1/11. Antepartum diagnosis of fetal intracranial hemorrhage due to maternal bernard-soulier syndrome.BACKGROUND: bernard-soulier syndrome, a lack of glycoprotein IB/IX, is a rare autosomal recessive bleeding disorder characterized by platelet dysfunction. women with bernard-soulier syndrome are at risk of being immunized against glycoprotein IB/IX, leading to severe isoimmune neonatal thrombocytopenia. CASE: A 26-year-old Japanese woman, gravida 1, para 0, with bernard-soulier syndrome presented at 35 weeks' gestation with changes in fetal heart rate patterns and ultrasonographic findings that strongly suggested fetal intracranial hemorrhage. Management was by cesarean hysterectomy and bilateral salpingo-oophorectomy at 36 weeks, but the neonate died 6 hours after birth. CONCLUSION: Maternal immunization to glycoprotein IB/IX during pregnancy can cause severe fetal thrombocytopenia and massive intracranial bleeding.- - - - - - - - - - ranking = 1keywords = thrombocytopenia (Clic here for more details about this article) |
2/11. Hemolytic uremic syndrome with intracranial hemorrhage following mitomycin C administration.A 50-year-old woman treated for breast cancer with mitomycin C developed severe hypertension, followed by deep coma 3 days later. Computed tomography of the brain showed frontoparietal intracranial hemorrhage accompanied by subarachnoid hemorrhage. The patient was diagnosed additionally with hemolytic uremic syndrome (HUS) based on hemolytic anemia with schistocytosis, thrombocytopenia, and acute renal failure. The patient underwent hemodialysis and plasmapheresis with no improvement. We present the pathologic findings of the general vessels, which has been reported rarely. This case represents the first reported intracranial hemorrhage in HUS following mitomycin C administration. We emphasize the need to control blood pressure in patients with HUS.- - - - - - - - - - ranking = 0.5keywords = thrombocytopenia (Clic here for more details about this article) |
3/11. Prenatal intracranial hemorrhage and neurologic complications in alloimmune thrombocytopenia.Neonatal alloimmune thrombocytopenia results from platelet-antigen incompatibility between mother and fetus, leading to antibody-mediated destruction of fetal platelets. With a prevalence of 1 in 1000 births, approximately 4000 infants born in the united states each year develop neonatal alloimmune thrombocytopenia. Ten to 20% of affected neonates develop intracranial hemorrhage, with 25 to 50% occurring prenatally. We report three infants who developed prenatal hemorrhage. One died in utero, and the other two had cerebral porencephaly and neurologic deficits. Infants with neonatal alloimmune thrombocytopenia have elevated risks of perinatal death and neurologic complications, including cerebral palsy, hypotonia, cortical blindness, developmental delay, seizures, and psychomotor retardation. We also report our retrospective review of the new england Medical Center neonatal intensive care unit between 1990 and 1999. Using current management guidelines, including treatment of the mother with a weekly infusion of high-dose (1-2 g/kg) intravenous immunoglobulin and/or corticosteroids, all eight infants with neonatal alloimmune thrombocytopenia did well.- - - - - - - - - - ranking = 565.97769130305keywords = alloimmune thrombocytopenia, neonatal alloimmune thrombocytopenia, neonatal alloimmune, alloimmune, thrombocytopenia (Clic here for more details about this article) |
4/11. Bleeding complications of platelet glycoprotein IIb/IIIa inhibitor abciximab (ReoPro ).Studies of patients scheduled for percutaneous coronary intervention with acute coronary syndrome have shown that the addition of intravenous glycoprotein (GP) IIb/IIIa inhibitors to aspirin and heparin is associated with a reduction in death or myocardial infarction compared to therapy with aspirin and heparin alone. The principle safety issue with GP IIb/IIIa inhibitors is the risk of bleeding, as the potent antiplatelet effect of these drugs may adversely affect hemostasis. In addition, antagonists of GP IIb/IIIa may increase the risk of thrombocytopenia. We report a case of abciximab-induced severe thrombocytopenia which led to fatal intra-cranial hemorrhage.- - - - - - - - - - ranking = 1keywords = thrombocytopenia (Clic here for more details about this article) |
5/11. Repeated antenatal intracranial haemorrhage: magnetic resonance imaging in a fetus with alloimmune thrombocytopenia.magnetic resonance imaging was used to show repeated antenatal intracranial haemorrhage in a fetus with alloimmune thrombocytopenia.- - - - - - - - - - ranking = 273.62054796122keywords = alloimmune thrombocytopenia, alloimmune, thrombocytopenia (Clic here for more details about this article) |
6/11. Fatal intracranial hemorrhage in a pregnant patient with autoimmune thrombocytopenic purpura.thrombocytopenia in pregnancy is a frequent cause of hematological consultation. Autoimmune thrombocytopenic purpura results from platelet destruction due to autoantibodies. Spontaneous intracranial hemorrhage is a rare but devastating complication of these patients. We present a fatal case of intracranial hemorrhage in a 18 week pregnant woman diagnosed with autoimmune thrombocytopenia. The clinical course and treatment of this unusual clinical complication is discussed in relation to the world literature.- - - - - - - - - - ranking = 0.5keywords = thrombocytopenia (Clic here for more details about this article) |
