Summary Summary: Trauma, shock, and sepsis can lead to the activation of humoral and cellular mechanisms which in health promote blood clot formation, inflammation, and tissue repair. In patients with infections a substantial decrease of the antithrombin (AT) activity can be found which correlates with the severity of the underlying disease. In adults with septic shock an attenuation of DIC and decreased mortality can be achieved by AT administration. AT substitution is at present one of the promising options in the therapy of patients with SIRS in order to terminate DIC, prevent pulmonary microvascular obstruction, and possibly increase survival. The additional use of heparin was therapeutically not effective in shock patients with DIC. AT bound to glycosaminoglycans is able to liberate prostacyclin from human endothelial cells. Thus, intravenous heparin may compete with the physiological receptor of AT and inhibit prostacyclin release. Fresh frozen plasma and coagulation factor concentrates are indicated for balanced substitution of haemostasis in patients with bleeding and at clinically relevant risk of bleeding. In any case, procoagulant concentrate administration has to be preceded by inhibitor (AT) treatments for prevention of DIC or thromboembolism.