Marx F J, Hofstetter A, Schilling A
Urologe A. 1977 Jul;16(4):241-3.
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.
在泌尿道脓毒症中，通常源自革兰氏阴性菌的内毒素可通过激活凝血引发止血的原发性紊乱，直至临床上出现明显的消耗性凝血病。该反应由内毒素诱导的粒细胞、内皮细胞和血小板改变所触发，从而释放促凝血活性，这可能导致弥漫性血管内凝血并损害重要器官。继发性高纤维蛋白（原）溶解可对止血产生额外的负面影响。泌尿道脓毒症中止血的继发性紊乱是由于肝脏功能受损（凝血因子产生减少、活化凝血因子清除减少）和肾脏功能受损（尿毒症毒素导致血小板病）所致。泌尿道脓毒症治疗引起的止血紊乱包括肠外营养中的K缺乏性维生素症，伴有影响肠道细菌生长的抗生素，以及羧苄青霉素引起的血小板功能和纤维蛋白形成改变。
