Damage Control Resuscitation: Directly Addressing the Early Coagulopathy of Trauma

Abstract

Rapid progress in trauma care occurs when the results of translational research are promptly integrated into clinical practice. Experience with a high volume of severely injured casualties expedites the process.1 Historically, these conditions have converged during times of conflict, improving the care of combat casualties and subsequently that of civilian trauma patients.1,2 In the most severely injured casualties, we know that when the lethal triad of hypothermia, acidosis, and coagulopathy are present, death is imminent.3 Current teaching is to avoid reaching these conditions by using “damage control surgery.”4–6 However, conventional resuscitation practice for damage control focuses on rapid reversal of acidosis and prevention of hypothermia, and surgical techniques focus on controlling hemorrhage and contamination. Direct treatment of coagulopathy has been relatively neglected, viewed as a byproduct of resuscitation, hemodilution, and hypothermia, and delayed by blood banking logistics. Damage control resuscitation addresses the entire lethal triad immediately upon admission to a combat hospital.7,8 By demonstrating that in the severely injured the coagulopathy of trauma is present at admission, recent studies have brought back to light the importance of treating this disorder at an earlier stage.9–12 Reports of lactated Ringer's solution and normal saline increasing reperfusion injury and leukocyte adhesion lead one to conclude that the standard crystalloid-based resuscitation guidelines in prehospital trauma life support (PHTLS) and advanced trauma life support (ATLS) may worsen the presenting acidosis and coagulopathy in severely injured trauma patients, and possibly increase ARDS, SIRS, and MOF.13–17 The safety of withholding PRBCs in hemodynamically stable patients has been demonstrated,18 and the risks associated with blood transfusion are well described.19,20 Further, massive transfusion in military and civilian casualties has been associated with an increased risk of death.21–23 Taken together, these observations suggest that the most severely injured may need a resuscitative approach tailored specifically to their needs. However, even in the largest civilian academic trauma centers, patients with injuries at the outer limits of survivability, such as those massively transfused with more than 10 units of RBCs in the first 24 hours, are uncommon and constitute only 1% to 2% of the patient population, making it difficult to develop and test new resuscitation concepts.21 Because 7% of combat casualties require massive transfusion, we have had just such an opportunity to observe the effects of new resuscitation strategies in the combat hospitals of Iraq and Afghanistan. The military munitions used in Southwest Asia can inflict severe multisystem injuries on both combatants and civilians. These patients frequently present to American military medical personnel shortly after being wounded. Unlike civilian systems, where treatment of coagulopathy is often limited by standard blood bank logistics, in Iraq we frequently have immediate access to PRBCs and thawed AB or A plasma, and rapid access to apheresis platelets, prepooled cryoprecipitate, fresh whole blood, and rFVIIa, as indicated.24–29 Thus, the opportunity to formally evaluate the immediate and direct treatment of the coagulopathy of trauma is available. The trauma patients who are most severely injured (approximately 10%) also represent the majority of in-hospital trauma deaths. Considerable attention has been directed toward the technical details of damage control surgery and reversing the acidosis and hypothermia present at admission. Less attention has been directed toward reversing the coagulopathy related to blood loss that is present at the same time. Clinical experience in Operation Iraqi Freedom and Operation Enduring Freedom suggests that coagulopathy may be present at the time of admission before significant resuscitative fluid has been given, as a consequence of acidosis-induced coagulation factor dysfunction, coagulation factor consumption, and hypothermia-induced failure of platelet activation. Failure to recognize and immediately address the coagulopathy found in severely injured patients can be linked to several factors. Most studies of trauma-induced coagulopathy have measured the laboratory changes that happen in the OR or ICU after dilution with crystalloid and PRBCs, and have concluded that the coagulopathy could be fully explained by the resuscitation and/or hypothermia.30 The goal of shock resuscitation efforts in the past has been largely to support blood pressure and urine output and to reverse the metabolic derangements associated with the ischemia associated with acute blood loss.31,32 Although these goals are obviously important, the studies supporting this concept were based on controlled animal hemorrhage studies, and the results were not evaluated in randomized human trials.33–35 Additionally, the potential benefits