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Short Bowel Syndrome
Dr.Neelam Ahirwar
Objectives
 Definition
 Etiology
 Clinical manifestation
 Management
 prognosis
 Complication
Definition
 It is a malabsorpative state that may
follow massive resection of small intestine.
 There is no specific intestinal length at
which SBS well clinically present.
 The small intestine of the neonate is about
250 cm in length, 750 cm in adult.
 Infants have more favorable long term
prognosis.
 Factors that influence the length of time
until child independent of TPN
 Extent/ location of resection.
 Presence or absence of colon
 Presence /Absence of ICV.
 Degree of adaptation in remaining bowel.
 Extent of residual bowel disease or
complications e.g. adhesions, strictures
Etiology
 Congenital anomalies :
 Intestinal Atresia .
 Gastroschisis
 omphalocele
 Hirschsprung’s disease,
 Acquired :
Resection of bowel:
 NEC ,
 Crohn’s disease
 volulus,
 tumor ,
 radiation enteritis,
 ischemic injury
Manifestation
 Fluid & electlytes
imbalance.
 Steatorrhea
 Wt loss and malnutrition.
 Minerals def: Ca, Mg, Iron,
zinc, B12, fat soluble vit.
 Malabsorption of CHO and
protein.
 Metabolic acidosis.
 Gastric acid hypersecretion.
 Cholelithiasis.
 Liver disease, cholestasis.
 Bone disease.
 Complications related to
TPN.
Reduction of functioning bowel mass to below min
necessary to balance supply & demand of essential
body needs leading to intestinal failure manifested
as:
Manifestation related to site of
resection
 Duodenal resection
 Jejunal resection
 Ileal resection
 Loss of the ileocecal valve
 Colon
Duodenal resection
 Protein , CHO, fat maldigestion
 Ca, mg, iron, folate malabsorption
 Fat soluble vit deficiency
Jejunal resection
 CHO Malabsorption.
 Water soluble vit defiency .
 Malabsorption is transient (ileal
adaptation).
Ileal resection
 Steatorrhea as bile salts not absorbed.
 Cholesterol stones secondary to loss of bile
acids.
 Fat soluble vit def.
 B12 def
 Loss of ileal brake, decrease transit time
causing diarrhea.
Loss of the ileocecal valve
 Bacterial overgrowth: allows bacteria to
flux into ilium
 Rapid transit time that exacerbate
malabsorption.
Colon
 Role of The Colon:
 water absorption.
 It gives additional length, it slows transit time
and slows gasteric empting,
 But
 Deconjugation of bile acids by colonic bacteria &
secondary secretory diarrhea.
 lactic acidosis: conversion of CHO by
lactobacillus to D-lactic acid lead to high AG
metabolic acidosis,
Intestinal adaptation
 Starts 24-48 hrs post-op, (enteral feeds
as early as possible).
 Lasts up to 11-12 years .
 Change in morphorogy and functional
capacity.
Change in morphorogy
 Macroscopic
 Increase in length
 Microscopic
 Villus: increase height and diameter
 Crypt: elongation
 Epithelial cell life cycle: increase proliferation
 decrease apoptosis.
Change in functional capacity
 Increase absorption per unit length
 Upregulation of sodium glucose
transporter.
Lab investigation
 Blood
 U&E, bone profile, & mg, PRN then biweekly
 CBC, triglycerides, cholesterol Weekly
 Folate, vit B12, copper, zinc, Monthly
 Blood gas and AG for suspected lactic
acidosis.
Microbiology
 If sepsis suspected; blood & urine c/s
 Cultures from both the central and
peripheral sites.
 Consider opportunistic infections, so search
for fungal infection.
Imaging Studies
To assess for potential complications,
 Infection
 Abdominal ultrasonography to look for fungal balls in
the kidney
 Bowel obstruction
 Plain radiography.
 Barium imaging of the bowel
 Liver disease
 Abdominal US to study the liver, biliary tract, &
presence of ascites.
Management
 During early period after intestinal
resection, TPN to prevent fluid and
electrolytes imblance.
 Stomal & fecal losses replaced q 2 hrs with
solution separate from TPN.
 May develop gastric hypersecretion so give
H2 blocker
Management
 The goals of nutritional therapy
 1.Maintain adequate nutrition
 2.Promote intestinal adaptation
 3.Avoid complications
 TPN for the first 7-10 days
 TPN :30 kcal/kg/day
 Enteral feeding when hemodynamic
stable and fluid management stable.
 Continuous enteral feeds: to prevent
osmotic diarrhea.
 Bolus feeds less well tolerated.
 Formula osmolality should be < 310
mosm/kg.
Composition
 Protien hydrolysate or elemental diets
 Complex carbohydrate is better than
simple carbohydrate
 Oxalate restriction in patient with an
intact colon and fat malabsorption to avoid
stone formation.
 Lipid
 Medium-chain triglycerides
 Better absorbed in the presence of bile acid or
pancreatic insufficiency.
 Long-chain triglycerides : more effective
in stimulating intestinal adaptation
 Mix MCT + LCT
 Indications for continued parental
nutrition
 Poor weight gain or loss of maintenance weight.
