Zerbino D D, Lukasevich L L
Arkh Patol. 1983;45(12):13-20.
Examinations of 43 section observations of shock established that the role of the syndrome of disseminated intravascular blood coagulation (DIBC) in the development of shock was variable: in some cases it caused the shock condition (embolism with amniotic waters, premature desquamation of the placenta), in others it is its consequence (hemorrhagic, cardiogenic shock). Morphogenesis of the DIBC syndrome is different depending on its role in the development of the shock condition. The DIBC syndrome as the cause of shock is characterized by completeness of thrombus formation processes and the presence of thrombi consisting of fibrin and/or formed blood elements. The time of formation of microthrombi in various organs is approximately the same and coincides with the period of shock development in the clinical picture. The characteristic morphological features of DIBC as the consequence of the shock include incomplete thrombus formation processes with the presence of pre-thrombi and/or strands and filaments of fibrin, involvement of the adrenals, the presence of the phenomenon of fibrin lining of vascular walls. The time of development of intravascular coagulation does not coincide with shock occurrence and may be different in various parts of the microcirculatory bed.
对43例休克切片观察的研究表明,弥散性血管内凝血(DIBC)综合征在休克发展过程中的作用各不相同:在某些情况下,它会引发休克状态(羊水栓塞、胎盘早期剥离),而在其他情况下,它是休克的后果(出血性、心源性休克)。DIBC综合征的形态发生取决于其在休克状态发展中的作用,因而有所不同。作为休克病因的DIBC综合征的特征是血栓形成过程完整,且存在由纤维蛋白和/或血液有形成分构成的血栓。不同器官中微血栓的形成时间大致相同,且与临床表现中休克发展的时期相符。作为休克后果的DIBC的特征性形态学表现包括血栓形成过程不完整,存在血栓前体和/或纤维蛋白条索及细丝,肾上腺受累,血管壁出现纤维蛋白衬里现象。血管内凝血的发展时间与休克发生不一致,且在微循环床的不同部位可能有所不同。