Background: Cholestatic jaundice and liver enzyme abnormalities have been reported in neonatal septicaemia; the course, pattern, and outcome of such hepatobiliary dysfunction have not been described.
Methods: One hundred fifty-three neonates with blood culture–positive sepsis were recruited from the neonatal intensive care unit of an urban hospital. Liver function tests were done on day 3 and day 10 in all of the cases. In babies with abnormal results (direct bilirubin >20% of total with a minimum level of 2 mg/dL or alanine aminotransferase [ALT] >50 U/L), tests were repeated weekly for 1 month and then fortnightly for 3 months or until normalization of values. Anthropometry was recorded at all of these visits.
Results: Klebsiella pneumoniae was the commonest organism, isolated in 95.4% of subjects. Eighty-three (54.2%) subjects had hepatobiliary dysfunction in the form of either cholestatic jaundice (n = 65 [42.5%]) or derangement in ALT (n = 57 [37.3%]). The onset of cholestasis was seen by day 3 of sepsis in 80% (n = 52), with maximum value of direct bilirubin seen by the 10th day in 90% (n = 58). Only 15% (n = 10) continued to have cholestatic jaundice beyond 30 days of onset of sepsis, and it resolved by 60 days. Hepatic enzyme abnormalities followed a more protracted course: onset by day 10 in 95%, peak value by day 38 in 90%, and normalisation by 60 days in 82% of subjects. The prevalence of any hepatobiliary dysfunction was found less frequently in babies who died as compared with survivors (43.4% vs 56.7%; P < 0.01). The weight, length, and head circumference during follow-up visits were comparable between neonates with or without hepatobiliary dysfunction.
Conclusions: Hepatobiliary dysfunction is common in Gram-negative neonatal septicaemia. The onset of abnormalities is early in most cases but ultimately resolve within 2 to 3 months after sepsis. The presence of conjugated hyperbilirubinemia in neonatal sepsis may carry a better prognosis in terms of survival and has no significant effect on growth during early infancy.
*Department of Paediatrics
†Department of Microbiology
‡Department of Pathology, University College of Medical Sciences, University of Delhi and GTB Hospital, Delhi, India.
Address correspondence and reprint requests to Dr Dheeraj Shah, MD, DNB, MNAMS, Associate Professor, Department of Paediatrics, University College of Medical Sciences and GTB Hospital, Dilshad Garden, Delhi 110095, India (e-mail: email@example.com).
Received 8 June, 2011
Accepted 20 August, 2011
The authors report no conflicts of interest.