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`a v a i l a b l e a t w w w . s c i e n c e d i r e c t . c o m
`
`The Surgeon, Journal of the Royal Colleges
`of Surgeons of Edinburgh and Ireland
`
`w w w . t h e s u r g e o n . n e t
`
`Short bowel syndrome
`
`Claire L. Donohoe, John V. Reynolds*
`
`Department of Surgery, Trinity Centre for Health Sciences, Trinity College Dublin, St James’ Hospital, Dublin 8, Ireland
`
`a r t i c l e i n f o
`
`a b s t r a c t
`
`Article history:
`Received 17 February 2010
`Accepted 13 June 2010
`
`Keywords:
`Short bowel syndrome
`Intestinal adaptation
`Intestinal failure
`Intestinal transplant
`Parenteral nutrition
`Intestinal lengthening
`
`is a state of malabsorption following intestinal
`The short bowel syndrome (SBS)
`resection where there is less than 200 cm of intestinal length. The management of short
`bowel syndrome can be challenging and is best managed by a specialised multidisci-
`plinary team. A good understanding of the pathophysiological consequences of resec-
`tion of different portions of the small intestine is necessary to anticipate and prevent,
`where possible, consequences of SBS. Nutrient absorption and fluid and electrolyte
`management in the initial stages are critical to stabilisation of the patient and to
`facilitate the process of adaptation. Pharmacological adjuncts to promote adaptation are
`in the early stages of development. Primary restoration of bowel continuity, if possible,
`is the principle mode of surgical treatment. Surgical procedures to increase the surface
`area of the small intestine or improve its function may be of benefit in experienced
`hands, particularly in the paediatric population. Intestinal transplant is indicated at
`present for patients who have failed to tolerate long-term parenteral nutrition but
`with increasing experience, there may be a potentially expanded role for its use in the
`future.
`ª 2010 Royal College of Surgeons of Edinburgh (Scottish charity number SC005317) and
`Royal College of Surgeons in Ireland. Published by Elsevier Ltd. All rights reserved.
`
`Introduction
`
`The short bowel syndrome is a malabsorptive state usually
`following massive resection of the small intestine.1 It gener-
`ally occurs when there is less than 200 cm of bowel in situ.2
`Intestinal failure may be defined as a condition where faecal
`energy loss occurs and the patient is unable to increase oral
`intake or absorptive capacity sufficiently to maintain their
`nutritional status by the enteral route alone. These patients
`may become dependent on parenteral nutrition support to
`maintain their energy balance. Malabsorption of macronutri-
`ents and micronutrients may predominate as a clinical
`manifestation, whereas other patients may struggle to main-
`tain fluid and electrolytes homeostasis.
`
`Newer definitions of the syndrome have been proposed
`in order to better define and diagnose patients according to their
`likely requirement for surgical intervention and to evaluate new
`therapies.1 These definitions are included in Table 1.
`
`Epidemiology
`
`the syndrome is
`The exact population prevalence of
`unknown. However, this may be estimated from numbers of
`patients on home total parenteral nutritioneof whom
`approximately one quarter to one-third have short bowel
`syndrome. Thus the estimated population prevalence is
`approximately 1 per million.3 SBS is more likely to occur in
`
`* Corresponding author. Tel.: þ353 872271250.
`E-mail address: reynoljv@tcd.ie (J.V. Reynolds).
`1479-666X/$ e see front matter ª 2010 Royal College of Surgeons of Edinburgh (Scottish charity number SC005317) and Royal College of
`Surgeons in Ireland. Published by Elsevier Ltd. All rights reserved.
`doi:10.1016/j.surge.2010.06.004
`
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`271
`
`Table 1 e Proposed consensus definitions of Short bowel
`syndrome and intestinal failure.1
`
`Short bowel syndrome-intestinal failure results from surgical
`resection, congenital defect or disease-associated loss of
`absorption and is characterised by the inability to maintain
`protein-energy, fluid, electrolyte or micronutrient balances
`when on a conventionally accepted, normal diet.
