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Short Bowel
Syndrome
Objectives
 At the end of this session every participant should be
able:-
 To explain the about the general concept of Short
bowel syndrome
 To explain the different causes short bowel syndrome
 To explain pathophysiology of short bowel sydrome
 To elaborate different medical and surgical approaches
towards Short bowl syndrome
Introduction
 The small intestine is a tubular structure that extends from
the pylorus to the cecum.
 The estimated length measure about 4 to 6 meters.
 Duodenum length about 20cm and the remaining about 40%
making the jejunum and 60% making up the ileum.
 Small intestine has a well adapted epithelium in which
absorption and secretion occur.
 8 to 9 L of fluid enter the small intestine daily.
 consists of salivary, gastric, biliary, pancreatic, and intestinal
secretions. Of which 80% is absorbed in the small intestine
and 1.5l will be absorbed in the large intestine.
Introduction
 The intestinal function depend on several factors including,
length of the presence of the ileocecal valve, the residual
segment left in case of resection.
 The jejunum is the site of absorption of most macronutrients
and minerals. GI hormones that are critical for gut function,
such as cholecystokinin and secretin, are also produced in
the jejunum.
 The ileum is essential for the absorption of carbohydrates,
proteins, fluids, and electrolytes. Bile acids, vitamin B12, and
the fat-soluble vitamins (A, D, E, K) are primarily absorbed in
the ileum.
What is Short bowel syndrome
 Short bowel syndrome (SBS) is a clinical condition in which
there is inadequate length of functional intestine to sustain
normal enteral nutrition as a result of massive small bowel
resection.
 Short bowel syndrome (SBS) in adults is defined as less than
180 to 200 centimeters of remaining small bowel (normal
length 275 to 850 cm) leading to the need for nutritional and
fluid supplements.
 For paediatrics remaining with less than 25% of the small
intestine.
Short Bowel syndrome
 Short bowel syndrome (SBS) is the main cause of chronic
intestinal failure (IF), defined as ‘the reduction of gut
function below the minimum necessary for the absorption
of macronutrients and/or water and electrolytes, such that
intravenous supplementation is required to maintain health
and/or growth.
Condition which can lead to
SBS
 Massive small bowel resection as in superior mesenteric
artery ischaemia.
 Multiple sequential resections.
 Recurrent Crohn’s disease—common cause.
 necrotising enterocolitis in neonates and children.
 Intestinal atresia.
 Midgut volvulus. X
 Radiation enteritis.
Anatomical subtypes SBS
 End jejunostomy
 Jejunocolic anastomosis
 Jejunal ileal Anasomosis,(the ileocecal valve is
preserved)
Anatomical subtypes of
SBS
Pathophysiology of SBS
The primary pathophysiological mechanism of chronic
intestinal failure secondary to SBS is intestinal malabsorption
due to the loss of intestinal absorptive surface and more
rapid intestinal transit.
 Resection of less than 50% of the small intestine is
generallywell tolerated. However, clinically significant
malabsorption occurs when greater than 50% to 80% of the
small intestine has been resected.
 Among adult patients who lack a functional colon, lifelong
TPN dependence is likely to persist if there is less than 100
cm of residual small intestine.
 Among infants with short bowel syndrome, weaning from
TPN-dependence has been achieved with as little as 10 cm
of residual small intestine.
Pathophysiology of SBS
 Other determinants of the severity of malabsorption
1. include the presence or absence of an intact colon,The colon has
the capacity to absorb large fluid and electrolyte loads and
nutrient assimilation by absorbing short chain fatty acids.
2. intact ileocecal valve by delaying transit of chyme from the small
intestine into the colon, that is thereby prolonging the contact time
between nutrients and thesmall-intestinal absorptive mucosa.
3. Third, healthy, rather than diseased, residual small intestine.
4. Resection of jejunum is better tolerated than resection of ileum,
as the capacity for bile salt and vitamin B 12 absorption is specific
to the ileum.
