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INTRODUCTION

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Shock is defined as the inadequate delivery of oxygen to tissues leading to cellular dysfunction and injury. In 1872 Gross described shock as a “rude unhinging of the machinery of life.”1 Although this definition is less than precise, to this day it illustrates the physiologic derangements of decompensated shock. Significant hypoperfusion and cellular injury may occur despite normal systemic blood pressure, so equating shock with hypotension and cardiovascular collapse is a vast oversimplification and results in delayed recognition of early shock, when intervention is most effective at preventing end-organ dysfunction.

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Shock is most precisely defined as inadequate delivery of oxygen and nutrients and removal of metabolites necessary for normal tissue and cellular function. The initial cellular injury that occurs is reversible. However, the injury will become irreversible if tissue hypoperfusion is prolonged or severe enough such that, at the cellular level, compensation is no longer possible. Rapid recognition of the patient in shock and the prompt institution of steps to correct shock is a critical skill for the trauma surgeon. Surgeons caring for injured patients must frequently initiate active treatment empirically, prior to a definitive diagnosis of the cause of shock.

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The management of the patient in shock has been an integral component of the surgeon’s realm of expertise for centuries. Bernard suggested that an organism attempts to maintain constancy in the internal environment despite external forces that attempt to disrupt the milieu intérieur.2 In the intact animal, the failure of physiologic systems to buffer the organism against these external forces results in the shock state. In addition, recent serial analysis of the genomic response to severe injury further identifies that the patients able to most rapidly restore homeostasis have the best outcomes.3 Cannon described the “fight or flight response” generated by elevated levels of catecholamines in the bloodstream and introduced the term homeostasis in 1926. He spent 2 years on the battlefields of Europe and published his classic monograph, Traumatic Shock, in 1923. Cannon’s observations led him to propose that shock was due to a disturbance of the nervous system that resulted in vasodilatation and hypotension. He proposed that secondary shock with its attendant capillary permeability leak was caused by a “toxic factor” released from the tissue.4,5 Interestingly, Cannon is also credited with first proposing deliberate hypotension in patients with penetrating wounds of the torso to minimize internal bleeding since “if the pressure is raised before the surgeon is ready to check the bleeding that may take place, blood that is sorely needed may be lost.”6

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Blalock documented that shock after hemorrhage was associated with reduced cardiac output and that hemorrhagic shock was due to volume loss, not a “toxic factor.”7 He also noted, however, that toxins could be important initiators of shock. In 1934, Blalock proposed the following four categories of shock that are still utilized today: hypovolemic, vasogenic, cardiogenic, ...

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