`Intestinal failure results from obstruction, dysmotility, surgical
`resection, congenital defect, or disease-associated loss of
`absorption and is characterised by the inability to maintain
`protein-energy, fluid, electrolyte or micronutrient balance.
`
`women (2:1), most likely due to the shorter length of the small
`intestine in women.4
`Short bowel syndrome (SBS) results from resection of
`unviable intestine secondary to vascular
`insufficiency,
`Crohn’s disease, malignancy or radiation in adults.3 In the
`paediatric population congenital intestinal anomalies such as
`gastroschisis or atresia, or necrotising enterocolitis lead to
`insufficient intestinal length to maintain nutrition.5
`
`Colon in continuity
`
`The concept of colon in continuity is important to under-
`standing the adaptation process which occurs in short bowel
`syndrome. The colon becomes an important digestive organ
`after loss of a critical mass of small bowel. It can help
`compensate for the lack of small bowel by reabsorbing water,
`electrolytes and short-chain fatty acids. By hormonal mech-
`anisms, it can slow intestinal transit and stimulate intestinal
`adaptation. Up to 65% of carbohydrate intake may be lost in
`the faeces if not degraded by colonic bacteria.6 The flora of the
`colon ferment malabsorbed carbohydrates to short-chain
`fatty acids, which when absorbed, can provide up to 500 kcal/
`day.7 Medium chain fatty acids are water soluble and thus can
`be absorbed in the colon and these may be used as dietary
`supplements in cases of long-chain fatty acid malabsorption,
`which is not usually the case in SBS as these patients have
`intact pancreatic function. Accordingly, patients who have
`a jejunostomy and therefore, no colon in continuity, do not
`have the ability to reabsorb large amounts of gastrointestinal
`secretions. If they lose a critical mass of jejunum (with
`<100 cm remaining) they may have a net secretory response
`to food.
`
`Pathophysiology
`
`Loss of the ileocaecal valve
`
`Consequences of the SBS arise from an inability to absorb
`adequate macro- and/or micronutrients. There may be an
`inability to maintain nutritional intake and this may include
`vitamin and mineral deficiencies or could result in fluid and
`electrolyte imbalances. Additionally, loss of gastrointestinal
`hormonal production may alter bowel motility, transit and
`gastroduodenal emptying. The degree of functional impair-
`ment is dependent on a number of factors: length of intestine,
`segments of intact bowel, the absorptive quality of the
`remnant bowel, and inter-individual variability in efficiency of
`absorptive capacity and adaptation. Patients at greatest risk
`for developing malabsorption are summarised in Table 2.
`
`Normal intestinal physiology
`
`The normal small bowel length is estimated to be approxi-
`mately 600 cm. Macronutrients such as carbohydrate,
`nitrogen and fat are predominantly absorbed within the first
`100e150 cm of jejunum. The gastrointestinal tract processes
`8e9 L of fluid per day. The majority of water ingested is
`reabsorbed and over 80% of this absorption occurs in the small
`bowel with only 100e200 ml of fluid egested in faecal
`material daily.
`
`Table 2 e Patients at highest risk of developing short
`bowel syndrome.28
`Anastomosis
`
`PLUS length of residual
`small intestine
`
`Duodenostomy or jejunoileal
`Jejunocolic or ileocolic
`End jejunostomy
`
`<35 cm
`<60 cm
`<115 cm
`
`If the ileocaecal valve is resected, small bowel bacteria may
`overgrow due to small intestine dilation and slower motility.8
`Bacterial overgrowth has several negative consequences
`including competition for nutrients, inflammation, gastroin-
`testinal bleeding, bacterial translocation and endotoxaemia,
`liver injury and D-lactic acidosis.9
`
`Jejeunal resection
`
`Most of the food absorbed daily is absorbed by the long villi of
`the jejunum, where most of the digestive enzymes are
`concentrated.10 Following resection there is an initial and
`temporary reduction in nutrient absorption, until
`the
`remaining small intestine can adapt. In addition, hypertonic
`solutions, such as that provided by naso-enteral feeding, can
`exacerbate fluid losses by stimulating fluid secretion by the
`jejunum.11 Loss of jejunum also means loss of gastrointestinal
`feedback hormones, which can lead to rapid gastric emptying
`of liquids, which may then overwhelm the absorptive capacity
`of the remaining small bowel.
