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Damage Control Resuscitation: the New Face of Damage Control

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Damage Control Resuscitation: the New Face of Damage Control REVIEW ARTICLE Damage Control Resuscitation: The New Face of Damage Control Juan C. Duchesne, MD, FACS, FCCP, Norman E. McSwain, Jr., MD, FACS, Bryan A. Cotton, MD, FACS, John P. Hunt, MD, MPH, FACS, Jeff Dellavolpe, MD, Kelly Lafaro, MD, MPH, Alan B. Marr, MD, FACS, Earnest A. Gonzalez, MD, FACS, Herb A. Phelan, MD, FACS, Tracy Bilski, MD, FACS, Patrick Greiffenstein, MD, James M. Barbeau, MD, JD, Kelly V. Rennie, MD, Christopher C. Baker, MD, FACS, Karim Brohi, MD, FRCS, FRCA, Donald H. Jenkins, MD, FACS, and Michael Rotondo, MD, FACS amage control resuscitation has become a topic of in- These temporized patients would then undergo continued resus- Dcreasing relevance and popularity over the past several citation and aggressive correction of their coagulopathy, hypo- years. Hemorrhage accounts for 30% to 40% of trauma thermia, and acidosis in the intensive care unit (ICU) before fatalities and is the leading cause of preventable death in returning to the operating room (OR) for the definitive repair of trauma.1 Damage control resuscitation (DCR) is a treatment their injuries. This approach has been shown to lead to better- strategy that targets the conditions that exacerbate hemor- than-expected survival rates for abdominal trauma,3–10 and its rhage in trauma patients. New data from both civilian medical application has now been extended to include thoracic surgery3 centers and military operations in the Iraq and Afghanistan and early fracture care.4–8 conflicts have allowed for a reappraisal of the resuscitation Discussions of damage control surgery usually center techniques of the trauma victim. The emergence of the idea of on the type and timing of surgical procedures. Recently, DCR has fostered controversy regarding its overall efficacy, methods of resuscitation of patients with exsanguinating its associated mortality, and the scientific basis of such a hemorrhage have come under increasing scrutiny for their strategy. This article attempts to answer some of the overar- ability to adequately correct the acidosis, hypothermia, and 9,10 ching questions associated with the acute care and resuscita- coagulopathy seen in these patients. DCR is a concept that tion of the trauma patient. Topics reviewed and discussed will has been popularized by the military and is now being studied include DCR and surgery, transfusion ratios, permissive hy- in the civilian setting. DCR differs from current resuscitation approaches by attempting an earlier and more aggressive potension, recombinant factor VIIa (rFVIIa), hypertonic fluid correction of coagulopathy and metabolic derangement. The solutions, and the destructive forces of hypothermia, acidosis, concept centers around the assumption that coagulopathy is and coagulopathy. We will also investigate some of the actually present very early after injury, and earlier interven- implications of DCR as they pertain to the future of resusci- tions to correct it in the most severely injured patients may tation and the optimization of trauma care in the future. lead to improved outcomes. DCR centers on the application Originally coined by the US Navy in reference to tech- of several key concepts, namely, the permissive hypotension, niques for salvaging a ship, which had sustained serious dam- the use of blood products over isotonic fluid for volume age,2 the term “damage control” has been adapted to truncating replacement, and the rapid and early correction of coagulopa- initial surgical procedures on severely injured patients to provide thy with component therapy.11 This resuscitation strategy only interventions necessary to control hemorrhage and contam- begins from ground zero in the emergency room (ER) and ination to focus on reestablishing a survivable physiologic status. continues through the OR and into the ICU. Understanding the physiologic sequelae of exsangui- Submitted for publication December 22, 2008. nating hemorrhage and the complex interaction of hypother- Accepted for publication July 19, 2010. mia, acidosis, and coagulopathy is central to an appreciation Copyright © 2010 by Lippincott Williams & Wilkins for the potential benefits of DCR.12 In addition, as with any From the Tulane School of Medicine Health Science Center (J.C.D., N.E.M., J.D., K.L., K.V.R.), New Orleans, Los Angeles; University of Texas Health new therapy, there exists some controversy with regard to its Science Center (B.A.C., E.A.G.), Houston, Texas; Louisiana State University efficacy, impact on outcomes, and the scientific evidence Health Science Center (J.P.H., A.B.M., P.G., J.M.B., C.C.B.), New Orleans, behind the strategy. This review will examine the basis and Los Angeles; University of Texas Southwestern Medical