Fluid Choice for Resuscitation in Trauma

The “ideal” fluid replacement regimen in trauma patients is still discussed controversially. Aside from blood, several nonblood alternatives—including crystalloids, hypertonic solutions, albumin, and nonprotein (synthetic) colloids—are available to correct hypovolemia in the trauma patient. Interpretation of the literature is difficult because of variations in study design, patient population, target for volume replacement, end points, and type of fluids. Metaanalyses are not very helpful because patients of all types, not just trauma patients, and very old studies are included. Reviewing the meager literature on this issue, the choice of fluid therapy in trauma patients engenders the most controversy. Recommendations for fluid resuscitation in trauma patients are more likely based on “personal guidelines” than on research results. It is imperative to continue the search for substances that are effective in avoiding development of posttrauma multiorgan dysfunction syndrome and that are without detrimental side effects. Trauma is the fourth leading cause of death in the United States. Volume deficits are often present in trauma patients (Fig. 1) and may result in the development of posttrauma multiple organ failure in the intensive care unit (ICU). In addition to apparent blood loss, fluid deficits may also occur secondary to generalized alterations of the endothelial barrier, resulting in diffuse capillary leakage and fluid shift from the intravascular to the interstitial compartment. Adequate volume therapy appears to be fundamental in the management of the trauma patient. In a prospective review of 111 consecutive patients who died in hospital after admission for treatment of injuries, the most common defect in patients’ care was related to inadequate fluid resuscitation. Trauma patients are definitely different from cardiac surgery patients, patients with malignancies undergoing surgery, or septic patients; thus, volumereplacement strategies should be considered separately for these patients. Besides (hypo-, iso-, and hypertonic) crystalloids, human albumin (HA), and various synthetic colloids (e.g., dextrans, gelatins, hydroxyethyl starch [HES] preparations) are available to treat trauma-related volume deficits. In recent years, the crystalloid/colloid dispute has been enlarged to a colloid/colloid debate because, aside from the natural colloid albumin, several synthetic colloids are increasingly used as plasma substitutes in the trauma patient. Aggressive prehospital fluid administration (“in the field”) has been common practice for more than 25 years in trauma patients. Some recent studies, however, have shown that early volume restoration in certain types of trauma before definite hemostasis has been performed may result in accelerated blood loss, hypothermia, and dilutional coagulopathy. It has been recommended that volume replacement should not be started early (concept of “permissive hypotension,” “scoop and run” principle). This review is not designed to intensify the controversy between delayed fluid resuscitation and early (field) volume replacement because different emergency care systems make a comparison between countries almost impossible; subsequently, no clear general recommendation can be given. Instead, this review is aimed to recall the options for volume replacement in trauma patients. Pathophysiology of Shock in the Trauma Patient Hemorrhage-related hypovolemia after trauma can be divided into three phases: • Phase I is the period from injury to operation for control of bleeding (predefinite care), • Phase II is the period immediately during and after surgery, and • Phase III is the period of the trauma patient in the ICU (postdefinite care). Trauma-related hypovolemia may be associated with flow alterations that are inadequate to fulfill the nutritive role of the circulation. Many of the manifestations of organ failure after successful primary resuscitation after trauma may result from peripheral, microcirculatory derangements. In spite of achieving “normal” systemic hemodynamics, it is not guaranteed that perfusion in all organs and tissues is maintained as well. During low output Figure 1. Reasons of in-hosptal trauma death. CNS, central nervous system. (Data derived from Sauaia et al.) International TraumaCare (ITACCS) www.itaccs.com 58 syndrome, the organism tries to compensate perfusion deficits by redistribution of flow to vital organs (e.g., heart, brain) resulting in an underperfusion of other organs (e.g., splanchnic bed, kidney). Inflammatory mediators and vasopressors are released in this situation and are of particular importance for development of impaired perfusion. Recent evidence suggests that the endothelium is not only a passive barrier between the circulating blood and the tissue, but may also be markedly involved in the regulation of microcirculatory blood flow by producing important regulators of the vascular tone (e.g., prostaglandins, nitric oxide, endothelins, angiotensin II). The regional regulation of blood flow is likely due to a balance between systemic mechanisms (e.g., the autononous nervous system) and other more locally active blood flow regulators. One important approach to improve perfusion in this situation appears to be the use of adequate volume. Our pathophysiologic knowledge of the importance of the endothelium in modulating microcirculation and inflammation has increased; however, the influence of different volume-replacement strategies on endothelial function has still to be elucidated. Goals of Volume Replacement in the Trauma Patient The primary goal of volume administration is to guarantee stable systemic hemodynamics and microcirculation by rapidly restoring circulating plasma volume (Table 1). Excessive fluid accumulation, particularly in the interstitial tissue, should be avoided. The infused fluid may stay in the intravascular compartment or equilibrate with the interstitial/intracellular fluid compartments. Different mechanisms are involved in the control of volume and composition of each compartment including the antidiuretic hormone and the renin-angiotensin systems. The principal action of these systems is to retain water to restore water or intravascular volume deficits, to retain sodium to restore intravascular volume, and to increase hydrostatic perfusion pressure by vasoconstriction. Increased activity of these systems is known to occur in stress situations, such as trauma. If water or intravascular volume deficits and the stress-related stimuli are additive, volume therapy may inhibit this process through counterregulatory mechanisms. Antidiuretic hormone production depends on sufficient extracellular volume, in particular of the intravascular compartment. Administration of a restricted amount of crystalloid could replace a water deficit, but the replacement of an intravascular volume deficit would require much more volume to inhibit the activation of this system. Thus, it can be expected that replacement of only water (crystalloids) will not inhibit the normal response of antidiuretic hormone and renin-angiotensin, whereas administering a combination of crystalloids and colloids (replacement of water deficit and simultaneous maintainance of a sufficient intravascular volume) may achieve this goal. One important aspect of fluid therapy in the traumatized patient is the risk of inducing interstitial edema. Tissue edema is related to an imbalance in the sum of the Starling forces across capillary membranes or an increase in protein permeability, by which an increase in fluid flux to the interstitial space is promoted. A decrease in membrane integrity, an increase in hydrostatic pressure, and a decrease in intravascular colloid oncotic pressure (COP) will induce fluid movement across the microvascular membrane and may produce interstitial fluid accumulation (e.g., pulmonary edema). Moreover, endothelial swelling may also occur by which organ perfusion is further disturbed. Thus, the choice of fluid for correcting hypovolemia in trauma patients should take this regulatory issue into account. Fluid Choice in Trauma Resuscitation The choice of fluid therapy engenders the most controversy, and an examination of the body of literature on this subject results in confusion. Volume replacement in the trauma patient should not only aim at increasing the circulating intravascular volume, adverse effects, effects on inflammation, perfusion and tissue oxygenation should be considered as well. The different fluids show varying effects on the volume compartments (Table 2).