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Published on: September 20, 2019
Total Parenteral Nutrition-Induced Cholestasis: Prevention and Management
Sue V Beath1, Deirdre A Kelly1
1The Liver Unit, Birmingham Children's Hospital, Steelhouse Lane, Birmingham, West Midlands, B4 6NH, UK.
Insights
Cholestasis during total parenteral nutrition (TPN) involves multiple liver injury pathways, especially in children. Prevention focuses on risk identification, monitoring, and managing inflammation to avoid serious liver complications.
Area of Science:
- Hepatology
- Pediatric Gastroenterology
- Clinical Nutrition
Background:
- Cholestasis is a critical complication in patients receiving total parenteral nutrition (TPN).
- Multiple pathogenic pathways converge on the hepatic acinus, leading to liver injury.
- Type 3 intestinal-associated liver disease presents with fibrosis, portal hypertension, and jaundice.
Purpose of the Study:
- To elucidate the multifactorial nature of cholestasis in TPN patients.
- To highlight the increased susceptibility of children to TPN-associated liver disease.
- To outline strategies for the prevention and management of TPN-induced cholestasis.
Main Methods:
- Review of pathogenic mechanisms leading to cholestasis in TPN.
- Analysis of clinical manifestations including liver function tests, fibrosis, portal hypertension, and jaundice.
- Identification of risk factors and preventative measures.
Main Results:
- TPN-associated cholestasis results from converging pathogenic pathways affecting the liver.
- Children are more vulnerable to developing severe liver disease (Type 3 IALD) compared to adults.
- Temporary elevations in liver function tests can occur.
Conclusions:
- Prevention is paramount and involves identifying high-risk patients and scenarios.
- Meticulous monitoring and personalized TPN solutions are essential.
- Prompt management of inflammatory events with antibiotics and line locks can mitigate liver injury.
Abstract:
When cholestasis occurs in patients receiving total parenteral nutrition, it is the result of many pathogenic pathways converging on the hepatic acinus. The result may be a temporary rise in liver function tests. The resulting fibrosis, portal hypertension, and jaundice are hallmarks of type 3 intestinal-associated liver disease to which children are more susceptible than adults. The key to prevention is in identifying high-risk scenarios, meticulous monitoring, and personalized prescription of parenteral nutrition solutions combined with an active approach in reducing the impact of inflammatory events when they occur by prompt use of antibiotics and line locks.
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