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INTRODUCTION

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. Hemorrhagic shock is an important contributor to postresuscitation organ failure and late mortality.1 Resuscitation of traumatic shock, 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.

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., burns, sepsis), often requiring aggressive fluid therapy, are discussed in other chapters (see Chapter 151, “Sepsis,” and Chapter 217, “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.

PATHOPHYSIOLOGY

Hemorrhagic shock creates 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. Hemorrhagic shock triggers a complex range of physiologic responses that may temporarily 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 will 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 tissue hypoxia, 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.2,3 However, acidosis does not, by itself, have a significant effect on coagulation until the pH decreases below 7.0.4

The normal total circulating volume of an adult is approximately 7% of ideal body weight or about 5 L for an average 70-kg adult patient divided into about 3 L of plasma and 2 L of red blood cell volume (Table 13-1). Replacement of lost blood with room temperature isotonic unbuffered crystalloid contributes to hypothermia, hemodilution, and acidosis.

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