Traumatic Hemorrhagic Shock: Advances In Fluid Management

Traumatic Hemorrhagic Shock: Advances In Fluid Management (Trauma CME)

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Table of Contents
Table of Contents
  1. Abstract
  2. Case Presentations
  3. Introduction
  4. Critical Appraisal Of The Literature
  5. Epidemiology
  6. Etiology and Pathophysiology
    1. Resuscitation Injury
  7. Differential Diagnosis
  8. Prehospital Care
  9. Emergency Department Evaluation
  10. Diagnostic Studies
    1. Laboratory Testing
    2. Bedside Ultrasound
    3. Diagnostic Radiography And Computed Tomography Scans
  11. Treatment
    1. Which Fluid Is Best For Resuscitation?
      1. Normal Saline
      2. Albumin And Other Colloids
      3. Hypertonic Saline
      4. Hypertonic Saline-Dextran
    2. Timing And Goals Of Resuscitation From Hemorrhagic Shock
      1. Managing Coagulopathy Of Trauma
    3. The Role Of Tranexamic Acid In Hemorrhagic Shock
  12. Special Circumstances
  13. Controversies And Cutting Edge
  14. Disposition
  15. Summary
  16. Risk Management Pitfalls For Traumatic Hemorrhagic Shock
  17. Case Conclusion
  18. Clinical Pathway For Resuscitation In Hemorrhagic Shock
  19. Tables and Figures
    1. Figure 1. The Vicious Cycle Of Fluid Administration
    2. Figure 2. Coagulopathy Chart
    3. Table 1. Comparison, By Conflict, Of Killed In Action, Died Of Wounds, And Case Fatality Rates (As Of 2006)
    4. Table 2. Differential Diagnosis For Shock In Trauma
    5. Table 3. Classes Of Shock By ATLS® Designation*
    6. Table 4. Examples Of Massive Transfusion Protocols
  20. References


A number of concerns have been raised regarding the advisability of the classic principles of aggressive crystalloid resuscitation in traumatic hemorrhagic shock. This issue reviews the advances that have led to a shift in the emergency department (ED) protocols in resuscitation from shock state, including recent literature regarding the new paradigm for the treatment of traumatic hemorrhagic shock, which is most generally known as damage control resuscitation (DCR). Goals and endpoints for resuscitation and a review of initial fluid choice are discussed, along with the coagulopathy of trauma and its management, how to address hemorrhagic shock in traumatic brain injury (TBI), and new pharmacologic treatment for hemorrhagic shock. The primary conclusions include the administration of tranexamic acid (TXA) for all patients with uncontrolled hemorrhage (Class I), the implementation of a massive transfusion protocol (MTP) with fixed blood product ratios (Class II), avoidance of large-volume crystalloid resuscitation (Class III), and appropriate usage of permissive hypotension (Class III). The choice of fluid for initial resuscitation has not been shown to affect outcomes in trauma (Class I).

Case Presentations

In the middle of your Saturday overnight shift, you are called to see a patient who drove himself to the hospital with a stab wound to the left upper back. This 19-year old male states that he was on the way to church when he was accosted by “2 dudes” who stabbed him “out of the blue.” He said he may have run into something with his car while trying to get away from them. You find the patient awake, but sluggish. He is speaking and his airway appears patent. Breath sounds are equal bilaterally. The patient’s initial vital signs are: heart rate of 140 beats per minute, blood pressure of 80/50 mm Hg, respiratory rate of 20 breaths per minute, temperature of 97°F (36.1°C), and SpO2 of 100% on room air. He reports only the single injury and when he is fully undressed, no other signs of trauma are found. Peripheral pulses are palpable, and on close inspection, the wound appears to be bleeding only minimally. The trauma surgeon is notified and is en route to assist. Initial FAST examination is negative. Two 18-gauge IVs are placed, lab work is drawn, and 2 L of lactated Ringer solution are administered. The blood pressure rapidly rises to 110/75 mm Hg, and the patient starts to complain of shortness of breath. Chest x-ray reveals a large hemothorax, and the patient’s blood pressure drops to 75/55 mm Hg. You begin to wonder if your initial resuscitation is really helping this patient.

