CHAPTER 11 PREHOSPITAL FLUID RESUSCITATION: WHAT TYPE, HOW MUCH, AND CONTROVERSIES

Mark Newell, Vincente Gracias, Michael Rotondo

Fluid resuscitation is a vital treatment in the care of hypotensive trauma patients. Restoration of effective circulating blood volume improves oxygen delivery, thereby diminishing the untoward effects of shock at the cellular and organ level. However, fluid resuscitation, in and of itself, is not a panacea. Whereas restoration of effective circulating blood volume is essential, the method of supplying fluid is more controversial and complicated by several confounding factors. The inability to deliver definitive care in the field, the heterogeneity of patient populations, the variability in mechanism of injury, and the level of in-field hemorrhage control make precise study of the topic challenging. Therefore, the debate persists concerning the type, the amount, and the timing of fluid administration. The purpose of this chapter is to provide insight in the use of fluid resuscitation of trauma patients in the prehospital setting.

EPIDEMIOLOGY

If trauma is the leading cause of civilian death in Americans aged less than 45 years and the fourth leading cause of death in the United States for all ages,¹ hemorrhagic shock is the primary physiologic defect leading to death. Volume deficits develop not only as a result of blood loss, but also due to diffuse capillary-endothelial leak and fluid shifts from the intravascular to the interstitial space.² These deficits, and the attendant hypoperfusion, potentially lead to multiple organ dysfunction, failure, and death.²

Aggressive fluid administration has been mainstay therapy in trauma patients for over 40 years. Estimates of the numbers of trauma patients in the United Kingdom given prehospital intravenous fluid range from 8.6 to 65 patients per 100,000 population per year.³ However, for the last 15 years this practice, especially in the setting of uncontrolled hemorrhage, has been questioned.

CAUSES OF SIGNIFICANT HEMORRHAGE

The causes of hemorrhage vary depending on the mechanism of injury. In blunt trauma, bleeding usually emanates from solid organs such as the spleen and liver, mesenteric blood vessel tears, pelvic and femur fractures, thoracic bleeding from lung lacerations or intercostal vessel bleeding from rib fractures, or external causes such as scalp lacerations. Uncontained bleeding from aortic transection and cardiac rupture usually leads to exsanguination at the scene. When the wounding mechanism is secondary to penetrating trauma, uncontrolled major vascular injury usually is the source of the hemorrhage.

DIAGNOSIS/ASSESSMENT

In the prehospital setting, emergency medical technicians perform an immediate assessment of the trauma victim in the form of a primary and secondary survey. This assessment includes an evaluation of the patient for life-threatening conditions that need to be promptly addressed. The patency of the airway is initially evaluated. This is followed by auscultation of breath sounds assessing for pneumothoraces or hemothoraces. Attention is then turned to the circulation. Central and peripheral pulses are assessed. Obvious sources of external bleeding are controlled. The patient’s blood pressure is measured. Because definitive care cannot be rendered at the scene, a “scoop and run” rather than a “stay and stabilize” philosophy should be evoked. Attempts at intravascular cannulation should not delay transfer to the trauma center.

CLASSES OF HEMORRHAGIC SHOCK

Hemorrhage is the most common cause of shock in the injured patient.⁴ Shock is defined as the presence of inadequate organ perfusion and tissue oxygenation.⁴ In the presence of inadequate oxygen for normal aerobic metabolism, anaerobic metabolism occurs leading to lactic acidosis. If this process continues, cellular membranes lose their integrity leading to cellular swelling, progressive cellular damage, and ultimately, cellular death.⁴

Hemorrhage, an acute loss of circulating blood volume, is classified based on the percentage of blood volume loss. Specific hemodynamic, respiratory, central nervous system, urinary, and integumentary changes occur given the degree of shock (Table 1). Whereas class I hemorrhage is associated with minimal clinical symptoms and requires little, if any, volume replacement, class IV hemorrhage is immediately life-threatening, necessitates blood transfusion, and usually calls for surgical intervention to halt ongoing bleeding.⁴

Table 1 Classification of Hemorrhagic Shock

MANAGEMENT

Access

The basic management principles to follow in hemorrhagic shock are to stop the bleeding and replace the volume loss. Establishing a patent airway with adequate ventilatory exchange and oxygenation is the first priority. Supplemental oxygen is supplied while external bleeding is controlled. Two large-caliber (minimum of 16-gauge) peripheral intravenous catheters are inserted, preferably in the antecubital veins.⁴ Intravenous access should not delay transport of the patient to the trauma center.

