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1/60. Prognostic factors and management in pregnancies complicated with severe kell alloimmunization: experiences of the last 13 years.

    Because of the recent referral of an anti-Kell sensitized pregnant woman, whose fetus became severely anemic despite intensive antepartum surveillance, the prevalence and characteristics of fetal Kell isoimmunization were reviewed and analyzed. Cases with Kell and RhD alloimmunization requiring intrauterine intravascular transfusions (IUT) at the Mount Sinai Medical Center during the 13-year period ending March 1998 were compared. Thirty-six fetuses with RhD and 5 with Kell isoimmunization required IUTs. Lower fetal and neonatal hematocrit levels were observed in the RhD group. A significantly higher incidence of polyhydramnios was found among fetuses with Kell isoimmunization and the maternal serum titers were much lower than those in the RhD group. DeltaOD450 values did not reliably reflect the Kell sensitized fetus's condition. There were no intrauterine deaths or neonatal direct hyperbilirubinemia in the Kell group, and the hemolytic disease of the newborn was more severe in the RhD group. Although the course of the hemolytic disease in our cases of Kell isoimmunization showed a better prognosis than that in the RhD group, the importance of this condition should not be underestimated, and differences in the pathophysiology of Kell and RhD alloimmunization should be taken into consideration during the management of these cases.
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2/60. Death due to thrombotic thrombocytopenic purpura in pregnancy: case report with review of thrombotic microangiopathies of pregnancy.

    maternal death during pregnancy, although uncommon, may result from a broad range of conditions. In this paper, a case of thrombotic thrombocytopenic purpura diagnosed by postmortem examination is presented. Thrombotic thrombocytopenic purpura is one of a subset of diseases that result in the formation of microthrombi within the vasculature, either as a primary or secondary manifestation. Other conditions included in the differential diagnosis during pregnancy are hemolytic uremic syndrome, systemic lupus erythematosus, preeclampsia-eclampsia and the hellp syndrome, acute fatty liver of pregnancy, antiphospholipid antibody syndrome, and disseminated intravascular coagulation. The histologic manifestations of these diseases can be similar and in most cases do not provide adequate information to accurately differentiate these diseases in the postmortem period. This paper addresses the need for clinical history (i.e., symptomatology, trimester of onset) and antemortem laboratory testing in addition to a thorough autopsy to accurately differentiate among the conditions named previously. In the absence of an adequate clinical history and antemortem laboratory testing, the more general diagnosis of "thrombotic microangiopathy of pregnancy" is acceptable.
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3/60. Intra-uterine death due to umbilical cord thrombosis secondary to antiphospholipid syndrome.

    This is a case of intra-uterine death due to a thrombotic event on the fetal side of circulation in a woman who was subsequently diagnosed with antiphospholipid syndrome.
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4/60. Maternal blood coagulation factor XIII is associated with the development of cytotrophoblastic shell.

    We analysed the early implantation tissues of normal women and of a patient with congenital factor xiii deficiency in order to study the role of maternal subunit A of factor XIII (XIIIA) in the development of extravillous cytotrophoblast. The patient had received adequate administration of factor xiiia concentrate only up to 7 weeks of gestation (wG). Her pregnancy was maintained until the latter half of 8 wG, but was terminated by intrauterine fetal death at 9 wG. Immunohistochemical staining of cytokeratin, XIIIA and subunit S of factor XIII was performed in the early implantation tissues of normal women and of this patient. Numerous well-formed cytotrophoblastic shells and Nitabuch's layers were detected in implantation tissues at 7-8 wG in normal women, and XIIIA was present in the intercellular space in well-formed cytotrophoblastic shells, while the cytotrophoblastic shells and Nitabuch's layers in this patient's implantation tissue were poorly-formed. Furthermore, XIIIA was not detected around them. It is suggested that when the maternal plasma activity of factor XIII is low, the concentration of XIIIA at the placental bed is also low, leading to the insufficient formation of cytotrophoblastic shell and therefore an increased probability of miscarriage in patients with congenital factor xiii deficiency.
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5/60. Neonatal cerebral ischaemia with elevated maternal and infant anticardiolipin antibodies.

