A fetal inflammatory response is protective for chronic lung disease. Neonatal sepsis is strongly associated with chronic lung disease, and the infecting organism is important. Coagulase-negative staphylococcal infection confers a risk for chronic lung disease similar to that of other bacteremias. Candidemia confers the greatest risk of chronic lung disease.

The risk of perinatal transmission of hepatitis C virus (HCV) from a cohort of 95 human immunodeficiency virus (HIV)-negative intravenous drug users (IVDU) is described, 89 of whom were positive for antibodies to HCV (anti-HCV). Infection, defined as the presence of HCV RNA in a serum sample collected from an infant at any time during follow-up, was detected in six of 63 (9.5%) infants born to HCV antibody-positive viraemic mothers. No mother who was HCV RNA negative at delivery transmitted HCV to her infant. Hepatitis C virus antibodies became undetectable in uninfected infants by 15 months, but persisted in all HCV-infected infants throughout follow-up. An abnormal alanine aminotransferase (ALT) level was observed on at least one occasion in all HCV-infected infants and in six occasions in uninfected infants. Two of the six HCV-infected infants became HCV RNA negative during follow-up by 27 and 29 months. Both of these infants had a large ALT elevation (mean peak ALT 398U l-1) at around 12 months of age. Analysis of a range of potential risk factors revealed that maternal HCV RNA load was important in predicting transmission, but suggested that other factors play a role in perinatal transmission from mother to child. No difference was found between mothers who transmitted HCV to their infants and those who did not for HCV genotype, duration of drug use, duration of methadone use, methadone dose, history of alcohol abuse, past hepatitis B virus (HBV) infection, mode of delivery, maternal and gestational age, birth weight and incidence of breast-feeding. Mothers who transmitted HCV to their infants had a longer duration between membrane rupture and delivery than the mothers who did not transmit (P = 0.03). HCV RNA was not detected in breast milk and colostrum samples from 38 viraemic mothers, including two who transmitted HCV to their infant.

Over a 7 year study period, 82 infants were identified who had necrotising enterocolitis (NEC). A case-control study of the 74 preterm infants was performed to determine those factors which contributed to the development of NEC. The 35 infants with NEC and gestation between 30-36 weeks, when compared with control infants matched for gestational age, had significantly lower birthweight centiles, cord pH, and 1 minute Apgar scores. By contrast, there were no significant differences between the 39 infants with NEC and controls in the 25-29 week group, except that fewer babies with NEC had received breast milk. The eight term babies all appeared to have an obvious predisposing event. We thus propose a model in which susceptibility to NEC is dependent on gestational age. In the 25-29 week range all babies are at risk on the basis of extreme prematurity. In the 30-36 week range asphyxiated and growth retarded babies are at increased risk, while at term a major predisposing event appears to be required.

Most estimated fetal weight formulas have been derived and tested with larger fetuses, yet accuracy in predicting birth weight is more critical at the limit of viability. Complete data from 142 pregnancies in which delivery took place within 7 days of an ultrasonographic examination were used to create an appropriate formula for fetuses less than 1000 g and compare it with 10 currently available formulas. Our formula (In [BW] = 0.66 x 1n [HC] + 1.04 x 1n [AC] + 0.985 x 1n [FL]) was significantly more accurate than all other formulas and also performed better on a prospective cohort of 27 fetuses with estimated fetal weight less than 1000 g. Of the existing formulas, the Hadlock formula (using head circumference, abdominal circumference, femur length) was the most accurate, being significantly more accurate than all but the Woo formula with all but the Woo formula.