Coagulopathy in Severe Sepsis: Interconnectivity of Coagulation and the Immune System.

Abstract

Disseminated intravascular coagulation (DIC) remains a challenging complication of infection with inadequate treatment and significant morbidity and mortality rates. Review of the English-language literature. Disseminated intravascular coagulation arises from the immune system's response to microbial invasion, as well as the byproducts of cell death that result from severe sepsis. This response triggers the coagulation system through an interconnected network of cellular and molecular signals, which developed originally as an evolutionary mechanism intended to isolate micro-organisms via fibrin mesh formation. However, this response has untoward consequences, including hemorrhage and thrombosis caused by dysregulation of the coagulation cascade and fibrinolysis system. Ultimately, diagnosis relies on clinical findings and laboratory studies that recognize excessive activation of the coagulation system, and treatment focuses on supportive measures and correction of coagulation abnormalities. Clinically, DIC secondary to sepsis in the surgical population presents a challenge both in diagnosis and in treatment. Biologically, however, DIC epitomizes the crosstalk between signaling pathways that is essential to normal physiology, while demonstrating the devastating consequences when failure of local control results in systemic derangements. This paper discusses the pathophysiology of coagulopathy and fibrinolysis secondary to sepsis, the diagnostic tools available to identify the abnormalities, and the available treatments.