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A Shock Toxin That Produces Disseminated Intravascular Coagulation and Multiple Organ Failure

 

作者: Robert,   Hardaway Yvonne,  

 

期刊: The American Journal of the Medical Sciences  (OVID Available online 2001)
卷期: Volume 322, issue 4  

页码: 222-228

 

ISSN:0002-9629

 

年代: 2001

 

出版商: OVID

 

关键词: Shock;Septic shock;Traumatic shock;Disseminated intravascular coagulation;Multiple organ failure;Acute respiratory distress syndrome

 

数据来源: OVID

 

摘要:

ObjectiveTo introduce a new concept in the etiology and treatment of traumatic and septic shock. It describes 3 types of shock: (1) hypovolemic shock, (2) traumatic shock, and (3) septic shock.BackgroundThe mortality of septic shock in both total number and mortality rate has been increasing over the past 40 years despite major advances in diagnosis and treatment, including a number of “magic bullets.” Trauma is the No. 1 cause of death in persons under the age of 44 and the No. 3 cause of all deaths. Traumatic shock has been assumed to be caused by hypovolemia; however, many traumatic shock patients die with a normal blood volume, usually after several days. Septic shock in pigs using an injection of killedEscherichia coliorganisms produced disseminated intravascular coagulation (DIC). Control pigs treated with plasminogen activator survived. Septic shock in humans also treated with plasminogen activator showed excellent results. Traumatic shock studied in pigs showed excellent results with plasminogen activator. A normal blood volume was maintained with the use of intravenous fluids. Traumatic shock in humans also treated by plasminogen activator showed excellent results. The improvement in Pao2and other parameters demonstrated in these studies provides a new possibility in the treatment of trauma and/or sepsis induced acute respiratory distress syndrome (ARDS). DIC is almost always present in traumatic and septic shock and probably in the course of ARDS and multiple organ failure. The DIC is probably initiated by tissue cell or bacterial cell destruction, which liberates a thrombogenic aminophospholipid that forms the inner layer of all cell walls.

 

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