Pediatric Nutrition in Practice

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Malabsorptive Disorders and Short Bowel Syndrome 185


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chain fatty acids, especially butyrate, are known to
promote glucagon-like peptide-2 release.
Long-chain triglycerides are poorly absorbed
by patients with a reduced absorptive surface. In
case of small intestinal bacterial overgrowth
(SIBO), bacteria metabolize and inactivate bile
acids, preventing the solubilization necessary for
long-chain triglyceride digestion.
Medium-chain triglycerides (MCT) are rapidly
hydrolyzed by pancreatic lipase and are less de-
pendent on an extensive absorptive surface for
adequate absorption. They are water soluble, and
can be absorbed intact directly into the portal
circulation [9]. Excessive intake of MCT can
cause diarrhea and ketosis, while MCT do not
provide essential fatty acids. Current clinical
prac t ice is based on for mu las conta i ni ng no more
than 60% MCT as fat.
Whether the molecular form of the nitrogen
taken up might inf luence PN duration and/or the
occurrence of non-IgE-mediated sensitization
and allergic enteritis remains debated. A link be-
tween SIBO, abnormal mucosal permeability and
protein sensitization is possible, but the use of el-
emental diets (amino acid-based formulas) is not
clinically established ( table  3 ). Patients with di-
lated, poorly motile segments of the small bowel
should benefit first from an approach aiming to
reduce bowel dilatation and SIBO, with subse-
quent bacterial translocation [10].
Hydrolyzed protein formulas (HPF) have been
used for many years and have changed the inci-
dence and outcome of PDI during the last decades.
HPF have been evaluated by comparison with in-
tact protein infant formulas in a crossover study of
60 days duration on 10 infants with SBS [11]. No
effect of formula type was observed on growth, ni-
trogen absorption or mucosal permeability. In gen-
eral, HPF are lactose free and contain MCT [11, 1 2].
Elemental amino acid-based formulas
(EAABF) have been introduced more recently
for infants suffering from severe allergic diseases.
It is not yet established whether this type of for-
mula may inf luence the outcome of SBS. A ben-

Ta b l e 3. Small intestinal bacterial overgrowth


General remarks



  • Several factors intrinsic to SBS predispose to SIBO and
    explain its high prevalence in this patient population

  • Poorly motile segments of the small bowel in close proximity
    to the colon are common in patients with SBS and dysmotility,
    and the intestinal stasis and contamination that results
    promotes abnormal growth of bacteria in the small intestine

  • The link between SIBO, translocation, cholestasis, portal
    fibrosis and cirrhosis is now clearly established

  • SIBO may significantly compromise digestive and absorptive
    functions and may delay or prevent weaning from PN

  • Traditional clinical tests for overgrowth may be unreliable

  • Management may include surgery if advocated; antibiotic
    therapy should be carefully selected to avoid resistance

  • The intestinal microbiota plays an important role in intestinal
    adaptation and should be preserved as much as possible

  • The use of probiotics might offer potential based on
    experimental evidence, but there is a lack of sufficient data
    from human studies. The use of D-lactate producing
    probiotics should be avoided

  • D-Lactic acidosis is secondary to bacterial hypermetabolism,
    especially in the colon, as a consequence of intestinal
    malabsorption


Definition
CFU per milliliter of bacteria in the proximal small bowel



  • Overgrowth of >10^5 CFU/ml

  • Overgrowth of >10^3 CFU/ml provided that the species of
    bacteria isolated from the jejunal aspirate are those that
    normally colonize the large bowel or provided that those
    same species are absent from the saliva and gastric juice

  • Breath hydrogen testing


Caused by small intestine stasis from:



  • Intestinal obstruction (e.g. stenosis, narrowed anastomosis)

  • Blind loop from terminolateral anastomosis

  • Dilated and poorly motile segments of the small bowel in
    close proximity to the colon


Consequences



  • Small intestinal mucosal injury with villous atrophy and
    subsequent malabsorption

  • Increased small intestinal mucosal permeability

  • IgE-mediated sensitization and allergic enteritis

  • Gram-negative sepsis from bacterial translocation

  • Portal inflammation, cholestasis, fibrosis and end-stage liver
    disease (cirrhosis)


Management
Reversal or removal of any predisposing condition(s)



  • Redo anastomosis

  • Enteroplasty

    • Small intestinal tapering and lengthening (Bianchi
      procedure)

    • Serial transverse enteroplasty (STEP procedure)
      Appropriate nutritional support/replacement
      Suppression or eradication of the contaminating bacterial flora



  • Intermittent bowel decontamination with antibiotics

  • Use of probiotics (Lactobacillus rhamnosus GG,
    Saccharomyces boulardii, etc.)


CFU = Colony-forming unit.


Koletzko B, et al. (eds): Pediatric Nutrition in Practice. World Rev Nutr Diet. Basel, Karger, 2015, vol 113, pp 182–189
DOI: 10.1159/000360339

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