Cases reported "Fetomaternal Transfusion"

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1/41. A proven case of materno-foetal transfusion determined by cytogenetic and dna analysis.

    We report a case of materno-foetal transfusion in a phenotypically normal male foetus after death in utero at the 35th week of gestation. We have used cytogenetic and polymerase chain reaction (PCR) microsatellite analysis to determine the presence of maternal cells in foetal blood collected by intracardiac puncture. In the intracardiac blood sample, maternal cells were estimated to comprise between 5 and 10% of nucleated foetal blood cells. When there is a suspicion of foetal genetic pathology, it is necessary to be aware that the foetal blood karyotype may be misrepresentative, as the analysed blood cells can indeed be of maternal origin.
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2/41. Acute intrapartum fetoplacental transfusion in monochorionic twin pregnancy.

    BACKGROUND: The risk of antenatal fetofetal transfusion in monochorionic twin pregnancies has been noted, but possible acute intrapartum transfusion has not been studied extensively. Acute fetoplacental transfusion after the birth of the first twin can be disastrous to the second twin, so it deserves description. CASES: We present three cases of acute intrapartum fetoplacental transfusion after successful deliveries of first twins. After the births of their cotwins, the second twins rapidly deteriorated and were born severely hypovolemic and anemic. CONCLUSION: The risk of acute intrapartum transfusion should be kept in mind when planning delivery of monochorionic twins.
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3/41. 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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4/41. Incidental diagnosis and tempestive therapy in a case of neonatal alloimmune thrombocytopenia due to anti-HPA-5b.

    Neonatal alloimmune thrombocytopenia (NAIT) is usually attributable to HPA-1a antibodies. The authors report a case of incidentally diagnosed thrombocytopenia in a small for gestational age infant. A NAIT was suspected and she was successfully treated with intravenous IgG. The direct and indirect platelet suspension immunofluorescence test (PSIFT) in maternal blood suggested alloimmunization to HPA-5b. Empiric treatment with IgG could be useful in case of clear suspect even in absence of confirmed diagnosis.
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5/41. 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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6/41. Fetal-maternal bleed in the second trimester of pregnancy. A report of two cases.

    Two cases of nontraumatic fetal-maternal bleeding occurred in the second trimester. Both presented with mild, lower quadrant tenderness similar to round ligament pain, illustrating the potential for a misdiagnosis.
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7/41. A case of maternal reaction due to fetomaternal transfusion.

    We present here a case of maternal reaction to fetomaternal transfusion complicated by subchorionic hemorrhage. A 40-year-old woman, gravida 2, para 0, was admitted to our hospital at 25 weeks' gestation because of high blood pressure. On the morning of 32 weeks and 2 days' gestation, she developed sudden onset nausea, dyspnea and regular uterine contractions. blood pressure was 80/50 mmHg and pulse was 110 beats/minute. At this time, her WBC, hemoglobin and platelets were decreased significantly. Two hours after onset, the patient's condition improved spontaneously. Increased serum alpha-fetoprotein level (3.0 multiple of median) was observed. She was suggested to be a case of acute fetomaternal transfusion.
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8/41. Idiopathic chronic fetomaternal haemorrhage resulting in hydrops--a case report.

    INTRODUCTION: We report a case of idiopathic chronic fetomaternal haemorrhage (FMH) that developed in the late trimester. CLINICAL PRESENTATION: The patient presented with decreased fetal movement at 38 weeks gestation. Antenatal follow-up was uneventful with normal serial ultrasound performed at 22 and 35 weeks. Prior to delivery, the cardiotocography (CTG) was abnormal with decreased baseline variability and late deceleration. Emergency lower segment caesarean section was performed. Upon delivery, a hydropic neonate with a haemoglobin level of 3.9 g/dL was noted. The Kleihauer-Betke test was positive, confirming FMH. OUTCOME: The neonate later developed intraventricular haemorrhage (IVH) and spastic cerebral palsy on follow-up. DISCUSSION: It is possible for FMH to occur late at the third trimester leading to detrimental effect. The fact that FMH can occur without antecedent risk factors underscores the importance of further research, and a high index of suspicion.
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9/41. Massive fetomaternal hemorrhage and oxytocin contraction test: case report and review.

    We present a case of a nulliparous woman who underwent oxytocin contraction test because of abnormal cardiotocograph. She delivered a severely anemic neonate due to severe fetomaternal hemorrhage. Fetal ultrasonography and Doppler studies of the umbilical arteries may not be helpful, while its worthy to perform flow cytometry for detection of fetal cells in maternal circulation when there is strong clinical suspicion. Management of massive fetomaternal hemorrhage requires immediate delivery by Caesarean section if the gestational age is suitable. Alternatively, for very premature fetuses could be used serial fetal intravascular transfusions if there are the necessary facilities and experienced personnel.
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10/41. Massive antenatal fetomaternal hemorrhage: evidence for long-term survival of fetal red blood cells.

    BACKGROUND: Massive fetomaternal hemorrhage (FMH) can lead to life-threatening anemia. Quantification based on flow cytometry with anti-hemoglobin F (HbF) is applicable in all cases but underestimation of large fetal bleeds has been reported. A large FMH from an ABO-compatible fetus allows an estimation of the life span of fetal red blood cells (RBCs) in the maternal circulation. CASE REPORT: The mother went to the obstetrician twice antepartum owing to symptoms assumed to be preeclampsia; that, however, was not found. She later delivered by cesarean section owing to diminished fetal movements. No fetal weight gain was observed during the last 2 weeks of pregnancy. STUDY DESIGN AND methods: Fetal RBCs were quantified by flow cytometry with anti-HbF, anti-Fy(a), anti-s, and anti-Jk(b) on a regular basis. RESULTS: The infant had anemia at delivery and an FMH was determined to be 314 /- 17 mL ( /- SD) of whole blood. It is assumed that the two antenatal visits were associated with the FMH. Postpartum follow-up showed that fetal RBCs in the maternal circulation were detectable with anti-HbF up to 119 days. Quantification by flow cytometry based on anti-HbF was in agreement with quantification based on anti-Fy(a), anti-s, and anti-Jk(b), although they were less sensitive. CONCLUSION: ABO-compatible fetal RBCs from an FMH had a life span in the maternal circulation close to that of adult RBCs.
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