Which practice is a major risk factor for neonatal cholestasis in premature infants?

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Multiple Choice

Which practice is a major risk factor for neonatal cholestasis in premature infants?

Explanation:
Long-term parenteral nutrition disrupts the normal enterohepatic circulation and bile flow, which is especially problematic in premature infants whose hepatobiliary systems are immature. When gut feeds are limited or delayed, the absence of enteral stimulation reduces cholecystokinin release and gallbladder contraction, leading to bile stasis. Over weeks of intravenous nutrition, the liver accumulates conjugated bilirubin, producing neonatal cholestasis associated with parenteral nutrition. This risk rises with the duration of PN, which is why prolonged PN is the most important factor in premature infants developing cholestasis. Prolonged phototherapy helps manage unconjugated bilirubin and does not drive cholestasis. Postnatal CMV infection can cause liver inflammation and cholestasis in some cases, but it is not the primary driver in the typical premature neonate with PN-related cholestasis. Maternal diabetes affects neonatal metabolic risk more broadly and is not a major contributor to PN-associated cholestasis. To reduce risk, clinicians aim to shorten PN duration when feasible and advance enteral feeding as early as tolerated, with strategies like using lipid emulsions that may mitigate PN-associated liver injury.

Long-term parenteral nutrition disrupts the normal enterohepatic circulation and bile flow, which is especially problematic in premature infants whose hepatobiliary systems are immature. When gut feeds are limited or delayed, the absence of enteral stimulation reduces cholecystokinin release and gallbladder contraction, leading to bile stasis. Over weeks of intravenous nutrition, the liver accumulates conjugated bilirubin, producing neonatal cholestasis associated with parenteral nutrition. This risk rises with the duration of PN, which is why prolonged PN is the most important factor in premature infants developing cholestasis.

Prolonged phototherapy helps manage unconjugated bilirubin and does not drive cholestasis. Postnatal CMV infection can cause liver inflammation and cholestasis in some cases, but it is not the primary driver in the typical premature neonate with PN-related cholestasis. Maternal diabetes affects neonatal metabolic risk more broadly and is not a major contributor to PN-associated cholestasis.

To reduce risk, clinicians aim to shorten PN duration when feasible and advance enteral feeding as early as tolerated, with strategies like using lipid emulsions that may mitigate PN-associated liver injury.

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