Hemorrhage is the leading cause of preventable death on the battlefield. Damage Control Resuscitation (DCR) works synergistically with Damage Control Surgery (DCS) and prioritizes non-surgical interventions that reduce morbidity and mortality due to trauma and hemorrhage. DCR aims to restore homeostasis and prevent or mitigate tissue hypoxia and coagulopathy. This is accomplished through aggressive hemorrhage control and blood transfusion with products that provide the functionality of Whole Blood (WB). Crystalloids are avoided to reduce dilutional coagulopathy.

For other topics related to Military Medicine, please see our posts on TCCC and Recent Updates, Prolonged Field Care, Blast Injuries, Inhalation Injuries, Abdominal Stab Wounds, and Emergency Resuscitative Thoracotomy.

The major principles of DCR include:

  • Recognition of casualties requiring DCR
  • Optimization of Fluids
  • Blood product transfusion

Adjunctive therapies during DCR include:

  • Relatively hypotensive resuscitation: to avoid re-bleeding (target sBP 80-90mmHg)
  • Compressive/hemostatic dressings and devices
  • Empiric use of TXA: if given early reduces mortality in trauma
  • Prevention of acidosis and hypothermia
  • Expeditious delivery to definitive surgical control

There is now strong retrospective evidence in both civilian and military trauma populations that patients requiring massive transfusion (MT) benefit from a higher ratio of plasma and platelets to red cells (e.g., 1 unit plasma: 1 unit platelets: 1 unit of Packed RBCs [PRBCs]). MT at a 1:1:1 ratio is associated with improved survival. The practice of giving large amounts of crystalloid or RBCs alone in the initial resuscitation period is no longer the standard of care for major trauma.

We will first review the blood products and pharmacologic adjuncts available for DCR, then the general approach to DCR in the combat environment. We will end off the post with pediatric considerations.

Blood products for DCR

Red Blood Cells

  • Standard RBC units:
    • Stored up to 42 days under refrigeration in additive solution
  • “frozen” RBCs:
    • Stored frozen with glycerol cryoprotectant for up to 10 years at <-65°C, then thawed and rinsed in an automated process
    • Require 1.5h and specialized equipment to prepare


  • Fresh Frozen Plasma (FFP)
    • Stored frozen and thawed “on demand”
      • Delay in treatment >30 mins with FFP
    • Pre-thawed and stored refrigerated for up to 5 days (so-called “thawed plasma”)
      • Typically results in significant waste due to the 5-day post-thaw shelf life
    • “liquid” (never frozen) plasma
      • Stored for 26 days in Citrate Phosphate Dextrose (CPD) anticoagulant solution, or 40 days in Citrate Phosphate Dextrose Adenine (CPDA-1)
    • Freeze-Dried Plasma (FDP)
      • Relatively rapid reconstitution and availability
      • Considered functionally interchangeable with other plasma products for trauma

Note: Although group AB plasma is classically considered the only universally compatible plasma, it is now widely recognized that A plasma can be considered universal. The US military, as well as
many civilian trauma centers, routinely use A plasma as universal emergency release plasma.


  • Traditional
    • Stored at room temperature (20-24°C), under constant agitation, for maximum of 5 days
  • Cold-stored Platelets (CSP)
    • Stored refrigerated (1-6°C), maintained without agitation for up to 3 days in plasma
    • Refrigerated storage better preserves platelet hemostatic function and reduces risk of bacterial growth
    • Cold-stored platelets in platelet additive solution (CSP-PAS) or plasma retain function for at least 15 days
    • Functionally interchangeable with traditionally stored platelets

Whole Blood (WB)

  • In deployed environments, the inability to supply blood components due to logistical constraints led to the use of WB collected onsite from “walking blood banks”
  • This collected WB is not prospectively tested for Transfusion-Transmitted Diseases
    • Recipients of these products must be tested at 3, 6 and 12 months to monitor for disease transmission
  • WB delivers all the components of blood in the correct ratio and is independently associated with improved survival
  • The availability of Type-Specific WB may be limited due the constrained pool of donors
  • Low Titer Group O Whole Blood (LTOWB) is considered the universal donor
  • Cold-Stored WB (CWB) will provide platelet hemostatic function during the first 2 weeks of storage
  • Platelet function is moderately reduced during the remaining shelf life (21 days for CPD WB and 35 days for CPDA WB)

damage control

Pharmacologic Adjuncts

Hemostatic pharmaceutical adjuncts to limit blood loss are a subject of considerable investigation.