About 50 minutes later, EMS arrives with a pedestrian struck by a car. EMS states that this 24-year-old male was the victim of a hit-and-run accident in which the driver apparently backed over him after first clipping him with the car and knocking him to the ground. When you walk into the patient’s room, you find him awake and angry, complaining of pain in his right upper quadrant. He is on a backboard, wearing a cervical collar, and has obvious bruising to the right chest and abdomen. His airway is patent and his breath sounds are equal bilaterally. The patient’s initial vital signs are: heart rate of 125 beats per minute, blood pressure of 120/80 mm Hg, respiratory rate of 20 breaths per minute, temperature of 98°F (36.6°C), and SpO2 of 94% on room air. Per EMS, the patient was hypotensive on their arrival, with initial blood pressure of 80/40 mm Hg, but it rapidly improved with 2 L of crystalloid given in the field. A second large-bore IV is placed and labs are drawn. The FAST examination reveals significant hemoperitoneum. He then becomes diaphoretic, and repeat blood pressure is now 75/40 mm Hg. The nurse asks if you want 2 more liters of crystalloid…


Resuscitation from shock state is a central part of emergency medicine practice. For many years, the gold standard of treatment was the rapid restoration of circulating volume with crystalloid solutions to normal, or even supraphysiologic, levels. Research over the past 30 years has yielded significant improvements in the treatment of various etiologies of shock, including the treatment of septic shock, using variations on early goal-directed therapy first described by Rivers et al.1 However, all types of shock are not the same, and different etiologies require different approaches. Intravascular losses that result from third spacing, as in sepsis or pancreatitis, are primarily water and electrolytes. Aggressively replacing these losses with crystalloid before irreversible damage occurs makes perfect sense. In contrast, losses from hemorrhage include water, electrolytes, colloids, clotting factors, platelets, and blood cells. Additionally, there are inflammatory and immune responses to hemorrhage and tissue injury that result in third spacing, causing further losses. The complexity inherent in the management of these losses is just now beginning to be understood.

This issue of Emergency Medicine Practice focuses on advances in knowledge that should fundamentally change how we treat trauma patients in hemorrhagic shock. The best available evidence from the literature suggests that we must shift away from the paradigms that have guided emergency clinicians in the past. The following questions provide a guide to the changing landscape:

  • What is resuscitation injury?
  • What fluid is best for resuscitation?
  • When should fluid resuscitation start, and once initiated, what should the endpoints be?
  • How should the coagulopathy of trauma be managed?
  • What is the most appropriate role of pharmacologic management?

Current standard resuscitation methods are probably appropriate for more than 90% of trauma patients.2 This review is primarily intended to address the needs of the most critically injured patients who are in hemorrhagic shock. Even in the largest civilian academic trauma centers, these patients are uncommon, constituting only 1% to 2% of all trauma presentations.2 Nonetheless, since hemorrhagic shock is a leading preventable cause of death, implementation of effective treatment strategies for this small population can improve overall trauma survival.

Critical Appraisal Of The Literature

A search of PubMed was carried out using the following combinations of key words: hemorrhagic shock, fluid management, shock, resuscitation, hypertonic saline, trauma-hemorrhage, damage control resuscitation, trauma, and coagulopathy. More than 300 articles were reviewed, which provided the background for further literature review. The Cochrane Database of Systematic Reviews was also consulted, and the combination of these resources served as the foundation of this evidence-based review. Until recently, research in the treatment of hemorrhagic shock was of questionable quality, limited to animal data, or driven by expert opinion. Particularly in the United States (US), there are significant difficulties in conducting randomized controlled trials with trauma patients where consent is not readily available and who may be part of a vulnerable population. As a result, the only Level I evidence reviewed in this article is from abroad.

