Certain trauma-related terminology must be understood and utilized in order to effectively communicate with surgeons during trauma resuscitations or surgeries in which blood loss is occurring. Hemorrhage classifications I-IV, damage control resuscitation, and damage control surgery are terms that quickly convey critical information between surgeons and anesthesia personnel, ensuring a common understanding of the various interventions that may be required to resuscitate a trauma or surgical patient experiencing bleeding. The ACS identifies four classes of hemorrhage. Understanding this classification scheme promotes more effective communication between surgeons and anesthesiologists.
Class I hemorrhage is the volume of blood that can be lost without hemodynamic consequence. The heart rate does not change and the blood pressure does not decrease in response to losing this volume of blood. In most circumstances, this volume represents less than 15% of circulating blood volume. The typical adult has a blood volume equivalent to 70 mL/kg. A 70-kg adult can be presumed to have nearly 5 L of circulating blood. Children are considered to have 80 mL/kg and infants, 90 mL/kg blood volume. Intravenous fluid is not required if the bleeding is controlled, as in brief, controlled bleeding encountered during an elective surgical procedure.
Class II hemorrhage is the volume of blood, that, when lost, prompts sympathetic responses to maintain perfusion; this usually represents 15-30% of circulating blood volume. The diastolic blood pressure will increase (a reflection of vasoconstriction) and the heart rate will increase to maintain cardiac output. Intravenous fluid or colloid is usually indicated for blood loss of this volume. Transfusions may be required if bleeding continues, suggesting progression to class III hemorrhage.
Class III hemorrhage represents the volume of blood loss (30-40% of circulating blood volume) that consistently results in decreased blood pressure. Compensatory mechanisms of vasoconstriction and tachycardia are not sufficient to maintain perfusion and meet the metabolic demands of the body. Metabolic acidosis will be detected on arterial blood gas analysis. Blood transfusions are necessary to restore tissue perfusion and provide oxygen to tissues. The patient may transiently respond to fluid boluses given in response to hemorrhage; however, if bleeding persists or given time for the fluid bolus to redistribute, the blood pressure will decline. Surgeons should be advised when this pattern persists, particularly during elective surgical cases where the development of shock is not expected. Class III hemorrhage may prompt an intervention such as a damage control procedure (see below).
Class IV hemorrhage represents life-threatening hemorrhage. When more than 40% of circulating blood volume is lost, the patient will be unresponsive and profoundly hypotensive. Rapid control of bleeding and aggressive blood-based resuscitation (ie, damage control resuscitation) will be required to prevent death. Patients experiencing this degree of hemorrhage will likely develop a trauma-induced coagulopathy, require massive blood transfusion, and experience a high likelihood of death.
Coagulation abnormalities are common following major trauma, and trauma-induced coagulopathy is an independent risk factor for death. Recent prospective clinical studies suggest that in up to 25% of major trauma patients, trauma-induced coagulopathy is present shortly after injury and before any resuscitative efforts have been initiated. In one report, acute traumatic coagulopathy was only related to the presence of a severe metabolic acidosis (base deficit ≥6 mEq/L) and appeared to have a dose-dependent relationship with the degree of tissue hypoperfusion; 2% of patients with base deficits less than 6 mEq/L developed coagulopathy compared with 20% of patients with base deficits greater than 6 mEq/L. Although injury severity scores were likely high in those developing coagulopathy, only the presence of the metabolic acidosis correlated to developing trauma-induced coagulopathy.
Global tissue hypoperfusion appears to have a key role in the development of trauma-induced coagulopathy. During hypoperfusion, the endothelium releases thrombomodulin and activated protein C to prevent microcirculation thrombosis. Thrombomodulin binds thrombin, thereby preventing thrombin from cleaving fibrinogen to fibrin. The thrombomodulin-thrombin complex activates protein C, which then inhibits the extrinsic coagulation pathway through effects on cofactors V and VIII (Figure 39-2). Activated protein C also inhibits plasminogen activator inhibitor-1 proteins, which increases tissue plasminogen activator, resulting in hyperfibrinolysis (Figure 39-3). One prospective clinical study found the following effects of hypoperfusion on coagulation parameters: (1) progressive coagulopathy as base deficit increases; (2) increasing plasma thrombomodulin and falling protein C (indicating activation of the protein levels with increasing base deficit), supporting the argument that the anticoagulant effects of these proteins in the presence of hypoperfusion are related to the prolongation of prothrombin and partial thromboplastin times; and (3) an influence of early trauma-induced coagulopathy on mortality.
