Objective: Hypoxic ischaemia and inflammatory damage have both been implied in the pathogenesis of white matter injury. These two mechanisms may not be mutually exclusive. Our hypothesis was that a fetal inflammatory response (FIR) might reduce the electrocortical activity in preterm infants.
Methods: FIR was defined as inflammation of the fetal vessels in the chorionic plate or the umbilical cord. Forty-eight infants with gestational age less than 33 weeks were included: 17 with FIR and 31 without inflammation. Amplitude-integrated EEG (aEEG) was recorded on the first day of life. The median aEEG recording time was 1.8 h. Minimum amplitude (minA) was measured. Cerebral tissue oxygenation saturation was measured with near-infrared spectroscopy (c-TOI, Hamamatsu NIRO 300).
Results: FIR infants had a significantly lower gestational age (27.1 ± 2.6 vs 29.6 ± 2.6 weeks; p = 0.03) and body weight (1032 ± 432 vs 1359 ± 509 g, p = 0.03). There were no differences in surfactant therapy, mechanical ventilation, inotropics, or clinical parameters (blood pressure, pCO2, pH, haemoglobin, satO2). In five infants the background activity was continuous, discontinuous in 37, and burst suppression in six. Only one with burst suppression had FIR. The median minA was 3 μV (1; 7.5). MinA was normally distributed after logarithmic transformation. There was a positive linear correlation between minA and c-TOI (r = 0.4, p = 0.005) and gestational age (r = 0.4, p = 0.01). Surprisingly, when controlled for c-TOI (p = 0.02) and gestational age, FIR tended to be associated with highest minA (3.6 μV; 95% CI 3.0 to 4.4) versus 3.0 μV; 95% CI 2.6 to 3.5; p = 0.13).
Conclusion: Apparently, FIR does not suppress electrical activity, but reduced cerebral oxygenation is associated with low minA.
Funding: This work was supported by the Ludvig og Sara Elsass Foundation.