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KEY POINTS

KEY POINTS

  • In shock, there is an imbalance between substrate delivery (supply) and substrate requirements (demand).

  • In the neuroendocrine response to shock, the hypothalamus releases corticotrophin-releasing hormone, causing pituitary release of adrenocorticotropin hormone followed by adrenal cortex release of cortisol.

  • Shock-activated neutrophils and their products may produce bystander cell injury and organ dysfunction.

  • Because it is difficult to measure oxygen debt during resuscitation of trauma patients, surrogate parameters such as base deficit and serum lactate are measured.

  • Crystalloid solutions pass relatively freely across the vascular endothelium and damaged endothelial glycocalyx layer in shock, and this can result in pronounced expansion of the extracellular fluid compartment.

  • Lyophilized plasma is compatible with all blood types and can be stored at room temperature for up to 2 years, and its reconstitution requires less than 6 minutes.

  • The principles of damage control resuscitation are permissive hypotension, restriction of crystalloid resuscitation, earlier blood and component resuscitation in appropriate ratios, and goal-directed correction of any coagulopathy.

  • Exceptions to damage control resuscitation include elderly patients and those with traumatic brain injuries.

  • Viscoelastic assays of coagulation such as thromboelastography and rotational thromboelastometry are now commonly used to correct any coagulopathies during resuscitation.

  • Forms of shock include hypovolemic, neurogenic, cardiogenic, septic, obstructive, and traumatic.

A MODERN HISTORY OF SHOCK

In 1872, Dr. Samuel Gross, the American trauma surgeon immortalized in the Thomas Eakins painting, The Gross Clinic, described shock as a “rude unhinging of the machinery of life.”1 Although imprecise, this rendering of the shock state elegantly characterizes the manifestation of the physiologic derangements of decompensated shock. More precisely, shock is the inadequate delivery of oxygen to and removal of potentially toxic metabolites from tissues, which leads to cellular dysfunction and injury. Significant tissue hypoperfusion and cellular injury may occur despite normal systemic blood pressure; 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. Therefore, understanding oxygen kinetics, the principle physiologic derangements that occur during shock, host responses to malperfusion, and ways to diagnose and reverse shock states can improve the outcome of injured and critically ill patients.

The initial cellular injury that occurs as a result of tissue malperfusion and dysoxia is reversible. However, cellular injury will become irreversible if tissue hypoperfusion is prolonged or severe enough such that compensation is no longer possible. Rapid recognition of the patient in shock and the prompt institution of steps to correct shock are critical skills for the trauma surgeon and team.

The management of the patient in shock has been integral to the surgeon’s expertise for centuries. In 1854, the French physiologist Claude Bernard suggested that an organism attempts to maintain constancy in the internal environment despite external forces that attempt to disrupt the milieu intérieur2; this idea was later refined into the concept of ...

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