  • Tranexamic Acid
    • Strong evidence demonstrates significant improvement in survival following the early use of TXA, but only when given with 3 hours of injury, after which mortality is higher.
  • rFVIIa
    • No longer recommended
    • Not shown to reduce mortality and may increase risk of adverse events
  • Prothrombin Complex Concentrates (PCCs)
    • Only indicated for urgent warfarin reversal
    • Not adequately studied in a broad trauma population
  • Fibrinogen concentrate
    • Has not been studied adequately in trauma patients either

Management Principles for DCR

These principles apply to both the prehospital and medical treatment facility phases of care, though the exact resources and treatments may differ between phases. For more information on prehospital care in the combat environment, please see our posts on Introduction to TCCC and TCCC 2018 updates.

Recognition of Casualties Requiring DCR

  • Massive transfusion = cumulative ≥10 RBC units in initial 24h post-injury
    • These casualties have increased risk of morbidity and mortality due to exsanguination
    • Ideally, these patients should be rapidly identified, and hemostasis established at the earliest level of care possible
  • Robust pre-hospital data are lacking, but several factors predict the need for MT in trauma. In a casualty with serious injuries, 3/4 features below indicates 70% predicted risk of MT and 85% risk if 4/4:
    • sBP < 110mmHg
    • HR > 105 bpm
    • Hct < 32%
    • pH < 7.25
  • Other risk factors associated with MT or need for aggressive resuscitation:
    • Injury pattern
      • Above-the-knee traumatic leg amputation esp. if concomitant pelvic injury, multi-amputation, penetrating injury to chest or abdomen
    • >2 regions positive on FAST scan
    • Lactate concentration on admission >2.5
    • Admission INR ≥ 1.2-1.4
    • BD > 6 mEq/L
    • Near Infrared Spectroscopy (NIR)-derived StO2< 75% (in practice, rarely available)
  • Recognition of clinical patterns associated with need for MT is essential for effective triage. These include:
    • Uncontrolled truncal or junctional bleeding
    • Uncontrolled major bleeding secondary to large soft tissue injuries
    • Proximal, bilateral, or multiple amputations
    • Mangled extremity
    • Clinical signs of coagulopathy (e.g., paucity of clots, petechial bleeding)
    • Severe hypothermia
  • Laboratory evaluation such as viscoelastic testing (Thromboelastography [TEG] or Rotational Thromboelastometry [ROTEM®]) may also facilitate early identification of patients who will require MT, although this technology is not widely available in the deployed setting

Note: Many point-of-care coagulation tests that measure PT/INR have linear ranges only between INR 2.0-3.0 and are unreliable in clinical conditions characterized by loss of fibrinogen. These devices should not be relied upon to evaluate the coagulation function in trauma patients.

Optimization of Fluids

  • Blood products are preferred for hemorrhagic shock resuscitation
  • The order of priority for fluid administration should be:
    • Whole blood (Group O low titer preferred)
    • Blood components = 1:1:1 ratio
      • Hospital setting: cryoprecipitate is available and should be added to create 1:1:1:1
        ratio to supply fibrinogen and other clotting factors (Factors VIII, XIII, and vWF)
    • RBCs plus plasma = 1:1 ratio
    • Plasma with or without RBCs
    • RBCs alone
  • Volume resuscitation with crystalloid or colloid should be used sparingly given the potential for harm
  • During prolonged evacuations and in the absence of available blood products, crystalloid and non-blood colloid fluids may be needed for casualties at risk of imminent death
    • Administration should be balanced against risk of worsening coagulopathy
    • RBCs or plasma alone are preferable to crystalloids and colloids
    • Albumin provides effective and more physiologic volume expansion than other colloids
      • Consider supplementing with fibrinogen concentrate and TXA, if available
    • Hextend or Hespan should be avoided as these worsen coagulopathy
    • Hypertonic Saline should only be used for casualties with TBI and evidence of increased ICP
    • Crystalloid infusion should be the last resort in the severely bleeding casualty
  • Casualties at low risk of developing shock should not receive IV fluids or adjunctive medications

