Cases reported "Fetal Hypoxia"

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1/16. 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.
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2/16. 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.
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3/16. 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.
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4/16. Four cases of the ex utero intrapartum treatment (EXIT) procedure: anesthetic implications.

    The ex utero intrapartum treatment (EXIT) procedure is a method of maintaining utero-placental circulation during cesarean section to gain time to secure a potentially obstructed fetal airway. Four cases of the EXIT procedure are described with special reference to the maternal anesthetic technique. Deep volatile anesthesia (approximately 2 MAC) with isoflurane or sevoflurane for a prolonged period of time, in three cases in combination with an intravenous nitroglycerin infusion, was used to ensure a fully relaxed uterus during the procedure. All mothers were maintained hemodynamically stable with preserved utero-placentary perfusion. It was possible to intubate the tracheas of two fetuses, whereas in the other two tracheostomies had to be performed. Fetal gas exchange was not negatively affected during the EXIT procedure as evidenced by normal blood gas values in the umbilical artery at the time of delivery. After reducing the concentration of volatile anesthetic, delivery of the neonate and administration of oxytocin, uterine contractility was promptly re-established and there were no signs of uterine atony in the postoperative period. All four neonates survived the procedure without complications.
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5/16. Endothelial, inducible and neuronal nitric oxide synthase in congenital pulmonary lymphangiectasis.

    Abnormal growth and development of lymphatic pulmonary structures leads to severe hypoxia in congenital pulmonary lymphangiectasis (CPL). This case study aims to determine the cellular source and topographical distribution of the nitric oxide synthases in CPL. It studies the post mortem tissue of a term newborn with the clinical course and histological findings of CPL and three controls without pulmonary pathology. It was found that endothelial cells of pulmonary arteries and lymphatic structures stained significantly more for endothelial nitric oxide synthase protein in the CPL patient compared to the controls. The authors conclude that synthesis of endothelial nitric oxide synthase is upregulated in vascular and lymphatic endothelial cells in congenital pulmonary lymphangiectasis.
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6/16. Sinusoidal fetal heart rate pattern due to massive feto-maternal transfusion.

    A 30-year-old woman presented with mild abdominal discomfort and decreased fetal movements in the 34th week of her third pregnancy. fetal monitoring revealed a sinusoidal heart rate pattern, and abdominal delivery was promptly performed, with the newborn having a hematocrit of 7% due to massive fetomaternal transfusion. Fetal resuscitation was followed by a favorable outcome. The sinusoidal heart rate is discussed, with emphasis on the need for proper and prompt recognition of its significance.
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7/16. 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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8/16. Temporal relationships of neuropathologic conditions caused by perinatal asphyxia.

    The neuropathologic conditions in 120 perinatal deaths attributed to fetal or newborn asphyxia were examined. central nervous system necrosis was present in 16 of these deaths. The approximate time of asphyxial insult was established by determining the duration of the process, based on the findings of neuronal necrosis, macrophage response, or an astrocyte response, in conjunction with clinical data. The time of the asphyxial insult for the 16 perinatal deaths was as follows: antepartum fetal asphyxia, two cases; antepartum-intrapartum fetal asphyxia, five cases; intrapartum fetal asphyxia, four cases; and neonatal asphyxia, five cases. These observations indicate that an asphyxial insult may occur in the antepartum period, in the prodromal period of preterm labor, in the intrapartum period, and in the neonatal period. Five to ten percent of the asphyxial insults in each reproductive time period were initially sublethal, allowing necrosis of the brain of the fetus or newborn to develop.
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9/16. Critical tricuspid insufficiency due to papillary muscle rupture. A result of prenatal hypoxic insult.

    Fatal tricuspid insufficiency secondary to papillary muscle rupture due to prenatal hypoxic insult occurred in a full-term newborn. The diagnosis of flail tricuspid valve should be considered when fetal distress is encountered in a newborn with persistent hypoxemia. prenatal diagnosis of this condition combined with prompt delivery, prostaglandin E1 therapy, and possible surgical repair of the tricuspid valve may improve chances of survival.
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10/16. hydranencephaly after maternal butane-gas intoxication during pregnancy.

    A newborn infant who suffered intra-uterine anoxia is described, whose mother inhaled butane gas accidentally during the sixth month of pregnancy. The infant was born at 39 weeks. ultrasonography and neuroradiological studies (CT scan and angiography) showed an almost complete absence of both cerebral hemispheres. The thalamus, brainstem and cerebellum were preserved. These findings were compatible with hydranencephaly. The authors believe that the malformation was due to intra-uterine anoxia occurring during fetal brain-development.
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