Presented at the Neonatal Society 2007 Spring Meeting.
Philpott A1, Aladangady N1,2
1 Neonatal Unit, Homerton University Hospital NHS Foundation Trust, London, UK
2 Barts and the London School of Medicine, Queen Mary University London, UK
Background: Studies on conjugated hyperbilirubinaemia (CH) in preterm infants is limited. In the mid-1980s CH was reported as 3% in infants less than 1500g (1).
Aims: 1. To study the incidence of CH in preterm infants of less than 32 weeks gestation. 2. To study the associated factors and natural history of CH in the preterm infant.
Methods: Infants with CH (total bilirubin >100 μmol/l with a conjugated fraction of greater than 20% on more than one plasma sample) were identified from the hospital biochemistry database over a 5-year period (Jan 99 – December 03). Each case was compared with a gestational age and sex matched control infant identified from the neonatal unit admission book. Details of birth weight and ethnicity were recorded and antenatal Doppler ultrasound scan results were obtained from the fetal medicine database. Clinical data pertaining to CRIB II score, ventilation, feeding (enteral/parenteral), gastrointestinal (GI) examination, and proven bacterial infection were collected by retrospective case note analysis. Biochemical data was recorded on liver and thyroid functions, coagulation profile and urinary reducing substances. The study was approved by the East London Research Ethics Committee.
Results: During the study period 40 babies developed CH, resulting in an incidence of 6.0% in babies born at <32 wks gestation and increasing to 11.2% of babies born at <27 wks gestation. Mean birth weight was 843g (IQR 615-900g) and gestational age 26.6weeks (IQR 25-28weeks), with a male:female ratio of 22:18. CH was first noted on day 28 (mean value) (IQR 11-81d) with a peak value on day 44 (IQR 17-96d), and resolution of CH on day 85 (IQR 29-189d). On univariate analysis there was no difference in gestational age, sex, CRIB II scores or ethnicity (p>0.1) between the study and control groups. Significant differences were found in birth weight (p<0.02), abnormal antenatal Doppler scans (p<0.001), duration of ventilation (p<0.001), insertion of a central line for parenteral nutrition (p<0.01), duration of parenteral nutrition (p<0.001), day of starting enteral feeds (p<0.001), day of attaining full feeds (p<0.03), proven infection (p<0.02) and proven gastrointestinal complications (p<0.001). There was no association between the development of CH and maternal breast milk feeding (p>0.1). Basic biochemical investigations and liver ultrasound scans were normal in all of the neonates studied.
Conclusion: The extremely preterm neonate is at high risk of developing CH. In a preterm population <32 weeks gestation who develop CH with normal examination and baseline investigations, and a prolonged period of parenteral nutrition the cause is unlikely to be significant or permanent liver disease.
References
1. Brown DC Ir Med J 1991; 84(2): 56-7