[Basics in the pathophysiology of sepsis]

Within the recent years preclinical and clinical investigations to a great extend increased the pathophysiological understanding what is going on in patients with severe sepsis. It became evident, that not the initiating infection by itself is the main reason for the severity and limited prognosis in sepsis. More important is the unbalanced reaction of the patient's organism to this infection, which is reflected in a mainly cytokine driven inflammation, the so called systemic inflammatory response syndrome, with its consequences. In the context of this syndrome released mediators, in part together with toxins from infectious microorganisms, result in a systemic activation of haemostasis. In the centre of our pathophysiologic model are the activations of the monocyte/macrophage-system and of the endothelium. This results in the activation of plasmatic cascades including the coagulation and fibrinolysis systems. The observed activation of haemostasis and inhibition of fibrinolysis in patients with sepsis by themselves interact with leukocytes and endothelium and play an important role in the progressive derangement of microcirculation. This is clinically reflected in organ dysfunctions. Within a single individual patient there is increased fibrin formation, decreases in coagulation factors, inhibitors and platelets, as well as defects of the fibrinolytic system in parallel that may clinically result in disseminated intravascular coagulation with the risk of bleeding complications in addition to organ dysfunctions.