Blood Product Transfusion

  • “Golden hour boxes” or similar isothermal transport devices containing blood components should be available on patient transport vehicles
  • WB (Group O low titer preferred) or blood components 1:1:1 should be transfused when shock is present or expected
    • Blood products fully tested for TTDs should be used whenever possible
    • Personnel transfused with blood products collected in the deployed setting must be followed up with infectious disease testing at 3, 6, and 12 months
  • During transfusion:
    • Frequent reassessment to gauge adequacy of resuscitation and to diagnose adverse reactions
    • Calcium (10ml amp 10% calcium chloride, or 30ml 10% calcium gluconate) should be
      given to patients in shock after ~4u citrated blood products
    • Blood products should ideally be warmed to 37°C
  • As the casualty stabilizes, resuscitation by component ratios should be replaced by “goal-directed” therapy guided by PT/INR, aPTT, and viscoelastic testing (ROTEM® or TEG)


Adjunctive Therapies

Hypotensive Resuscitation

  • In casualties without CNS injury, resuscitation prior to surgical control of bleeding focuses on maintaining sBP ~80-90mmHg
    • Reduces re-bleeding by minimizing intravascular hydrostatic pressure
  • Changes in mental status or pulse quality have been used to detect impending hypotensive shock
    • Not adequately tested
    • Can be misleading due to use of analgesics and sedatives (e.g. ketamine)
  • Hypotensive resuscitation should not be used with CNS injury because of associated adverse outcomes
    • Casualties with CNS injury benefit from avoidance of even transient hypotension and hypoxia

Compressive/hemostatic dressings and devices

Prevent further hemorrhage with direct pressure, topical hemostatic dressings, and/or tourniquets, if possible, to minimize the risk of shock.

  • Extremity injury:
    • Tourniquets (e.g., Combat Application Tourniquet, Special Operations Forces Tactical Tourniquet)
      • May be responsible for saving more wounded service members in Iraq and Afghanistan than any other single medical intervention
    • Superficial wounds: hemostatic dressings (e.g., Combat Gauze or Celox gauze)
    • Junctional (axillary, neck, and groin) hemorrhage:
      • Junctional tourniquets (e.g., Combat Ready Clamp, SAM® Junctional Tourniquet, Junctional Emergency Treatment Tool, and XSTAT™ device
    • Truncal internal hemorrhage: Non-compressible
      • Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) may be an effective technique for truncal hemorrhage control in expert hands
      • Limited literature, not yet widely available

 Empiric use of TXA

  • In casualties at high risk of hemorrhagic shock, TXA reduces mortality if given within three hours of injury
  • TXA given > 3 hours post-injury increases the risk of mortality
  • Dose: 1g IV TXA over 10min, then 1g over 8h

Prevention of acidosis and hypothermia

  • Metabolic acidosis in acute trauma is due to inadequate tissue perfusion leading to lactic acid production
    • Best addressed with WB or equal ratio blood components
    • Crystalloid resuscitation exacerbate acidosis and should be avoided
  • Hypothermia is multifactorial:
    • Causes include cold exposure, cold resuscitation fluids, significant blood loss, and shock
      • Warm the casualty with passive or active methods as available and indicated including “space blankets” (e.g. HPMK), heated fluids, fluid blankets, forced-air warmers, warmed environment, warmed inhaled gases via ventilator, etc.
    • NOTE: With injuries treated with tourniquets, the extremity distal to the tourniquet should be exposed and cooled relative to core temperature to preserve the ischemic limb’s viability