Risk Management Pitfalls For Traumatic Hemorrhagic Shock

  1. “The patient said she couldn’t be pregnant.” All women of childbearing age who arehypotensive should have a pregnancy test done to exclude ruptured ectopic pregnancy.
  2. “The patient might be bleeding, but he is rockstable as long as he is getting fluids.” Resuscitation is not a substitute for definitive bleeding control.
  3. “This trauma victim is paralyzed, so he must be in neurogenic shock.” Hypotensive victims of trauma must have hemorrhagic shock ruled out definitively.
  4. “She was bleeding out. I had to address that first.” Trauma care goes ABC for a reason. There is nothing wrong with addressing circulation early, but airway and breathing come first.
  5. “I read this awesome thing about permissive hypotension. I thought it was the way to go for everyone.” Permissive hypotension is contraindicated in patients with TBI.
  6. “I know I can get this patient’s blood pressure back to normal if I attach him to the rapid infuser.” Normalizing blood pressure is contraindicated in patients who have ongoing bleeding.
  7. “Trauma management is a cookbook. You just do the same thing for everyone and wait for the cavalry.” This is an abdication of responsibility and means we are not maximizing the patient’s chance for survival.
  8. “Blood products are dangerous and this guy is only mildly hypotensive. I’m just going to give him 2 L of crystalloid and see what happens. I know all bleeding stops eventually.” Failing to recognize hemorrhagic shock and initiate treatment will leave your patient far behind the 8-ball.
  9. “I read about early goal-directed therapy for sepsis and I saw the Surviving Sepsis guidelines. Clearly the right treatment for shock is 6 L of crystalloid empirically.” Treatment of shock must be tailored to the etiology of shock and to the specific patient. Large-volume crystalloid resuscitation is discouraged in hemorrhagic shock.
  10. “This old guy syncopized and it’s not clear why. I suspect his low blood pressure is just his baseline.” Consider gastrointestinal bleeding and aneurysmal rupture as etiologies of hypotension and syncope. Early appropriate treatment and endoscopic or surgical bleeding control will help this patient.

Tables and Figures

Figure 1. The Vicious Cycle Of Fluid Administration


Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.

To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study, will be included in bold type following the reference, where available. In addition, the most informative references cited in this paper, as determined by the author, will be noted by an asterisk (*) next to the number of the reference.

