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Initial evaluation of shock in the adult trauma patient and management of NON-hemorrhagic shock

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 brain injury as the leading cause of death from trauma [2,3].

This topic will review the evaluation of shock in the adult trauma patient, focusing on recognition of shock, basic initial management, and acute interventions needed to treat non-hemorrhagic causes of shock. General management of the adult trauma patient, management of hemorrhagic shock, and other aspects of shock, including the pathophysiology and differential diagnosis, are discussed separately. (See "Initial management of trauma in adults" and "Initial management of moderate to severe hemorrhage in the adult trauma patient" and "Definition, classification, etiology, and pathophysiology of shock in adults".)


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]. The pathophysiology of shock is discussed in greater detail separately. (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: Nov 2017. | This topic last updated: Nov 13, 2017.
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