7/11. Fulminant hemophagocytic syndrome with a high interferon gamma level diagnosed as macrophage activation syndrome.A 26-year-old woman presented with general fatigue, persistent fever, nuchal lymphadenitis, thrombocytopenia, and liver damage. From the bone marrow finding, we diagnosed her condition as hemophagocytic syndrome. Steroid pulse therapy, cyclosporin A treatment, and combined chemotherapy generated no response. The patient showed severe mucosal bleeding, rapidly experienced multiple organ failure, and finally died of a brain hemorrhage on the 13th hospital day. Epstein-Barr virus, cytomegalovirus, human herpes virus type 6, human parvovirus B19, and herpes simplex virus were not detected. Autopsied samples of the spleen, bone marrow, and liver showed extreme proliferation of activated macrophages, so-called histiocytes, without lymphoid malignancy. The interferon gamma level at presentation was prominently high. The continuously elevated levels of ferritin and soluble interleukin 2 receptor were correlated with the catastrophic outcome. The disease in our case mimicked infantile hemophagocytic lymphohistiocytosis. However, there was neither a family history of the disease nor a mutation in the perforin gene. So, it is reasonable to categorize our case as macrophage activation syndrome. Although our patient lacked arthritis or eruption, we cannot deny the possibility that an oligoarthritis type of systemic-onset juvenile rheumatoid arthritis or, considering the patient's age, adult-onset Still disease lies at the base of our case.- - - - - - - - - - ranking = 0.5keywords = thrombocytopenia (Clic here for more details about this article) |
8/11. Characteristics of six newborn infants with postnatal findings of severe intracranial haemorrhage.OBJECTIVE: The objective of this study was to study the characteristics of newborn infants with postnatal findings of severe neonatal intracranial haemorrhage. methods: All the records of babies who underwent surgery from 1997 to 2002 for intracranial haemorrhage were reviewed. These were correlated with their antenatal records to see if fetal intracranial haemorrhage had been detected at the 20 weeks' screening scan or any other incidental scan e.g. growth scan. The perinatal records were also reviewed to see if there was associated birth trauma such as instrumentation or obstetric manoeuvres at delivery. RESULTS: Six cases of severe intracranial haemorrhage were diagnosed postnatally. Of these, only 1 case was detected antenatally on ultrasound scan. None of the cases were due to birth trauma. Three babies were found to have clotting factor deficiency. One of them subsequently developed cerebral palsy. One baby was diagnosed to have alloimmune thrombocytopenia. One case underwent an emergency Caesarean section for non-reassuring fetal status. Extensive intracranial haemorrhage, attributed to hypoxia, was found. The baby died. CONCLUSIONS: Our study suggests that neonatal intracranial haemorrhages are not exclusively due to birth trauma. The study also shows that fetal intracranial haemorrhage may not be detected antenatally by the routine practice. The causes in our study included clotting deficiency, alloimmune thrombocytopenia and hypoxia.- - - - - - - - - - ranking = 109.44821918449keywords = alloimmune thrombocytopenia, alloimmune, thrombocytopenia (Clic here for more details about this article) |
9/11. Fetomaternal alloimmune thrombocytopenia presenting as intracerebral bleeding in utero.Feto-maternal alloimmune thrombocytopenia is a serious fetal disorder resulting from platelet antigen incompatibility between the mother and the fetus. Intracranial bleeding is the most serious complication of alloimmune thrombocytopenia and can result in severe disability and death in utero. The authors report a case of intracerebral hemorrhage in utero resulting from alloimmune thrombocytopenia.- - - - - - - - - - ranking = 383.06876714571keywords = alloimmune thrombocytopenia, alloimmune, thrombocytopenia (Clic here for more details about this article) |
10/11. pregnancy in mother with Glanzmann's thrombasthenia and isoantibody against GPIIb-IIIa: Is there a foetal risk?Glanzmann's thrombasthenia (GT) is a rare autosomal recessive platelet disorder caused by qualitative or quantitative abnormalities of a platelet glycoprotein complex (GPIIb-IIIa) leading to excessive bleeding. Platelet transfusions are the first-line therapy for severe or persistent bleeding and surgery. Isoantibody against GPIIb-IIIa complexes present on normal platelets can be observed in Glanzmann's thrombasthenia type I patients after platelet transfusion possibly leading to platelet transfusion refractoriness. pregnancy in Glanzmann's thrombasthenia type I women is rare, and severe bleeding can be observed in the peripartum or late postpartum period. Moreover, pregnancy can contribute to the maternal isoimmunization by the passage of the foetal cells into the maternal circulation. The transplacental passage of the maternal isoantibodies can induce moderate to severe foetal thrombocytopenia. We discuss here the case of in utero death at 31 weeks of gestation due to intracranial haemorrhage in an immunized mother and review the literature. Presence of isoantibody prior to gestation or detected during the index pregnancy must be taken into account in evaluating risk for the mother and the foetus.- - - - - - - - - - ranking = 0.5keywords = thrombocytopenia (Clic here for more details about this article) |
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