`
`Ileal resection
`
`Under normal physiological conditions most of the 8e9 L of
`secretions which are secreted by the small intestine are
`reabsorbed by the ileum. Absorption of vitamin B12 and bile
`salts occur at the ileum. Bile acids and fats are absorbed and
`pass directly to the liver via the enterohepatic circulation. If
`there is less than 100 cm of ileum left in situ the ability to
`reabsorb secretions is exceeded and there is a net secretory
`response to food. The loss of enterohepatic circulation will
`lead to bile salt deficiency and fat malabsorption.12 Feedback
`mechanisms usually detect malabsorption, termed the ileal-
`colonic brake. For example, malabsorbed fat reaching the
`
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`ileum usually causes a delay in gastric emptying and intes-
`tinal
`transit
`times in order to increase gut absorptive
`capacity.13 However, ileal resection may lead to loss of these
`hormonal feedback checks including peptide YY, glucagon-
`like peptide-I and neurotensin.14
`
`Consequences
`
`Increased secretions, reduced absorption of nutrients and
`fluid and loss of hormonal feedback mechanisms all combine
`to create diarrhoea with a high osmotic load.15 Simple
`carbohydrates which are digested to sugars contribute to the
`osmotic load and favour small bacterial overgrowth. Products
`of this overgrowth again contribute to osmotic diarrhoea.
`Therefore, these patients should have higher protein and fat
`content in their diet instead of simple carbohydrates.
`
`Adaptation
`
`Following resection of large amounts of small intestine, the
`gastrointestinal
`tract undergoes a process of adaption
`whereby the ileum can increase slightly in length and diam-
`eter and adapts functionally to absorb macronutrients. This
`evolves over a one to two year period. Experimental models
`show epithelial hyperplasia 24e48 h after resection.16e18 The
`length of villi and thus the absorptive area increases. Animal
`models show that this process is stimulated by enteral
`nutrition by providing energy for enterocyte reproduction and
`stimulate the release of trophic factors.19 Fat-stimulated
`glucagon-like peptide-II can lead to hyperplasia.20,21 A number
`of other growth and trophic factors have been implicated in
`the process in animal models including enteroglucagon,
`epidermal growth factor, glutamine, growth hormone, chole-
`cystokinin, gastrin, neurotensin,
`leptin and insulin-like
`growth factor.14,22,23 Few studies have been carried out in
`humans. Trophic hormone release is stimulated more effec-
`tively by fat than either protein or carbohydrate in animal
`models.24 In patients with a jejunostomy, limited adaptation
`occurs and they are less likely to require less nutritional
`support with time.25
`The process of adaptation is gradual and can take place
`over up to two years.26 Thus those who require parenteral
`nutrition support may achieve independence as the adapta-
`tion process compensates. However, studies have shown that
`of those who require this support in the home setting only 20%
`become parenteral nutrition independent in the long-term.27
`
`Prognosis
`
`The likelihood of being able to resume a normal oral diet after
`resection of large amounts of the small bowel can be predicted
`by certain parameters. Factors favouring the ability to resume
`oral nutrition include adequate length of the remaining bowel;
`the presence of colon and intact ileocaecal valve, and co-
`morbidities. The prognosis may be good where there is an
`intact duodenum, a jejunal length of greater than 200 cm, and
`an intact colon. The likelihood of requiring long-term paren-
`is high if there is less than 50e60 cm
`teral nutritional
`
`remaining jejunum even if there is colon in continuity.28 If the
`colon is not present, the bowel can only adapt if there is at
`least 100 cm of small intestine remaining. The adaptation
`process means that up to 70% of those with SBS initially
`requiring total parenteral nutrition can be successfully
`weaned off and converted to complete enteral nutrition.
