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Nutritional management of infants with short bowel syndrome.
Semin Perinatol. 2007 Apr; 31(2):104-11.SP

Abstract

The prevalence of short bowel syndrome appears to be increasing because of more aggressive surgical and medical approaches to the management of neonatal intraabdominal catastrophies. Hence, a large cohort of neonates with intestinal failure occupies neonatal intensive care units, requiring chronic total parenteral nutrition (TPN) in hopes that the residual bowel will adapt, thereby permitting weaning of TPN. Alternatively, when there is no hope for adaptation, these infants are maintained on TPN in hopes that they will grow to a size and state of general health satisfactory for either isolated intestinal transplant when liver function is preserved or combined liver-intestinal transplantation when the liver is irreparably damaged. Thus, it is imperative to provide enough parenteral nutrition to facilitate growth while minimizing TPN constituents predisposing to liver damage. Liver disease associated with intestinal failure (IFALD) seems to occur due to a variety of host factors combined with deleterious components of TPN. Host factors include an immature bile secretory mechanism, bile stasis due to fasting, and repeated septic episodes resulting in endotoxemia. Many constituents of TPN are associated with liver damage. Excessive glucose may result in fatty liver and/or hepatic fibrosis, excessive protein may lead to reduced bile flow, and phytosterols present in intravenous lipid may produce direct oxidant damage to the liver or may impede cholesterol synthesis and subsequent bile acid synthesis. Parenteral strategies employed to minimize TPN damage include reducing glucose infusion rates, reducing parenteral protein load, and reducing parenteral lipid load. Furthermore, preliminary studies suggest that fish oil-based lipid solutions may have a salutary effect on IFALD. Ultimately, provision of enteral nutrition is imperative for preventing or reversing IFALD as well as facilitating bowel adaptation. While studies of trophic hormones are ongoing, the most reliable current method to facilitate adaptation is to provide enteral nutrition. Continuous enteral feeding remains the mainstay of enteral nutrition support.

Authors+Show Affiliations

Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229-3039, USA. jackie.wessel@cchmc.orgNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

17462495

Citation

Wessel, Jacqueline J., and Samuel A. Kocoshis. "Nutritional Management of Infants With Short Bowel Syndrome." Seminars in Perinatology, vol. 31, no. 2, 2007, pp. 104-11.
Wessel JJ, Kocoshis SA. Nutritional management of infants with short bowel syndrome. Semin Perinatol. 2007;31(2):104-11.
Wessel, J. J., & Kocoshis, S. A. (2007). Nutritional management of infants with short bowel syndrome. Seminars in Perinatology, 31(2), 104-11.
Wessel JJ, Kocoshis SA. Nutritional Management of Infants With Short Bowel Syndrome. Semin Perinatol. 2007;31(2):104-11. PubMed PMID: 17462495.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nutritional management of infants with short bowel syndrome. AU - Wessel,Jacqueline J, AU - Kocoshis,Samuel A, PY - 2007/4/28/pubmed PY - 2007/6/26/medline PY - 2007/4/28/entrez SP - 104 EP - 11 JF - Seminars in perinatology JO - Semin Perinatol VL - 31 IS - 2 N2 - The prevalence of short bowel syndrome appears to be increasing because of more aggressive surgical and medical approaches to the management of neonatal intraabdominal catastrophies. Hence, a large cohort of neonates with intestinal failure occupies neonatal intensive care units, requiring chronic total parenteral nutrition (TPN) in hopes that the residual bowel will adapt, thereby permitting weaning of TPN. Alternatively, when there is no hope for adaptation, these infants are maintained on TPN in hopes that they will grow to a size and state of general health satisfactory for either isolated intestinal transplant when liver function is preserved or combined liver-intestinal transplantation when the liver is irreparably damaged. Thus, it is imperative to provide enough parenteral nutrition to facilitate growth while minimizing TPN constituents predisposing to liver damage. Liver disease associated with intestinal failure (IFALD) seems to occur due to a variety of host factors combined with deleterious components of TPN. Host factors include an immature bile secretory mechanism, bile stasis due to fasting, and repeated septic episodes resulting in endotoxemia. Many constituents of TPN are associated with liver damage. Excessive glucose may result in fatty liver and/or hepatic fibrosis, excessive protein may lead to reduced bile flow, and phytosterols present in intravenous lipid may produce direct oxidant damage to the liver or may impede cholesterol synthesis and subsequent bile acid synthesis. Parenteral strategies employed to minimize TPN damage include reducing glucose infusion rates, reducing parenteral protein load, and reducing parenteral lipid load. Furthermore, preliminary studies suggest that fish oil-based lipid solutions may have a salutary effect on IFALD. Ultimately, provision of enteral nutrition is imperative for preventing or reversing IFALD as well as facilitating bowel adaptation. While studies of trophic hormones are ongoing, the most reliable current method to facilitate adaptation is to provide enteral nutrition. Continuous enteral feeding remains the mainstay of enteral nutrition support. SN - 0146-0005 UR - https://www.unboundmedicine.com/medline/citation/17462495/Nutritional_management_of_infants_with_short_bowel_syndrome_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0146-0005(07)00031-6 DB - PRIME DP - Unbound Medicine ER -