Damage Control Resuscitation

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Damage Control Resuscitation:
The New Face of Damage Control
J. trauma Volume 69(4), October 2010, pp 976-990

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Damage Control Resuscitation

  1. 1. Damage Control Resuscitation:The New Face of Damage Control Volume 69(4), October 2010, pp 976-990
  2. 2. Hemorrhage accounts for 40% of all trauma-associated deaths.Damage control resuscitation (DCR) is atreatment strategy that targets the conditionsthat exacerbate hemorrhage in trauma patients.Topics reviewed and discussed will include DCRand surgery, transfusion ratios, permissivehypotension, recombinant factor VIIa (rFVIIa),hypertonic fluid solutions, and the destructiveforces of hypothermia, acidosis, andcoagulopathy.
  3. 3. Damage Control Originally coined by the US Navy in reference to techniques for salvaging a ship.
  4. 4. “Damage control” has been adapted to truncating initial surgical procedures on severely injured patients to provide only interventions necessary to control hemorrhage and contamination to focus on reestablishing a survivable physiologic status.These temporized patients would then undergo continued resuscitation and aggressive correction of their coagulopathy, hypothermia, and acidosis in the ICU before returning to the OR for the definitive repair of their injuries.
  5. 5. Discussions of damage control surgery usually center on the type and timing of surgical procedures.Recently, methods of resuscitation of patients with exsanguinating hemorrhage have come under increasing scrutiny for their ability to adequately correct the acidosis, hypothermia, and coagulopathy seen in these patients.
  6. 6. DCR differs from current resuscitationapproaches by attempting an earlier and moreaggressive correction of coagulopathy andmetabolic derangement.DCR centers on the application of several keyconcepts, the permissive hypotension, the useof blood products over isotonic fluid for volumereplacement, and the rapid and early correctionof coagulopathy with component therapy.
  7. 7. PERMISSIVE HYPOTENSION
  8. 8. PERMISSIVE HYPOTENSION Keep the blood pressure low enough to avoid exsanguination while maintaining perfusion of end organs. Injection of a fluid that will increase blood pressure has dangers in itself. If the pressure is raised before the surgeon is ready to check bleeding, blood that is sorely needed may be lost.
  9. 9. Endpoint of resuscitation before definitive hemorrhage control was a systolic pressure of 70 to 80 mmHg, using a crystalloid/ colloid mixture as his fluid of choice. Cannon WB. JAMA. 1918;70:618.“When the patient must wait for a considerable period, elevation of his SBP to 85 mmHg is all that is necessary … and when profuse internal bleeding is occurring, it is wasteful of time and blood to attempt to get a patient’s blood pressure up to normal. One should consider himself lucky if a systolic pressure of 80 to 85 mmHg can be achieved and then surgery undertaken.” Beecher HK. U.S. Government Printing Office; 1952:6
  10. 10. Regardless of the victim’s blood pressure, survival was better in their urban “scoop and run” rapid transport system when no attempt at prehospital resuscitation was made. Immediate vs. delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331:1105–1109.
  11. 11. Trauma patients without definitive hemorrhage control should have a limited increase in blood pressure until definitive surgical control of bleeding can be achieved.
  12. 12. ISOTONICCRYSTALLOIDS
  13. 13. ISOTONIC CRYSTALLOIDSIsotonic fluid administration in large boluses for acute hemorrhagic loss or severe traumatic injury requiring massive transfusion is the optimal therapy.
  14. 14. Crystalloids can cause dilutional coagulopathyand do little for the oxygen carrying capacity neededto correct anaerobic metabolism and the oxygendebt associated with shock.The use of unwarmed fluids can also be implicatedas a major cause for hypothermia.Crystalloids have been associated withhyperchloremic acidosis and the worsening oftrauma patients existing acidosis.Isotonic, hypotonic, and colloid solutions given post-injury have been shown to leak and cause edemawith only a fraction remaining within theintravascular system.
  15. 15. HYPERTONIC SALINE
  16. 16. HYPERTONIC SALINEHTS attractive for its ability to raise blood pressure quickly at much lower volumes of infusion than isotonic fluids and, thus, potentially easier to use and transport into combat.
  17. 17. HTS with dextran (HSD)Risks and concerns associated with HSD Uncontrolled bleeding Hyperchloremic acidosis Central pontine myelinolysis (CPM) – Keeping serum Na <155 and not raising >10 mEq/d
  18. 18. COMPONENTS OF COAGULOPATHY
  19. 19. TRAUMA• Fluid administration Hemorrhage• Operative exposure Coagulopathy Acidosis Hypothemia
  20. 20. Hypothermia Severe hypothermia is associated with a high mortality. Most cases of hypothermia – ER: resuscitation period – OR: exposure of the peritoneum Hypothermic patients were hypocoagulable with body temperatures < 34.0°C
  21. 21. Acidosis Metabolic acidosis is the predominant physiologic defect resulting from persistent hypoperfusion. Acidosis at pH < 7.2 is associated with decreased contractility and cardiac output, vasodilation, hypotension, bradycardia, increased dysrhythmias, and decreased blood flow to the liver and kidneys. Acidosis can also act synergistically with hypothermia in its detrimental effect on the coagulation cascade.
  22. 22. More sensitive measures of the adequacy ofcellular oxygenation are the base deficit andserum lactate.The base deficit and lactate serve as a usefulguide for the adequacy of resuscitationefforts.Lactate has been demonstrated to have thebest association with hypovolemic shock anddeath and is a useful marker as an endpoint ofresuscitation.
  23. 23. Injury and Ischemia Hypoperfusion Base Deficit > -6 Endothelium Endothelium expresses releases tPA thrombomodulin (TM) TM complexes with thrombin Hyperfibrinolysis Protein C pathway activated Fibrinogen Depletion Extrinsic pathway inhibitedTrauma-Induced SystemicCoagulopathy anticoagulation
