Disseminated Intravascular Coagulation: Objective Clinical and Laboratory Diagnosis, Treatment, and Assessment of Therapeutic Response

Abstract

Current concepts of the etiology, pathophysiology, clinical and laboratory diagnosis and management of fulminant and low-grade disseminated intravascular coagulation (DIC) have been presented. Considerable attention has been devoted to interrelationships within the hemostasis system. Only by clearly understanding the 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. Objective clinical and laboratory criteria for diagnosis of DIC have been delineated, thus avoiding needless confusion and empirical decisions regarding the diagnosis. Many therapeutic decisions to be made are controversial and will remain so until more is published about specific therapeutic modalities and survival patterns. Also, therapy must be highly individualized depending on the nature of DIC, age, etiology of DIC, site and severity of hemorrhage or thrombosis, and hemodynamic and other clinical parameters. Also presented are clear criteria for severity of DIC and objective criteria for defining a response to therapy. Also, since it is often difficult for the individual physician to decide when to stop expensive therapy, objective criteria by which therapy may be stopped when continuation is likely fruitless are presented as a guideline.

Changes in blood acid-base balance parameters and coagulation profile during diarrhea in calves

“…In broad terms, there are two major pathways that may cause DIC: (i) a systemic inflammatory response which activates the cytokine network and coagulation cascade (such as in severe sepsis and major trauma) and/or (ii) release or exposure of pro-coagulant material into the blood stream (such as in cancer or obstetric patients) (Levi et al 1997). Disseminated intravascular coagulation is a continuously progressing process, it can be subdivided into three phases: phase I -compensated activation of the haemostatic system, phase II -decompensated activation of the haemostatic system, phase III -full-blown DIC (Bick 1996). The pathologic process is characterized by widespread fibrin deposition in the microcirculation with subsequent ischemic damage, and by the development of a hemorrhagic diathesis caused by the consumption of procoagulans and hyperactivity of fibrinolysis (Morris 1990).…”

Alterations in some blood coagulation parameters in naturally occurring cases of canine babesiosis

“…Levels of significance were determined by non-parametric tests (Mann-Whitney U test, STATISTICA for Windows, version 5.1 release, StatSoft, Inc. 1984-1996. Any P value of 0.05 or lower was considered to be significant.…”

“…This could be a function of inhibitor breakdown and/or liver dysfunction affecting inhibitor production in dogs with babesiosis. Early and prolonged decreases in AT III activity are well documented during a systemic inflammatory response (Bick, 1996), suggesting that AT III activity could be the consequence of systemic inflammation resulting from babesiosis. Decreased AT III activity was also indicative of chronic DIC in babesiosis.…”

Disseminated Intravascular Coagulation in Obstetrics: Ethiopathogenesis and up to date Management Strategies

“…A prolonged PT and aPTT is seen in 50-69% of cases (50) . This condition is related to the consumption of the coagulation factors.…”