Cases reported "fetal hypoxia"

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1/62. Fetal seizures causing increased heart rate variability during terminal fetal hypoxia.

    Fetal seizures together with both abnormal breathing movements and fluctuations in fetal blood pressure and heart rate resulting in increased fetal heart rate variability have been observed in brain-damaged fetal sheep shortly after an asphyxial insult. We report a clinical example of convulsions and increased heart rate variability during terminal fetal hypoxia. ( info)

2/62. fetal heart rate during a maternal grand mal epileptic seizure.

    Although maternal ingestion of antiepileptic drugs is strongly suspected of causing congenital defects, particularly oral clefts, the effect of epilepsy itself or a combined effect of drug intake and epilepsy have not been excluded as etiological factors. Very little is known about fetal oxygenation during a maternal grand mal epileptic seizure. We describe two cases in which fetal heart rate was recorded during a maternal epileptic seizure during labor. The first fetus became clearly asphyctic as judged from the fetal heart rate recording: immediately after the epileptic seizure there was a 13-minute continuous bradycardia wave with decreased short-term variability. After the bradycardia a phase of tachycardia with decreased short-term and long-term variability occurred. In the other fetus there was only a short period of bradycardia, which was followed by a phase of tachycardia and decreased short-term and long-term variability. Both fetuses were vigorous at birth 43 and 87 minutes, respectively, after the epileptic seizures of their mothers. We conclude that a maternal grand mal epileptic seizure can be ominous to the fetus. It is therefore important that epileptic seizures are controlled by optimal medication throughout pregnancy. ( info)

3/62. Legionnaire's disease complicating pregnancy: a case report with intrauterine fetal demise.

    OBJECTIVE: Legionnaire's disease complicating pregnancy is an unusual event that can seriously compromise both the mother and the fetus. CASE REPORT: We describe one case of such association, with an unfavourable intrauterine fetal outcome, secondary to acute placental insufficiency, related to infection. DISCUSSION: It is important in these high risk pregnancies complicated by acute pneumonia to take into consideration the diagnosis, as early as possible, and the appropriate treatment or the careful monitoring of fetal wellbeing. ( info)

4/62. Expectant management of placenta accreta following stillbirth at term: a case report.

    placenta accreta is a rare complication of pregnancy with high rates of morbidity and mortality. We report a case of expectant management. This strategy may prevent catastrophic postpartum haemorrhage requiring peripartum hysterectomy. ( info)

5/62. Bilateral thalamic lesions in a newborn with intrauterine asphyxia after maternal cardiac arrest--a case report with literature review.

    Hypoxic-ischemic brain damage in preterm and term infants is one major cause of neonatal neurologic morbidity. Depending on the gestational age and the extent of hypoxia, different pathologic findings have been observed. Hypoxic-ischemic lesion of the thalamus is the least common form of cerebral injury. Although long-term outcome with spastic or extrapyramidal cerebral palsy is known, clinical features in the neonatal period are not well described.We report an infant with bilateral hypoxic-ischemic thalamic lesions after maternal cardiac arrest at 28 weeks of gestation. Clinical features and diagnostic results of our patient are compared to information given in the literature to define the clinical entity of hypoxic-ischemic thalamic lesions in neonates better. ( info)

6/62. Extensive hepatic necrosis in a premature infant.

    A fatal case of fulminant hepatic failure that occurred in the neonatal period is reported in a premature infant born after 27 4/7-weeks' gestation. Immediately after birth the infant had severe hypoxia and hypotension resulting from birth asphyxia, hypovolemic shock, and septicemia. At autopsy, histological appearance of the liver showed virtually total hepatocellular necrosis without features of fibrosis. Although the exact cause of hepatocellular injury cannot be fully ascertained, it is assumed that hypoxia and hypotension must have been the predominant factors leading to massive hepatic necrosis. ( info)

7/62. Short-acting beta-adrenergic blockade and the fetus. A case report.

    An infant was born to a woman who received intravenous esmolol for intrapartum supraventricular tachyarrhythmia. Despite the very short acting and cardio-selective beta-1 adrenergic blockade induced by that agent, neonatal effects can occur up to 48 hours after delivery. ( info)

8/62. The clinical diagnosis of asphyxia responsible for brain damage in the human fetus.

    OBJECTIVE: Our objective was to review the clinical findings in infants who died in the perinatal period with brain damage attributable to asphyxia. STUDY DESIGN: The neuropathologic findings in 208 perinatal deaths have been reviewed. Thirty cases (22 fetal, eight newborn) had evidence of white matter or neuronal necrosis due to asphyxia. The clinical course of the pregnancy in 22 cases with brain damage attributable to fetal asphyxia were examined. RESULTS: The diagnosis of asphyxia was confounded by several factors: (1) asphyxia may occur at any time in the last half of pregnancy, (2) 50% of the antepartum asphyxia occurred when the pregnancy had no risk factors, (3) periodic fetal assessment in the complicated preterm pregnancies failed to identify the asphyxial episodes in the remaining cases of antepartum asphyxia, and (4) indicators of fetal asphyxia in the cases of intrapartum fetal asphyxia were obtained after the central nervous system injury had occurred. CONCLUSION: These findings highlight the difficulty in the diagnosis of fetal asphyxia at a stage that could permit intervention to prevent brain damage. ( info)

9/62. Severe newborn encephalopathy unrelated to intrapartum hypoxic events: 3 case reports.

    INTRODUCTION: Newborn encephalopathy is an important clinical problem associated with considerable morbidity and mortality and is pertinent in the assignment of blame in obstetrics litigation. CLINICAL PICTURE: We report 3 babies with severe neonatal encephalopathy. OUTCOME: In all 3 cases, intrapartum hypoxic insult was unlikely to be a significant contributing factor towards the development of neonatal encephalopathy. The aetiology was unclear in the first 2 cases and there was antecedent antenatal cause of feto-maternal haemorrhage in the last case. CONCLUSION: Prevention of neonatal encephalopathy was not possible in these 3 cases. We recommend that umbilical cord blood gases be clearly documented in such cases to reduce unnecessary obstetrics litigation of intrapartum asphyxia as the significant contributing factor to the poor neonatal outcome. Clinicians must have a high index of suspicion of antecedent causes and perform the necessary investigations to elucidate the aetiology of the neonatal encephalopathy. ( info)

10/62. 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. ( info)
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