  1. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345(19):1368-1377. (Prospective randomized; 263 patients)
  2. * Holcomb JB, Jenkins D, Rhee P, et al. Damage control resuscitation: directly addressing the early coagulopathy of trauma. J Trauma. 2007;62(2):307-310. (Review)
  3. Sauaia A, Moore FA, Moore EE, et al. Epidemiology of trauma deaths: a reassessment. J Trauma. 1995;38(2):185-193. (Cross-sectional)
  4. Cannon WB. The preventative treatment of wound shock. JAMA. 1918;70(9):618-621. (Guideline)
  5. Beecher HK. Preparation of battle casualties for surgery. Ann Surg. 1945;121(6):769-792. (Guideline)
  6. Fogelman MJ, Wilson BJ. A different concept of volume replacement in traumatic hypovolemia: observations on injured man and animal. Am J Surg. 1960;99:694-701. (Animal study)
  7. Shires T, Coln D, Carrico J, et al. Fluid therapy in hemorrhagic shock. Arch Surg. 1964;88:688-693. (Animal study)
  8. American College of Surgeons. Advanced Trauma Life Support for Doctors. Eighth edition. Chicago, IL: American College of Surgeons; 2008. (Guideline)
  9. Alam HB, Rhee P. New developments in fluid resuscitation. Surg Clin North Am. 2007;87(1):55-72, vi. (Review)
  10. Cotton BA, Guy JS, Morris JA, Jr, et al. The cellular, metabolic, and systemic consequences of aggressive fluid resuscitation strategies. Shock. 2006;26(2):115-121. (Guideline)
  11. Knoferl MW, Angele MK, Ayala A, et al. Do different rates of fluid resuscitation adversely or beneficially influence immune responses after trauma-hemorrhage? J Trauma. 1999;46(1):23-33. (Animal study)
  12. Shah KJ, Chiu WC, Scalea TM, et al. Detrimental effects of rapid fluid resuscitation on hepatocellular function and survival after hemorrhagic shock. Shock. 2002;18(3):242-247. (Animal study)
  13. * Bickell WH, Wall MJ, Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331(17):1105-1109. (Prospective; 598 patients)
  14. Pope AM, Institute of Medicine (U.S.). Fluid resuscitation: state of the science for treating combat casualties and civilian injuries. Washington, D.C.: National Academy Press; 1999. (IOM report/review)
  15. Butler F. Fluid resuscitation in tactical combat casualty care: brief history and current status. Journal of Trauma-Injury Infection & Critical Care. 2011;70(5):s11-s12. (Guideline)
  16. Gawande A. Casualties of war--military care for the wounded from Iraq and Afghanistan. N Engl J Med. 2004;351(24):2471-2475. (Commentary)
  17. Holcomb JB, Stansbury LG, Champion HR, et al. Understanding combat casualty care statistics. J Trauma. 2006;60(2):397-401. (Review)
  18. Lang F, Busch GL, Ritter M, et al. Functional significance of cell volume regulatory mechanisms. Physiol Rev. 1998;78(1):247-306. (Review)
  19. Rhee P, Burris D, Kaufmann C, et al. Lactated Ringer’s solution resuscitation causes neutrophil activation after hemorrhagic shock. J Trauma. 998;44(2):313-319. (Review)
  20. Alam HB, Stanton K, Koustova E, et al. Effect of different resuscitation strategies on neutrophil activation in a swine model of hemorrhagic shock. Resuscitation. 2004;60(1):91-99. (Animal study)
  21. Rhee P, Koustova E, Alam HB. Searching for the optimal resuscitation method: recommendations for the initial fluid resuscitation of combat casualties. J Trauma. 2003;54(5 Suppl):S52-62. (Review)
  22. Ashbaugh DG, Bigelow DB, Petty TL, et al. Acute respiratory distress in adults. Lancet. 1967;2(7511):319-323. (Case series; 12 patients)
  23. Ablove RH, Babikian G, Moy OJ, et al. Elevation in compartment pressure following hypovolemic shock and fluid resuscitation: a canine model. Orthopedics. 2006;29(5):443-445. (Animal study)
  24. Balogh Z, McKinley BA, Cocanour CS, et al. Supranormal trauma resuscitation causes more cases of abdominal compartment syndrome. Arch Surg. 2003;138(6):637-642; discussion 642-633. (Retrospective; 156 patients)
  25. Sasser S, Varghese M, Kellermann A, et al. Prehospital trauma care systems. Geneva: World Health Organization, 2005.
  26. Liberman M, Mulder D, Lavoie A, et al. Multicenter Canadian study of prehospital trauma care. Ann Surg. 2003;237(2):153-160. (Prospective; 9405 patients)
  27. Seamon MJ, Fisher CA, Gaughan J, et al. Prehospital procedures before emergency department thoracotomy: “scoop and run” saves lives. J Trauma. 2007;63(1):113-120. (Retrospective; 180 patients)