`However, after two years of parenteral nutrition the proba-
`bility of intestinal failure is 94%.28 Intestinal conditions that
`run counter to successful adaptation include Crohn’s disease,
`radiation enteritis, carcinoma or pseudo-obstruction. These
`patients do not seem to mount an adequate adaptation
`response to loss of intestinal function.
`Citrulline is a non-protein amino acid produced by intes-
`tinal mucosa. Thus plasma levels indicate whether there is
`functioning mucosa present. Crenn et al. used plasma citrul-
`line levels to predict whether patients with short bowel
`syndrome after two years would go on to develop permanent
`intestinal failure. In a study of 57 patients, a plasma citrulline
`level of <20 mmol/L had a positive predictive of 95% and a level
`greater than this, an 86% negative predictive value for
`permanent intestinal failure.29 These results were recently
`replicated in over 500 patients with intestinal
`failure
`conditions.30
`The reason it is critical to try to wean patients back onto
`enteral nutrition is due to the high complication rate associ-
`ated with long-term parenteral nutrition use. In a series of 68
`patients with intestinal insufficiency 32.4% died e half due to
`the consequences of intestinal failure or home parenteral
`nutrition. Those with lower survival tended to be those on
`total parenteral nutrition, those with less than 50 cm of intact
`bowel, those with an end enterostomy or those in whom the
`aetiology of short bowel syndrome was radiation enteritis or
`ischaemia. In this series of patients the survival rate was 88%
`at 3 years and 78% at five years.27 However, it must be noted
`that the majority of these patients died from their underlying
`condition rather than to directly due to complications of
`parenteral nutrition.
`
`Complications of short bowel syndrome
`
`A: Early
`
`Early complications include dehydration and electrolyte
`derangements. Intra-venous fluid supplementation (to either
`enteral or parenteral nutrition) may be required to maintain
`the patient’s hydration status. In particular, magnesium,
`calcium and potassium may be difficult to control in patients
`with SBS.
`Electrolytes are secreted in high concentrations by the
`jejunum and ileum and if there is inadequate intestinal
`length, there may be net electrolyte losses. Knowledge of
`electrolyte physiology is important to effectively supplement
`electrolytes. Total body electrolyte levels of magnesium and
`potassium may be reduced even if serum levels are main-
`tained. Thus, excess electrolyte losses may be diagnosed by
`reduced urinary electrolyte levels. Oral electrolyte replace-
`ment can be problematic as it can cause osmotic diarrhoea
`necessitating intra-venous supplementation. Replacement
`should be done slowly as an abrupt increase in plasma levels
`
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`273
`
`removes the stimulus for active electrolyte uptake in the loop
`of Henle thus increasing urinary excretion and further
`depleting body stores. Cellular uptake is slow and therefore
`repletion requires sustained correction. Electrolyte correction
`is of particular importance to prevent potentially life-threat-
`ening arrhythmias developing.
`Hypomagnesaemia is a particular problem with jejunos-
`tomies. It is compounded by the hyperaldosteronism which
`occurs secondary to dehydration. Magnesium salts may
`worsen diarrhoea and thus parenteral supplementation may
`be required. Vitamin D supplementation may increase intes-
`tinal absorption of magnesium. Hypercalcaemia secondary to
`hyperparathyroidism in response to low serum magnesium
`levels should be anticipated and corrected.
