Background: Persistent pulmonary hypertension of the newborn (PPHN) affects systemic oxygenation and may worsen brain injury in infants with neonatal encephalopathy (NE). Evidence suggests that higher cerebral regional oxygenation (crSO2) indicates derangement in cerebral autoregulation, energy metabolism, and blood flow following NE. Our aim was to evaluate the impact of PPHN on crSO2, in infants with NE treated with therapeutic hypothermia (TH).
Methods: We retrospectively evaluated infants with NE and PPHN vs without PPHN, between 2018-2022. Linear regression analysis was performed to evaluate the impact of PPHN on crSO2 and total MRI score, adjusted for perinatal factors.
Results: 164 infants were analyzed, including 19(12%) with PPHN and 145(88%) without. PPHN-infants had significantly higher crSO2 during rewarming and post-rewarming compared to non-PPHN infants (87 ± 6 vs 80 ± 6, p = 0.001; 87 ± 5 vs 80 ± 7, p = 0.008, respectively), and a significantly higher total MRI score [7(2-19) vs 1(0-3), p < 0.001]. PPHN was significantly associated with higher crSO2 during rewarming (b = 6.21, 95% CI 2.37-10.04, p = 0.002) and post-rewarming (b = 8.60, 95% CI 2.28-14.91, p = 0.009), and total MRI score (b = 7.42, 95% CI 4.88-9.95, p < 0.001).
Conclusions: PPHN was associated with higher crSO2 during and after rewarming, and worse brain MRI score, indicating a significant impact of PPHN on brain injury in infants with NE undergoing TH.
Impact: Cerebral oxygenation was significantly higher in infants with neonatal encephalopathy (NE) and persistent pulmonary hypertension (PPHN) compared to infants without PPHN, during the rewarming and post-rewarming periods of therapeutic hypothermia (TH). PPHN is associated with brain injury in infants with NE undergoing TH. In infants with NE and PPHN, monitoring of cerebral oxygenation would help detect infants at higher risk of adverse outcomes.