  28. Cotton BA, Jerome R, Collier BR, et al. Guidelines for prehospital fluid resuscitation in the injured patient. J Trauma. 2009;67(2):389-402. (Guideline)
  29. Guly HR, Bouamra O, Spiers M, et al. Vital signs and estimated blood loss in patients with major trauma: testing the validity of the ATLS classification of hypovolaemic shock. Resuscitation. 2011;82(5):556-559.
  30. Heffernan DS, Thakkar RK, Monaghan SF, et al. Normal presenting vital signs are unreliable in geriatric blunt trauma victims. J Trauma. 2010;69(4):813-820.
  31. Tremblay LN, Rizoli SB, Brenneman FD. Advances in fluid resuscitation of hemorrhagic shock. Can J Surg. 2001;44(3):172-179. (Review)
  32. Hartmann AF. Theory and practice of parenteral fluid administration. JAMA. 1934;103(18):1349-1354. (Review)
  33. White SA, Goldhill DR. Is Hartmann’s the solution? Anaesthesia. 1997;52(5):422-427. (Review)
  34. Anderson YS, Curtis NJ, Hobbs JA, et al. High serum D-lactate in patients on continuous ambulatory peritoneal dialysis. Nephrol Dial Transplant. 1997;12(5):981-983. (Prospective; 26 patients)
  35. Shires GT, Browder LK, Steljes TP, et al. The effect of shock resuscitation fluids on apoptosis. Am J Surg. 2005;189(1):85-91. (Animal study)
  36. Ayuste EC, Chen H, Koustova E, et al. Hepatic and pulmonary apoptosis after hemorrhagic shock in swine can be reduced through modifications of conventional Ringer’s solution. J Trauma. 2006;60(1):52-63. (Animal study)
  37. Santry HP, Alam HB. Fluid resuscitation: past, present, and the future. Shock. 2010;33(3):229-241. (Review)
  38. Rizoli SB, Kapus A, Fan J, et al. Immunomodulatory effects of hypertonic resuscitation on the development of lung inflammation following hemorrhagic shock. J Immunol. 1998;161(11):6288-6296. (Review)
  39. Alam HB, Sun L, Ruff P, et al. E- and P-selectin expression depends on the resuscitation fluid used in hemorrhaged rats. J Surg Res. 2000;94(2):145-152. (Animal study)
  40. Todd SR, Malinoski D, Muller PJ, et al. Lactated Ringer’s is superior to normal saline in the resuscitation of uncontrolled hemorrhagic shock. J Trauma. 2007;62(3):636-639. (Animal study)
  41. Rizoli SB. Crystalloids and colloids in trauma resuscitation: a brief overview of the current debate. J Trauma. 2003;54(5 Suppl):S82-S88. (Review)
  42. Schierhout G, Roberts I. Fluid resuscitation with colloid or crystalloid solutions in critically ill patients: a systematic review of randomised trials. BMJ. 1998;316(7136):961-964. (Review)
  43. Choi PT, Yip G, Quinonez LG, et al. Crystalloids vs. colloids in fluid resuscitation: a systematic review. Crit Care Med. 1999;27(1):200-210. (Systematic review)
  44. * Finfer S, Bellomo R, Boyce N, et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004;350(22):2247-2256. (Prospective randomized double-blind; 6997 patients)
  45. Devlin JW, Barletta JF. Albumin for fluid resuscitation: implications of the Saline versus Albumin Fluid Evaluation. Am J Health Syst Pharm. 2005;62(6):637-642. (Commentary)
  46. Perel P, Roberts I. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev. 2007(4):CD000567. (Systematic review)
  47. Myburgh J, Cooper DJ, Finfer S, et al. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med. 2007;357(9):874-884. (Prospective randomized double-blind; 460 patients)
  48. Jacob M, Chappell D. Saline or albumin for fluid resuscitation in traumatic brain injury. N Engl J Med. 2007;357(25):2634-2635; author reply 2635-2636. (Commentary)
  49. Bunn F, Trivedi D, Ashraf S. Colloid solutions for fluid resuscitation. Cochrane Database Syst Rev. 2008(1):CD001319. (Systematic review)
  50. Velasco IT, Pontieri V, Rocha e Silva M Jr, et al. Hyperosmotic NaCl and severe hemorrhagic shock. Am J Physiol. 1980;239(5):H664-673. (Animal study)
  51. Junger WG, Coimbra R, Liu FC, et al. Hypertonic saline resuscitation: a tool to modulate immune function in trauma patients? Shock. 1997;8(4):235-241. (Review)
  52. Ciesla DJ, Moore EE, Gonzalez RJ, et al. Hypertonic saline inhibits neutrophil (PMN) priming via attenuation of p38 MAPK signaling. Shock. 2000;14(3):265-269; discussion 269-270. (Cell study)
  53. Ciesla DJ, Moore EE, Zallen G, et al. Hypertonic saline attenuation of polymorphonuclear neutrophil cytotoxicity: timing is everything. J Trauma. 2000;48(3):388-395. (Cell study)
