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Published on: December 1, 2012
Nutritional management of infants with short bowel syndrome
Jacqueline J Wessel1, Samuel A Kocoshis
1Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229-3039, USA. jackie.wessel@cchmc.org
Insights
Short bowel syndrome is rising, often requiring total parenteral nutrition (TPN). Strategies to minimize TPN-induced liver damage (IFALD) and promote bowel adaptation are crucial for infant survival and growth.
Area of Science:
- Neonatology
- Pediatric Gastroenterology
- Surgical Nutrition
Background:
- Short bowel syndrome prevalence is increasing due to advances in neonatal care.
- Neonates with intestinal failure require chronic total parenteral nutrition (TPN) for growth and adaptation.
- Intestinal failure-associated liver disease (IFALD) is a significant complication of TPN.
Purpose of the Study:
- To review the causes and management of IFALD in neonates with intestinal failure.
- To discuss strategies for minimizing TPN-induced liver damage.
- To highlight the importance of enteral nutrition for bowel adaptation and IFALD prevention/reversal.
Main Methods:
- Review of current literature on short bowel syndrome, TPN, and IFALD.
- Analysis of host factors and TPN components contributing to IFALD.
- Evaluation of parenteral and enteral nutrition strategies.
Main Results:
- IFALD results from a combination of host factors (immature bile secretion, bile stasis, sepsis) and TPN components (excessive glucose, protein, phytosterols in lipids).
- Parenteral strategies to minimize IFALD include reducing glucose, protein, and lipid loads.
- Preliminary evidence suggests fish oil-based lipid solutions may benefit IFALD.
Conclusions:
- Minimizing TPN constituents and optimizing delivery are key to preventing IFALD.
- Enteral nutrition is essential for promoting bowel adaptation and reversing IFALD.
- Continuous enteral feeding is the current standard for nutritional support in these infants.
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.
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