Types of Fluid

Crystalloid

A crystalloid is a solution of small nonionic or ionic particles. They are freely permeable to the vascular membrane and are distributed mainly in the interstitial space. As such, only one-third of the volume of crystalloid infused expands the intravascular space. This accounts for the need to provide at least three times more volume of crystalloid than the volume of blood lost. Because of decreased colloid osmotic pressure secondary to decreased serum protein concentration from hemorrhage, capillary leaks, and crystalloid replacement, this ratio of volume of crystalloid infused to blood volume lost may even approach 7–10:1.⁵

Depletion of both the interstitial fluid volume and the intravascular space following severe injury may be a reason to use crystalloids for fluid resuscitation, which restore volume to both spaces.⁶ Animal and human studies demonstrating improved survival from shock when utilizing isotonic fluid and blood versus blood transfusion alone support this view. Other advantages of crystalloid use in prehospital fluid resuscitation include its negligible cost in comparison to other resuscitative fluids, immediate availability, and long-term storage capacity.

Given the predilection of crystalloid to primarily fill the interstitial space, tissue edema is common and may have deleterious effects. In head-injured patients, increased brain edema may adversely affect outcome. Gas exchange may be impaired secondary to pulmonary edema. Endothelial and red cell edema impair microcirculation and tissue oxygen exchange, potentially contributing to multiple organ dysfunction.⁵

According to Advanced Trauma Life Support (ATLS) guidelines, fluid resuscitation of the trauma patient begins with a 2-L bolus of crystalloid, usually lactated Ringer’s (LR) solution. LR is an isotonic fluid that contains L-lactate and D-lactate in a 50:50 mixture. The L-lactate is metabolized in the liver to bicarbonate, thereby providing additional buffer. Although the D-lactate isomer is thought to be a cause of acidosis, studies have shown that resuscitation with LR does not lead to increased lactic acid levels.⁷ However, normal saline (NS), another isotonic crystalloid, can induce a hyperchloremic acidosis when given in large volumes because of its concentration of chloride ions (154 mEq/l).⁶ Healey et al.⁷ suggest, in their animal model of massive hemorrhage, increased survival rate in animals resuscitated with LR and blood relative to those animals that received NS and blood. This difference was thought to be secondary to the profound acidosis occurring in the NS/blood group.

Because LR has a lower osmolality than plasma (273 mOsm/l vs. 285–295 mOsm/l), large volumes of LR can reduce serum osmolality and contribute to cerebral edema. For this reason, NS may be the preferred resuscitative fluid in head-injured patients.⁶

Hypertonic sodium chloride (HS) in concentrations ranging from 3% to 7.5% has been used for the treatment of hypovolemic shock.² Because of its elevated osmolality (2400 mOsm/l in 7.5%), HS produces an increase in intravascular volume that far exceeds the infused volume⁶ (Table 2). The cardiovascular effects of HS include improved myocardial contractility, decreased systemic and pulmonary vascular resistance, mobilization of tissue edema into the blood compartment, and reduction in venous capacitance.^2,⁶ These effects are transient, however, so HS has been mixed with colloids (dextran or hydroxyethyl starch) to prolong its efficacy, especially when used for small volume resuscitation.

Table 2 Effect on Plasma Volume Expansion of Various Solutions

Volume Infused (ml)	Fluid Infused	Plasma Volume Expansion (ml)
1000	D₅W	100
1000	Lactated Ringer’s	250
250	7.5% hypertonic saline	1000
500	5% albumin	375
100	25% albumin	450
500	6% hetastarch	750

Modified from Rizoli SB: Crystalloids and colloids in trauma resuscitation: a brief overview of the current debate. J Trauma 54:S82–S88, 2003.

HS decreases intracranial pressure (ICP), primarily in areas of the brain with an intact blood-brain barrier.⁸ Cooper et al.,⁹ in a double-blind, randomized controlled trial of hypotensive patients with severe traumatic brain injury, studied the effects of prehospital resuscitation with hypertonic saline versus Ringer’s lactate on neurological outcome. These investigators did not find a significant difference in 3- or 6-month extended Glasgow Outcome Scores between the two groups.

Immunomodulatory effects of HS, either immunostimulatory or immunosuppressive depending on the concentration, have been described. HS affects nuclear activation, protein synthesis and proliferation, polymorphonuclear leukocyte function, and cytoskeleton polymerization. In animal models of hemorrhage, these effects have been associated with reduced organ dysfunction and improved survival.⁸

Despite its benefits, a meta-analysis evaluating the effect of HS compared to isotonic crystalloid on 30-day outcome in trauma patients failed to show a survival advantage.¹ As such, the role of HS in prehospital fluid resuscitation has yet to be defined.

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