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Circulatory shock has a high mortality. Severe hemorrhage after injury carries a mortality rate of 30% to 40% and is responsible for almost 50% of deaths occurring within 24 hours of injury.1,2 Septic shock has a mortality of up to 50%.3 Resuscitation, starting in the prehospital setting and continuing throughout the victim's care in the ED and on into the hospital, has the goal of restoring the necessary level of tissue perfusion and oxygenation for survival while simultaneously limiting further volume loss.

Intravascular volume depletion is a common feature of circulatory shock; crystalloids, colloids, and blood products (packed red blood cells and plasma) are the primary volume expanders to reverse intravascular volume depletion. This chapter focuses on the issues related to fluid and blood resuscitation in traumatic shock, with an emphasis on hemorrhagic shock. Processes that cause loss of plasma fluid and electrolytes (e.g., dehydration, burns, sepsis), often requiring aggressive fluid therapy, are discussed in other chapters (see chapters 150, "Toxic Shock Syndromes," 151, "Sepsis," and 216, "Thermal Burns").

The principal objectives of fluid and blood resuscitation in traumatic shock are: (1) to restore intravascular volume sufficient to maintain oxygen-carrying capacity and tissue perfusion for adequate cellular oxygen delivery, and (2) to prevent or correct derangements in coagulation.


Circulatory shock is a state of impaired oxidative metabolism and homeostasis due to inadequate oxygen delivery to meet metabolic demand, and hypoperfusion leading to inadequate cellular waste removal. Acute shock triggers a complex range of physiologic responses that compensate for intravascular volume loss and maintain perfusion to the most important vascular beds. Shock also produces a global insult to the vascular endothelium that activates the coagulation and inflammatory systems (Figure 13-1). When uncorrected, coagulopathy, additional inflammation, and organ system damage result.

FIGURE 13-1.

Endothelium-mediated activation of the triad of hypoxia, inflammation, and coagulation. [©Kevin R. Ward, MD.]

While moderate transient hypoperfusion may be well tolerated, prolonged or severe hypoperfusion leads to accumulation of oxygen debt and progressive cellular and organ dysfunction. If rapid and severe, sudden cardiovascular collapse and death may occur.

Coagulopathy observed in trauma victims, termed trauma-induced coagulopathy, is ascribed to a combination of factors beginning with loss of coagulation factors from hemorrhage, followed by hemodilution from crystalloid resuscitation, and then exacerbated by acidosis (evidenced by a base deficit) and hypothermia that occur during the course of ongoing hemorrhage and resuscitation.4 These same principles also apply to other causes of shock.5 However, acidosis does not, by itself, have a significant effect on coagulation until the pH decreases below 7.0.6

The lethal triad of hypothermia, hemodilution, and acidosis can be viewed a partially iatrogenic based on the type of resuscitation provided. The ...

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