`Loss of negative feedback to gastric secretions in SBS leads
`to transient hypergastrinaemia and thus gastric hypersecre-
`tion for up to 6 months following resection.31 The consequence
`of this may be peptic ulceration and oesophagitis and therefore
`prophylactic gastric protection is important. Proton pump
`inhibitors have been shown to improve water absorption.32
`
`B: Late
`
`related
`Chronic complications from SBS include TPN-
`complications, bacterial overgrowth, micronutrient deficiency
`and metabolic complications. Parenteral nutrition bypasses
`first pass liver metabolism and longterm TPN can lead to
`steatosis, cholestasis and cirrhosis. Recurrent episodes of
`sepsis from line infections, bacterial overgrowth and biliary
`stasis all contribute to the development of liver disease.33
`Fifteen percent of patients on TPN for greater than one year
`develop end-stage cirrhosis which carries with it a 100% two-
`year mortality rate.34 More than 50% of those on TPN for more
`than 5 years develop complicating liver disease. This may be
`minimised but not eradicated by reducing excess dextrose and
`lipid feeding. Moreover patients with SBS seem to develop
`cholestatic liver disease at a greater rate versus other long-
`term TPN patients. This is postulated to be due to recurrent
`sepsis from bacterial overgrowth or lack of supplementary
`enteral nutrition in SBS patients. In one study, liver biopsies
`demonstrated chronic cholestasis in 65% after 6 months of
`TPN in patients with a bowel remnant of less than 50 cm.35
`Gallstones and related problems are also more common due
`to the interrupted enterohepatic circulation, which alters bile
`composition.12
`The other major complication of parenteral nutrition is
`catheter related. Sepsis accounted for one-third of the deaths
`in a series of SBS patients with a 50% 5-year mortality rate.28 On
`average SBS patients on TPN had one hospitalisation per year
`for infection. Occlusion of the delivery catheter by thrombosis
`is not an uncommon problem with an incidence of 0.2 episodes
`per 1000 catheter days. If catheter thrombosis is not due to
`malpositioning then it is a risk factor for developing superior
`vena cava thrombosis and mandates warfarin prophylaxis.
`Bacterial overgrowth can lead to carbohydrate malab-
`sorption and episodes of sepsis from bacterial translocation. It
`should be suspected in SBS patients with blind loops or no
`ileocaecal valve and pyrexia of unknown origin or refractory
`diarrhoea or weight loss.36 Bacteria can interfere with chylo-
`micron formation and thus decrease absorption of fatty acids.
`
`An inflammatory response may lead to loss of intestinal
`architecture and further loss of absorptive capacity or may
`even present as a colitis or ileitis.37 Prevention is by regular
`bowel washout using a gastrotomy tube or treatment with
`short courses of broad spectrum antibiotics. Some patients
`will require courses of antibiotic every month. The role of
`probiotics in this setting is unproven. A low carbohydrate diet
`decreases the nutrient source for intestinal flora.
`The greatest risk of developing a micronutrient deficiency
`is after
`the transition to enteral
`feeding. The degree
`of malabsorption is not easily predictable. In patients with a
`short length of small intestine serum levels of magnesium,
`calcium, zinc, selenium and fat soluble vitamins should be
`measured every 3 months.38 If there are any concerns about
`large amounts of enteral losses, urinary excretion of the water
`soluble electrolytes may give a better indication of total body
`stores. Since water soluble vitamins are absorbed in the
`proximal jejunum they are rarely deficient. If there is greater
`than 60 cm of terminal ileum resected it must be anticipated
`that B12 supplementation will be required.39 Resection of the
`proximal jejunum may lead to folate deficiency. Patients
`should undergo yearly bone density monitoring.