Mechanism of trauma-induced coagulopathy. During periods of tissue hypoperfusion, thrombomodulin (TM) released by the endothelium complexes with thrombin. The thrombin-TM complexes prevent cleavage of fibrinogen to fibrin and also activate protein C (PC), reducing further thrombin generation through cofactors V and VIII. (Reproduced, with permission, from Brohi K, Cohen MJ, Davenport RA: Acute coagulopathy of trauma: mechanism, identification and effect. Curr Opin Crit Care 2007;13:680.)
Mechanism of hyperfibrinolysis in tissue hypoperfusion. Tissue plasminogen activator (tPA) released from the endothelium during hypoperfusion states cleaves plasminogen to initiate fibrinolysis. Activated protein C (aPC) consumes plasminogen activator inhibitor-1 (PAI-1) when present in excess, and reduced PAI-1 leads to increased tPA activity and hyperfibrinolysis. FDPs, fibrin degradation products; PC, protein C; TM, thrombomodulin. (Reproduced, with permission, from Brohi K, Cohen MJ, Davenport RA: Acute coagulopathy of trauma: Mechanism, identification and effect. Curr Opin Crit Care 2007;13:680.)
Trauma-induced coagulopathy is not solely related to impaired clot formation. Fibrinolysis is an equally important component as a result of plasmin activity on an existing clot. Tranexamic acid administration is associated with decreased bleeding during cardiac and orthopedic surgeries, presumably because of its antifibrinolytic properties. A randomized control study involving 20,000 trauma patients with or at risk of significant bleeding found a significantly reduced risk for death from hemorrhage when tranexamic acid therapy (loading dose, 1 g over 10 min followed by an infusion of 1 g over 8 h) was initiated within the first 3 h following major trauma. Figure 39-4 demonstrates the benefit of initiating this therapy in relation to the time of injury.
Influence of tranexamic acid in preventing death from bleeding. Outcomes ratios (OR) of tranexamic acid with 95% confidence interval (green area) on the x-axis and time (h) to treatment on the y-axis demonstrate improved survival if tranexamic acid therapy is initiated within 3 h of injury. The area of the curve to the left of OR 1.0 demonstrates the benefits of therapy, while that to the right demonstrates harm from intervention. (Reproduced, with permission, from Roberts I, Shakur H, Afolabi A, 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;377:1096.)
Early coagulopathy of trauma is associated with increased mortality. Administering blood products in equal ratios early in resuscitation has become an accepted approach to correction of trauma-induced coagulopathy. This balanced approach to transfusion, 1:1:1 (red blood cell:fresh frozen plasma:platelet), is termed damage control resuscitation. Although the 1:1:1 combination attempts to replicate whole blood, it results in a pancytopenic solution with only a fraction of whole blood’s hematocrit and coagulation factor concentration. Red blood cells will over time improve oxygen delivery to ischemic, hypoperfused tissues. Fresh frozen plasma provides clotting factors V and VIII along with fibrinogen, which improves clotting, possibly due to overwhelming of the thrombin-thrombomodulin complex. Platelets and cryoprecipitate, although included in the 1:1:1 massive transfusion protocol, are probably not necessary in the initial phase of resuscitation, given the normal platelet and fibrinogen levels noted in early coagulopathy. Additional platelet transfusions may be beneficial if the resuscitation is prolonged, as is typical for most major trauma resuscitations, or if a recalcitrant coagulopathy is noted with coagulation studies. The use of crystalloid fluids in early trauma resuscitation has markedly decreased with the increased emphasis upon early blood product administration.
Most trauma centers have early-release type O-negative blood available for immediate transfusion to patients with severe hemorrhage. Depending on the urgency of need for transfusion, administration of blood products typically progresses from O-negative to type-specific, then to crossmatched units as the acute need decreases. Patients administered uncrossmatched O-negative blood are those deemed at high risk of requiring massive transfusion. As the amount of uncrossmatched blood administered increases beyond 8 units, attempts to return to the patient’s native blood type should not be pursued and type O blood should be continued until the patient is stabilized.
Military experience treating combat-wounded soldiers and civilians has provided great insight into trauma resuscitation and trauma-induced coagulopathy. As the use of blood and blood products has evolved, the 1:1:1 transfusion ratio has been uniformly adopted to address the frequent incidence of trauma-induced coagulopathy. Retrospective analysis of severely wounded solders found improved survival when this transfusion protocol was utilized. Consequently, hemostatic resuscitation has been rapidly adopted by civilian trauma centers, which have reported similar survival benefits for civilian patients with severe trauma. Nevertheless, using traditional definitions, this approach is not “evidence based” from randomized clinical trials.