    A baby girl born by elective lower segment caesarean section was found to have left-sided focal seizures at 48 hours after birth. Her mother had previously had a neonatal death at 26 weeks' gestation and another child born at 32 weeks' gestation had a congenital right hemiplegia with a left middle cerebral artery infarct on CT scan. The mother had raised anticardiolipin IgG antibodies at the time of delivery of her second child, with no thrombotic symptoms. Therefore, during this pregnancy, she had been treated with low molecular weight heparin and aspirin. The baby's mother had raised IgG and IgM anticardiolipin antibodies and the baby had IgG anticardiolipin antibodies at the upper range of normal 4 days after delivery. The seizures were controlled with phenobarbitone and phenytoin. CT and MRI scans showed evidence of cerebral ischaemia. A repeat MRI scan at 4 months of age was normal, anticonvulsants were discontinued, and her latest neurological examination at 5 months was normal.
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6/60. Thromboembolism during pregnancy. Risks, challenges, and recommendations.

    pregnancy is an important risk factor for venous thrombosis, and venous thromboembolism is a leading cause of preventable death in pregnancy. Diagnosis of venous thromboembolism is complicated in that the symptoms of dyspnea and lower extremity edema are relatively common complaints of pregnant patients. physicians should maintain an appropriately high index of suspicion and request diagnostic imaging in a timely manner. Diagnosis of deep venous thrombosis with Doppler ultrasonography of the lower extremity poses no health risk to the fetus, but other radiographic studies pose a low radiation risk to the fetus. Because anticoagulant therapy poses a greater health risk to mother and fetus than does the radiation required for the diagnosis of pulmonary embolism, clinicians should aggressively pursue objective evidence of venous thromboembolism. Once the diagnosis is made, anticoagulation with intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin should be used prepartum followed by warfarin therapy after delivery.
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7/60. prenatal diagnosis of a subdural hematoma associated with reverse flow in the middle cerebral artery: case report and literature review.

    To our knowledge this is the first reported case of a subdural hematoma, related to fetal autoimmune thrombocytopenia, diagnosed prenatally by ultrasound. The underlying etiology was hidden maternal autoimmune thrombocytopenia. This disease, which is as serious as alloimmune thrombocytopenia, causes severe fetal thrombocytopenia, which carries with it a high risk of intracranial hemorrhage and recurrence in subsequent pregnancies. Only 14 cases of fetal subdural hematomas have been reported in the literature. The etiologies of these cases were principally traumatic, or due to disorders of hemostasis. Their prognoses were generally poor, with 50% resulting in fetal death in utero and the remaining 50% demonstrating post-natal sequelae. The presence of reverse flow in the middle cerebral artery is rare and its association with a subdural hematoma unusual. Abnormalities found on cerebral Doppler studies indicate an adaptive response to a fetal condition for which the prognosis is then very poor. Monitoring fetuses at risk for hemorrhage by ultrasound imaging and Doppler studies enables us to detect indicators of a worsening prognosis before the ultrasound appearance of morphological hemorrhage. The development of intracranial hemorrhage raises difficult management issues during the index pregnancy and in subsequent pregnancies.
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8/60. Homozygous factor v Leiden mutation in a woman with multiple adverse pregnancy outcomes.

    We report a case with one intrauterine fetal death (IUFD) at 32 weeks of gestation, one premature delivery at the same week, and one abortion of unknown etiology at 12 weeks of gestation. We discuss that the presence of homozygosity for factor v Leiden may be associated with placental insufficiency in this woman. Application of anticoagulant therapy may have been beneficial in her current pregnancy.
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9/60. Two cases of acute leukaemia in pregnancy.

    2 cases of acute leukaemia which developed in the course of pregnancy are reported. The first was a 34-year-old woman who presented with acute myeloblastic leukaemia late in the second trimester and received combination chemotherapy. A normal male infant was delivered. The second patient, aged 24 years, presented with acute lymphoblastic leukaemia early in the second trimester and was treated with the same regime. Pre-eclamptic toxaemia developed at 29 weeks gestation. Intra-uterine death was confirmed 1 week later.
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10/60. Fetal splenic rupture following transfusion.

    BACKGROUND: splenic rupture in the newborn is a rare complication in erythroblastosis fetalis. There are no reports of splenic rupture in the fetus affected by hemolytic disease of the newborn. CASE: A 41-year-old gravida 3, para 2-0-0-2 with severe rhesus alloimmunization was managed with serial intrauterine transfusions resulting in fetal death after the fourth procedure. autopsy findings revealed intra-abdominal clotted blood and splenic capsular defects consistent with splenic rupture. CONCLUSION: Fetal splenic rupture might occur in hemolytic disease of the newborn associated with splenomegaly. Acute hemodynamic changes with increased intra-abdominal pressure from intrauterine transfusion might precipitate splenic rupture. (Obstet Gynecol 2001;97:824-5.
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