Physiology and spontaneous
adaptation
 The acute phase (4-6 weeks)
Gastric hypersecretion can result in diarrhea with important fluid and
electrolyte loss. The challenge during this phase is to compensate
dehydration and monitor the micro- and macronutrient deficiencies.
 The adaptation phase(Up to 2 years)
Morphological adaptation (hypertrophy of intestinal crypts), the onset of
compensatory hyperphagia, a change in microbiota composition, and
endocrine hormone production and secretion. All these physiological
adaptations improve the energy, fluid, and electrolyte balances and may allow
reducing or even weaning from PN.
Physiology and spontaneous
adaptation
 stationary phase
takes place after the spontaneous adaptation phase and several long-
term complications can then appear (such as oxalate lithiasis in
patients with colon in continuity) in addition to the risk of malnutrition
and parenteral nutrition complications
Clinical presentations
 The most common signs, symptoms, and findings include
1. malnutrition
2. weight loss
3. diarrhea
4. steatorrhea
5. dehydration
6. vitamin deficiencies
7. electrolyte imbalance
Managements
1. Total parenteral nutrition.
2. Fat and fibre free but protein rich liquid diet with essential fatty acids.
3. Diarrhoea is controlled by loperamide.
4. Oral cholestyramine to bind bile salts is needed in massive resection which
includes ileum.
5. Parenteral vitamin B12 injection regularly.
6. H2 antagonists/PPIs/somatostatin (to reduce secretions from stomach, liver
and pancreas).
7. Octreotide reduces the secretion and reduces GI motility.
8. Fluid and electrolyte management.
9. Control of diarrhoea.
Managements cont
Role of Glucagon-like peptide 1 (GLP-1)
 GLP-1 analogs has been assessed for the treatment of SBS
patients, due to their effect on gastric emptying.
The administration of exendin-4, a GLP-1 receptor agonist, and
liraglutide, a GLP-1 analog , both approved for the treatment of
type 2 diabetes.
 These pilot studies have shown encouraging results, including a
slowing of gastric emptying, a reduction in stoma output, and an
improved absorption.
Managements cont
Role of Glucagon-like peptide 2 (GLP-2)
 GLP-2 is another proglucagon-derived peptide secreted by the L-cells
of the diffuse enteroendocrine system in response to nutrient
ingestion.
 This endogenous hormone increases villus height and crypt depth,
thus enhancing intestinal absorption. It also increases transit time
and mesenteric blood flow and has a beneficial effect on the barrier
function and immune protection.
 Teduglutide is a GLP-2 analog resulting from the substitution of a
single amino acid compared to endogenous GLP2 thus delaying its
degradation.
Surgical management
 restoring the digestive continuity should be considered in all patients with
enterostomy, and performed whenever possible, 3 to 6 months after the last
resection.
 Bianchi Procedure
Bianchi15 originally described an intestinal lengthening procedure in which the
mesenteric vascular bed is separated into two systems.
The dilated small intestine is split into two parallel segments, each with its own
blood supply, and the ends are approximated ,This resulted in a 50% decreased
diameter of the small intestine and increased length by 200%.
Surgical management
 Serial transverse enteroplasty(STEP Preocedure)
In contrast to the Bianchi procedure, dilated small intestine is serially
stapled in a transverse fashion to create a narrower lumen and longer
intestinal length . The STEP procedure improved enteral feeding
tolerance, resulting in significant catch-up growth, and was not
associated with increased mortality.1

Other options
 Small bowel transplantation
 Antiperistaltic colonic interposition into the small bowel
segment
 Mucosal stem cell transplantation using enterocytes
without lymphoid tissue
Late Complications of SBS
 Gallstone formation due to altered bile metabolism.
 Urinary calculi due to increased oxalate level.
 Recurrent bacterial enteritis.
 Fulminant hepatic failure often can occur.
 Osteomalacia, tetany, hypomagnesaemia.
