Cases reported "Fetal Death"

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1/21. 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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2/21. Intrauterine fetal death caused by pit viper venom poisoning in early pregnancy.

    Poisonous snakebite is a rare complication of pregnancy. It has been suggested that snakebite poisoning during pregnancy may cause fetal loss. We report a case of intrauterine fetal death after a poisonous snakebite in the first trimester of pregnancy. A 29-year-old pregnant Japanese woman was admitted to hospital after being bitten by a pit viper on her right heel. The patient was at 10 weeks of gestation. In response to the bite, her right leg became extremely swollen, and paralysis of the right oculomotor nerve was observed. Intravenous administration of cepharanthine, ulinastatin, hydrocortisone sodium succinate, gabexate mesylate and antibiotics was started. Laboratory data suggested the presence of rhabdomyolysis. One week after admission, although she improved clinically and symptomatically, transvaginal ultrasonography revealed intrauterine fetal death. No vaginal bleeding was observed. A dilatation and curettage was performed. The patient made an uneventful recovery and was discharged from hospital 17 days after the snakebite. Consistent with other reports, in the first trimester intrauterine fetal death may especially occur when the mother has systemic symptoms, although its mechanism remains unclear.
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3/21. amniotic fluid embolism with second trimester pregnancy termination: a case report.

    PURPOSE: Describe the diagnosis, clinical features, pathophysiology, treatment and anesthetic management of amniotic fluid embolism (AFE) in a patient undergoing second trimester pregnancy termination. CLINICAL FEATURES: A 30-yr-old gravida 2, para 1, woman was admitted for a dilatation and evacuation procedure for underlying intra-uterine fetal demise in her second trimester of pregnancy. hypotension, shock, respiratory arrest, pulseless electrical activity, hemorrhage, disseminated intravascular coagulopathy, requiring cardiopulmonary resuscitation and blood transfusion complicated her intraoperative care. AFE was considered the most likely cause of this intraoperative event. CONCLUSIONS: It is now recognized that the pathophysiological features of AFE are similar to a type-1 hypersensitivity reaction ranging from mild systemic reaction to anaphylaxis and shock. AFE has a high maternal and fetal morbidity and mortality rate, requiring prompt recognition and treatment. In patients with cardiovascular instability, the treatment of AFE is similar to anaphylaxis requiring aggressive fluid hydration, cardiopulmonary resuscitation, administration of blood products and the use of vasopressors.
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4/21. cyclophosphamide for lupus during pregnancy.

    Severe systemic lupus erythematosus often requires the use of cyclophosphamide in women of reproductive age. As cyclophosphamide is generally avoided during pregnancy because of its teratogenic risk, its impact on fetal survival is poorly understood. This is a case series of lupus patients exposed to cyclophosphamide during pregnancy. We reviewed pregnancies in patients with lupus seen at a large university hospital between October 1986 and September 2003. The pregnancies were evaluated prospectively for cyclophosphamide exposure, lupus activity, and fetal outcome. Comparison was made between pregnancies with severe lupus requiring cyclophosphamide and those that did not. We identified four pregnancies with cyclophosphamide exposure. Two pregnancies were inadvertently exposed to cyclophosphamide early in the first trimester; both resulted in first trimester miscarriages. Two patients were administered cyclophosphamide for severe lupus nephritis and thrombocytopenia during the second trimester. Soon after the administration of cyclophosphamide, both pregnancies ended with fetal demise. Pregnancies exposed to cyclophosphamide for severe lupus flare resulted in a higher rate of fetal losses than pregnancies with severe lupus but not requiring the drug (100% versus 31.25%). In conclusion we present four pregnancies exposed to cyclphosphamide, each ending with pregnancy loss. Based on our experience, the survival of the fetus is strongly in doubt when cyclophosphamide is required to treat lupus in the mother.
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5/21. fetal death in a patient with intrahepatic cholestasis of pregnancy.

