Page 65 - JSOM Winter 2019
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Therefore, we propose use of an additional mnemonic acro-  which can be confused with hemorrhagic shock. Later, during
              nym, SMART, to assist with the recall of key strategies in the re-  prolonged field care, other causes of shock may have to be
              suscitation of casualties with hemorrhage in trauma. Providers   considered, including sepsis and venous thromboembolism.
              should be taught to initiate the use of this mnemonic acronym
              when caring for a patient with visible catastrophic hemorrhage   With  greater  understanding  of  the  underlying  processes  has
              or a patient with traumatic injuries who, on structured assess-  come clearer evidence for treatment strategies that address
              ment (e.g., by using the MARCH or C-ABCDE approach), is   these problems. In 2016, Rossaint et al.  published the up-
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              suspected of being at risk of life-threatening hemorrhage.  dated European guideline for the management of major
                                                                 bleeding and coagulopathy after trauma. Recent revision of
                                                                 the Tactical Combat Casualty Care guidelines also included
              Management of Hemorrhagic Shock
              in Trauma Patients                                 specific evidence-based recommendations about the hierar-
                                                                 chy  of early  blood-product  administration  to patients  with
              The pathogenesis of the coagulopathy that occurs in patients   hemorrhagic shock.  The 2016 European guideline includes
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              after traumatic injury is complex but has been increasingly   39 evidence-based recommendations that cover all aspects of
              well described in recent years. Brohi et al.  in 2003 observed   care, from initial resuscitation through quality management
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              that there is a coagulopathy seen in trauma patients that can-  strategies. Key recommendations include that evidence-based
              not be attributed solely to the adverse effects of fluid replace-  treatment algorithms are implemented and that checklists are
              ment given during resuscitation. The authors suggested the   used to guide patient care.
              traumatic  process  itself  results  in  the  release  of  factors  that
              contribute to this coagulopathy. Hess et al.  in 2008 described   SMART Mnemonic Acronym: Recommendations
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              some of the complex mechanisms that contribute to this co-
              agulopathy. After traumatic injury, tissue factors are released   S – Start the clock
              that initiate both coagulation and fibrinolysis. The hypoperfu-  •  Minimize the time from point of injury to surgical con-
              sion that results from untreated severe hemorrhage then causes   trol of bleeding.
              acidosis, which, in turn, leads to additional imbalance of nor-  •  Minimize time to resuscitation with blood products.
              mal clotting mechanisms. This coagulopathy contributes to   Life-threatening bleeding must be stopped as quickly as possi-
              additional bleeding and, hence, worsening tissue perfusion.   ble by whatever means, including surgical intervention. Death
              Hypoperfusion, in turn, causes a reduction in oxygen delivery,   of trauma patients who have suffered significant torso injury
              leading to tissue ischemia and accumulation of lactate. This   occurs  very  rapidly,  and  so  the  time  from  injury  to  hemor-
              has been described as causing an “oxygen debt.”  Although   rhage control must be minimized.  Shackelford et al.  have
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              such a debt can lead to irreversible organ failure, it has also   also highlighted the beneficial impact of early blood product
              been suggested that it causes failure of endothelial function   administration on survival.
              which, combined with acute traumatic coagulopathy, may     – Stop the bleeding
              constitute “blood failure.”  The early use of blood products   •  Tourniquet use
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              to restore blood function toward normal is a key strategy to   •  Immediate bleeding control procedure
              minimize the ischemic insult to all organs.        The reintroduction of effective field limb tourniquets has led
                                                                 to a demonstrable improvement in survival for patients with
              Injudicious resuscitation attempts with room temperature crys-  life-threatening hemorrhage from the extremities.  For the
              talloid fluids can then lead to hemodilution and hypothermia,   management of junctional hemorrhage, other techniques and
              both of which can cause further disruption  of coagulation.   devices have become available, and so the use of these devices
              Early treatment, therefore, is directed at stopping bleeding,   is emphasized in this mnemonic.
              maintaining tissue perfusion with the optimum resuscitation   M – Maintain perfusion
              fluids available, countering hyperfibrinolysis, preventing hy-  •  Fluid therapy in the hypotensive bleeding patient
              pothermia, and titrating blood products to further maintain   •  Target systolic blood pressure of 100mmHg
              perfusion and replace clotting components. Emerging evidence   If there are any delays in time to hemorrhage control, then
              from the Afghanistan conflict emphasizes the survival bene-  organ perfusion must be maintained with appropriate prod-
              fit of blood-product administration as soon as possible after   ucts. Failure to maintain perfusion causes critical reduction
              injury.  Prehospital administration of plasma reduces 30-day   in oxygen delivery to vital organs, and so care providers must
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              mortality when used by civilian air medical transport teams.    instigate fluid therapy with the optimum available fluid to
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              These actions can be summarized as follows:        maintain critical perfusion. Although a strategy of hypoten-
                                                                 sive resuscitation may be appropriate for a short duration
                •  Start the clock and stop the bleeding         in patients without evidence of traumatic brain injury, pro-
                •  Maintain perfusion                            longed or profound hypotension below 100 mmHg should be
                •  Administer antifibrinolytics                  avoided.  If blood pressure monitoring is unavailable in par-
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                •  Retain heat                                   ticularly austere environments, then providers should consider
                •  Titrate blood products and calcium; think of alternative   loss of radial pulses as a trigger to initiate fluid therapy but
                  causes of shock
                                                                 should monitor for return of pulses to avoid excessive fluid
              A vital strategy in the resuscitation of shocked patients with   administration.
              traumatic injuries in any environment, but particularly in aus-  A – Administer tranexamic acid
              tere and resource-poor healthcare settings, is to monitor the   •  Tranexamic acid for a patient who is bleeding or at risk
              patient’s  response  to resuscitation  and always  consider  that   of significant hemorrhage
              there may be alterative causes of shock. Shock due to ten-  The CRASH 2 trial demonstrated a clear survival benefit for
              sion pneumothorax may develop rapidly in severely injured   patients with traumatic injuries at risk of significant hemor-
              patients, or they may experience neurogenic shock, both of   rhage when tranexamic acid was administered within 3 hours

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