Damage control resuscitation (DCR)
Historically, first described by Rotondo et al in 1993. In that study, although no significant differences were identified between the 22 patients with definitive laparotomy (DL) vs 24 damage control surgery (DC) (with actual survival rates were similar, ~ 55% DC vs. 58% DL), in a subset of 22 patients with major vascular injury and two or more visceral injuries (maximum injury subset), survival was markedly improved in patients treated with damage control (77% vs 11%) (Fisher's exact test, p < 0.02).
Three main phases - damage control surgery aimed to arrest bleeding to limit risk of contamination, Operative time should be limited to 90 min to minimise risk of hypothermia, coagulopathy, and acidemia (Riha et al, 2013); transfer to ICU for resuscitation to normalize tissue oxygen delivery, and resolve acidosis and coagulopathy; and then back to OR again for definitive repair of injuries temporized during damage control surgery.
Four mechanisms of trauma-associated coagulopathy (besides dilutional effect of IV fluids) (Pohlman et al, 2015):
1) a qualitative platelet defect (particularly after traumatic brain injury [TBI])
2) diffuse endothelial cell injury
3) depletion of coagulation factors and platelets through hemorrhage and deposition into injuries,
4) consumption of platelets and coagulation factors secondary to disseminated intravascular coagulation (DIC) or hyperfibrinolysis
Why acidemia is bad? (Pohlman et al, 2015):
Acidemia diminishes coagulation factor enzymatic activity, depletes fibrinogen and reduces the number of circulating platelets.
Acidemia also
(1) decreases cardiac contractility, causes dysrhythmias, which, in effect, may cause cardiogenic shock on hypovolemic shock in the exsanguinating patient.
(2) desensitizes peripheral vasculature adrenergic receptors to endogenous catecholamines disabling compensatory mechanisms in response to hemorrhagic shock
(3) stimulates inflammation, and suppresses immunity
Why hypothermia is bad? (Pohlman et al, 2015): The enzymatic specificity constants of coagulation factors in hemostatic pathways and platelet activity are negatively affected to a significant degree by hypothermia. Coagulation factor activity is reduced approximately 10%–15% for each 1 °C drop in temperature
Although damage control surgery and resuscitation was initially described following abdominal injury, the basic principle has been extended to all aspects of trauma care
Resuscitation
Massive Transfusion (MT): ≥10 units of packed red blood cells within a 24-hour period
The physiology supporting the 1:1:1 (FFP:platelets:PCs) approach is based on the basis of dilutional coagulopathy with conventional transfusion especially so associated with crystalloid (3:1, 3L of crystalloid with 1L of blood).
Neal et al (2012) - Crystalloid resuscitation in a ratio greater than 1.5:1 per unit of PRBCs transfused was independently associated with a higher risk of MOF, ARDS, and ACS.
Holcomb et al (2015) - RCT (n = 680 with major traumatic bleeding) FFP: platelets: PC of 1:1:1 vs 1:1:2.
No significant differences in terms of mortality at 24 hours (12% in 1:1:1 vs 17% in 1:1:2) or at 30 days (22% vs 26% respectively) but patients given 1:1:1 were significantly more likely to have adequate hemostasis (86% vs 78%) and had fewer exsanguination deaths at 24 hours (9% vs 15%).
Other retrospective studies:
Bergman et al (2007) - combat-related trauma, 1:1.4 plasma to RBC ratio is independently associated with improved survival to hospital discharge, primarily by decreasing death from hemorrhage.
Complications of massive transfusion of PCs:
1) Dilution thrombocytopenia
2) Lower fibrinogen levels (give cryoprecipitate)
3) electrolyte abnormalities
4) TRALI/MOF
Platelets:
Every 50 × 109/L increase in admission platelet count decreases odds of death at 6 h decrease by 17% (p=0.03, 95% CI 0.70–0.99), whereas any platelet transfusion within the first 24 h is associated with a lower mortality in injured patients compared to patients who do not receive platelets (p-value less than 0.05).
