Early management of SBS includes replacement of fluid and electrolytes.
Enteral feeding should begin once the patient stabilizes.
Continuous enteral feeding is preferred.
For enteral feedings, hypoallergenic protein hydrolysate formulas or breast milk are usually best tolerated
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
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.
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.