Perinatal infection increases the risk of neonatal neurologic injury. Our objective is to determine whether histologically confirmed chorioamnionitis and funisitis is associated with fetal metabolic acidosis.

This is a retrospective cohort study of all infants 34 weeks or less born at a single tertiary hospital admitted to the neonatal intensive care unit (NICU) between April 1999 and September 2002. Maternal and neonatal records and placental pathology reports were reviewed.

There were 392 infants at 23 to 34 weeks' gestational age admitted to the NICU during this period of whom 354 had placental pathology reported; 259 infants had umbilical cord gases available. These neonates were placed into 3 groups: group 1 (208 infants) had no signs of placental infection, group 2 (59 infants) had isolated chorioamnionitis, and group 3 (87 infants) had both chorioamnionitis and funisitis. The gestational age (30.2 ± 2.8, 28.3 ± 3.4, 27.8 ± 2.8 weeks, P < .01) and birth weight (1358 ± 520, 1242 ± 547, 1103 ± 381 g, P < .01) were significantly higher in group 1. There was an increase in neurologic morbidity in groups 2 and 3 (25.2%, 34.4%, 43.7%), which was not significant when corrected for gestational age. Groups 2 and 3 had a small but significant increase in umbilical arterial pH (7.25 ± 0.10, 7.29 ± 0.10, 7.30 ± 0.08, P < .01) and base excess (−3.5 ± 3.6, −2.2 ± 3.6, −2.3 ± 2.7 mmol/L, P=.02). When a single pathologist reviewed all placentas with any inflammation and staged them on the basis of the degree of the fetal inflammatory response, no relationship was found between the degree of fetal inflammation and umbilical arterial pH (stage 1, 7.27 ± 0.09; stage 2, 7.30 ± 0.09; stage 3, 7.30 ± 0.08; P=.41) or base excess (stage 1, −2.82 ± 3.47 mmol/L; stage 2, −1.95 ± 3.17 mmol/L; stage 3, −2.23 ± 3.07 mmol/L; P=.62). When stepwise multiple linear regression was performed, neither histologic chorioamnionitis nor histologic funisitis were associated with a change in umbilical cord pH or base excess.

Intrauterine infection, as confirmed by histologic chorioamnionitis and funisitis, is not associated with fetal metabolic acidosis. Intrauterine infection may represent a nonhypoxic form of encephalopathy that produces neurologic morbidity by a mechanism independent of hypoxia-ischemia leading to metabolic acidosis.