pediatrics. 2008;121(3): e678–86.
61. Mertes N, Grimm H, Fürst P, Stehle P. Safety and effi cacy of a new parenteral lipid emulsion (SMOFlipid) in surgical patients: a ran­domized, double-blind, multicenter study. Ann Nutr Metab. 2006;50(3):253–9.
62. Schiano T, Klang M, Quesada E, Scott F, Tao Y, Shike M. Thiamine status in patients receiving long-term home parenteral nutrition. Am J Gastroenterol. 1996;91(12):2555–9.
63. Wolman S, Anderson G, Marliss E, Jeejeebhoy K. Zinc in total par­enteral nutrition: requirements and metabolic effects. Gastroenterology. 1979;76:458–67.
64. Lane H, Lotspeich C, Moore C, Ballard J, Dudrick S, Warren D. The effect of selenium supplementation on selenium status of patients receiving chronic total parenteral nutrition. J Parenter Enteral Nutr. 1987;11:177–82.
65. Vantini I, Benini L, Bonfante F, Talamini G, Sembenini C, Chiarioni G, et al. Survival rate and prognostic factors in patients with intes­tinal failure. Dig Liver Dis. 2004;36:46–55.
66. Amiot A, Messing B, Corcos O, Panis Y, Joly F. Determinants of home parenteral nutrition dependence and survival of 268 patients with non-malignant short bowel syndrome. Clin Nutr. 2012;23:1–7. Elsevier Ltd.
67. Bines JE. Intestinal failure: a new era in clinical management. J Gastroenterol Hepatol. 2009;24 Suppl 3:S86–92.
68. Briones E, Iber F. Liver and biliary tract changes associated with total parenteral nutrition: pathogenesis and prevention. J Am Coll Nutr. 1995;14:219–28.
69. Cavicchi M, Beau P, Crenn P, Degott C, Messing B. Prevalence of liver disease and contributing factors in patients receiving home parenteral nutrition for permanent intestinal failure. Ann Intern Med. 2000;132(7):525–32.
70. Lowry S, Brennan M. Abnormal liver function during parenteral nutrition: relation to infusion excess. J Surg Res. 1979;26:300.
71. Lindor K, Burnes J. Ursodeoxycholic acid for the treatment of home parenteral nutrition-associated cholestasis. Gastroenterology. 1991;101:250–3.
72. Spagnuolo M, Iorio R, Vegnente A, Guarino A. Ursodeoxycholic acid for treatment of cholestasis in children on long-term total par­enteral nutrition: a pilot study. Gastroenterology. 1996;111:716–9.
73. Buchman A, Moukarzel A, Goodson B, Herzog F, Pollack P, Reyen L, et al. Catheter-related infections associated with home
. Cited 20 Sep 2012. Elsevier Inc.
http://www.ncbi.nlm.nih.gov/
parenteral nutrition and predictive factors for the need for cath­eter removal in their treatment. J Parenter Enteral Nutr. 1994; 18:297–302.
74. Buchman A, Misra S, Moukarzel A, Ament M. Catheter thrombosis and superior/inferior vena cava syndrome are rare complications of long term parenteral nutrition. Clin Nutr. 1994;13(6):356–60.
75. Moukarzel A, Haddad I, Ament M, Buchman A, Reyen L, Maggioni A, et al. 230 patient years of experience with home long-term par­enteral nutrition in childhood: natural history and life of central venous catheters. J Pediatr Surg. 1994;29(10):1323–7.
76. Leiby J, Purcell H, Demaria J, Kraut E, Sagone A, Metz E. Pulmonary embolism as a result of Hickman catheter-related thrombosis. Am J Med. 1989;86:228–31.
77. Gould J, Carloss H, Skinner W. Groshong catheter-associated sub­clavian venous thrombosis. Am J Med. 1993;95:419–23.
78. Buchman A, Sohel M, Brown M, Jenden D, Ahn C, Roch M, et al. Verbal and visual memory improve after choline supplementation in long-term total parenteral nutrition: a pilot study. J Parenter Enteral Nutr. 2001;25:30–5.
79. DiBaise JK, Young RJ, Vanderhoof JA. Intestinal rehabilitation and the short bowel syndrome: part 1. Am J Gastroenterol. 2004; 99(7):1386–95.
80. Drucker D, Erlich P, Asa S, Brubaker P. Induction of intestinal epi­thelial proliferation by glucagon-like peptide 2. Proc Natl Acad Sci U S A. 1996;93(15):7911–26.
81. Joly F, Dray X, Corcos O, Barbot L, Kapel N, Messing B. Tube feeding improves intestinal absorption in short bowel syndrome patients. Gastroenterology. 2009;136(3):824–31. AGA Institute American Gastroenterological Association.
82. Vanderhoof J. Short bowel syndrome. Neonatal Gastroenterol. 1996;23:377–86.
83. McIntyre P, Fitchew M, Lennard-Jones J. Patients with a jejunos­tomy do not need a special diet. Gastroenterology. 1986;91:25–33.
84. Lennard-Jones J. Review article: practical management of the short bowel. Aliment Pharmacol Ther. 1994;8:563–77.
85. Cosnes J, Lamy P, Beaugerie L, Le Quintrec M, Gendre J, Le Quintrec Y. Adaptive hyperphagia in patients with postsurgical mal­absorption. Gastroenterology. 1990;99(6):1814–9.
86. Aly A, Barany F, Kollberg B, Monsen U, Wisen O, Johansson C. Effect of an H2-receptor blocking agent on diarrhoeas after exten­sive small bowel resection in Crohn’s disease. Acta Med Scand. 1980;207:119–22.
87. Jacobsen O, Ladefoged K, Stage J, Jarnum S. Effects of cimetidine on jejunostomy effl uents in patients with severe short-bowel syn­drome. Scand J Gastroenterol. 1986;21(7):824–8.
88. Jeppesen P, Staun M, Tjellesen L, Mortensen P. Effect of intrave­nous ranitidine and omeprazole on intestinal absorption of water, sodium, and macronutrients in patients with intestinal resection. Gut. 1998;43:763–9.
89. Williams N, Evans P, King R. Gastric acid secretion and gastrin production in the short bowel syndrome. Gut. 1985;26(9):914–9.
90. Cooper J, Williams N, King R, Barker M. Effects of a long-acting somatostatin analogue in patients with severe ileostomy diarrhoea. Br J Surg. 1986;73(2):128–31.
91. Kusuhara K, Kusunoki M, Okamoto T, Sakanoue Y, Utsunomiya J. Reduction of the effl uent volume in high-output ileostomy patients by a somatostatin analogue, SMS 201–995. Int J Colorectal Dis. 1992;7(4):202–5.
92. Rodrigues C, Lennard-Jones J, Thompson D, Farthing M. The effects of octreotide, soy polysaccharide, codeine and loperamide on nutrient, fl uid and electrolyte absorption in the short-bowel syn­drome. Aliment Pharmacol Ther. 1989;3(2):159–69.
93. Sukhotnik I, Khateeb K, Krausz MM, Sabo E, Siplovich L, Coran AG, et al. Sandostatin impairs postresection intestinal adaptation in a rat model of short bowel syndrome. Dig Dis Sci. 2002;47(9): 2095–102.