Patologia emocoagulativa e suo trattamento in corso di sepsi

The host response to infection involves soluble mediators ( components of flogosis, clotting factors) and cells(platelets, endothelial cells and monocites) and is a continuum of complex and very organized chain reactions that have as objective the elimination of pathogenic threat, and the restitution ad integrum of the host. However if the response is excessive , the host response turn on its bearer and causes the organ dysfunction. In sepsis there is a strong cross-talk between flogosis and coagulation. In septic patients the primary activation of haemostasis is associated to thrombocytopenia with a variable incidence from 36%-60%. There is an attenuation of anticoagulant mechanism, including P C; AT, and the fibrinolitic way. In patients affected by two organ failure septic shock, the recommended therapy comprise the use of activated recombinant protein c. We analyzed the effect of activated recombinant protein c in a limited group of patients in ICU on coagulation cascade. In particular we studied coagulation parameter variation of septic patients. Despite a deep knowledge on coagulation cascade, poor information are available on VWF role on septic coagulation modifications. Four patients were enrolled in our study that lasted 28 days. Our study suggest that high VWF:Ag e VWF:CBA levels remain elevated during all the period evaluated. Moreover thrombocytopenia is not correlated to VWF levels. Clinical features are quite different from Moskowitz Syndrome characterized by platelets number decrease associated with high molecular weights consumption as cause-effect. VWF level trend probably correlates with endothelium injury. In fact we can assume that persistent high levels of VWF confirm a continuous and severe endothelium injury causing a multiorgan failure. VWF dosage trend may be an important prognostic index. Future improvements may include propeptide and ADAMTS13 dosage, though VWF multimers distribution does not seem to be well-matched with significant deficits of this metalloproteasi.