Tranexamic acid (TXA)
In a Cochrane review, Henry et al (2011) showed that TXA decreases the need for blood transfusion by one-third in patients undergoing high-risk elective surgery
Permissive hypotension:
Landmark study: Bickell et al (1994) NEJM - hypotensive patients who received no IV fluid administration prior to OR and were allowed a lower blood pressure in the pre-hospital and emergency room phases had a higher survival than those who were treated with more fluids targeting a “normal” systolic blood pressure (70% vs 62%, p = 0.04). Extrapolation to blunt trauma (especially with TBI?)
Rationale of permissive hypotension
(1) decreasing the incidence and severity of dilutional coagulopathy and
(2) avoiding the hypothetical “pop the clot” effect, which occurs when the fresh and unstable clot sealing a vascular laceration is dislodged when the intravascular pressure increases.
(3) decreases inflammatory cascade, which is exacerbated in response to IV fluids administration
In an animal study, permissive hypotension >90 - 120 min is associated with worse end-organ damage (Li et al, 2011)
Definitive surgery
Definitive repair of injuries temporized during damage control surgery usually starts 24 to 48 hours following initial injury.
References:
Historically, first described by Rotondo et al in 1993. In that study, although no significant differences were identified between the 22 patients with definitive laparotomy (DL) vs 24 damage control surgery (DC) (with actual survival rates were similar, ~ 55% DC vs. 58% DL), in a subset of 22 patients with major vascular injury and two or more visceral injuries (maximum injury subset), survival was markedly improved in patients treated with damage control (77% vs 11%) (Fisher's exact test, p < 0.02).
Three main phases - damage control surgery aimed to arrest bleeding to limit risk of contamination, Operative time should be limited to 90 min to minimise risk of hypothermia, coagulopathy, and acidemia (Riha et al, 2013); transfer to ICU for resuscitation to normalize tissue oxygen delivery, and resolve acidosis and coagulopathy; and then back to OR again for definitive repair of injuries temporized during damage control surgery.
Four mechanisms of trauma-associated coagulopathy (besides dilutional effect of IV fluids) (Pohlman et al, 2015):
1) a qualitative platelet defect (particularly after traumatic brain injury [TBI])
2) diffuse endothelial cell injury
3) depletion of coagulation factors and platelets through hemorrhage and deposition into injuries,
4) consumption of platelets and coagulation factors secondary to disseminated intravascular coagulation (DIC) or hyperfibrinolysis
Why acidemia is bad? (Pohlman et al, 2015):
Acidemia diminishes coagulation factor enzymatic activity, depletes fibrinogen and reduces the number of circulating platelets.
Acidemia also
(1) decreases cardiac contractility, causes dysrhythmias, which, in effect, may cause cardiogenic shock on hypovolemic shock in the exsanguinating patient.
(2) desensitizes peripheral vasculature adrenergic receptors to endogenous catecholamines disabling compensatory mechanisms in response to hemorrhagic shock
(3) stimulates inflammation, and suppresses immunity
Why hypothermia is bad? (Pohlman et al, 2015): The enzymatic specificity constants of coagulation factors in hemostatic pathways and platelet activity are negatively affected to a significant degree by hypothermia. Coagulation factor activity is reduced approximately 10%–15% for each 1 °C drop in temperature
Although damage control surgery and resuscitation was initially described following abdominal injury, the basic principle has been extended to all aspects of trauma care
Resuscitation
Massive Transfusion (MT): ≥10 units of packed red blood cells within a 24-hour period
The physiology supporting the 1:1:1 (FFP:platelets:PCs) approach is based on the basis of dilutional coagulopathy with conventional transfusion especially so associated with crystalloid (3:1, 3L of crystalloid with 1L of blood).
Neal et al (2012) - Crystalloid resuscitation in a ratio greater than 1.5:1 per unit of PRBCs transfused was independently associated with a higher risk of MOF, ARDS, and ACS.