Expeditious delivery to definitive surgical control

  • In general, every effort should be made to deliver the critically injured casualty to the highest available level of care as rapidly as possible
  • Only absolutely necessary procedures should be performed
  • Interventions in the prehospital setting should be balanced against the need to expeditiously deliver the patient to definitive care
  • DCS at Role 2 forward surgical units should only focus on control of hemorrhage and contamination

Pediatric Considerations

  • No prospective studies of transfusion resuscitation in pediatric trauma. Most major children’s centers extrapolate from adult literature and are using similar DCR strategies
  • For children < 30kg, transfusions of RBC units, FFP, or apheresis platelets should be given in “units” of 10-15 ml/kg. One unit of cryoprecipitate is typically administered for every 10kg body weight
  • Blood volume in children can be estimated at between 60-80ml/kg; therefore, a 30kg child may have a TOTAL blood volume of 1800-2400mL
  • Over-resuscitation contributes to morbidity and mortality
  • Whole blood may be the better (safer, more convenient) choice:
    • Full oxygen delivery capacity
    • Full hemostatic functionality
    • Supports more accurate volume dosing compared to component therapy
  • Massive transfusion = ≥40ml/kg of blood products in 24 hours.
    • Children are at high risk of developing hypocalcemia, hypomagnesaemia, metabolic acidosis, hypoglycemia, hypothermia, and hyperkalemia during MTs
      • Frequent monitoring and correction of acid/base status, electrolytes, and core temperature is essential during resuscitation
  • Tranexamic Acid:
    • Limited retrospective data demonstrating benefit in pediatric trauma
    • Studies in pediatric cardiac, orthopedic, and cranial surgeries showing overall safety and decreased transfusion requirements
    • No prospectively validated dosing available for pediatric trauma
      • Commonly used in elective surgery: loading dose 10-100 mg/kg IV, then 5-10 mg/kg/hour infusion
    • UK Royal College of Pediatrics and Child Health recommends:
      • Loading dose of 15mg/kg (up to 1 gm), then 2mg/kg/hr over 8 hours (up to 1gm)
  • Viscoelastic clot testing (e.g., TEG or ROTEM®) can be utilized to direct transfusion requirements as in adults
  • Prolonged CPR > 20-30min is generally futile in children with traumatic cardiac arrest; even in-hospital traumatic cardiac arrests have a very high mortality after 20-30 min



DCR prioritizes non-surgical interventions that reduce morbidity and mortality due to trauma and hemorrhage. DCR aims to restore homeostasis and prevent or mitigate tissue hypoxia and coagulopathy.

The major principles of DCR include:

  • Recognition of casualties requiring DCR
  • Blood product transfusion, optimization of fluids

Adjunctive therapies during DCR include:

  • Relatively hypotensive resuscitation: to avoid re-bleeding (target sBP 80-90mmHg)
  • Compressive/hemostatic dressings and devices
  • Empiric use of TXA: if given early reduces mortality in trauma
  • Prevention of acidosis and hypothermia
  • Expeditious delivery to definitive surgical control



For full reference list, please refer to first reference.

