A review of septic shock.
The mortality of septic shock, both in percentage of septic shock cases and total number of septic shock cases, has been increasing over the past several decades. This is despite major advances in diagnosis and treatment. The basic cause of traumatic and septic shock has only partially been elucidated. This review presents information about the basic cause and mechanism of septic shock as well as a new treatment based on this information. Data sources include research papers on the subject of septic shock from 1875 until the present. These papers numbered more than 10,000, most of which are not included in the reference list because many are duplicative. The main result of the review of literature is that all of a wide variety of treatments of septic shock have not resulted in a lowering of mortality, but in fact have increased it. Another toxin (in addition to endotoxin and its secondarily induced host mediators) is proposed. This toxin causes disseminated intravascular coagulation, which may obstruct the microcirculation of any and all organs, producing multiple organ failure by microclots. These microclots may be lysed by plasminogen activator and circulation to the organs restored.
Hardaway
R M
RM
Department of Surgery, Texas Tech University Health Sciences Center, El Paso, USA.
D000818:Animals; D017152:Antibodies, Antiphospholipid / Q000097:blood; D004195:Disease Models, Animal; D004211:Disseminated Intravascular Coagulation / Q000209:etiology / Q000503:physiopathology; D004285:Dogs; D006801:Humans; D010960:Plasminogen Activators / Q000627:therapeutic use; D011817:Rabbits; D012772:Shock, Septic / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D013552:Swine; D014568:Urokinase-Type Plasminogen Activator / Q000627:therapeutic use
D017152:Antibodies, Antiphospholipid; D010960:Plasminogen Activators; D014568:Urokinase-Type Plasminogen Activator