Cases reported "Fetomaternal Transfusion"

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1/69. Massive fetomaternal hemorrhage: how long should children with good evolution be controlled? A case report.

    We report on a term infant with a severe fetomaternal hemorrhage that caused a serious anemia that was surmounted after several transfusions. After the initial complications, such as persistent pulmonary circulation, severe anemia and thrombocytopenia, the outcome was good. We discuss the importance of a long-term follow-up of affected children, as well as their mothers. No clear parameters for a real prognosis are available. A follow-up is needed in order to detect possible complications in neurological development.
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2/69. Fetal complication after external cephalic version at term: case report and literature review.

    We report a case of fetal distress following external cephalic version at term, which resulted in delivery by emergency cesarean section of an anemic, acidemic infant. The characteristics of the fetal heart rate tracing, the clinical findings, and a positive Kleihauer-Betke test after delivery suggest that fetomaternal hemorrhage or placental abruption was the most likely cause of the fetal distress. We review the incidence of the reported fetal complications after external version.
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3/69. anemia due to massive chronic foetomaternal hemorrhage.

    We report a case of massive chronic foetomaternal hemorrhage. The labor course was uncomplicated. The newborn presented with pallor. tachypnea, and moderate hepatosplenomegaly. The initial hemoglobin was 6.5 g/dl. The Kleihauer-Betke stain on a maternal blood sample was 12%, which is equivalent to 540 ml of fetal blood in the maternal circulation. A clot in the umbilical vein was demonstrated sonographically. The possible association of foetomaternal hemorrhage with umbilical vein thrombosis is discussed.
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4/69. prenatal diagnosis of acute massive fetomaternal hemorrhage.

    We present here 2 cases of acute and 2 cases of chronic massive fetomaternal hemorrhage. A sinusoidal fetal heart rate pattern may indicate chronic fetomaternal hemorrhage, but, when increased variability is observed in fetal monitoring, maternal hemoglobin F should be measured to exclude acute fetomaternal hemorrhage.
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5/69. Massive feto-maternal hemorrhage as a cause of perinatal mortality and morbidity.

    11 cases of massive feto-maternal hemorrhage (FMH) detected at the Leuven blood transfusion Center are described. Based on these case reports, a review is given of the various theoretical and practical problems related to this complication, e.g. the relative frequency of perinatal mortality and morbidity due to massive FMH, the causes and pathogenesis, the symptoms and diagnosis, the clinical varieties, and the pathophysiology as seen in the fetus and newborn. Finally, the indications for looking for large FMHs are described, and the therapeutic implications when this complication is discovered.
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6/69. The importance of simple microscopy.

    A case of severe neonatal anaemia, the cause of which was found to be severe fetomaternal haemorrhage is presented. The diagnosis was confirmed by simple microscopic examination of the maternal blood using the technique of acid elution, the Kleihauer-Betke test. In the differential diagnosis of anaemia of a newborn, the diagnosis of fetomaternal haemorrhage must be considered and the simple Kleihauer-Betke test should be performed on the maternal blood as soon as possible.
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7/69. Massive fetomaternal transplacental hemorrhage as a perinatology problem, role of ABO fetomaternal compatibility--case studies.

    BACKGROUND: Massive fetomaternal transplacental hemorrhage is not simply a problem of possible alloimunization in Rh incompatibility but also endangers the fetus (newborn) by massive anemization. Bleeding from placental vessels can occur after small trauma to the gravid uterus with mild or no clinical signs (bleeding or spotting, pain, hypertonus). The rupture of anchoring villi related to early uterine contractions is also possible. In the case of slow blood loss, the fetus reacts by adequate or inadequate compensatory reactions (hydrops fetus). Rapid and massive blood loss is followed by perinatal hypoxic damage and finally death. Our goal was to map out the diagnostic and therapeutic possibilities in regard to specific neonatal care. CASE REPORT: We evaluated four cases of fetomaternal transfusion during a 2-year period with special regard to postpartum adaptation of the newborn and the perinatal outcome. The incidence of adverse outcomes following massive fetomaternal transplacental hemorrhage was 50% (2 of 4). There was one perinatal death and one infant was affected by spastic quadriplegia. CONCLUSIONS: For diagnosis, it is possible to use cardiotocography (decreased variability, sinusoid pattern), ultrasound (biophysical profile) and special hematological tests for quantitative determination of fetal erythrocytes in the maternal blood. For the treatment of such cases one should consider premature termination of pregnancy or intraumbilical transfusion.
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8/69. Detection of massive transplacental haemorrhage by flow cytometry.

