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38 - Disorders of Coagulation in Pregnancy

from Section 5 - Late Pregnancy – Maternal Problems

Cara C. Heuser
Affiliation:
Department of Obstetrics & Gynecology, University of Utah Health Sciences Center, Salt Lake City, UT, USA
D. Ware Branch
Affiliation:
Department of Obstetrics & Gynecology, University of Utah Health Sciences Center & Intermountain Healthcare, Salt Lake City, UT, USA
Philip Steer
Affiliation:
Imperial College London
Carl Weiner
Affiliation:
University of Kansas
Bernard Gonik
Affiliation:
Wayne State University, Detroit
Stephen Robson
Affiliation:
University of Newcastle
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Summary

Introduction

The human hemostatic system involves a number of complex and highly regulated processes. In turn, these processes are interwoven with other important systemic and cellular systems (e.g., immune, hematologic, nutritional/gastrointestinal, and cardiovascular) and are thus sensitive to myriad biologic influences and events. During states of blood vessel injury the hemostatic system must be quick, localized, and reliable. Unfortunately, there are many inherited, acquired, and physiologic conditions that can disrupt the hemostatic system and lead to suboptimal or inappropriate clot formation. The chapter focuses on thrombophilias and nonphysiologic thrombi (thrombosis not required for hemostasis) as they relate to the pregnant woman.

Several national organizations, including the American College of Obstetricians and Gynecologists (ACOG) and the American College of Chest Physicians (ACCP) have published guidelines regarding thrombosis and pregnancy. These will be referred to throughout this chapter.

Hemostatic System

In the normally functioning hemostatic system, coagulation is mediated by a cascade of extracellular clotting factors and cellular components that seal breached endothelium with fibrin–platelet plugs. This process can be thought of as having four essential phases:

  • 1. Platelet plug formation, mediated by exposure of endothelial proteins, including von Willebrand factor (vWF), which bind and recruit platelets to the site of injury.

  • 2. Clotting cascade and fibrin plug formation, initiated by endothelial tissue factor binding to factor VII and leading, via a number of redundant pathways, to thrombin-mediated conversion of fibrinogen to fibrin.

  • 3. Termination of clot formation by endogenous anticoagulants, including proteins C and S.

  • 4. Fibrinolysis, during which plasmin degrades the cross-linked fibrin polymers, resulting in the formation of fibrin degradation products (FDPs).

  • Effect of Pregnancy on Hemostasis

    The normal physiology of pregnancy causes important changes in the hemostatic system, resulting in a hypercoagulable state. These changes include:

  • • decrease by 60–70% in the level of protein S, with nadir around delivery

  • • increases by 20–1000% in fibrinogen, vWF, factors II, VII, VIII, IX, and X levels

  • • increases in the levels of antifibrinolytic plasminogen activation inhibitor 1 (PAI-1) and PAI-2

  • • progressive platelet activation

  • Although these changes may have evolved to protect the mother from excessive blood loss at delivery, they also increase the likelihood of pathologic thrombus formation.

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    Information
    High-Risk Pregnancy: Management Options
    Five-Year Institutional Subscription with Online Updates
    , pp. 1085 - 1107
    Publisher: Cambridge University Press
    First published in: 2017

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