616 - Lactic acid levels and their evolution as a predictor of brain injury and death in neonates with hypoxic ischemic encephalopathy (HIE): a retrospective chart review

Publication Number: 616.5920

Kathryn L. McCracken, Irish Health Service Executive South Network (UCC), beaconsfield, Cork, Ireland; Aisling Garvey, Cork University Maternity Hospital, Cork, Cork, Ireland; Brian Walsh, Infant Centre, University College Cork, Cork, Cork, Ireland; Deirdre Murray, University College Cork, Cork, Cork, Ireland; Vicki Livingstone, University College Cork, Cork, Cork, Ireland; Geraldine B. Boylan, University College Cork, Cork, Cork, Ireland; Eugene M. Dempsey, University College Cork, Cork, Cork, Ireland

Background: Hypoxic ischemic encephalopathy (HIE) is a serious complication of fetal asphyxia during labour defined as a form of neonatal encephalopathy following ischemia encompassing characteristic lesions on MRI. HIE has an incidence rate of approximately 1.5 per 1000 births. Blood lactate levels can be detected prior to clinical deterioration, suggesting it may be used as a predictor of ischemic outcomes and allow earlier intervention. In this study, “HIE outcomes” refers to severity of HIE development, long term effects on neurodevelopment, brain abnormality on MRI, and other adverse complications including death.

Objective: To investigate if lactate values and the rate of lactate clearance were predictive of brain injury and/or death in term infants with HIE.

Design/Methods: Retrospective chart review conducted at Cork University Maternity Hospital (CUMH) Primary Care Centre.117 term infants admitted to the NICU of Cork University Maternity Hospital, Ireland (2017–2022) for management of HIE were reviewed and 107 infants were included. 10 infants were omitted due to incomplete chart data. Lactate values at birth, 6, 12, 24, 36, 48 and 72 hours after birth were recorded, The primary outcome was the combined outcome of death or MRI abnormality.

Results: Preliminary results demonstrate that infants who had a poor outcome (n=38) had significantly lower Apgar scores at 1min (p=0.012) and more severe Sarnat stages (p < 0.001) compared to those in the good outcome group. Poor outcome was associated with higher lactate at birth compared to the good outcome group (median(IQR): 13.5(9.2-15.9)mmol/L) versus 9.5(6.9-11.5)mmol/L; p-value = 0.003). This is associated with an optimal cut-off point of >13.2mmol/L with an AUC of 0.68. Similarly, at 12 hours of age, the median lactate was 6.4(5.0-9.7)mmol/L in the poor outcome group and 3.3(2.2-4.4)mmol/L in the good outcome (p < 0.001). Optimal cut-off point at 12 hours of age was >5.6mmol/L with an AUC of 0.81. Interestingly, there was no difference in lactate clearance for combined outcome of death or abnormality on MRI but there was a difference in the 48 hour clearance rate for the secondary outcome of mortality. Median lactate clearance at 48h in the infants who survived was significantly higher than those who did not survive (median(IQR): 1.76(1.61-1.84) versus 1.28(0.62-1.58), p-value=0.010).

Conclusion(s): Lactate values are an important biomarker in patients with HIE. Higher lactate levels at birth and 12 hours are associated with worse outcome and death. Slower lactate clearance rates over 48 hours are associated with mortality but not brain injury.

Table 1. Clinical and demographic characteristics of the infants overall and by primary outcome group, n=109


Table 2. Comparison of lactate values between the primary outcome groups
Lactate values were significantly higher at birth, 6, 12, 24 and 36 hours after birth for the poor outcome group when compared to the good outcome group (Table 2).

Table 3. Diagnostic accuracy of lactate values to predict a poor outcome for the primary outcome