    BACKGROUND: Treatment with ursodeoxycholic acid in intrahepatic cholestasis of pregnancy reduces concentration of transaminases and bile acids in maternal serum, and is thought to reduce fetal death. We report a case of fetal death in a patient with intrahepatic cholestasis of pregnancy who had responded well to ursodeoxycholic acid, demonstrated by a low bile level. CASE: A young nulliparous woman presented with intrahepatic cholestasis of pregnancy at 28 weeks of gestation. transaminases and bile acids decreased after ursodeoxycholic acid administration. The patient was discharged from the hospital until delivery and received biochemical markers and conventional fetal monitoring twice weekly. Due to low bile acid values (< 13 UI/L) and unfavorable cervix, the patient was followed up expectantly. fetal death occurred at 39 weeks and 3 days, although cardiotocograph testing results were normal the day before. CONCLUSION: When lung maturity is achieved for patients with intrahepatic cholestasis of pregnancy, delivery should be considered.
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6/21. Six cases of massive feto-maternal bleeding causing intra-uterine fetal death.

    Six patients in whom intra-uterine fetal death (IUFD) near term resulted from massive feto-maternal hemorrhage are reported. Two of the mothers were Rh-negative, which necessitated the administration of large volumes of anti-D. In order to detect such patients, the Kleihauer-Betke test should be performed in all cases of IUFD of unknown etiology.
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7/21. Fetal exsanguination following intrauterine angiographic assessment and selective termination of a hydrocephalic, monozygotic co-twin.

    Selective termination by intracardiac potassium chloride injection was performed in twins discordant for hydrocephaly at 20 weeks' gestation. Because of the potential for vascular anastomoses to exist between the twins, fetal angiography was performed prior to the selective termination procedure. Determination of vascular connections between the fetuses was hindered by fetal bradycardia following intracardiac administration of contrast material. Selective termination was performed without difficulty using intracardiac potassium chloride (KCl) to produce asystole in the twin with hydrocephaly. The unaffected fetus appeared active and had a normal heart rate during and immediately after the procedure. However, both twins were found to have died the following day. Pathologic examination documented several vascular anastomoses between the monochorionic, diamniotic fetuses. A likely cause of death was exsanguination of the normal twin into the abnormal one. This case illustrates the difficulties encountered in selective termination of monozygotic twins and, to our knowledge, represents the first reported use of intrauterine fetal angiography.
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8/21. Intravenous immunoglobulin treatment of pregnant patients with recurrent pregnancy loss caused by antiphospholipid antibodies and Rh immunization.

    A patient with antiphospholipid antibodies and nine consecutive fetal deaths and a severely Rh-immunized woman with one previous live birth and seven fetal/neonatal deaths achieved live births after antepartum administration of intravenous immunoglobulin. This agent shows promise as a new treatment for patients with previous repetitive fetal deaths from immunologic causes.
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9/21. Consumption coagulopathy associated with intrauterine fetal death: the role of heparin therapy.

    A gravida with intrauterine fetal death who developed progressive chronic consumption coagulopathy was treated with heparin. When serial fibrinogen levels fell below 100 mg% and the prothrombin time was significantly prolonged, intravenously injected heparin corrected hypofibrinogenemia. A safe delivery followed administration of oxytocin. The authors emphasize the infrequent need for heparin therapy in the majority of cases of the intrauterine fetal death syndrome. Therapeutic guidelines for its use in selected cases are reviewed.
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10/21. Premature closure of the ductus arteriosus causing intra-uterine death. A case report.

    A case of hydrops fetalis with intra-uterine death after premature closure of the ductus arteriosus because of inhibition of premature labour by the administration of indomethacin is presented. The physiology of acute and chronic intra-uterine constriction of the ductus arteriosus and the effects of indomethacin on the fetal circulation are discussed. Mention is also made of the moral conflict confronting the doctor in the management of an affected fetus during the third trimester.
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