Skip to main content
ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #229006
Title: Course and outcome of parenteral nutrition-associated cholestasis in neonates

Author
item WILLIS, THERESA - BAYLOR COLLEGE MED
item CARTER, BETH - BAYLOR COLLEGE MED
item ROGERS, STEFANIE - BAYLOR COLLEGE MED
item HAWTHORNE, KELI - BAYLOR COLLEGE MED
item Abrams, Steven

Submitted to: Pediatric Academic Society
Publication Type: Abstract Only
Publication Acceptance Date: 2/15/2008
Publication Date: 5/5/2008
Citation: Willis, T.C., Carter, B.A., Rogers, S.P., Hawthorne, K.M., Abrams, S.A. 2008. Course and outcome of parenteral nutrition-associated cholestasis in neonates [abstract]. Electronic-Pediatric Academic Societies. Abstract no. 5823.3. Available: http://www.abstracts2view.com/pas/view.php?nu=PAS08L1_77.

Interpretive Summary:

Technical Abstract: Parenteral nutrition-associated cholestasis (TPN-Chol) leads to significant morbidity and mortality. To assess the safety and effectiveness of potential interventions, it is necessary to evaluate the natural history of TPN-Chol. This retrospective review was undertaken to evaluate the typical course of TPN-Chol. We assessed the maximum conjugated bilirubin (CB), time to resolution of cholestasis, incidence of sepsis, and overall outcomes. We reviewed the medical records of all Level III NICU patients at Texas Childrens Hospital with likely TPN-chol, defined as conjugated bilirubin (CB) greater than or equal to 2 mg/dL, who had ever received Ursodeoxycholic acid (Actigal) between Jan 2006 and April 2007. These criteria identified infants with at least minimal bowel function, since Ursodeoxycholic acid is given to all enterally-fed babies with probable TPN-chol. Infants transferred to our hospital after 60 days of age, or with cholestasis clearly unrelated to TPN (e.g., biliary atresia, metabolic disease) were excluded. Of 66 patients who met the study criteria, there were 10 deaths and 1 transplant. Five deaths were directly associated with liver failure. Maximum CB in babies who died/transplant was 14.8 +/- 2.3 mg/dL vs. 7.9 +/- 1.0 mg/dL p= 0.007 in babies who recovered (All data are Mean +/- SEM). Forty-four percent of babies with CB greater than or equal to 10 died vs 7% of babies with CB less than 10 mg/dL (p < 0.01). There was no significant relationship between maximum CB and birthweight, gender, or positive blood cultures (BDC). After taking into account maximum CB, cholestatic babies with a history of positive BDC occurring after the development of CB were more likely to die/transplant than those without a positive BDC, p < 0.05. Of 41 babies with positive culture, 11 died vs 0 deaths among the 23 without positive BDC (p= 0.03). Of the 66 babies with CB greater than or equal to 2, 89% developed a CB greater than or equal to 4 (n=59). Among survivors, mean time to resolution (CB < 2 mg/dL) for babies with a max CB greater than or equal to 4 mg/dL was 48.4 +/- 4.8 days (n=42). TPN-chol is common in our NICU with an average of 4 new diagnoses each month among babies able to tolerate some enteral nutrition. Infants with max CB >2 mg/dL have high rates of morbidity and mortality and the near certainty of progression to a CB > 4 mg/dL. A maximum CB greater than or equal to 10 mg/dL is associated with approximately a 50% mortality/transplant rate. Interventions to decrease CB may be considered for babies with a CB greater than or equal to 2 mg/dL.