Holcomb et al (2015) - RCT (n = 680 with major traumatic bleeding) FFP: platelets: PC of 1:1:1 vs 1:1:2.
No significant differences in terms of mortality at 24 hours (12% in 1:1:1 vs 17% in 1:1:2) or at 30 days (22% vs 26% respectively) but patients given 1:1:1 were significantly more likely to have adequate hemostasis (86% vs 78%) and had fewer exsanguination deaths at 24 hours (9% vs 15%).
Other retrospective studies:
Bergman et al (2007) - combat-related trauma, 1:1.4 plasma to RBC ratio is independently associated with improved survival to hospital discharge, primarily by decreasing death from hemorrhage.
Complications of massive transfusion of PCs:
1) Dilution thrombocytopenia
2) Lower fibrinogen levels (give cryoprecipitate)
3) electrolyte abnormalities
4) TRALI/MOF
Platelets:
Every 50 × 109/L increase in admission platelet count decreases odds of death at 6 h decrease by 17% (p=0.03, 95% CI 0.70–0.99), whereas any platelet transfusion within the first 24 h is associated with a lower mortality in injured patients compared to patients who do not receive platelets (p-value less than 0.05).
Tranexamic acid (TXA)
In a Cochrane review, Henry et al (2011) showed that TXA decreases the need for blood transfusion by one-third in patients undergoing high-risk elective surgery
Permissive hypotension:
Landmark study: Bickell et al (1994) NEJM - hypotensive patients who received no IV fluid administration prior to OR and were allowed a lower blood pressure in the pre-hospital and emergency room phases had a higher survival than those who were treated with more fluids targeting a “normal” systolic blood pressure (70% vs 62%, p = 0.04). Extrapolation to blunt trauma (especially with TBI?)
Rationale of permissive hypotension
(1) decreasing the incidence and severity of dilutional coagulopathy and
(2) avoiding the hypothetical “pop the clot” effect, which occurs when the fresh and unstable clot sealing a vascular laceration is dislodged when the intravascular pressure increases.
(3) decreases inflammatory cascade, which is exacerbated in response to IV fluids administration
In an animal study, permissive hypotension >90 - 120 min is associated with worse end-organ damage (Li et al, 2011)
Definitive surgery
Definitive repair of injuries temporized during damage control surgery usually starts 24 to 48 hours following initial injury.
References:
- Riha GM, Schreiber MA. Update and new developments in the management of the exsanguinating patient. J Intensive Care Med 2013;28(1):46-57.
- Rotondo MF, Schwab CW, McGonigal MD, Phillips GR, Fruchterman TM, Kauder DR, et al. 'Damage control': an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma. 1993;35(3):375-82
- Neal MD, Hoffman MK, Cuschieri J, Minei JP, Maier RV, Harbrecht BG, et al. Crystalloid to packed red blood cell transfusion ratio in the massively transfused patient: when a little goes a long way. J Trauma Acute Care Surg 2012;72(4):892-8.
- Borgman MA, Spinella PC, Perkins JG, Grathwohl KW, Repine T, Beekley AC, 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):805-13.
- Holcomb JB, Tilley BC, Baraniuk S, Fox EE, Wade CE, Podbielski JM, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA 2015;313(5):471-82. Epub 2015/02/04.
- Pohlman TH, Walsh M, Aversa J, Hutchison EM, Olsen KP, Lawrence Reed R. Damage control resuscitation. Blood Rev 2015;29(4):251-62.
- Henry DA, Carless PA, Moxey AJ, O'Connell D, Stokes BJ, Fergusson DA, et al. Anti-fibrinolytic use for minimising perioperative allogeneic blood transfusion. The Cochrane Database Syst Rev 2011(3):CD001886. doi: 10.1002/14651858.CD001886.pub4.
- Li T, Zhu Y, Hu Y, Li L, Diao Y, Tang J, et al. Ideal permissive hypotension to resuscitate uncontrolled hemorrhagic shock and the tolerance time in rats. Anesthesiology. 2011;114(1):111-9.
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