Cerebral Oxygen Saturation and Extraction in Preterm Infants With Transient Periventricular Echodensities

Abstract

OBJECTIVE: Our aim was to determine regional cerebral tissue oxygen saturation and fractional tissue oxygen extraction in preterm infants with transient periventricular echodensities. We hypothesized that as a result of reduced cerebral perfusion, regional cerebral tissue oxygen saturation will be lower and fractional tissue oxygen extraction will be higher during the first days after birth. PATIENTS AND METHODS: This was a prospective, observational study of 49 preterm infants (gestational age median: 30.1 weeks [26.0–31.8 weeks]; birth weight median: 1220 g [615–2250 g]). We defined transient periventricular echodensities as echodensities that persisted for >7 days. Regional cerebral tissue oxygen saturation was measured on days 1–5, 8, and 15 after birth. Fractional tissue oxygen extraction was calculated as (transcutaneous arterial oxygen saturation − regional cerebral tissue oxygen saturation)/transcutaneous arterial oxygen saturation. RESULTS: Transient periventricular echodensities were found in 25 of 49 infants. During the first week we found no difference between the 2 groups for cerebral tissue oxygen saturation and fractional tissue oxygen extraction values. On day 15 after birth, cerebral tissue oxygen saturation was lower in preterm infants with transient periventricular echodensities (66%) compared with infants without echodensities (76%) (P = .003). Fractional tissue oxygen extraction in infants with transient periventricular echodensities (0.30) was higher than fractional tissue oxygen extraction in infants without transient periventricular echodensities (0.20) (P < .001). The differences could not be explained by confounding variables. CONCLUSIONS: Persistent transient periventricular echodensities may be associated with increased cerebral oxygen demand after the first week after birth, which is contrary to our hypothesis. Cerebral oxygenation may be involved in the recovery of perinatal white matter damage.