  54. Bunn F, Roberts I, Tasker R, et al. Hypertonic versus near isotonic crystalloid for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev. 2004(3):CD002045. (Systematic review)
  55. Cooper DJ, Myles PS, McDermott FT, et al. Prehospital hypertonic saline resuscitation of patients with hypotension and severe traumatic brain injury: a randomized controlled trial. JAMA. 2004;291(11):1350-1357. (Prospective randomized double-blind; 229 patients)
  56. Kramer GC, Perron PR, Lindsey DC, et al. Small-volume resuscitation with hypertonic saline dextran solution. Surgery. 1986;100(2):239-247. (Animal study)
  57. Maningas PA, Bellamy RF. Hypertonic sodium chloride solutions for the prehospital management of traumatic hemorrhagic shock: a possible improvement in the standard of care? Ann Emerg Med. 1986;15(12):1411-1414. (Review)
  58. Wade CE, Kramer GC, Grady JJ, et al. Efficacy of hypertonic 7.5% saline and 6% dextran-70 in treating trauma: a meta-analysis of controlled clinical studies. Surgery. 1997;122(3):609-616. (Meta-analysis)
  59. Rizoli SB, Rhind SG, Shek PN, et al. The immunomodulatory effects of hypertonic saline resuscitation in patients sustaining traumatic hemorrhagic shock: a randomized, controlled, double-blinded trial. Ann Surg. 2006;243(1):47-57. (Prospective randomized double-blind; 27 patients)
  60. Riddez L, Drobin D, Sjostrand F, et al. Lower dose of hypertonic saline dextran reduces the risk of lethal rebleeding in uncontrolled hemorrhage. Shock. 2002;17(5):377-382. (Animal study)
  61. Bruttig SP, O’Benar JD, Wade CE, et al. Benefit of slow infusion of hypertonic saline/dextran in swine with uncontrolled aortotomy hemorrhage. Shock. 2005;24(1):92-96. (Animal study)
  62. * Bulger EM, May S, Kerby JD, et al. Out-of-hospital hypertonic resuscitation after traumatic hypovolemic shock: a randomized, placebo controlled trial. Ann Surg. 2011;253(3):431-441. (Prospective randomized double-blind; 853 patients)
  63. Baker AJ, Rhind SG, Morrison LJ, et al. Resuscitation with hypertonic saline-dextran reduces serum biomarker levels and correlates with outcome in severe traumatic brain injury patients. J Neurotrauma. 2009;26(8):1227-1240.
  64. * Bulger EM, May S, Brasel KJ, et al. Out-of-hospital hypertonic resuscitation following severe traumatic brain injury: a randomized controlled trial. JAMA. 2010;304(13):1455-1464.(Prospective randomized double-blind; 1331 patients)
  65. Wiggers HC, Goldberg H, Roemhild F, et al. Impending hemorrhagic shock and the course of events following administration of dibenamine. Circulation. 1950;2(2):179-185. (Animal study)
  66. Shoemaker WC, Appel PL, Kram HB, et al. Prospective trial of supranormal values of survivors as therapeutic goals in high-risk surgical patients. Chest. 1988;94(6):1176-1186. (Prospective randomized, 184 patients)
  67. Sakles JC, Sena MJ, Knight DA, et al. Effect of immediate fluid resuscitation on the rate, volume, and duration of pulmonary vascular hemorrhage in a sheep model of penetrating thoracic trauma. Ann Emerg Med. 1997;29(3):392-399. (Animal study)
  68. Holmes JF, Sakles JC, Lewis G, et al. Effects of delaying fluid resuscitation on an injury to the systemic arterial vasculature. Acad Emerg Med. 2002;9(4):267-274. (Animal study)
  69. Stern SA, Dronen SC, Birrer P, et al. Effect of blood pressure on hemorrhage volume and survival in a near-fatal hemorrhage model incorporating a vascular injury. Ann Emerg Med. 1993;22(2):155-163. (Animal study)
  70. Stern SA, Kowalenko T, Younger J, et al. Comparison of the effects of bolus vs. slow infusion of 7.5% NaCl/6% dextran-70 in a model of near-lethal uncontrolled hemorrhage. Shock. 2000;14(6):616-622. (Animal study)
  71. Kowalenko T, Stern S, Dronen S, et al. Improved outcome with hypotensive resuscitation of uncontrolled hemorrhagic shock in a swine model. J Trauma. 1992;33(3):349-353; discussion 361-342. (Animal study)
  72. Mapstone J, Roberts I, Evans P. Fluid resuscitation strategies: a systematic review of animal trials. J Trauma. 2003;55(3):571-589. (Systematic review)
  73. Badjatia N, Carney N, Crocco TJ, et al. Guidelines for prehospital management of traumatic brain injury 2nd edition. Prehosp Emerg Care. 2008;12 Suppl 1:S1-S52. (Guideline)
