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Initial evaluation and management of shock in adult trauma

Christopher Colwell, MD
Section Editor
Maria E Moreira, MD
Deputy Editor
Jonathan Grayzel, MD, FAAEM


Shock refers to inadequate tissue perfusion, which manifests clinically as hemodynamic disturbances and organ dysfunction. At the cellular level, shock results from insufficient delivery of required metabolic substrates, principally oxygen, to sustain aerobic metabolism.

In the setting of trauma, loss of circulating blood volume from hemorrhage is the most common cause of shock. Inadequate oxygenation, mechanical obstruction (eg, cardiac tamponade, tension pneumothorax), neurologic dysfunction (eg, high-spinal cord injury), and cardiac dysfunction represent other potential causes or contributing factors [1]. Shock is a common and frequently treatable cause of death in injured patients and is second only to traumatic brain injury as the leading cause of death from trauma [2,3].

This topic review will discuss the evaluation and initial management of shock in the trauma patient. The initial management of the trauma patient, a general overview of shock, including pathophysiology and differential diagnosis, and discussions of the management of shock in other clinical circumstances are presented elsewhere. (See "Initial management of trauma in adults" and "Definition, classification, etiology, and pathophysiology of shock in adults" and "Evaluation and management of suspected sepsis and septic shock in adults" and "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction".)


The pathophysiology of shock primarily relates to an imbalance in oxygen supply and demand. Patients in shock suffer from a critical reduction in the oxygen available to the mitochondria. Adenosine triphosphate (ATP) can still be synthesized by anaerobic glycolysis but at only 5 to 10 percent of the normal rate [4]. Anaerobic glycolysis results in the accumulation of pyruvate, which is converted to lactate [5]. (See "Definition, classification, etiology, and pathophysiology of shock in adults".)

The compensatory physiologic responses to acute hemorrhage attempt to maintain adequate oxygen delivery to tissues. Stimulation of the sympathetic nervous system results in an increased heart rate, vasoconstriction, and increased ventricular contractility. As the shock state progresses, vital organ (eg, brain and heart) perfusion can only be maintained at the expense of nonvital organs. If the process is not reversed, progressive lactate production leads to worsening systemic metabolic acidosis, which along with hypoxemia ultimately causes the loss of peripheral vasoconstriction and cardiovascular collapse.


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Literature review current through: Sep 2016. | This topic last updated: Dec 11, 2015.
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