 Bleeding diathesis, peripheral neuropathy
references

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short bowel syndrome.pptx Dr. Tarimo BM UDSM MCHAS 2023

  • 2. Objectives  At the end of this session every participant should be able:-  To explain the about the general concept of Short bowel syndrome  To explain the different causes short bowel syndrome  To explain pathophysiology of short bowel sydrome  To elaborate different medical and surgical approaches towards Short bowl syndrome
  • 3. Introduction  The small intestine is a tubular structure that extends from the pylorus to the cecum.  The estimated length measure about 4 to 6 meters.  Duodenum length about 20cm and the remaining about 40% making the jejunum and 60% making up the ileum.  Small intestine has a well adapted epithelium in which absorption and secretion occur.  8 to 9 L of fluid enter the small intestine daily.  consists of salivary, gastric, biliary, pancreatic, and intestinal secretions. Of which 80% is absorbed in the small intestine and 1.5l will be absorbed in the large intestine.
  • 4. Introduction  The intestinal function depend on several factors including, length of the presence of the ileocecal valve, the residual segment left in case of resection.  The jejunum is the site of absorption of most macronutrients and minerals. GI hormones that are critical for gut function, such as cholecystokinin and secretin, are also produced in the jejunum.  The ileum is essential for the absorption of carbohydrates, proteins, fluids, and electrolytes. Bile acids, vitamin B12, and the fat-soluble vitamins (A, D, E, K) are primarily absorbed in the ileum.
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  • 6. What is Short bowel syndrome  Short bowel syndrome (SBS) is a clinical condition in which there is inadequate length of functional intestine to sustain normal enteral nutrition as a result of massive small bowel resection.  Short bowel syndrome (SBS) in adults is defined as less than 180 to 200 centimeters of remaining small bowel (normal length 275 to 850 cm) leading to the need for nutritional and fluid supplements.  For paediatrics remaining with less than 25% of the small intestine.
  • 7. Short Bowel syndrome  Short bowel syndrome (SBS) is the main cause of chronic intestinal failure (IF), defined as ‘the reduction of gut function below the minimum necessary for the absorption of macronutrients and/or water and electrolytes, such that intravenous supplementation is required to maintain health and/or growth.
  • 8. Condition which can lead to SBS  Massive small bowel resection as in superior mesenteric artery ischaemia.  Multiple sequential resections.  Recurrent Crohn’s disease—common cause.  necrotising enterocolitis in neonates and children.  Intestinal atresia.  Midgut volvulus. X  Radiation enteritis.
  • 9. Anatomical subtypes SBS  End jejunostomy  Jejunocolic anastomosis  Jejunal ileal Anasomosis,(the ileocecal valve is preserved)
  • 11. Pathophysiology of SBS The primary pathophysiological mechanism of chronic intestinal failure secondary to SBS is intestinal malabsorption due to the loss of intestinal absorptive surface and more rapid intestinal transit.  Resection of less than 50% of the small intestine is generallywell tolerated. However, clinically significant malabsorption occurs when greater than 50% to 80% of the small intestine has been resected.  Among adult patients who lack a functional colon, lifelong TPN dependence is likely to persist if there is less than 100 cm of residual small intestine.  Among infants with short bowel syndrome, weaning from TPN-dependence has been achieved with as little as 10 cm of residual small intestine.
  • 12. Pathophysiology of SBS  Other determinants of the severity of malabsorption 1. include the presence or absence of an intact colon,The colon has the capacity to absorb large fluid and electrolyte loads and nutrient assimilation by absorbing short chain fatty acids. 2. intact ileocecal valve by delaying transit of chyme from the small intestine into the colon, that is thereby prolonging the contact time between nutrients and thesmall-intestinal absorptive mucosa. 3. Third, healthy, rather than diseased, residual small intestine. 4. Resection of jejunum is better tolerated than resection of ileum, as the capacity for bile salt and vitamin B 12 absorption is specific to the ileum.
