478 - Neonates treated with therapeutic hypothermia: is the absence of cord blood acidosis a marker for encephalopathy due to causes other than hypoxic-ischemic encephalopathy?

Poster Number: 478
Publication Number: 478.343

Marie-Coralie Cornet, UCSF Benioff Children's Hospital San Francisco, San Francisco, CA, United States; Michael Kuzniewicz, Kaiser Permanante, Los Gatos, CA, United States; Heather Forquer, Kaiser Permanente - Division of Research, Oakland, CA, United States; Emily Hamilton, McGill University, Montréal, PQ, Canada; Thomas B. Newman, UCSF, San Carlos, CA, United States; Aaron Scheffler, University of California, San Francisco, School of Medicine, San Francisco, CA, United States; Amy P. Murtha, UCSF Benioff Children's Hospital San Francisco, San Francisco, CA, United States; Yvonne W. Wu, University of California, San Francisco, School of Medicine, San Francisco, CA, United States

Background: Neonatal encephalopathy (NE) is a heterogeneous condition. Therapeutic hypothermia (TH) improves outcomes in neonates with NE due to presumed hypoxic-ischemic encephalopathy (HIE). Acidosis is a sign of prolonged perinatal hypoxemia. In both clinical and research settings, the worst pH or base deficit from either cord or infant blood gas analysis within the first hour of age is used to determine the presence of acidosis and perinatal HIE. Because the cord and infant blood gases are typically combined in this way, it is unknown how often infants undergoing TH lack cord blood acidosis, and whether these infants differ from other infants undergoing TH.

Objective: Among infants who received TH, to compare the clinical characteristics of those with and without cord blood acidosis.

Design/Methods: Among all 306,261 infants born within Kaiser Permanente Northern California at ≥ 35weeks gestation between 2011 to 2019, we identified those who received TH for presumed HIE. We abstracted maternal demographics, prenatal and perinatal conditions, cord blood gas, delivery complications, intubation, laboratory results and brain MRI findings from electronic records. Cord blood acidosis was defined as pH < 7.00 or base deficit ≥12. For all infants undergoing TH, we reviewed medical records to confirm the presence of encephalopathy and seizures (electrographic or focal clonic).

Results: Of 430 infants who received TH for presumed HIE (population incidence 1.4 per 1,000), 391 (92%) had a cord gas analysis. Cord acidosis was present in 197 of 391 (50%) infants with available cord gas. Infants with no cord acidosis were more likely to be exposed to maternal chorioamnionitis (37% vs. 19%, P < 0.001) and epidural analgesia (69% vs. 51%, P < 0.001) than infants with cord acidosis. Infants without cord acidosis were more often intubated, but the rate moderate/severe encephalopathy, seizure frequency, and length of stay was similar in the two groups (Table). Infants with no cord acidosis had less renal and hepatic injury than those with cord acidosis. Perinatal arterial ischemic stroke was also more common in those without cord acidosis (22% vs 8%; p=0.04).Conclusion(s): Half of infants undergoing TH have no evidence of cord acidosis. These infants may have a distinct underlying pathophysiology, including a higher rate of stroke on brain MRI. Further studies are needed to assess the efficacy of neuroprotective treatments for NE based on underlying pathophysiology.
Clinical characteristics of neonates with and without cord acidosis (pH < 7.00 or base deficit ≥12) among neonates treated with TH for suspected HIEData are presented as median (IQR) for continuous measures, and % for categorical measures.