Shock is a pathophysiologic state triggered by failure to adequately deliver oxygen to the cellular level and perpetuated by the cellular response to ischemia. Shock can be caused by a wide variety of conditions and, once initiated, can become a rapidly fatal downward spiral. Shock is a leading cause of both early and late mortality following traumatic injury. Although shock is easily diagnosed in the clinical setting, effective treatment is complex and dynamic and may require the utmost resources of the hospital and its personnel. Clinical indicators of shock include:

The term shock was first used to describe the pathophysiology occurring after injury by the English surgeon Guthrie in 1815, in On Gunshot Wounds of the Extremities.<sup>28 Peterson C.G., Haugen F.P. Hemorrhagic shock and the nervous system Am J Surg 1963 ;  106 : 233-239

Cliquez ici pour aller à la section Références</sup> In a description in 1872, Gross<sup>14 Gross S.G.   A system of surgery: Pathological, diagnostic, therapeutic, and operative Philadelphia: Lea & Febiger (1872). 

Cliquez ici pour aller à la section Références</sup> described shock as “a rude unhinging of the machinery of life.” Early speculation on the cause of shock included theories of systemic toxins released by injured muscle tissue and vagal hyperactivity producing loss of vasomotor tone and cardiac exhaustion. In the late 1900s, Crile and then Blalock in the 1930s demonstrated definitively that hypovolemia was the leading contributor to shock after injury. The concept of an irreversible deficit at the cellular level was first proposed in the early 1940s by Wiggers. Modern research has focused on the role of shock in producing organ system dysfunction and, once again, on circulating systemic toxins, now referred to as inflammatory mediators.<sup>2 Anderson R.N., Vaslef S.N. Shock Textbook of Surgery Philadelphia: WB Saunders (1997).  68-69

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