The Changing Landscape of Trauma Care, Part 2

Introduction

For decades, virtually all injury was treated with open operative surgery. Resuscitation was based on the belief that large-volume crystalloid infusion to raise blood pressure (BP) to normal was the optimal therapy. Advanced trauma life support teaching was that 2 L of crystalloid fluid should be the initial resuscitation for all trauma patients, and those who failed to respond should receive additional crystalloid fluid. Patients did not receive a blood transfusion until later in treatment, and fresh frozen plasma (FFP) and platelets were not given until 10 U of blood had been administered. Regardless of the fluid infused, the goal of initial resuscitation was to raise BP to a normal level. During the time I (TS) was chair of the emergency medicine department at the State University of New York’s Kings County Hospital, I remember administering liters of crystalloid fluid preoperatively, believing it was not safe to operate until the patient had been what we termed “adequately resuscitated.”

However, as early as 1918, Walter B. Cannon, MD, correctly observed that fluid therapy without hemostasis was not wise, and numerous animal studies since then also raised serious questions about this approach. This article points out the revolutionary changes in the thinking and practice of resuscitation that have occurred in the last 20 years. We now realize that raising BP to normal only perpetuates hemorrhage. Hypotension treated with additional volume resuscitation without surgical control of hemorrhage creates a cycle leading to dilution of clotting factors and red blood cells (RBCs), recurrent hypotension, and ultimately death.

The realization that early blood transfusion is probably the wisest course is a concept that has only been in clinical practice for less than 15 years. Major trauma centers now routinely keep type O negative blood in the ED refrigerators so that it is instantly available.

Our understanding of trauma coagulopathy also has changed dramatically. Once thought to be simply a consequence of hypotension and hypothermia, we now realize that coagulopathy following trauma is far more complicated and likely occurs in concert with the inflammatory response to serious injury. Regardless of its etiology, we have recognized that earlier administration of plasma and platelets following trauma prevents coagulopathy, and this approach is more beneficial than treating coagulopathy after it develops. There has been much debate about the optimal ratios of RBCs, plasma, and platelets, and the ideal ratio has yet to be determined. The idea that “one-size-fits-all” is almost certainly not the case: Different patients require different and more precise treatment strategies.

For years, we have relied on laboratory measurements of coagulation to guide transfusion therapy, but standard laboratory values often take over 30 minutes to obtain. In an extremely dynamic situation involving large-volume blood loss, this interval is too lax. A more personalized approach using rapidly available technology, such as thromboelastography (TEG), allows for real-time assessment of a multiplicity of coagulation dynamics and rapid correction of any abnormalities. Procoagulants such as factor 7A, prothrombin complex concentrate (PCC), and tranexamic acid (TXA) have a role. However, the data to support the use of these expensive agents is lacking. While they certainly can be life-saving, each of these components brings with it a risk of causing indiscriminate coagulation—even in areas of the body that are not injured. Moreover, their availability in nontrauma centers is either limited or not an option.

There is little question that our rapid advances in understanding resuscitation and transfusion practice has saved lives. Twenty years ago, intensive care units were populated by trauma patients who had received many liters of crystalloid fluid, and at least partly a consequence of the resuscitation experience, many had severe respiratory failure. Open abdomens were common and also a likely consequence of large-volume crystalloid use. While these problems have not entirely disappeared, they now occur much less frequently.

Standardizing trauma care has also helped enhance patient care a great deal. Most major trauma centers have a “massive transfusion” protocol which allows the blood bank to prepare coolers containing not only blood, but also plasma, platelets, and procoagulants. This practice obviates the need to order the components individually. Rapid access to technology such as TEG allows emergency physicians (EPs) and other trauma care professionals to precisely guide transfusion therapy, but this remains an area of intensely debated investigation. Hopefully, our understanding will continue to mature over the next few years.

Another area of trauma care that has rapidly evolved is the use of endovascular techniques for trauma hemostasis. The realization that we can obtain control of vascular injury without the need for a large open operation has revolutionized care. While endovascular techniques have been used for pelvic hemostasis since 1972, we now use it regularly in every body cavity. Splenic artery embolization was developed by our (TS) group in Brooklyn, New York in 1995, and its use has now expanded to other abdominal solid organ injuries.

Injuries to the thoracic aorta once required a thoracotomy, cardiopulmonary bypass, and open repair. Stent grafting is now the treatment of choice for these injuries, allowing for a minimally invasive solution, and permitting those with both aortic and many other injuries to receive care for all of these wounds much sooner than was possible in the past, when multiply injured patients were simply not considered candidates for early open repair.

Thoracotomy in the ED has been widely practiced for a variety of indications. While it is still the only available solution for injury to the heart and/or proximal pulmonary vasculature in a patient who is hemodynamically unstable and/or in extremis, other options now exist to obtain vascular inflow for patients bleeding in the abdomen or pelvis. The use of transfemoral balloons for aortic occlusion allows clinicians to temporize hemorrhage without a huge open operation, and resuscitative endovascular balloon occlusion of the aorta (REBOA), has only been available for the last several years. The exact indications, wisest strategy, length of time the balloon can be inflated, rate of complications, and who is the appropriate physician (eg, EP, intensivist, vascular surgeon) to insert it, all remain questions requiring resolution. Much more work is necessary to pursue the role that REBOA can have in the care of desperately injured trauma patients.

There has been a revolution in the care of severely injured patients. After 50 years of thinking that we knew the answers, we have come to realize that those answers were wrong. Newer resuscitation strategies, as well as new treatment strategies continue to evolve, allowing us to refine care of severely injured patients. Perhaps the one thing we have really learned is that we do not have all of the answers and that the discussion must continue if we are to do better at serving more trauma victims.