  74. Revell M, Greaves I, Porter K. Endpoints for fluid resuscitation in hemorrhagic shock. J Trauma. 2003;54(5 Suppl):S63-S67. (Review)
  75. Blair SD, Janvrin SB, McCollum CN, et al. Effect of early blood transfusion on gastrointestinal haemorrhage. Br J Surg. 1986;73(10):783-785. (Prospective; 50 patients)
  76. Kwan I, Bunn F, Roberts I. Timing and volume of fluid administration for patients with bleeding. Cochrane Database Syst Rev. 2003(3):CD002245. (Systematic review)
  77. Barbee RW, Reynolds PS, Ward KR. Assessing shock resuscitation strategies by oxygen debt repayment. Shock. 2010;33(2):113-122. (Review)
  78. Tisherman SA, Barie P, Bokhari F, et al. Clinical practice guideline: endpoints of resuscitation. J Trauma. 2004;57(4):898-912. (Guideline)
  79. Dutton RP, Mackenzie CF, Scalea TM. Hypotensive resuscitation during active hemorrhage: impact on in-hospital mortality. J Trauma. 2002;52(6):1141-1146. (Prospective randomized; 110 patients)
  80. Sondeen JL, Coppes VG, Holcomb JB. Blood pressure at which rebleeding occurs after resuscitation in swine with aortic injury. J Trauma. 2003;54(5 Suppl):S110-S117. (Animal study)
  81. Brandstrup B, Tonnesen H, Beier-Holgersen R, et al. Effects of intravenous fluid restriction on postoperative complications: comparison of two perioperative fluid regimens: a randomized assessor-blinded multicenter trial. Ann Surg. 2003;238(5):641-648. (Prospective randomized observerblinded; 172 patients)
  82. Martin M, Salim A, Murray J, et al. The decreasing incidence and mortality of acute respiratory distress syndrome after injury: a 5-year observational study. J Trauma. 2005;59(5):1107-1113. (Prospective; 1913 patients)
  83. Holcomb JB. Fluid resuscitation in modern combat casualty care: lessons learned from Somalia. J Trauma. 2003;54(5 Suppl):S46-S51. (Review)
  84. Krausz MM. Fluid resuscitation strategies in the Israeli army. J Trauma. 2003;54(5 Suppl):S39-S42. (Review)
  85. Rotondo MF, Zonies DH. The damage control sequence and underlying logic. Surg Clin North Am. 1997;77(4):761-777. (Review)
  86. MacLeod JB, Lynn M, McKenney MG, et al. Early coagulopathy predicts mortality in trauma. J Trauma. 2003;55(1):39-44. (Prospective; 7638 patients)
  87. Brohi K, Singh J, Heron M, et al. Acute traumatic coagulopathy. J Trauma. 2003;54(6):1127-1130. (Retrospective; 1088 patients)
  88. * Brohi K, Cohen MJ, Ganter MT, et al. Acute traumatic coagulopathy initiated by hypoperfusion: modulated through the protein C pathway? Ann Surg. 2007;245(5):812-818. (Prospective; 208 patients)
  89. Brohi K, Cohen MJ, Ganter MT, et al. Acute coagulopathy of trauma: hypoperfusion induces systemic anticoagulation and hyperfibrinolysis. J Trauma. 2008;64(5):1211-1217; discussion 1217. (Prospective; 208 patients)
  90. Hess JR, Holcomb JB, Hoyt DB. Damage control resuscitation: the need for specific blood products to treat the coagulopathy of trauma. Transfusion. 2006;46(5):685-686. (Review)
  91. Hess JR, Brohi K, Dutton RP, et al. The coagulopathy of trauma: a review of mechanisms. J Trauma. 2008;65(4):748-754. (Review)
  92. Darlington DN, Kheirabadi BS, Delgado AV, et al. Coagulation changes to systemic acidosis and bicarbonate correction in swine. J Trauma. 2011 Apr 15. Epub ahead of print. (Review)
  93. Tien H, Nascimento B, Jr, Callum J, et al. An approach to transfusion and hemorrhage in trauma: current perspectives on restrictive transfusion strategies. Can J Surg. 2007;50(3):202-209. (Review)
  94. Hebert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group. N Engl J Med. 1999;340(6):409-417. (Prospective randomized; 838 patients)
  95. Corwin HL, Gettinger A, Pearl RG, et al. The CRIT Study: anemia and blood transfusion in the critically ill - current clinical practice in the United States. Crit Care Med. 2004;32(1):39-54.
  96. Hirshberg A, Dugas M, Banez EI, et al. Minimizing dilutional coagulopathy in exsanguinating hemorrhage: a computer simulation. J Trauma. 2003;54(3):454-463. (Computer simulation)
  97. Borgman MA, Spinella PC, Perkins JG, et al. The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat support hospital. J Trauma. 2007;63(4):805-813. (Retrospective; 246 patients)
  98. Duchesne JC, Hunt JP, Wahl G, et al. Review of current blood transfusions strategies in a mature level I trauma center: were we wrong for the last 60 years? J Trauma. 2008;65(2):272-276; discussion 276-278. (Retrospective; 2746 patients)