    flow cytometry has been shown to be a more accurate and sensitive method than the Kleihauer-Betke test for the measurement of feto-maternal haemorrhage in Rh(D) incompatibility. This report describes the successful use of flow cytometry to detect and monitor the management of a massive transplacental haemorrhage (105 ml) of fetal Rh(D) positive cells in a Rh(D) negative woman. The report highlights the accuracy and reproducibility of the test and the stability of a blood sample when transferred 596 kilometres to a central testing facility.
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9/69. Doppler sonography for predicting fetal anemia caused by massive fetomaternal hemorrhage.

    Fetomaternal hemorrhage (FMH) can cause severe anemia in the fetus. Untreated, this may cause hydrops or even fetal death. However, correct diagnosis of FMH followed by blood transfusion can prevent these life-threatening consequences. We describe two cases in which fetal anemia was suspected because of maternal reporting of decreased or absent fetal movements, the detection of a sinusoidal heart rate pattern and increased blood flow velocities of the middle cerebral artery and umbilical vein. Together with the Betke-Kleihauer test showing fetal cells in the maternal circulation, this led to the correct diagnosis of severe fetal anemia caused by FMH. A cesarean section was performed within a few hours. Both neonates were severely anemic and received immediate blood transfusions. They are currently alive and well.
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10/69. autopsy findings in a series of five cases of fetomaternal haemorrhages.

    AIMS: Fetal blood cells enter the maternal circulation in up to 95% of pregnancies, but usually in minute volumes. Haemodynamically significant fetomaternal haemorrhage (FMH) is a much rarer event reported in approximately 1 in 2800 pregnancies. Most of the literature on this phenomenon emphasises the clinical aspects, and there is no comprehensive description of the autopsy findings. We present a series of five fatal FMH. The aim of this series is to highlight some of the autopsy findings that may prompt consideration of a diagnosis of FMH and lead to appropriate confirmatory testing and counselling of the affected couple. methods: The five cases were referred to the Children's Hospital at Westmead for full autopsy. A Kleihauer-Betke test was performed on the mother's blood within one week of delivery in each case. RESULTS: The infants ranged in age from 27 to 40 weeks gestation (mean 36.6 weeks) with a mean birth weight of 2793 g. The estimated volumes of fetal blood lost ranged from 443 to 104 mL (mean loss 243 mL). The estimated percentage of fetal blood volume loss was an average of 107% (i.e., greater than the entire blood volume of the fetus). No other causes of hydrops were identified. pallor was often noted, and in most cases the autopsies were markedly bloodless with large vessels collapsed. Where the brain:liver ratio could be applied, two fetuses showed a mild increase in ratio, while one infant showed moderate growth restriction with a ratio of 6.2:1 (normal ratio 2.8:1 on non-macerated fetuses over 28 weeks gestation). Placental abnormalities included thrombosis of the umbilical vein and intervillous 'haematomas' in two cases. The most striking microscopic feature was the presence of intravascular nucleated RBC within virtually all organs. Placental intervillous (i.e., within the maternal vascular compartment) nucleated red blood cells were also seen in all cases. CONCLUSIONS: The autopsy findings of FMH can be subtle and easily overlooked unless a high index of suspicion is maintained. The most reliable autopsy features are pallor, subcutaneous oedema or serous effusions, and intravascular nucleated red blood cells (RBC) in organs or more specifically in the placental intervillous space. In all cases of unexplained fetal death a Kleihauer-Betke test should be performed.
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