Select Abstracts From the 19th International Conference on Neonatal and Childhood Pulmonary Vascular Disease

https://doi.org/10.1002/pul2.70318 

1 Placental Abnormalities of Malperfusion, Inflammation, and Meconium are Associated With Persistent Pulmonary Hypertension of the Newborn

Tsoi SM, Gasper C, Maltepe E, Chidboy M, Ozarslan N, Blavelt CA, Buarpung S, Cheung S, Steurer M, Keller RL, Fineman JR, Gaw SL.

University of California, San Francisco, Department of Pediatrics, Pathology and Laboratory Medicine, and Obstetrics, Gynecology & Reproductive Sciences. San Francisco, California

Background/Hypothesis: Persistent pulmonary hypertension of the newborn (PPHN) is a cause of neonatal hypoxic respiratory failure due to the failed transition of the pulmonary vasculature after birth. Mechanisms of disease are unknown, but we hypothesize they are directly related to insults in the intrauterine environment. The objective of this study was to elucidate whether placental histopathology representative of intrauterine insults during pulmonary vascular development are associated with a diagnosis of persistent pulmonary hypertension of the newborn (PPHN), and compare placental histopathologic lesions across PPHN etiologies.

Materials and Methods: We conducted a case-control study of mother–infant dyads ≥ 35 weeks gestation who delivered at a tertiary care center between 2020–2025. Cases were infants diagnosed with PPHN and treated with inhaled nitric oxide; unaffected controls were infants without congenital anomalies. Placentas underwent blinded histopathologic review using standardized criteria. Multivariate logistic regression modeling was used to control for confounding maternal and infant factors.

Results: 106 placentas were analyzed (53 PPHN, 53 controls). Placental lesions were significantly more common in PPHN placentas, including fetal vascular malperfusion (30.2% vs 9.4%, p < 0.01), placental inflammation (66.0% vs 37.7%, p < 0.01), chronic presence of meconium (43.4% vs 15.2%, p < 0.01), and chorangiosis (7.6% vs 0%, p = 0.04). In adjusted analyses compared to controls, among 41 placentas with fetal development etiologies (e.g. congenital anomalies) of PPHN, fetal vascular malperfusion, placental inflammation and fetal inflammatory response were more common. Among 12 placentas with typical causes of PPHN (e.g. meconium aspiration syndrome), placental inflammation, maternal and fetal inflammatory responses, and meconium were more common.

Conclusions: PPHN placentas demonstrate lesions of malperfusion, inflammation, and chronic meconium, suggesting a complex interplay between intrauterine hypoxia and inflammation as a potential mechanism for the abnormal pulmonary vascular development and function seen in PPHN.

Read the full meeting abstract collection