This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Altshuler, G. Search for Related Content PubMed PubMed Citation Articles by Altshuler, G. Social Bookmarking                         What's this?

Some Placental Considerations Related to Neurodevelopmental and Other Disorders

Department of Pathology, The University of Oklahoma Health Sciences Center, The Children's Hospital of Oklahoma, Oklahoma Memorial Hospital, Oklahoma City, OK

Many newborns who appear normal at birth later manifest substantial neurologic and other disease. Pathologists are able to explain some of that sad enigma. Placental pathology frequently reveals the pathogenesis of cerebral palsy, mental retardation, and other neurodevelopmental disorders. This requires recognition of gross placental abnormalities and insightful light microscopic examination. Chorioamnionitis is now proven to be the major cause of premature onset of labor and prematurity. There is important need for investigation of pathogenetic processes associated with ascending intrauterine infection. Major complications therein include bacterially mediated fetal hypoperfusion resulting from placental and umbilical vasocontraction. Placentas of 10% of newborns have villitis of unknown etiology. The importance of villitis is incompletely known. The fetus may discharge meconium on more than one occasion, particularly so when the fetus is postmature. Clinicians may not recognize that fetal discharge has occurred if the event occurred 4 days or more prior to delivery. Intra-amniotic meconium associated with oligohydramnios probably causes placental and umbilical vasocontraction. Meconium probably thus contributes to the pathogenesis of pulmonary vasoconstriction, persistent fetal circulation, necrotizing enterocolitis, and damage of the fetal brain, liver, and kidneys. Fetal hypoxia and asphyxia may be acutely or chronically acquired. Major placental lesions associated with neonatal asphyxia include chronic ischemic change, nucleated red blood cells, intravillous hemorrhages, intimal vascular fibrin cushions, meconium staining, and intervillous fibrin. (J Child Neurol 1993;8:78-94).

Journal of Child Neurology, Vol. 8, No. 1, 78-94 (1993)
DOI: 10.1177/088307389300800111


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				J C Becher, J E Bell, J W Keeling, N McIntosh, and B Wyatt The Scottish perinatal neuropathology study: clinicopathological correlation in early neonatal deaths Arch. Dis. Child. Fetal Neonatal Ed., September 1, 2004; 89(5): F399 - F407. [Abstract] [Full Text] [PDF]

				B Hargitai, T Marton, and P M Cox BEST PRACTICE NO 178: Examination of the human placenta J. Clin. Pathol., August 1, 2004; 57(8): 785 - 792. [Abstract] [Full Text] [PDF]

				M C Hermansen Nucleated red blood cells in the fetus and newborn Arch. Dis. Child. Fetal Neonatal Ed., May 1, 2001; 84(3): 211F - 215. [Full Text]

				E. Petridou, M. Koussouri, N. Toupadaki, A. Papavassiliou, S. Youroukos, E. Katsarou, and D. Trichopoulos Risk Factors for Cerebral Palsy: A Case-Control Study in Greece Scand J Public Health, March 1, 1996; 24(1): 14 - 26. [Abstract] [PDF]