Using hemostatic resuscitation (ie, damage control resuscitation), blood and blood products are administered preemptively to address a presumed coagulopathy. Often coagulation status is not assessed until the patient stabilizes. Although this treatment approach appears to be effective in controlling trauma-induced coagulopathy, patients requiring this therapy may be exposed to unnecessary additional units of blood or blood products. An alternative approach that relies on thromboelastography (TEG) may allow more goal-directed transfusion of blood and blood products and is increasingly utilized in trauma resuscitations. The formation and stability of a clot represents interactions between the coagulation cascades, platelets, and the fibrinolytic system, all of which can be demonstrated with TEG (Figure 39-5). As TEG use during trauma resuscitation becomes more routine, the current 1:1:1 hemostatic resuscitation ratio will likely undergo modification to proportionately less fresh frozen plasma, and the use of antifibrinolytic therapy will likely increase.
Thromboelastograph (TEG). The graph begins as a straight line until clot formation begins (the enzymatic stage of clotting). As a clot forms, increasing resistance develops on the strain gauge, creating a splaying of the graph. The pattern of the graph suggests the status of fibrinogen stores (α angle) and platelet function (maximum amplitude, MA). Eventually, fibrinolysis will occur as demonstrated by decreasing MA. Deficiencies of various clotting components will affect each phase of the TEG whereas increased fibrinolysis will be demonstrated by an earlier decline in the maximum amplitude. ACT, activated clotting time; EPL, Ly30, K, R, values related to rate of clot breakdown. (Reproduced, with permission, from Kashuk JL, Moore EE, Sawyer M, et al: Postinjury coagulopathy management: Goal directed resuscitation via POC thrombelastography. Ann Surg 2010;251:604.)
Administration of blood products must be done with consideration for potential hazards that may result from transfusion. Although blood-borne diseases such as acquired immunodeficiency syndrome, hepatitis B, and hepatitis C are usually thought of as the highest transfusion-related risks, the incidence of such infections has decreased 10,000-fold due to better screening tests of donors and donated units (see Chapter 51). Noninfectious transfusion reactions are now the leading complication of transfusion and represent a more than 10-fold greater risk than blood-borne infection. Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related death reported to the U.S. Food and Drug Administration. However, although the bleeding trauma patient is at risk for a transfusion-related reaction, that risk is minimal compared with the far greater likelihood of death from exsanguination. The most prudent approach for blood product utilization in the bleeding trauma patient is to administer the blood products that are necessary, based on laboratory studies, clinical evidence of significant bleeding, and the degree of hemodynamic instability that can be directly attributed to hemorrhage.
Massive Transfusion Protocols
Delay in obtaining blood products other than red blood cells is common in both civilian and military settings. Clinical evidence supports the need for, and benefit of, established massive transfusion protocols (MTPs), allowing the blood bank to assemble blood products in prescribed ratios to support hemostatic resuscitation. With MTPs in place, hemostatic resuscitation can continue until the demand for blood products stops. An MTP-driven, blood-based resuscitation, rather than a crystalloid-based resuscitation, improves survival from trauma, reduces total blood product utilization in the first 24 h following injury, reduces acute infectious complications (severe sepsis, septic shock, and ventilator-associated pneumonia), and decreases postresuscitation organ dysfunction (an 80% decrease in odds of developing multisystem organ failure).
It is important to establish which personnel are empowered to invoke use of the MTP, given the expense and implications for the blood bank in terms of blood inventory, personnel training and availability, and disruption of routine blood bank duties. Establishing an MTP benefits both the patient, through improved survival and fewer complications, and the institution, through more efficient and effective processes for utilizing critical blood bank resources.
Initiating an MTP for all trauma patients is impractical; however, delaying request for an MTP until the patient has undergone a thorough trauma evaluation may increase the risk of morbidity and mortality. The assessment of blood consumption (ABC) score is an attempt to predict which patients are likely to require an MTP. The ABC score assigns 1 point for the presence of each of four possible variables: (1) penetrating injury; (2) systolic blood pressure less than 90 mmHg; (3) heart rate greater than 120 beats per minute; and (4) positive results of a focused assessment with sonography for trauma (FAST) evaluation. The FAST evaluation is a bedside ultrasonography screening examination performed by surgeons and emergency department physicians to assess the presence or absence of free fluid in the perihepatic and perisplenic spaces, pericardium, and pelvis. Patients with ABC scores of 2 or higher are likely to require massive transfusion. This scoring system has been validated in multiple level 1 trauma centers and is now relatively commonplace in trauma evaluations.