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Published on: November 20, 2015
Placental Evidence of Intrauterine Stress: Mechanisms, Timing, and Links to Perinatal Brain Injury
Charlotte F Kim1, Chrystalle Katte Carreon2
1Department of Pathology and Immunology, Baylor College of Medicine, Texas Children's Hospital, 6621 Fannin St., MC-1195, Houston, TX 77030, USA.
Placental examination is frequently performed following adverse fetal or neonatal neurologic outcomes to elucidate the cause or timing of injury. In practice, however, the placenta more often serves as a biologic archive of fetal stress, adaptation, and reduced physiologic reserve rather than a definitive record of injury. This review synthesizes current research linking placental pathology to perinatal brain injury, with emphasis on biological mechanisms and temporal interpretation. We examine how placental findings inform assessments of intrauterine stress, impaired placental or fetal perfusion, inflammation, and diminished placental reserve. Surrogate markers of fetal stress, including nucleated red blood cells and intrauterine meconium passage, provide contextual evidence regarding the duration and severity of intrauterine compromise but do not establish causality. Finally, we review acute circulatory disruption, chronic or intermittent impairment of fetal blood flow, umbilical cord-related pathology, and immune-mediated placental disorders that increase vulnerability to neurologic injury.
Placental examination is frequently performed following adverse fetal or neonatal neurologic outcomes to elucidate the cause or timing of injury. In practice, however, the placenta more often serves as a biologic archive of fetal stress, adaptation, and reduced physiologic reserve rather than a definitive record of injury. This review synthesizes current research linking placental pathology to perinatal brain injury, with emphasis on biological mechanisms and temporal interpretation. We examine how placental findings inform assessments of intrauterine stress, impaired placental or fetal perfusion, inflammation, and diminished placental reserve. Surrogate markers of fetal stress, including nucleated red blood cells and intrauterine meconium passage, provide contextual evidence regarding the duration and severity of intrauterine compromise but do not establish causality. Finally, we review acute circulatory disruption, chronic or intermittent impairment of fetal blood flow, umbilical cord-related pathology, and immune-mediated placental disorders that increase vulnerability to neurologic injury.

