Venous and Arterial Thrombosis:
Pathophysiological and Clinical Aspects
15th International Congress on Thrombosis Antalya, Turkey, October 16-21, 1998
Selected Plenary Lectures
Guest Editors: H. Coenraad Hemker, Maastricht; Sylviane Lévy-Toledano, Paris

Paper

Disseminated Intravascular Coagulation
Clinical and Pathophysiological Mechanisms and Manifestations
Rodger L. Bick, Banu Arun, Eugene P. Frenkel

Division of Hematology Oncology, Department of Medicine, University of Texas Southwestern Medical Center, Dallas, Tex., USA

Address of Corresponding Author

Haemostasis 1999;29:111-134 (DOI: 10.1159/000022493)

  Key Words

• Coagulopathy
• Thrombosis
• Hemorrhage
• Shock
• Disseminated intravascular coagulation

  Abstract

Disseminated intravascular coagulation (DIC) is a complex disorder, with pathophysiology being variable and highly dependent upon the triggering event(s), host response(s) and comorbid conditions. As a result of these complicated interactions, the clinical expression and laboratory findings are varied, thereby affecting the specifics of diagnosis and therapeutic approaches. The highly complex and variable pathophysiology of DIC often results in a lack of uniformity in clinical manifestations, a lack of consensus in the specific appropriate laboratory criteria of diagnosis, and a lack of specific therapeutic modalities. Indeed, recommendations for therapy are often difficult because the morbidity and survival is more dependent on the specific cause of DIC and because the generally used specific therapeutic approaches, which include for example heparin, low-molecular-weight-heparin antithrombin concentrate and protein C concentrate, have never been subjected to objective prospective randomized trials, except antithrombin concentrates. An analysis of the complex and varied pathophysiological events in DIC provide objective guidelines and criteria for the clinical diagnosis, the laboratory diagnosis, and the definition of severity. These data compounded by an understanding of complex and varied pathophysiology can be used for objective evaluation of therapeutic responses and results. DIC is an intermediary mechanism of disease usually seen in association with well-defined clinical disorders. The pathophysiology of DIC serves as an intermediary mechanism in many disease processes, which sometimes remain organ specific. This catastrophic syndrome spans all areas of medicine and presents a broad clinical spectrum that is confusing to many. Most physicians consider DIC to be a systemic hemorrhagic syndrome; however, this is only because hemorrhage is evident and often impressive. Less commonly appreciated is the profound microvascular thrombosis and sometimes, large vessel thrombosis. The hemorrhage is often simple to contend with in patients with fulminant DIC, but it is the small- and large-vessel thrombosis, with impairment in blood flow, ischemia, and associated end-organ damage that usually leads to irreversible morbidity and mortality. In conclusion, the pathophysiological 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 pathophysiological 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 which 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.

Copyright © 1999 S. Karger AG, Basel

  Author Contacts

Rodger L. Bick, MD, PhD, FACP
10455 North Central Expressway, Suite 109
Dallas, TX 75231 (USA)
Tel. +1 214 373 9350, Fax +1 214 373 9351

  Article Information

Number of Print Pages : 24
Number of Figures : 3, Number of Tables : 7, Number of References : 179