 Extensive stomal fluid and electrolyte losses
which cannot be replaced orally.
Pharmacologic therapy
 Decrease stomal secretory losses
 H2 blockers, PPI & octreotide
 ??loperamide
 Ursodeoxycholic acid: Improves bile acid–dependent bile
flow.
 Antibiotics used to prevent small-bowel overgrowth.
 Insufficient data regarding -glutamine affects clinical
outcomes in infants.
 GH in children with SBS may have some benefit in those
with low or limited GH responsiveness.
Surgical Care
 Surgical care is related to venous access (ie,
central line placement to provide TPN).
 Gastrostomy tube placement to provide for
enteral access.
Nontransplantation procedures
 To improve the surface area or to slow transit
emptying time.
 Bianchi procedure (intestinal tapering or
lengthening)
 Indicated in small bowel with bacterial
overgrowth ,dilated bowel and continued
malabsorption
 Cutting bowel longitudinally, and create a segment
of bowel twice length, half diameter without loss
of mucosal surface area.
Tapering Bowel lengthening
 Indications
 Impending or overt liver failure
 IV access loss
 Frequent central line related sepsis
 Intestinal failure
Small bowel transplantation
Prognosis
 Ultimately patient with SBS may be
successfully wean from TPN although the
entire process may take several years.
 Intestinal transplantation should be
consider as a last resort.
Complications
 Early complications
 Catheter related
complication
 chronic complications
 liver & biliary disease
 Bacterial overgrowth
 D-lactic acidosis,
 Nutritional def,
Bacterial overgrowth
 Defined as increased bacterial content in the
small intestine
 Occurs if no Ileum , dilated bowel loops with
hypomotility segment & strictures.
 Clinically: N, V, distension, FTT, increase hepatic
injury from TPN , GI blood loss
 Also common cause of clinical deterioration in a
previously stable patient with SBS.
 Diagnosed duodenal fluid analysis, culture, stool
c/s, H2 breath test.
 This well leads to CHO malabsorption,
worsening of osmotic diarrhea, and
increased risk of metabolic acidosis and
dehydration.
 Treatment with antibiotic , including
administration of metronidazole
alternating with oral gentamicin.
 Should be cycled on a weekly or biweekly
basis.
Conclusion
 Early management of SBS replacement of fluid and
electrolytes.
 Enteral feeding should begin once the patient
stabilizes.
 Continuous enteral feeding or is preferred.
 For enteral feedings, hypoallergenic protein
hydrolysate formulas or breast milk are usually best
tolerated
 Several pharmacological approaches have been tested
to enhance intestinal adaptation and improve feeding
tolerance. None of these approaches are proven to be
helpful, but studies are ongoing.
Thanks

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Short Bowel Syndrome.pptx

  • 2. Objectives  Definition  Etiology  Clinical manifestation  Management  prognosis  Complication
  • 3. Definition  It is a malabsorpative state that may follow massive resection of small intestine.  There is no specific intestinal length at which SBS well clinically present.  The small intestine of the neonate is about 250 cm in length, 750 cm in adult.  Infants have more favorable long term prognosis.
  • 4.  Factors that influence the length of time until child independent of TPN  Extent/ location of resection.  Presence or absence of colon  Presence /Absence of ICV.  Degree of adaptation in remaining bowel.  Extent of residual bowel disease or complications e.g. adhesions, strictures
  • 5. Etiology  Congenital anomalies :  Intestinal Atresia .  Gastroschisis  omphalocele  Hirschsprung’s disease,  Acquired : Resection of bowel:  NEC ,  Crohn’s disease  volulus,  tumor ,  radiation enteritis,  ischemic injury
  • 6. Manifestation  Fluid & electlytes imbalance.  Steatorrhea  Wt loss and malnutrition.  Minerals def: Ca, Mg, Iron, zinc, B12, fat soluble vit.  Malabsorption of CHO and protein.  Metabolic acidosis.  Gastric acid hypersecretion.  Cholelithiasis.  Liver disease, cholestasis.  Bone disease.  Complications related to TPN. Reduction of functioning bowel mass to below min necessary to balance supply & demand of essential body needs leading to intestinal failure manifested as:
  • 7. Manifestation related to site of resection  Duodenal resection  Jejunal resection  Ileal resection  Loss of the ileocecal valve  Colon
  • 8. Duodenal resection  Protein , CHO, fat maldigestion  Ca, mg, iron, folate malabsorption  Fat soluble vit deficiency
  • 9. Jejunal resection  CHO Malabsorption.  Water soluble vit defiency .  Malabsorption is transient (ileal adaptation).
  • 10. Ileal resection  Steatorrhea as bile salts not absorbed.  Cholesterol stones secondary to loss of bile acids.  Fat soluble vit def.  B12 def  Loss of ileal brake, decrease transit time causing diarrhea.
  • 11. Loss of the ileocecal valve  Bacterial overgrowth: allows bacteria to flux into ilium  Rapid transit time that exacerbate malabsorption.