  99. Mitra B, Mori A, Cameron PA, et al. Fresh frozen plasma (FFP) use during massive blood transfusion in trauma resuscitation. Injury. 2010;41(1):35-39. (Retrospective; 331 patients)
  100. Snyder CW, Weinberg JA, McGwin G, Jr, et al. The relationship of blood product ratio to mortality: survival benefit or survival bias? J Trauma. 2009;66(2):358-362; discussion 362-354. (Retrospective; 134 patients)
  101. Scalea TM, Bochicchio KM, Lumpkins K, et al. Early aggressive use of fresh frozen plasma does not improve outcome in critically injured trauma patients. Ann Surg. Oct 2008;248(4):578-584. (Prospective; 806 patients)
  102. Riskin DJ, Tsai TC, Riskin L, et al. Massive transfusion protocols: the role of aggressive resuscitation versus product ratio in mortality reduction. J Am Coll Surg. 2009;209(2):198-205. (Retrospective; 77 patients)
  103. Cotton BA, Gunter OL, Isbell J, et al. Damage control hematology: the impact of a trauma exsanguination protocol on survival and blood product utilization. J Trauma. 2008;64(5):1177-1182; discussion 1182-1173. (Retrospective; 211 patients)
  104. Dente CJ, Shaz BH, Nicholas JM, et al. Improvements in early mortality and coagulopathy are sustained better in patients with blunt trauma after institution of a massive transfusion protocol in a civilian level I trauma center. J Trauma. 2009;66(6):1616-1624. (Prospective; 116 patients)
  105. Duchesne JC, Kimonis K, Marr AB, et al. Damage control resuscitation in combination with damage control laparotomy: a survival advantage. J Trauma. 2010;69(1):46-52. (Retrospective; 196 patients)
  106. * Lin Y, Stanworth S, Birchall J, et al. Recombinant factor VIIa for the prevention and treatment of bleeding in patients without haemophilia. Cochrane Database Syst Rev. 2011(2):CD005011. (Systematic review)
  107. Carless PA, Henry DA, Moxey AJ, et al. Cell salvage for minimising perioperative allogeneic blood transfusion. Cochrane Database Syst Rev. 2010(3):CD001888. (Systematic review)
  108. Shakur H, Roberts I, Bautista R, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet. 2010;376(9734):23-32. (Prospective randomized doubleblind; 20,211 patients)
  109. Cap AP, Baer DG, Orman JA, et al. Tranexamic acid for trauma patients: a critical review of the literature. J Trauma. 2011;71(1):s9-s14. (Review)
  110. Duchesne JC, McSwain NE, Jr, Cotton BA, et al. Damage control resuscitation: the new face of damage control. J Trauma. 2010;69(4):976-990. (Review)
  111. Yu HP, Chaudry IH. The role of estrogen and receptor agonists in maintaining organ function after trauma-hemorrhage. Shock. 2009;31(3):227-237. (Review)
  112. Angele MK, Schwacha MG, Ayala A, et al. Effect of gender and sex hormones on immune responses following shock. Shock. 2000;14(2):81-90. (Review)
  113. Nickel EA, Hsieh CH, Chen JG, et al. Estrogen suppresses cardiac IL-6 after trauma-hemorrhage via a hypoxia-inducible factor 1 alpha-mediated pathway. Shock. 2009;31(4):354-358. (Animal study)
  114. Kozlov AV, Duvigneau JC, Hyatt TC, et al. Effect of estrogen on mitochondrial function and intracellular stress markers in rat liver and kidney following trauma-hemorrhagic shock and prolonged hypotension. Mol Med. 2010;16(7-8):254-261. (Animal study)
  115. Natanson C, Kern SJ, Lurie P, et al. Cell-free hemoglobinbased blood substitutes and risk of myocardial infarction and death: a meta-analysis. JAMA. 2008;299(19):2304-2312. (Meta-analysis)
  116. Voelckel WG, Raedler C, Wenzel V, et al. Arginine vasopressin, but not epinephrine, improves survival in uncontrolled hemorrhagic shock after liver trauma in pigs. Crit Care Med. 2003;31(4):1160-1165. (Animal study)
  117. Gonzales E, Chen H, Munuve R, et al. Valproic acid prevents hemorrhage-associated lethality and affects the acetylation pattern of cardiac histones. Shock. 2006;25(4):395-401. (Animal study)
  118. Szalay L, Shimizu T, Suzuki T, et al. Androstenediol administration after trauma-hemorrhage attenuates inflammatory response, reduces organ damage, and improves survival following sepsis. Am J Physiol Gastrointest Liver Physiol. 2006;291(2):G260-G266. (Animal study)
Publication Information

David Cherkas

Publication Date

November 2, 2011

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