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Intrahepatic cholestasis associated with parenteral nutrition in premature infants
Insights
Parenteral nutrition (PN) can cause liver issues like intrahepatic cholestasis in premature infants. Very low birth weight infants face higher risks, and longer PN duration increases cholestasis likelihood.
Area of Science:
- Neonatology
- Pediatric Gastroenterology
- Clinical Nutrition
Background:
- Premature infants often require parenteral nutrition (PN) due to feeding intolerance during respiratory distress.
- Intrahepatic cholestasis is a known complication associated with PN in infants.
Purpose of the Study:
- To investigate the incidence and risk factors of intrahepatic cholestasis in premature infants receiving PN.
- To identify clinical indicators for monitoring and managing PN-associated cholestasis.
Main Methods:
- Retrospective analysis of 62 premature infants (<2,000 gm birth weight) receiving PN.
- Monitoring for intrahepatic cholestasis defined as direct bilirubin ≥ 1.5 mg/dl.
- Correlation analysis of cholestasis onset with birth weight, gestational age, and duration of PN.
Main Results:
- 23% (14/62) of infants developed intrahepatic cholestasis.
- Infants <1,000 gm birth weight had a 50% incidence of cholestasis.
- Cholestasis onset averaged 42 days on PN and resolved upon PN discontinuation.
- Longer PN duration correlated with increased cholestasis risk, irrespective of gestational age or birth weight.
Conclusions:
- Parenteral nutrition is associated with intrahepatic cholestasis in premature infants, particularly those with very low birth weight.
- Direct bilirubin levels are effective for monitoring cholestasis onset and resolution.
- Prolonged PN administration increases the risk of developing cholestasis in this vulnerable population.
Abstract:
Sixty-two premature infants less than 2,000 gm birth weight received parenteral nutrition (PN) during periods of respiratory distress with feeding intolerance. Intrahepatic cholestasis (direct bilirubin greater than or equal to 1.5 mg/dl) associated with PN developed in 14 or 23% of these infants. The mean time on PN to onset of cholestasis was 42 days, and the cholestasis persisted as long as the infants continued to receive PN. All five infants who had serial follow-up laboratory studies showed an eventual return of direct bilirubin levels to normal. The direct bilirubin level appeared to be the best clinically available test to monitor for the onset and to follow the resolution of this complication. The very low birth weight infants less than 1,000 gm appeared to be at an increased risk of developing cholestasis with an incidence of 50%. However, there was no correlation between the length of time PN was administered to onset of cholestasis and the gestational age or birth weight of the infants. These tiny premature infants also received PN for significantly longer periods of time, and the longer the infusions were administered the greater was the risk of cholestasis developing.