  24. 24. TRAUMA-INDUCED COAGULOPATHYThe coagulopathy of trauma is one of the single most accurate predictors of prognosis in trauma and is one of the most significant challenges to any DCR effort.
  25. 25. In severely injured patients, coagulopathy canbe exacerbated during initial care, resuscitation,and stabilization.More than 5 units of pRBC will lead to adilutional coagulopathy, that prolongation ofthe PT was a sentinel sign of dilutionalcoagulopathy, and that this phenomenon occursearly.
  26. 26. A Blood- and Coagulation Factor- Based Resuscitation Strategy
  27. 27. Early Identification of Shock The combination of altered mental status, cool/clammy skin, and an absent radial pulse is a well-established triad, indicating hypovolemic shock. When examining vital signs, the shock index (SI= HR/SBP) is a better indicator of shock than hypotension and is more sensitive than individual vital signs analysis. Laboratory findings indicative of hypoperfusion include bicarbonate, base deficit, and lactate.
  28. 28. ABC Scoring1. Penetrating mechanism2. Positive FAST3. SBP ≦ 90 mmHg on arrival4. Heart rate ≧120 bpm on arrival Score ≧ 2 is 75% sensitive and 86% specific for predicting massive transfusion Early prediction of massive transfusion in trauma: Simple as ABC (assessment of blood consumption)? J Trauma. 2009;66:346–352.
  29. 29. DAMAGE CONTROL RESUSCITATION
  30. 30. Resuscitation With FFP Hewson et al. recommended that FFP and pRBCs be given at a ratio of 1:1 Crit Care Med. 1985;13:387–391. Hirshberg et al. concluded that to avoid coagulopathy, RBCs and FFP must be given in a 3:2 ratio. J Trauma. 2003;54:454–463. Patients receiving a “high” ratio of FFP to pRBC (1:1.4) had the lowest overall mortality rates and hemorrhage-related mortality rates and concluded that high FFP to RBC ratio is independently associated with improved survival to hospital discharge. J Trauma. 2007;63:805–813.
  31. 31. The optimal ratio of FFP to PRBC was 1:1 and that this should be given early in the course.
  32. 32. Resuscitation With Blood Fresh whole blood (FWB) was historically used in transfusion until it fell out of favor in the middle of the 20th century. By the late 1980s, component therapy had almost completely replaced whole blood therapy.
  33. 33. Theoretically, FWB replaces all the bloodcomponents lost to trauma, including platelets andfully functional clotting factors.In addition, the components of FWB are morefunctional than their stored counterparts.Separating blood into components results in dilutionand loss of about half of the viable platelets (88K/Lin 1 unit of component therapy vs. 150–400 K/L in500 mL of FWB), PRBCs (Hct 29% in componenttherapy vs. 38–50% in FWB), and clotting factorsdecreasing the coagulation activity of the separatedcomponents to 65% when giving a 1:1:1 ratio ofcomponent therapy.
  34. 34. FWB transfusion is currently primarily limited to the most severely injured military combat casualties.
  35. 35. Recombinant Factor VIIAThe rFVIIa is currently only approved by the FDA for the treatment of hemophilia, with all trauma uses being off-label.
  36. 36. 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;59:8–15; discussion 15–18. One arm of the trial evaluated its use in blunt trauma whereas the other assessed its utility in penetrating trauma. Although there was no change in mortality, the trial demonstrated a statistically significant reduction in transfusion required in the blunt trauma group, whereas the results for the penetrating trauma group showed no benefit.
  37. 37. Use of activated recombinant coagulation factor VII in patients undergoing reconstruction surgery for traumatic fracture of pelvis or pelvis and acetabulum: a double- blind, randomized, placebo-controlled trial. Br J Anaesth. 2005;94:586–591. In a cohort of patients requiring pelvic surgery demonstrated no significant reduction in transfusion requirement.
  38. 38. rFVIIa seems to be safe and possibly decreases transfusion in blunt trauma.rFVIIa has not shown any efficacy in penetrating trauma.
  39. 39. DAMAGE CONTROL SURGERY
  40. 40. DAMAGE CONTROL SURGERYVictims of penetrating torso trauma or multiple blunt trauma with hemodynamic instability are generally better served with abbreviated operations that control hemorrhage allowing for subsequent focus on resuscitation, correction of coagulopathy, and avoiding hypothermia.
  41. 41. Three Phases of Damage Control Surgery1. Initial operation with hemostasis and packing2. Transport to the ICU to correct the conditions of hypothermia, acidosis, and coagulopathy3. Return to the OR for definitive repair of all temporized injuries Ann Surg. 1988;208:362–370
  42. 42. In the case of laparotomy, once a damagecontrol approach has been initiated, the initialprocedure is directed toward controlling surgicalbleeding.Bleeding is controlled with either ligation ofvessels, balloon catheter tamponade, or packing.
  43. 43. Splenic and renal injuries are treated with rapidresections, non-bleeding pancreatic injuries aresimply drained, and liver injuries are packed.The treatment of hollow viscus perforationsincludes either a simple suture closure or rapidresection of the involved segment.No anastomoses are performed, and ostomiesare not matured.
  44. 44. At the completion of this portion of the procedure,the patient can either be transported to the ICUor to the interventional radiology suite forembolization of arterial hemorrhage that couldnot be controlled during the open procedure,such as pelvic fracture or liver traumainvolving the arterial circulation.
  45. 45. CONCLUSIONDCR focuses on early, aggressive correction of the components of the lethal triad, hypothermia, coagulopathy, and acidosis.This strategy must start in the ER and continue through the OR and ICU until the resuscitation is complete.

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