Center (H.A.P.), state of DCR, address some of the controversy of this strategy Dallas, Texas; The University of Mississippi Medical Center (T.B), Jackson, Mississippi; Royal London Hospital (K.B.), London, United Kingdom; Mayo of resuscitation and its relationship to damage control sur- Clinic (D.H.J.), Rochester, Minnesota; and The Brody School of Medicine at gery, and suggest its role in the future of resuscitation and the East Carolina University (M.R.), North Carolina. optimization of prognosis after trauma. Address for reprints: Juan C. Duchesne, MD, FACS, FCCP, Section of Trauma and Critical Care Surgery, Department of Surgery and Anesthesia, Tulane University School of Medicine, 1430 Tulane Avenue, SL-22, New Orleans, PERMISSIVE HYPOTENSION LA 70112-2699; email: [email protected]. The concept behind permissive hypotension involves DOI: 10.1097/TA.0b013e3181f2abc9 keeping the blood pressure low enough to avoid exsanguina- 976 The Journal of TRAUMA® Injury, Infection, and Critical Care • Volume 69, Number 4, October 2010 The Journal of TRAUMA® Injury, Infection, and Critical Care • Volume 69, Number 4, October 2010 Damage Control Resuscitation tion while maintaining perfusion of end organs. Although In 2006, Hirshberg et al.20 used computer modeling to hypotensive resuscitation is evolving into an integral part of demonstrate that the timing of resuscitation has different the new strategy of DCR, the practice itself is not a new effects on bleeding, with an early bolus delaying hemostasis concept. Walter Cannon and John Fraser remarked on it as and increasing blood loss and a late bolus triggering rebleed- early as 1918 when serving with the Harvard Medical Unit in ing. Animal models exploring the effect of fluid administra- France during World War I. They made the following obser- tion on rebleeding have been equally contradictory, with vations on patients undergoing fluid resuscitation: “Injection some demonstrating that limiting fluids reduces hemor- of a fluid that will increase blood pressure has dangers in rhage,21 whereas others demonstrate that fluids do not in- itself. Hemorrhage in a case of shock may not have occurred crease bleeding.22 Moreover, the limited use of fluids during to a marked degree because blood pressure has been too low resuscitation efforts is in direct opposition to guidelines put and the flow to scant to overcome the obstacle offered by the forth by the American College of Surgeons and the Advanced 23 clot. If the pressure is raised before the surgeon is ready to Trauma Life Support protocol. check any bleeding that may take place, blood that is sorely The discussion about the risks and benefits of permis- sive hypotension beg additional questions: even if one be- needed may be lost.”13 Dr. Cannon’s endpoint of resuscita- lieves that permissive hypotension is beneficial, it seems tion before definitive hemorrhage control was a systolic intuitive that some low threshold of safety should exist. How pressure of 70 mm Hg to 80 mm Hg, using a crystalloid/ low of a blood pressure can the injured patients tolerate? For colloid mixture as his fluid of choice. how long? Does this theoretical lower limit change when In World War II, Beecher promulgated Cannon’s hy- considering not only the initial hypotensive/hypoxic injury potensive resuscitation principles in the care of casualties but reperfusion injury as well? At the other end of the with truncal injuries. “When the patient must wait for a spectrum, at what level of blood pressure do we “pop the considerable period, elevation of his systolic blood pressure clot” off of spontaneously clotted vessels? Does this point ϳ (SBP) to 85 mm Hg is all that is necessary … and when vary with types of resuscitation fluid, time of onset, rate of profuse internal bleeding is occurring, it is wasteful of time resuscitation, and the nature of the wound? How does per- and blood to attempt to get a patient’s blood pressure up to missive hypotension come into play in the setting of multiple normal. One should consider himself lucky if a systolic injuries? Most of the work in this modality has been done in pressure of 80 mm Hg to 85 mm Hg can be achieved and then penetrating trauma. What is the role of permissive hypoten- surgery undertaken.”14 sion in blunt trauma? This is an especially pertinent question Although these anecdotal reports from earlier genera- in injuries where hypotension has been shown to be detri- tions of surgeons are interesting, more scientific attempts to mental, such as brain injury. This important point of conten- examine outcomes for permissive hypotension after serious tion that, in severe traumatic brain injury (TBI), denying injury have been mixed. The most well-known study that fluids can attenuate the injury by decreasing the intracerebral displayed a benefit for delayed aggressive fluid resuscitation perfusion pressure
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