Coagulopathy in sepsis — a new look at an old problem

 

Sepsis is a life-threatening condition characterized by a systemic response to microbial infection. Despite considerable progress in intensive care medicine, the incidence of sepsis and the number of sepsis-related deaths are increasing world-wide. There is a complex relationship between the coagulation, immune and inflammatory systems in sepsis. Activation of the coagulation cascade in sepsis is a result of a pathogen invasion and is a part of a immuno-inflammatory host response. In sepsis, the close cooperation of the immune and coagulation systems through cross signalling results in immunothrombosis. According to a recently described new theory, immunothrombosis is a immune response in which the local activation of coagulation facilitates the recognition and destruction of pathogens. Small amounts of clot formation are beneficial for the host because of bacteria trapping and prevention of the systemic spread of infection. Sepsis is a dynamic syndrome and in all patients with sepsis coagulation changes may progress from a normal profile to hypercoagulability and hypofibrinolysis, hyperfibrinolysis, and ultimately hypocoagulability.

 

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