Related Experiment Videos
Intrahepatic cholestasis with parental alimentation
Insights
Parenteral alimentation in infants can cause intrahepatic cholestasis, a liver condition. Discontinuing this treatment can reverse liver abnormalities, with no chronic dysfunction observed in survivors.
Area of Science:
- Pediatric Gastroenterology
- Hepatology
- Neonatal Intensive Care
Background:
- Parenteral alimentation (PA) is critical for critically ill infants lacking gastrointestinal function.
- Intrahepatic cholestasis is a potential complication of PA, particularly in prolonged use.
- Histologic changes in the liver are a key indicator of PA-associated complications.
Purpose of the Study:
- To examine the clinical and histologic evidence of intrahepatic cholestasis in infants receiving PA.
- To assess the reversibility of liver abnormalities after PA discontinuation.
- To determine the long-term hepatic function in surviving infants.
Main Methods:
- Review of clinical records and liver biopsies from eleven infants who received PA.
- Histologic examination for evidence of cholestasis, fibrosis, and hepatocyte membrane changes.
- Monitoring of liver function tests and correlation with PA treatment duration.
Main Results:
- All eleven infants showed histologic evidence of intrahepatic cholestasis.
- Marked cholestasis, fibrosis, and thickened hepatocyte limiting membranes were observed.
- Discontinuation of PA led to normalization of liver histology and function tests.
- Two surviving infants showed no chronic liver dysfunction after 2.5 years follow-up.
Conclusions:
- Intrahepatic cholestasis is a significant risk in infants receiving PA.
- Early detection and discontinuation of PA are crucial for reversing liver damage.
- Long-term hepatic function appears preserved in survivors after PA cessation.
Abstract:
From July 1971 to March 1975, elevan infants receiving total or partial parenteral alimentation at the University of Florida showed histologic evidence of intrahepatic cholestasis. The clinical records of these patients have been examined. These infants were critically ill and had protracted hospital courses with only two survivors. Liver biopsies demonstrated marked cholestasis with some fibrosis and thickening of the limiting membrane of the hepatocyte. In those patients in whom serial liver biopsies were obtained, hepatic histology returned toward normal, paralleling improvement in liver function studies, as intravenous alimentation was discontinued. Careful monitoring of the liver function tests is essential to detect this progressive abnormality as early as possible and discontinue intravenous alimentation. Follow-up as long as two and a half years in the two surviving patients has demonstrated no chronic dysfunction.