  1. LTC(P) Andrew P Cap, MC, USA; Heather F Pidcoke, MD, PhD; Philip Spinella, MD; LCDR Geir Strandenes, MC, Norwegian Special Forces; LTC Matthew A Borgman, MC, USA; COL Martin Schreiber, MC, USAR; COL (ret) John Holcomb, MC, USAR; COL Homer Chin-Nan Tien, MC, Canadian Forces; MAJ Andrew N Beckett, MC, Canadian Forces; Col. (ret) Heidi Doughty ,FRCP, FRCPath, RAMC; Col Tom Woolley, FRCA, RAMC; CAPT (ret) Joseph Rappold, MC, USN; Kevin Ward, MD; Col Michael Reade, MC Australian Defense Forces; MAJ Nicolas Prat, MC, French Army; COL Sylvain Ausset, MC, French Army; Bijan Kheirabadi, PhD; MAJ Avi Benov, MC, Israeli Defense Forces; MAJ Edward P. Griffin, USAF, MSC; LTC Jason B. Corley, MSC, USA; COL Clayton D. Simon, MC, USA; CAPT Roland Fahie, MSC, USN; Col (ret.) Donald Jenkins, USAF, MC; COL Brian Eastridge, MC, USAR; Col Stacy Shackelford, USAF, MC; CAPT Zsolt Stockinger, MC, USN. Damage Control Resuscitation – Combat Casualty Care – Clinical Practice Guideline. Joint Trauma System, 2017. Accessed 2019-02-/12. https://deployedmedicine.com/market/29/content/154
  2. Eastridge BJ, Mabry RL, Seguin P, et al. Death on the battlefield (2001-2011): implications for the future of combat casualty care. J Trauma Acute Care Surg, 2012. 73(6 Suppl 5): p. S431-7.
  3. Holcomb, J.B., Jenkins, D., Rhee, P., et al., Damage control resuscitation: directly addressing the early coagulopathy of trauma. J Trauma, 2007. 62(2): p. 307-10.
  4. Bjerkvig CK, Strandenes G, Eliassen HS, et al., “Blood failure” time to view blood as an organ: how oxygen debt contributes to blood failure and its implications for remote damage control resuscitation. Transfusion, 2016. 56 Suppl 2: p. S182-9.
  5. 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, placebocontrolled trial. Lancet, 2010. 376(9734): p. 23-32.
  6. 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): p. 805-13.
  7. Holcomb JB, Wade CE, Michalek JE, et al. Increased plasma and platelet to red blood cell ratios improves outcome in 466 massively transfused civilian trauma patients. Ann Surg, 2008. 248(3): p. 447-58.
  8. Stinger HK, Spinella PC, Perkins JG, et al. The ratio of fibrinogen to red cells transfused affects survival in casualties receiving massive transfusions at an army combat support hospital. J Trauma, 2008. 64(2 Suppl): p. S79-85; discussion S85.
  9. Shaz BH, Dente CJ, Nicholas J, et al. Increased number of coagulation products in relationship to red blood cell products transfused improves mortality in trauma patients. Transfusion, 2010. 50(2): p. 493-500.
  10. Agaronov M, DiBattista A, Christenson E, et al. Perception of low-titer group A plasma and potential barriers to using this product: A blood center’s experience serving community and academic hospitals. Transfus Apher Sci, 2016. 55(1): p. 141-5.
  11. Zielinski MD, Johnson PM, Jenkins D, et al. Emergency use of prethawed Group A plasma in trauma patients. J Trauma Acute Care Surg, 2013. 74(1): p. 69-74; discussion 74-5.
  12. Sharon R, Fiback, E. Quantitative flow cytometric analysis of ABO red cell antigens. Cytometry, 1991. 12(6): p. 545-9.
  13. Chhibber V, Greene M, Vauthrin M, et al. Is group A thawed plasma suitable as the first option for emergency release transfusion? (CME). Transfusion, 2014. 54(7): p. 1751-5; quiz 1750.
  14. Spinella PC, Perkins JG, Grathwohl Kw, et al. Warm fresh whole blood is independently associated with improved survival for patients with combat-related traumatic injuries. J Trauma, 2009. 66(4 Suppl): p. S69-76.
  15. Spinella PC, Dunne J, Beilman GJ, et al. Constant challenges and evolution of US military transfusion medicine and blood operations in combat. Transfusion, 2012. 52(5): p. 1146-53.
