Exsanguination: Reliable models to indicate damage control

History

Bailout/damage control surgery following trauma has developed as a major advance in surgical practice since the early 1980s. The principles of damage control surgery defied the traditional surgical teaching of definitive operative intervention and were slow to be adopted. Currently, damage control techniques developed by trauma surgeons have been used successfully to manage traumatic thoracic, abdominal, extremity, and peripheral vascular injuries. In addition, damage control surgery has been extrapolated for use in general, vascular, cardiac, urologic, and orthopedic surgery.

In 1983, Stone and associates were first to describe the “bailout” approach of staged surgical procedures for severely injured patients. This approach emerged after their observation that early death following trauma was associated with severe metabolic and physiologic derangements following severe exsanguinating injuries. Following massive transfusion (MT) exceeding two blood volumes in trauma and emergency surgery, severe physiologic derangement ensued and mortality rate was found to be greater than 60%. Profound shock along with major blood loss initiates the cycle of hypothermia, acidosis, and coagulopathy. It was at this time that hypothermia, acidosis, and coagulopathy were described as the “trauma triangle of death” or the “bloody vicious cycle.” A fourth component, dysrhythmia, which usually heralded the patient’s death, was later added by Asensio. Coagulopathy, acidosis, and hypothermia make the prolonged and definitive operative management of trauma patients dangerous. This new approach, now called “damage control,” describes the operative phase as multiphasic, in which reoperation occurs after correcting physiologic abnormalities.

Metabolic failure

Hypothermia is a consequence of severe exsanguinating injury and subsequent resuscitative efforts. Severe hemorrhage leads to tissue hypoperfusion and diminished oxygen delivery, which leads to reduced heat generation. Clinically significant hypothermia is important if the body temperature drops to less than 36° C for more than 4 hours. Hypothermia can lead to cardiac arrhythmias, decreased cardiac output, increased systemic vascular resistance, and left shift of the oxygen-hemoglobin dissociation curve. Hypothermia exerts a negative inotropic effect on the myocardium with depression of left ventricular contractility. The initial electrocardiographic change seen with hypothermia is sinus tachycardia, but as the core temperature decreases, progressive bradycardia ensues. The cardiac response to catecholamines may also be blunted in hypothermic hearts, and cold cardiac tissue poorly tolerates hypervolemia and hypovolemia. Hypothermia can also induce coagulopathy by inhibition of the coagulation cascade, of platelet activation, and of platelet function. Low temperature also impairs the host’s immunologic function. Hypothermia is aggravated by further heat loss resulting from either environmental factors or surgical interventions. The multidisciplinary team caring for trauma patients must make every effort to prevent heat loss and help to correct hypothermia.

More than 25% of trauma patients exhibit overt coagulopathy at the time of admission, and it is associated with a threefold increase in mortality risk. The causes of coagulopathy in patients with severe trauma are multifactorial, including consumption and dilution of platelets and coagulation factors, as well as dysfunction of platelets and the coagulation system. Clinical coagulopathy occurs because of hypothermia, platelet, and coagulation factor dysfunction that occurs at low temperatures, activation of the fibrinolytic system, and hemodilution following massive resuscitation. Platelet dysfunction is secondary to the imbalance between thromboxane and prostacyclin that occurs in a hypothermic state. Hypothermia and hemodilution produce an additive effect on coagulopathy. After replacement of one blood volume (5000 mL or 15 units of packed red blood cells [PRBCs]), only 30% to 40% of platelets remain in circulation. The prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen levels, and lactate levels are therefore not predictive of the severe coagulopathic state.

The predominant physiologic defect resulting from repetitive and persistent bouts of hypoperfusion is metabolic acidosis. Anaerobic metabolism starts when the shock stage of hypoperfusion is prolonged, leading to the production of lactate. Acidosis decreases myocardial contractility, cardiac output, functional clotting, and clot strength. Acidosis also worsens as a result of multiple transfusions, the use of vasopressors, aortic cross-clamping, and impaired myocardial performance. It is clear that a complex relationship exists among acidosis, hypothermia, and coagulopathy, and each factor compounds the other, leading to a high mortality rate once this cycle ensues and cannot be interrupted.