`Lactobacillus, Clostridium perfringens, Streptococcus
`bovis and other gram positive colonic bacteria ferment non-
`absorbed carbohydrate to D-lactic acid.40 This creates an acidic
`environment, rich in short-chain fatty acids, which supports
`the proliferation of the intestinal flora. If significant amounts
`of lactic acid are absorbed, a metabolic acidosis may develop
`which presents with encephalopathy, headache, ataxia and
`dysarthria.41 Broad-spectrum antibiotics against intestinal
`flora treat the bacterial overgrowth.40
`Oxalates normally bind to calcium. If fat is malabsorbed,
`calcium binds to free fatty acids, thus oxalate passes into the
`colon and is absorbed. This colonic absorption is enhanced by
`bile acid malabsorption. Higher serum levels and thus
`increased renal excretion increases the risk of developing
`nephrolithiasis. Other consequences of the SBS such as
`metabolic acidosis and a low urinary pH conditions favour
`nephrolithiasis.42
`Loss of a large amount of intestine may reduce serum
`citrulline concentrations to the extent that ammonia cannot
`be detoxified adequately via the urea cycle. If this is accom-
`panied by renal impairment, the excess ammonia may not be
`excreted. Arginine administration corrects ammonia levels.43
`
`Management strategy
`
`The goal of management of patients with short bowel
`syndrome is to allow them resume a normal lifestyle. To that
`end the provision of adequate macro- and micronutrients and
`sufficient fluid to prevent dehydration are basic pre-requi-
`sites. It is important to correct and prevent acid-base distur-
`bances. Steps in the management of SBS are summarised in
`Fig. 1.
`
`Early goals
`
`Where it is anticipated that a patients is susceptible to short
`bowel resection following massive bowel resection it is
`
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`
`Fig. 1 e Early management of short bowel syndrome.
`
`recommended to begin total parenteral nutrition within the
`first 24 h (Fig. 2). TPN will usually be required for the first 7e10
`days.44 A plan to measure and replace fluid losses and elec-
`trolytes every 2 h should be instituted, thus almost mandating
`high-dependency level care. Blood glucose levels should be
`monitored every 4 h and an insulin-sliding scale should
`be commenced if glucose levels are persistently elevated. Initial
`TPN requirements should be 25e35 kcal/kg/day, of which 1e1/
`5 g/kg/day should be provided as protein. Protein absorption is
`the nutrient which is least affected by reduction in gastroin-
`testinal function, thus there is no requirement for peptide
`based regimes. If less than 75 cm of jejunum remains the
`patient is likely to require longterm parenteral nutrition and
`saline supports. Supplemental fluid will be required parenter-
`ally if less than 100 cm of jejunum remains and oral rehydration
`solution will be necessary if less than 200 cm remains.25
`
`Once the patient is stable, enteral nutrition should be
`slowly introduced e initially at a low rate continuously. The
`initial rate should be 5% of the patient’s daily caloric intake.
`Enteral feeding rates can then be incrementally advanced
`every 3e7 days. The diet should be of high protein and fat
`content (providing 40% of daily caloric intake) to try to mini-
`mise osmotic diarrhoeal complications.45 If the underlying
`disease process involves inflammation of the intestine leading
`to reduced enzymmatic secretions, an elemental diet may be
`considered. If the colon is intact, fibre supplementation can be
`considered to slow intestinal transit. Parenteral nutrition
`should be concomitantly weaned as enteral nutrition is
`advanced. Continuous enteral nutrition via tube stimulates
`the adaptation process more than isocaloric amounts of
`nutrition delivered orally.46 Successfully weaning is indicated
`by the amount of enteral fluid loss. Enteral fluid loss reflects
`
`Fig. 2 e Non-transplant surgical treatment options.
`
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`275
`
`the degree of carbohydrate malabsorption. If there is a suspi-
`cion of excess fluid secretion as opposed to carbohydrate
`malabsorption being the cause of enteral
`losses, faecal
`content may be tested for glucose.
`Attempts to prevent liver disease arising as a complication
`of parenteral nutrition were formalised in one centre as an
`intestinal rehabilitation programme which involved aggres-
`sive use of enteral nutrition, control of bacterial overgrowth
`and prevention of catheter sepsis.47 It remains to be seen
`whether these results are generalisable in a non-specialist
`centre. Ursodeoxycholic acid has been used to treat chole-
`static liver disease and results in a series of children showed
`some improvement in liver disease.48 Results in adults show
`some benefits.49
`
`motility. These opiate-based medications can be addictive and
`thus should be weaned as soon as possible.