  16. Perkins JG, Cap AP, Spinella PC, et al. Comparison of platelet transfusion as fresh whole blood versus apheresis platelets for massively transfused combat trauma patients (CME). Transfusion, 2011. 51(2): p. 242-52.
  17. Blackbourne LH, Baer DG, Eastridge BJ, et al. Military medical revolution: prehospital combat casualty care. J Trauma Acute Care Surg, 2012. 73(6 Suppl 5): p. S372-7.
  18. Kragh JF, Jr., Aden JK, Steinbaugh J, et al. Gauze vs XSTAT in wound packing for hemorrhage control. Am J Emerg Med, 2015. 33(7): p. 974-6.
  19. Sims K, Montgomery HR, Dituro P, et al. Management of External Hemorrhage in Tactical Combat Casualty Care: The Adjunctive Use of XStat Compressed Hemostatic Sponges: TCCC Guidelines Change 15-03. J Spec Oper Med, 2016. 16(1): p. 19-28.
  20. Morrison JJ, Dubose JJ, Rasmussen TE. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study. Arch Surg, 2012. 147(2): p. 113-9.
  21. CRASH-2 collaborators, Roberts I, Shakur H,et al., The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial. Lancet, 2011. 377(9771): p. 1096-101, 1101 e1-2.
  22. Roberts I, Prieto-Merino D, Manno D. Mechanism of action of tranexamic acid in bleeding trauma patients: an exploratory analysis of data from the CRASH-2 trial. Crit Care, 2014. 18(6): p. 685.
  23. Boffard KD, Riou B, Warren B, et al. Recombinant factor VIIa as adjunctive therapy for bleeding control in severely injured trauma patients: two parallel randomized, placebo-controlled, double-blind clinical trials. J Trauma, 2005. 59(1): p. 8-15; discussion 15-8.
  24. Dutton RP, McCunn M, Hyder M, et al. Factor VIIa for correction of traumatic coagulopathy. J Trauma, 2004. 57(4): p. 709-18; discussion 718-9.
  25. Holcomb JB. Use of recombinant activated factor VII to treat the acquired coagulopathy of trauma. J Trauma, 2005. 58(6): p. 1298-303.
  26. Holcomb JB, Hoots K, Moore FA. Treatment of an acquired coagulopathy with recombinant activated factor VII in a damage-control patient. Mil Med, 2005. 170(4): p. 287-90.
  27. Hauser CJ, Boffard K, Dutton R, et al. Results of the CONTROL trial: efficacy and safety of recombinant activated Factor VII in the management of refractory traumatic hemorrhage. J Trauma, 2010. 69(3): p. 489-500.
  28. Schreiber MA, Perkins JG, Kiraly L, et al. Early predictors of massive transfusion in combat casualties. J Am Coll Surg, 2007. 205(4): p. 541-5.
  29. Ogura T, Nakamura Y, Nakano M, et al. Predicting the need for massive transfusion in trauma patients: the Traumatic Bleeding Severity Score. J Trauma Acute Care Surg, 2014. 76(5): p. 1243-50.
  30. Moore FA, Nelson T, McKinley Ba, et al. Massive transfusion in trauma patients: tissue hemoglobin oxygen saturation predicts poor outcome. J Trauma, 2008. 64(4): p. 1010-23.
  31. Brown JB, Lerner BE, Sperry JL, et al. Prehospital lactate improves accuracy of prehospital criteria for designating trauma activation level. J Trauma Acute Care Surg, 2016. 81(3): p. 445-52.
  32. Brohi K, Cohen MJ, Ganter Mt, et al. Acute coagulopathy of trauma: hypoperfusion induces systemic anticoagulation and hyperfibrinolysis. J Trauma, 2008. 64(5): p. 1211-7; discussion 1217.
  33. Leemann H, Lustenberger T, Talving P, et al. The role of rotation thromboelastometry in early prediction of massive transfusion. J Trauma, 2010. 69(6): p. 1403-8; discussion 1408-9.
  34. Doran CM, Woolley T, Midwinter MJ. Feasibility of using rotational thromboelastometry to assess coagulation status of combat casualties in a deployed setting. J Trauma, 2010. 69 Suppl 1: p. S40-8.
  35. Solvik UO, Roraas TH, Petersen PH, et al. Effect of coagulation factors on discrepancies in International Normalized Ratio results between instruments. Clin Chem Lab Med, 2012. 50(9): p. 1611-20.
  36. Kim SJ, Lee EY, Park R, et al. Comparison of prothrombin time derived from CoaguChek XS and laboratory test according to fibrinogen level. J Clin Lab Anal, 2015. 29(1): p. 28-31.
