Eclampsia may be associated with various focal neuro-logical features' that often resolve within a few hours or days, suggesting that their aetiology is different from that of the severe haemorrhage described in the early postmortem studies. We recently reported results of magnetic resonance imaging that implicate cerebral ischaemia in the cortical blindness of eclampsia,' and cerebral vasospasm has been described in angiographic studies of patients with eclampsia.2 We describe the experimental administration of nimodipine, a fairly selective cerebral vasodilator,3 to a moribund patient with eclampsia. Case report A 31 year old woman was admitted in the 38th week of her first pregnancy with the features of severe pre-eclampsia. Within a few hours she had a caesarean section, and immediately after delivery she was given a loading dose of phenytoin as prophylaxis against seizures. Seven hours postpartum she had a generalised convulsion. An additional 300 mg of phenytoin was given, but she had another convulsion, which was controlled by diazepam, one hour later. She had jaundice and stiffness of the neck, her coagulation variables were abnormal, and transaminases were raised. Fresh frozen plasma was given. Computed tomography 10 hours after delivery showed areas of low attenuation consistent with ischaemia or infarction Axial T2 weighted images of brain (spin echo 2000180). Left: image obtained before treatment, showing bilateral foci of high signal intensity in basal ganglia, right thalamus and insular cortex, and left temporal and parietal cortex extending into subjacent white matter; additional sections showed high signal intensity in pons, occipital lobes, and left cerebellar hemisphere. Right: image obtained four days later, after treatment with nimodipine, showing almost complete resolution ofchanges. Thin linear bands ofhigh signal intensity remain at boundary ofgrey and white matter ofpreviously affected areas in the brain stem and thalamus. There was no evidence of cerebral haemorrhage. Over the next four hours she had several generalised convulsions despite receiving an infusion of chlormethiazole and her phenytoin concentration being in the therapeutic range. She was given a transfusion of platelets because of worsening thrombocytopenia. Magnetic resonance imaging showed extensive areas ofhigh signal intensity consistent with cerebral ischaemia (figure). Seventeen hours after delivery, on the assumption that the relentless neurological deterioration was the potentially reversible consequence of vasospasm, we started an infusion of nimodipine at a rate of 1 mg/h for the first hour and then 2 mg/h while continuing the phenytoin and chlormethiazole. No further seizures occurred, and three hours after the introduction of nimodipine she was responding to verbal commands and moving her arms and legs equally. By 36 hours after delivery she was fully conscious and neurological examination gave normal results except for short term loss of memory. The infusion of nimodipine was stopped and the drug was given orall...
Summary Platelet behaviour was studied in groups of women suffering from mild and severe pre‐eclampsia, and compared with normal pregnant and non‐pregnant controls. Platelets from women with severe pre‐eclampsia were less responsive than normal to a variety of aggregating agents, and this impairment was significant in response to collagen and vasopressin. Women with severe pre‐eclampsia had raised plasma adenine nucleotide levels and lowered platelet 5‐hydroxytryptamine levels compared with the controls. Platelets from women with mild pre‐eclampsia showed only a slight difference from normal. These findings may be the result of platelets having undergone aggregation and disaggregation within the circulation, and suggest that platelets may be involved in the pathogenesis of pre‐eclampsia.
Factor VIII related antigen (VIIIRAg), Factor VIII coagulant activity (VIIIC), plasma uric acid, total plasma oestriol, plasma human placental lactogen (hPL) and urine oestrogen/creatinine ratio were measured in a group of 21 patients clinically suspected of fetal growth retardation and compared with normal pregnancy. Of the hormone assays, hPL was better than either oestriol or oestrogen/ creatinine ratio at distinguishing between normal and growth retarded pregnancies. Uric acid levels tended to be higher than normal in patients with fetal growth retardation, but the best means of distinguishing normal from growth retarded pregnancies proved to be the VIIIRAg/VIIIC ratio. This ratio was significantly elevated in fetal growth retardation compared with normal pregnancy, and the increase was evident as early as 30 weeks gestation. Using the VIIIRAg/VIIIC ratio test, the outcome of 17 of the 21 suspect pregnancies could be correctly predicted.
SummaryIn 26 women receiving either medroxyprogesterone acetate (Depo‐Provera) injections or combined oestrogen‐progestogen pills for contraception, tests of coagulation and fibrinolysis were performed before treatment, and after 8, 16 and 24 weeks of therapy. In the medroxyprogesterone group no significant changes were induced in fibrinogen, the vitamin K‐dependent factors, or antithrombin III. Plasminogen levels fell during therapy, and were significantly lower than pre‐treatment values after 16 and 24 weeks. By contrast, the 13 women receiving oral contraceptives showed raised levels of fibrinogen and plasminogen after 8 weeks of treatment, and of factors VII and X after 24 weeks. These data suggest that medroxyprogesterone acetate injections induce fewer changes in the blood coagulation system than oral contraceptives.
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