`Octreotide inhibits pancreatic secretions but also increases
`small bowel transit time. It should only be considered if more
`than 3 L of supplementary intra-venous fluid intake is
`required to maintain hydration. Octreotide decreases protein
`synthesis in the intestine and may potentially inhibit the
`adaptation process.59 Studies have shown that is does not
`decrease TPN requirements and therefore has no role to play
`in increasing nutrient absorption.
`Patients with steatorrhoea secondary to bile acid malab-
`sorption following ileal resection should have cholestyr-
`amine. This will bind bile salts and increase their
`enterohepatic circulation.
`
`Methods to promote adaptation
`
`the input of gastrointestinal
`Greater understanding of
`hormones in the process of adaptation has lead to attempts to
`promote adaptation. Glutamine and glucose are fuel sources
`for small intestinal enterocytes. Combinations of glutamine,
`growth hormones and diets high in carbohydrates have been
`used to aim to stimulate the adaptation process after uncon-
`trolled series reported some beneficial effects.50e52 However
`the benefits have not been replicated in controlled trials in
`humans.53e55
`Animal studies have suggested a role for the enter-
`oendocrine peptide, glucagon-like petide-2 in the bowel
`adaption response. A long-acting analogue of GLP-2, tedu-
`gluide is also available. A small (n ¼ 8) double blind RCT
`showed a modest improvement in intestinal absorption and
`nitrogen balance.21 GLP-2 treatment reduced faecal weight by
`approximately 1 kg/day, thus helping eleven parenteral
`nutrition-dependent SBS patients maintain their fluid and
`electrolyte balances with lower oral intake in a recent study.56
`There were no changes in intestinal morphology or body
`composition. A potential confounding factor for uncontrolled
`trials is that the amount of improvement due to adaptation
`without the GLP-2 stimulus is not known. A multi-centre
`placebo controlled randomised controlled trial using tedu-
`glutide is underway at present.57
`
`Oral rehydration solution
`
`Oral rehydration solution (ORS)may be required if there is less
`than 100 cm of residual jejunum in situ as net secretion will be
`greater than intake. The jejunum is permeable to salt, which is
`freely passively absorbed. The addition of glucose to a salt
`solution promoted further active salt absorption by solvent
`drag. The optimal NaCl concentration is that equal to small
`intestinal secretions (90 mmol.l).58 Patients should not drink
`plain water and should have ORS whenever thirsty.2 Studies in
`normal volunteers have shown that ORS can decrease intra-
`luminal duodenojejunal fluid flow rate.
`
`Pharmacological adjuncts
`
`Fluid management may be aided by introducing anti-motility
`agents to slow intestinal transit. Loperamide, diphenoxylate
`or codeine can successfully be combined to reduce intestinal
`
`Surgical treatment options
`
`Broadly speaking there are two categories of surgical
`management in short bowel syndrome: transplant and non-
`transplant. Non-transplant options aim to increase nutrient
`and fluid absorption by wither restoring intestinal continuity
`or by slowing intestinal transit or increasing intestinal surface
`area.60 In a series of 160 patients with SBS from one centre,
`28% underwent surgical treatment.60 Patients selected are
`usually those dependent on parenteral nutrition.61 In general
`terms the patient should be stable and their nutritional status
`should be optimised pre-operatively.61 These surgeries are
`often technically challenging due to the nature of the insult
`which led to the original intestinal resection. Restoration of
`intestinal continuity is a logical initial approach to minimising
`the effect of short bowel syndrome and has a relatively low
`morbidity and mortality. Bianchi et al. have described the
`technique of controllable expansion-recycle which they
`suggest should be used to promote adaptation prior to
`carrying out techniques using autologous intestinal tech-
`niques.62 A large bore tube is passed into the obstructed end of
`the distal jejunum and opened onto the abdominal wall as an
`end jejunostomy. A smaller tube is place into the colon and
`opened as an end colostomy onto the abdominal wall. Intes-
`tinal content is recycled via the two tubes at a slow rate. The
`jejunostomy tube can be occluded for periods to induce
`controlled bowel expansion. The system can be maintained
`for a number of months prior to definitive autologous intes-
`tinal reconstruction. There have been no studies published to
`support its efficacy.
