Pathological investigation of maternal deaths: a cause for concern.
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Careful study of reports prepared for the Confidential Enquiries into Maternal Deaths in England and Wales has made it clear that many maternal autopsy reports are not as informative as they might be. This is, in part at least, because no pathologist who does not work in a maternity unit can expect to see more than a handful of such deaths in a working lifetime. This paper describes briefly the particular features to look for at autopsy, stresses the importance of taking adequate material for histology and discusses some of the more significant histological findings, both of conditions which cause death and of those commonly associated with it.
Coagulation problems in pregnancy are primarily associated with overactivity of the intrinsic clotting system. This accounts for the increased incidence of thrombo-embolism during pregnancy. Where specific obstetric complications cause clotting problems the common underlying feature is usually placental pathology as in abruptio placentae, pre-eclampsia or hydatidiform mole. Abnormal activation of the clotting system is an early, and occasionally the first detectable feature of pre-eclampsia, but there is no evidence that this is a primary change. Therefore the role of anticoagulant treatment in the management of pre-eclampsia remains questionable. A new test for estimating factor VIII consumption is proving to be a sensitive index of early activation of the clotting system and can be used for the diagnosis of early pre-eclampsia.
The pathophysiologic mechanisms, clinical, and laboratory manifestations of DIC are complex in part due to interrelationships within the hemostasis system. Only by clearly understanding these extraordinarily complex pathophysiologic interrelationships can the clinician and laboratory scientist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. Many therapeutic decisions to be made are controversial and lack validation. Nevertheless, newer antithrombotic agents, and agents that can block, blunt, or modify cytokine activity and the activity of vasoactive substances appear to be of value. The complexity and variable degree of clinical expression suggests that therapy should be individualized depending on the nature of DIC, age, etiology of DIC, site and severity of hemorrhage or thrombosis and hemodynamics and other appropriate clinical parameters. At present, treatment of the triggering event, low-dose heparin or antithrombin concentrate and wise choice of components when indicated appear to be the most effective modes of therapy.
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Disseminated intravascular coagulation (DIC) is a manifestation of an underlying pathologic process such as cancer, infection, trauma, or obstetric catastrophe. It can manifest as thrombosis, bleeding, or both. To succeed, treatment must address the underlying cause.
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The possible predisposing causes of difibrination in the pregnant woman are discussed. Coagulation profiles and qualitative and quantitative assessment of fibrinolytic activity during labor, delivery and the early puerperium in normal pregnancies are presented. These factors were also studied in patients with abruptio placentae and prolonged intrauterine fetal death and in women whose pregnancies were terminated with intraamniotic infusion of hypertonic saline or prostaglandin F2alpha. The findings suggest that a minor degree of physiologic defibrination develops during normal labor that is qualitatively similar to, but of much lesser magnitude than, the pathologic defibrination syndrome commonly associated with abruptio placentae or prolonged intrauterine fetal death. Some degree of defibrination occurs in women undergoing saline abortion, similar to that of women during normal parturition, but does not usually reach clinically significant levels. The coagulation changes seen during prostaglandin abortion suggest that a minor degree of defibrination occurs that is substantially less than that seen during saline abortion. The findings presented form a basis for the rational management of defibrination in the pregnant woman.
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