  • 13. Physiology and spontaneous adaptation  The acute phase (4-6 weeks) Gastric hypersecretion can result in diarrhea with important fluid and electrolyte loss. The challenge during this phase is to compensate dehydration and monitor the micro- and macronutrient deficiencies.  The adaptation phase(Up to 2 years) Morphological adaptation (hypertrophy of intestinal crypts), the onset of compensatory hyperphagia, a change in microbiota composition, and endocrine hormone production and secretion. All these physiological adaptations improve the energy, fluid, and electrolyte balances and may allow reducing or even weaning from PN.
  • 14. Physiology and spontaneous adaptation  stationary phase takes place after the spontaneous adaptation phase and several long- term complications can then appear (such as oxalate lithiasis in patients with colon in continuity) in addition to the risk of malnutrition and parenteral nutrition complications
  • 15. Clinical presentations  The most common signs, symptoms, and findings include 1. malnutrition 2. weight loss 3. diarrhea 4. steatorrhea 5. dehydration 6. vitamin deficiencies 7. electrolyte imbalance
  • 16. Managements 1. Total parenteral nutrition. 2. Fat and fibre free but protein rich liquid diet with essential fatty acids. 3. Diarrhoea is controlled by loperamide. 4. Oral cholestyramine to bind bile salts is needed in massive resection which includes ileum. 5. Parenteral vitamin B12 injection regularly. 6. H2 antagonists/PPIs/somatostatin (to reduce secretions from stomach, liver and pancreas). 7. Octreotide reduces the secretion and reduces GI motility. 8. Fluid and electrolyte management. 9. Control of diarrhoea.
  • 17. Managements cont Role of Glucagon-like peptide 1 (GLP-1)  GLP-1 analogs has been assessed for the treatment of SBS patients, due to their effect on gastric emptying. The administration of exendin-4, a GLP-1 receptor agonist, and liraglutide, a GLP-1 analog , both approved for the treatment of type 2 diabetes.  These pilot studies have shown encouraging results, including a slowing of gastric emptying, a reduction in stoma output, and an improved absorption.
  • 18. Managements cont Role of Glucagon-like peptide 2 (GLP-2)  GLP-2 is another proglucagon-derived peptide secreted by the L-cells of the diffuse enteroendocrine system in response to nutrient ingestion.  This endogenous hormone increases villus height and crypt depth, thus enhancing intestinal absorption. It also increases transit time and mesenteric blood flow and has a beneficial effect on the barrier function and immune protection.  Teduglutide is a GLP-2 analog resulting from the substitution of a single amino acid compared to endogenous GLP2 thus delaying its degradation.
  • 19. Surgical management  restoring the digestive continuity should be considered in all patients with enterostomy, and performed whenever possible, 3 to 6 months after the last resection.  Bianchi Procedure Bianchi15 originally described an intestinal lengthening procedure in which the mesenteric vascular bed is separated into two systems. The dilated small intestine is split into two parallel segments, each with its own blood supply, and the ends are approximated ,This resulted in a 50% decreased diameter of the small intestine and increased length by 200%.
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  • 21. Surgical management  Serial transverse enteroplasty(STEP Preocedure) In contrast to the Bianchi procedure, dilated small intestine is serially stapled in a transverse fashion to create a narrower lumen and longer intestinal length . The STEP procedure improved enteral feeding tolerance, resulting in significant catch-up growth, and was not associated with increased mortality.1
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  • 23. Other options  Small bowel transplantation  Antiperistaltic colonic interposition into the small bowel segment  Mucosal stem cell transplantation using enterocytes without lymphoid tissue
  • 24. Late Complications of SBS  Gallstone formation due to altered bile metabolism.  Urinary calculi due to increased oxalate level.  Recurrent bacterial enteritis.  Fulminant hepatic failure often can occur.  Osteomalacia, tetany, hypomagnesaemia.  Bleeding diathesis, peripheral neuropathy