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2002, Number 6

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Cir Cir 2002; 70 (6)

Inflammation, endothelicen, and coagulation in sepsis. Current concepts

Carrillo-Esper R, González-Salazar JA

Language: Spanish
References: 69
Page: 433-441
PDF size: 67.09 Kb.


ABSTRACT

Objective: To review actual concepts concerning the pathophysiologic interrelation between infection, inflammation, and coagulation in severe sepsis. Material and methods: A summary of published medical literature from Medline search files and published reviews on severe sepsis pathogenesis. Results: Severe sepsis is one of the main causes of patient entry into the Intensive Care Unit and is associated with high morbimortality. Bacterial exotoxins and endotoxins activate the immune system, producing proinflammatory cytokines such as tumoral necrosis factor and several types of interleukins, which result in systemic inflammatory response whose objectives are to control and erradicate the infection process. If this process is uncontrolled by the antiinflammatory compensatory systemic response, it culminates in endothelial damage and coagulopathy secondary to expression of tisular factor, thrombomodulin consumption, and decreased levels of activated protein C, resulting in microvascular thrombosis, tisular hypoxia, and multiple organic dysfunction. Severe sepsis is characterized by a complex interaction among infection, coagulation, and inflammation that when uncontrolled results in microvascular thrombosis and multiple organic dysfunction.


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