Placental Pathology of Neonates Diagnosed with Encephalopathy Soon After Birth: A Retrospective Analytic Study

Abstract

Background: Placental pathology has been linked to neonatal encephalopathy (NE). Despite the high prevalence of NE in low- and middle-income countries (LMICs), there are limited published studies exploring this association from LMICs. Objective: To describe and analyze the histopathology of placentas from neonates diagnosed with encephalopathy shortly after birth. Methods: A retrospective analytic study was conducted on neonates diagnosed with encephalopathy at Klerksdorp/Tshepong (KT) hospital complex, South Africa from 1 December 2019 to 31 October 2022. Placentas from term and near-term neonates (birth weight ≥2000 grams) diagnosed with encephalopathy soon after birth were sent for histopathological examination. Neonates were grouped into those with encephalopathy with or without intrapartum hypoxia (IH) (base deficit ≥12 mmol/l). The severity of NE was assessed as mild, moderate and severe, according to Sarnat staging. The types and extent of placental lesions were compared between those with mild and moderate-to-severe encephalopathy and between cases with or without IH. Results: Out of 16,336 live births, 271 neonates were diagnosed with NE, and of these, 193 (71.2%) had NE with IH. Placental histopathology results were available for 239 neonates (88.2%). The median placental weight was 428 grams, with 46.6% of placentas weighing <10th percentile. Cord abnormalities were observed in 27.2% of placentas. Nearly all placentas (98.2%) exhibited at least one histopathological lesion. The most common microscopic placental lesions identified were maternal vascular malperfusion (MVM) (55.6%), fetal vascular malperfusion (55.1%), chorioamnionitis (41.2%), and villitis of unknown etiology (28.9%). There was a significant association between NE with IH and the presence of MVM, with an adjusted odds ratio of 3.24 (95% CI 1.19–8.79). No significant association was found between the presence or number of different placental lesions and the severity of NE. Factors associated with severity of any NE (with and without IH) included an Apgar score of less than 7 at 10 minutes (p<0.001) and pH <7.00 (p<0.001). Conclusion: A high proportion of neonates with encephalopathy showed evidence of intrapartum hypoxia. Almost all neonates with encephalopathy displayed at least one microscopic placental lesion. Furthermore, most placentas from neonates with NE exhibited abnormalities, indicating that placental pathology may play a significant role in the development of NE. A strong association was found between the presence of MVM and NE with IH.