Cases reported "Fetal Hypoxia"

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1/8. Posterior uterine rupture in a woman with a previous Cesarean delivery.

    A 33-year-old primipara with a previous low transverse Cesarean delivery underwent labor induction at 41 weeks' gestation with a 10-mg dinoprostone vaginal insert. Eleven hours later, with the cervix fully dilated, an emergency Cesarean delivery was performed because of repetitive variable decelerations followed by fetal bradycardia. A posterior uterine wall rupture extending from the fundus to the vagina was repaired in layers. The neonate had an apgar score of 2 and 4 and expired on the 7th day of life.
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2/8. Use of 31P magnetic resonance spectroscopy to characterize evolving brain damage after perinatal asphyxia.

    We investigated postasphyxial brain damage with 31P magnetic resonance spectroscopy (MRS) and correlated it with neurologic assessment and standard laboratory evaluation during the first 10 months of life in 1 infant, baby G. We compared these observations to 31P MRS data from 7 healthy term newborns, 1 normal infant examined serially over the first 8.5 months of life, and 5 other term infants following perinatal asphyxia. MRS noninvasively provides biochemical correlates of the evolution of brain damage following perinatal asphyxia and suggests that pH derived from the inorganic phosphate peak may serve as a marker for brain injury.
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3/8. Severe fetal brain injury without evident intrapartum asphyxia or trauma.

    Two appropriate-for-dates term infants were born after uncomplicated labors and atraumatic deliveries. They were depressed at birth, developed seizures on the first day of life, and followed clinical courses compatible with hypoxic-ischemic encephalopathy. However, the umbilical cord vessel pH and blood gases were normal. The children are now severely retarded and have cerebral palsy. These cases prove that the events of labor and delivery may not be responsible for all cases of brain damage in surviving children.
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4/8. Radiological colpocephaly: a congenital malformation or the result of intrauterine and perinatal brain damage.

    The term colpocephaly, meaning disproportional enlargement of the occipital horns of the lateral ventricles, was considered in the past to be a distinct congenital malformation acquired in early intrauterine life. During the last few years several cases were reported in whom a variety of intrauterine and perinatal causes could be associated with this radiological picture. We report on 9 children with radiological colpocephaly in whom intrauterine and/or perinatal injury to the developing brain seemed to be the cause of colpocephaly. It is evident from our observations that "radiological colpocephaly" is a non-specific finding caused frequently by CNS damage acquired during intrauterine and perinatal life.
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5/8. meconium peritonitis in stillbirths.

    meconium peritonitis is a sterile, chemical peritonitis resulting from perforation of the bowel in perinatal life. In stillbirths meconium peritonitis is extremely rare. We report the autopsy findings in three fetuses ranging from 21-39 weeks gestation in which meconium peritonitis was identified. Maternal history in two cases was suggestive of possible fetal hypoxia. No family history of cystic fibrosis was discerned. One fetus was hydropic and abdominal calcifications were noted on postmortem radiograph. Gross evidence of meconium in the peritoneal cavity, visceral adhesions, and serosal nodules were noted in two fetuses. Nodules of calcified meconium seen by microscopy were the only clues to diagnosis in the third fetus. The discovery of meconium peritonitis at autopsy may be the only residual evidence of antecedent bowel perforation. We suggest that intrauterine hypoxia may play a role in the development of meconium peritonitis in some cases.
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6/8. Postischemic hypervascularity of infancy: a stage in the evolution of ischemic brain damage with characteristic CT scan.

    One to 2 weeks after severe brain ischemia, four infants developed an unusual vascular lesion with a characteristic appearance on computed tomography that has not been reported previously. Restricted areas (most frequently the basal ganglia and thalamus) displayed increased attenuation, which enhanced further upon infusion of contrast medium. autopsy of one infant revealed that the CT abnormality corresponded to an extremely dense neovascular network which had almost completely replaced the parenchyma in that region. We postulate that this pathological change is a stage in the organization of ischemic brain damage reflecting the infant's vascular plasticity. Thus, hypoxia induces marked capillary proliferation in regions of normally high metabolism and capillary density. The CT pattern may prove useful in predicting the location and extent of sequelae to perinatal asphyxia.
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7/8. Quality of survival of infants with critical fetal reserve detected by antenatal cardiotocography.

    During the 8-year period 1973 to 1980, antenatal cardiotocographic monitoring was performed on 3,006 high-risk pregnancies selected from a total obstetric population of 37,856 patients. A critical fetal reserve was detected in 72 patients (2.3%) whose pregnancies resulted in 20 perinatal deaths and 52 infants who survived the neonatal period; 45 of these infants have been assessed at ages ranging from 2 months to 8 years, 9 months. growth was below the tenth percentile in 25.0% for weight, 23.3% for length, and 22.5% for head circumference at the review examination. Neurological abnormalities were detected in 12 infants but the abnormality was major in only four, including one who has familial interstitial polyneuropathy. The quality of survival of infants delivered of pregnancies complicated by critical fetal reserve is satisfactory; 93.2% had no neurological impairment likely to interfere with quality of life and indeed 13.5% had superior intelligence. Cardiotocographic evidence of critical fetal reserve does not signify that the fetus is doomed; delivery by cesarean section is indicated if the fetus is viable and has no ultrasonic evidence of untreatable major malformation.
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8/8. Congenital diencephalic and brain stem damage: neuropathologic study of three cases.

    Neuropathologic findings and clinical features of three patients with congenital brain stem damage are reported. All of the infants were premature (32 - 36 weeks' gestation) and experienced respiratory difficulty in the immediate postnatal period. One infant was moribund at deliver, dying 3 h after birth. In two infants who survived for 12 and 16 days, detailed neurologic examinations demonstrated multiple cranial nerve palsies with absence of facial expression. Autopsies revealed similar changes in the brains of all three infants: bilateral symmetrical lesions were found predominantly in the thalamus and brain stem. Histological features common to all three cases included prominent basophilic mineralized neurons, neuronal loss astrocytosis and axonal spheroids. necrosis was observed in two cases. These changes are most compatible with one or more episodes of total asphyxia during fetal life. This study supports the hypothesis that, in some cases, Mobius' syndrome is the result of intrauterine asphyxia.
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