`
`Methods to slow intestinal transit
`
`Segmental reversal of small bowel is one strategy to slow
`intestinal transit. There is not a great deal of evidence to
`support its use with only approximately 40 case reports
`reporting only short term follow-up results. If attempted it
`should be done after full adaptation has occurred. Approxi-
`mately 10 cm of intestine can be reversed as longer segments
`tend to obstruct. The reversed segment should be placed as far
`distally as possible to decrease the symptoms of obstruction.
`In one series of eight patients four weaned from total paren-
`teral nutrition at a median of 8 months of follow-up. Three
`patients had transient intestinal obstruction.63
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`t h e s u r g e o n 8 ( 2 0 1 0 ) 2 7 0 e2 7 9
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`A segment of colon interposed in either an isoperistaltic or
`antiperistaltic direction can be used to slow intestinal transit.
`Reports exist for just 12 patients, which included eleven infants
`under one year old, and reported no mortality or morbidity and
`good results in 4 of the children and in the one adult who
`underwent surgery.64e68 Between 8 and 24 cm of colon was
`used and the isoperistaltic segment had better outcomes.
`Intestinal valves act as a partial mechanical obstruction to
`disrupt the normal motility of the small intestine and prevent
`retrograde reflux of intestinal content. In those cases reported
`nipple valves or intussuscepted valves were used and most
`patients required surgery to remove the valve due to
`obstructive symptoms.60,69,70
`
`Methods to increase intestinal area
`
`The Longtitudinal Intestinal Lengthening and Tailoring (LILT)
`procedure has been used mainly in children to increase
`intestinal
`length, particularly where significantly dilated
`residual intestine with dysmotility and bacterial overgrowth is
`present.71 The intestine and its mesenteric arterial blood
`supply is divided longitudinally along its mesenteric border.
`This creates a double lumen which is reanastomosed, which
`increases the function but not the surface area of the
`remnant.72 Experience of this procedure has been recorded in
`over 100 cases, however, but experience in adult populations
`is limited. Patients not suitable are those with intestinal
`diameter <3 cm, with length of residual intestine <40 cm,
`length of dilated bowel <20 cm, those with hepatic failure.
`Devine et al. reported a series of 16 children with good
`outcomes reported e 14 were successfully weaned off paren-
`teral nutrition. There was improved stool volume and intes-
`tinal transit. There was a 10% rate of anastomotic stenosis.73 A
`further series of 53 paediatric patients showed that at long-
`term follow-up 79% remained parenteral nutrition free, with
`a high quality of life.74 In this same group of patients, the LILT
`procedure succeeded in restoring liver function parameters in
`those with liver fibrosis pre-operatively.75
`The Serial Transverse Enteroplasty (STEP) procedure
`utilises a series of transverse enterotomies with primary
`longtitudinal anastomosis to increase the intestinal area.76 A
`multi-institutional registry of STEP procedures reported 38
`cases, of whom 29 had short bowel syndrome.77 There was an
`increase in the percentage of calories taken enterally from
`31e67%. A single institution reported their experience of LILT
`(or the Bianchi) and STEP procedures in 64 patients of whom
`14 were adults.78 Both procedures were deemed successful in
`improving the ability to use enteral nutrition and treat
`complications of parenteral nutrition. There was a surgical
`c