title: [Septic shock in the urologic patient. II. Pathomechanisms of hemostatic disorders (author's transl)].
abstract: In urosepsis endotoxins usually deriving from gram-negative bacteria can initiate primary disturbances of hemostasis by activation of coagulation up to clinically manifest consumption coagulopathy. The reaction is triggered by an endotoxin induced alteration of granulocytes, endothelial cells, and platelets, thereby releasing procoagulant activities that possibly cause diffuse intravascular coagulation with impairment of vital organs. Additional negative effects on hemostasis can be caused by secondary hyperfibrino(geno)lysis. Secondary disturbances of hemostasis occur in urosepsis as a consequence of an impairment of liver (hypoproduction of coagulation factors, decrease of the clearance of activated coagulation factors) and kidney function (thrombocytopathy by uremic toxins). Disturbances of hemostasis induced by the treatment of urosepsis are the K-hypovitaminosis in parenteral feeding accompanied by antibiotics affecting the intestinal bacterial growth and the alteration of platelet function and fibrin formation by carbenicillin.
mesh_terms: D002228:Carbenicillin / Q000627:therapeutic use; D004211:Disseminated Intravascular Coagulation / Q000209:etiology; D006487:Hemostasis; D006801:Humans; D012772:Shock, Septic / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D014813:Vitamin K Deficiency / Q000209:etiology
chemical_list: D002228:Carbenicillin
vernacular_title: Urosepsis bis septischer Schock: II. Pathophysiologie der Hämostasestörungen.