The relation between cerebral oxygenation and lactate in infants with hypoxic-ischemic encephalopathy treated with hypothermia
Leanne Erkelens-de Vetten, Willemien S. Kalteren, Hendrik J. ter Horst, Arend F. Bos, Elisabeth M.W. Kooi
University of Groningen, University Medical Center Groningen, Beatrix Children’s Hospital, Division of Neonatology, Groningen, The Netherlands
Background and aims
In infants with moderate to severe hypoxic-ischemic encephalopathy (HIE), blood circulation is often compromised. Besides serum lactate, regional cerebral oxygen saturation (rcSO2) might be a marker for hemodynamic status. We aimed to examine the relation between rcSO2 and serum lactate, in relation to treatment with inotropes, in cooled infants with HIE during the first 4 days of life.
This is a retrospective cohort study. We included all cooled infants with cerebral NIRS measurements from 2010-2016. We correlated lactate levels and averaged rcSO2 values measured during periods between 6, 12, 24, 48, 72, and 96 hours after birth, in the entire group, and in subgroups of infants treated with and without inotropes.
Seventy-three infants were included in this study. Median GA was 40 weeks (min-max: 36-42), birth weight 3350 gr (1780-4990), 5’apgar score 3 (0-7), first lactate 17.5 mmol/L (1.9-71). All infants were sedated. Lactate and rcSO2 values are shown in table 1. Twenty-one infants received inotropes. Lactate, but not rcSO2, was persistently higher in the inotrope treated subgroup. Before 72hrs, we found no significant correlation coefficients between rcSO2 and lactate. Only at 72hrs, they correlated (rho=0.33, p=0.011). Within the subgroup of infants that received inotropes no significant correlations were found.
Although a higher lactate and the use of inotropes does not necessarily reflect poorer hemodynamics, these results may suggest that rcSO2 is a poor marker for hemodynamic status in HIE infants, possibly due to the decreased cerebral oxygen demand due to HIE, hypothermia and sedation.