  • 12. Colon  Role of The Colon:  water absorption.  It gives additional length, it slows transit time and slows gasteric empting,  But  Deconjugation of bile acids by colonic bacteria & secondary secretory diarrhea.  lactic acidosis: conversion of CHO by lactobacillus to D-lactic acid lead to high AG metabolic acidosis,
  • 13. Intestinal adaptation  Starts 24-48 hrs post-op, (enteral feeds as early as possible).  Lasts up to 11-12 years .  Change in morphorogy and functional capacity.
  • 14. Change in morphorogy  Macroscopic  Increase in length  Microscopic  Villus: increase height and diameter  Crypt: elongation  Epithelial cell life cycle: increase proliferation  decrease apoptosis.
  • 15. Change in functional capacity  Increase absorption per unit length  Upregulation of sodium glucose transporter.
  • 16. Lab investigation  Blood  U&E, bone profile, & mg, PRN then biweekly  CBC, triglycerides, cholesterol Weekly  Folate, vit B12, copper, zinc, Monthly  Blood gas and AG for suspected lactic acidosis.
  • 17. Microbiology  If sepsis suspected; blood & urine c/s  Cultures from both the central and peripheral sites.  Consider opportunistic infections, so search for fungal infection.
  • 18. Imaging Studies To assess for potential complications,  Infection  Abdominal ultrasonography to look for fungal balls in the kidney  Bowel obstruction  Plain radiography.  Barium imaging of the bowel  Liver disease  Abdominal US to study the liver, biliary tract, & presence of ascites.
  • 19. Management  During early period after intestinal resection, TPN to prevent fluid and electrolytes imblance.  Stomal & fecal losses replaced q 2 hrs with solution separate from TPN.  May develop gastric hypersecretion so give H2 blocker
  • 20. Management  The goals of nutritional therapy  1.Maintain adequate nutrition  2.Promote intestinal adaptation  3.Avoid complications
  • 21.  TPN for the first 7-10 days  TPN :30 kcal/kg/day  Enteral feeding when hemodynamic stable and fluid management stable.  Continuous enteral feeds: to prevent osmotic diarrhea.  Bolus feeds less well tolerated.  Formula osmolality should be < 310 mosm/kg.
  • 22. Composition  Protien hydrolysate or elemental diets  Complex carbohydrate is better than simple carbohydrate  Oxalate restriction in patient with an intact colon and fat malabsorption to avoid stone formation.
  • 23.  Lipid  Medium-chain triglycerides  Better absorbed in the presence of bile acid or pancreatic insufficiency.  Long-chain triglycerides : more effective in stimulating intestinal adaptation  Mix MCT + LCT
  • 24.  Indications for continued parental nutrition  Poor weight gain or loss of maintenance weight.  Extensive stomal fluid and electrolyte losses which cannot be replaced orally.
  • 25. Pharmacologic therapy  Decrease stomal secretory losses  H2 blockers, PPI & octreotide  ??loperamide  Ursodeoxycholic acid: Improves bile acid–dependent bile flow.  Antibiotics used to prevent small-bowel overgrowth.  Insufficient data regarding -glutamine affects clinical outcomes in infants.  GH in children with SBS may have some benefit in those with low or limited GH responsiveness.
  • 26. Surgical Care  Surgical care is related to venous access (ie, central line placement to provide TPN).  Gastrostomy tube placement to provide for enteral access.
  • 27. Nontransplantation procedures  To improve the surface area or to slow transit emptying time.  Bianchi procedure (intestinal tapering or lengthening)  Indicated in small bowel with bacterial overgrowth ,dilated bowel and continued malabsorption  Cutting bowel longitudinally, and create a segment of bowel twice length, half diameter without loss of mucosal surface area.
  • 29.  Indications  Impending or overt liver failure  IV access loss  Frequent central line related sepsis  Intestinal failure Small bowel transplantation
  • 30. Prognosis  Ultimately patient with SBS may be successfully wean from TPN although the entire process may take several years.  Intestinal transplantation should be consider as a last resort.
  • 31. Complications  Early complications  Catheter related complication  chronic complications  liver & biliary disease  Bacterial overgrowth  D-lactic acidosis,  Nutritional def,
  • 32. Bacterial overgrowth  Defined as increased bacterial content in the small intestine  Occurs if no Ileum , dilated bowel loops with hypomotility segment & strictures.  Clinically: N, V, distension, FTT, increase hepatic injury from TPN , GI blood loss  Also common cause of clinical deterioration in a previously stable patient with SBS.  Diagnosed duodenal fluid analysis, culture, stool c/s, H2 breath test.
  • 33.  This well leads to CHO malabsorption, worsening of osmotic diarrhea, and increased risk of metabolic acidosis and dehydration.  Treatment with antibiotic , including administration of metronidazole alternating with oral gentamicin.  Should be cycled on a weekly or biweekly basis.
  • 34. Conclusion  Early management of SBS replacement of fluid and electrolytes.  Enteral feeding should begin once the patient stabilizes.  Continuous enteral feeding or is preferred.  For enteral feedings, hypoallergenic protein hydrolysate formulas or breast milk are usually best tolerated  Several pharmacological approaches have been tested to enhance intestinal adaptation and improve feeding tolerance. None of these approaches are proven to be helpful, but studies are ongoing.