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Query: UMLS:C0917816 (mental retardation)
 15,867 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Some placental considerations related to neurodevelopmental and other disorders. 844 76

> Objective: To describe the perinatal characteristics of neurologically impaired infants with normal intrapartum fetal heart rate (FHR) patterns. Methods: In a registry of 300 neurologically impaired singleton term infants, a retrospective chart review was undertaken to analyze those patients with a normal intrapartum FHR pattern, i.e. reactive FHR pattern with a normal baseline rate throughout labor, and a subsequent finding of central nervous system impairment. Neonates with an abnormal intrapartum FHR pattern or a traumatic birth were excluded. In addition, the four criteria necessary for intrapartum asphyxia were as follows: arterial pH <7.00, Apgar score </=3 for 5 min, neonatal neurologic sequelae, such as seizures, and multiorgan system dysfunction. Infants were then categorized according to the timing of probable fetal injury. Results: Of the 300 infants in the registry, 24 (8%) neonates were identified. Six (25%) of these were considered postdates. Primary antenatal complications included early pregnancy bleeding (3 (13%)), cigarette and/or alcohol use (4 (17%)), and polyhydramnios (2 (8%)). Meconium was found in 12 patients (50%) during labor; of these, two (8%) patients had meconium aspiration syndrome and required extra corporeal membrane oxygenation (ECMO). None of the infants satisfied the four criteria for intrapartum asphyxia. Sixteen (67%) neonates were discharged with their mothers. The remaining eight neonates were admitted to the neonatal intensive care unit, and two (8%) neonatal deaths occurred due to meconium aspiration syndrome and sudden infant death syndrome. The long term neurologic outcome of the 22 survivors ranged from 3 to 14 years and included the following: developmental delay (10 (45%)), seizure disorder (7 (32%)), cerebral palsy (11 (50%)), and mental retardation (4 (17%)). None of these infants appeared to have been injured during labor. The probable timing of neurologic injury appeared to be early pregnancy (13 (54%)) or postnatally (11 (46%)). Conclusions: Infants who are later found to be neurologically impaired can have normal intrapartum FHR patterns during labor. These neurologic injuries seem to occur in early pregnancy or after birth. In the absence of fetal trauma, these findings suggest that a reactive intrapartum FHR pattern is not associated with intrapartum fetal asphyxia.
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PMID:Normal Fetal Heart Rate Pattern in the Brain-damaged Infant: A Failure of Intrapartum Fetal Monitoring? 968 57