  37. Duchesne JC, Barbeau JM, Islam TM, et al. Damage control resuscitation: from emergency department to the operating room. Am Surg, 2011. 77(2): p. 201-6.
  38. Butler FK, Holcomb JB, Schreiber MA, et al. Fluid Resuscitation for Hemorrhagic Shock in Tactical Combat Casualty Care: TCCC Guidelines Change 14-01–2 June 2014. J Spec Oper Med, 2014. 14(3): p. 13-38.
  39. Medby C. Is there a place for crystalloids and colloids in remote damage control resuscitation? Shock, 2014. 41 Suppl 1: p. 47-50.
  40. Kozek-Langenecker SA. Fluids and coagulation. Curr Opin Crit Care, 2015. 21(4): p. 285-91.
  41. Strandvik GF. Hypertonic saline in critical care: a review of the literature and guidelines for use in hypotensive states and raised intracranial pressure. Anaesthesia, 2009. 64(9): p. 990-1003.
  42. Joint Trauma System, Neurosurgery and Severe Head Injury CPG,02 Mar 2017. http://jts.amedd.army.mil/assets/docs/cpgs/JTS_Clinical_Practice_Guidelines_(CPGs)/Neurosurgery_Severe_Head_Injury_02_Mar_2017_ID30.pdf Accessed Mar 2018.
  43. Percival TJ, Rasmussen TE. Reperfusion strategies in the management of extremity vascular injury with ischaemia. Br J Surg, 2012. 99 Suppl 1: p. 66-74.
  44. Neff LP, Cannon JW, Morrison JJ, et al. Clearly defining pediatric massive transfusion: cutting through the fog and friction with combat data. J Trauma Acute Care Surg, 2015. 78(1): p. 22-8; discussion 28-9.
  45. Eckert MJ, Wertin TM, Tyner SD, et al. Tranexamic acid administration to pediatric trauma patients in a combat setting: the pediatric trauma and tranexamic acid study (PED-TRAX). J Trauma Acute Care Surg, 2014. 77(6): p. 852-8; discussion 858.
  46. Tzortzopoulou A, Cepeda MS, Shchumann R, et al. Antifibrinolytic agents for reducing blood loss in scoliosis surgery in children. Cochrane Database Syst Rev, 2008(3): p. CD006883.
  47. Schouten ES, van de Pol AC, Schouten AN, et al. The effect of aprotinin, tranexamic acid, and aminocaproic acid on blood loss and use of blood products in major pediatric surgery: a meta-analysis. Pediatr Crit Care Med, 2009. 10(2): p. 182-90.
  48. Basta MN, Stricker PA Taylor JA. A systematic review of the use of antifibrinolytic agents in pediatric surgery and implications for craniofacial use. Pediatr Surg Int, 2012. 28(11): p. 1059-69.
  49. Grassin-Delyle S, Couturier R, Abe E, et al. A practical tranexamic acid dosing scheme based on population pharmacokinetics in children undergoing cardiac surgery. Anesthesiology, 2013. 118(4): p. 853-62.
  50. Health, R.C.o.P.a.C. Major trauma and the use of tranexamic acid in children: Evidence statement. 2012 [cited 2016 July 14]; http://www.rcpch.ac.uk/system/files/protected/page/Major Trauma and the Use of Tranexamic Acid in Children – Evidence Statement 2012-11.pdf.
  51. Nylund CM, Borgman MA, Holcom JB, et al. Thromboelastography to direct the administration of recombinant activated factor VII in a child with traumatic injury requiring massive transfusion. Pediatr Crit Care Med, 2009. 10(2): p. e22-6.
  52. Inaba K, Rizoli S, Veigas PV, et al. 2014 Consensus conference on viscoelastic test-based transfusion guidelines for early trauma resuscitation: Report of the panel. J Trauma Acute Care Surg, 2015. 78(6): p. 1220-9.
  53. Matos RI, Watson RS, Nadkarni VM, et al. Duration of cardiopulmonary resuscitation and illness category impact survival and neurologic outcomes for in-hospital pediatric cardiac arrests. Circulation, 2013. 127(4): p. 442-51.
Richard Hoang

Richard Hoang

Dr. Richard Hoang is a 5th year Emergency Medicine Resident at the University of Ottawa with a variety of academic interests including military medicine, trauma, simulation, and FOAMed.