Abstract

Premature birth remains a pressing public health issue, with approximately one in every ten pregnancies in the United States ending in preterm delivery. Globally, an estimated 15 million infants are born prematurely each year, and tragically, nearly one million of these newborns die within the first day of life. Despite notable advancements in perinatal and neonatal care, respiratory distress syndrome (RDS) continues to be one of the leading causes of perinatal morbidity and mortality. RDS affects not only premature infants but can also occur in full-term neonates. One particularly severe and often fatal manifestation of RDS is the atelectatic form of pneumopathy—a non-inflammatory lung condition characterized by incomplete lung expansion and alveolar collapse. This form of pneumopathy leads to significant systemic complications, including profound effects on the central nervous system. The current study explores the morphological and morphometric alterations in the brains of 138 neonates who died due to the atelectatic form of pneumopathy. Through detailed histopathological and morphometric analyses, the research focuses on assessing the extent of neuronal degeneration, proliferation of glial cells (gliocytes), vascular irregularities, and expansion of the perivascular spaces. These findings underscore the detrimental impact of severe pulmonary dysfunction on the developing brain. By shedding light on the neuropathological consequences of neonatal RDS, the study offers valuable insights that could inform future therapeutic approaches and preventive strategies in neonatal intensive care.

Key words: Distress syndrome, atelectasis, distelectasis, pneumopathy, hyaline membrane