EXSANGUINATION: RELIABLE MODELS TO INDICATE DAMAGE CONTROL

Published on 20/03/2015 by admin

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CHAPTER 59 EXSANGUINATION: RELIABLE MODELS TO INDICATE DAMAGE CONTROL

Alicia M. Mohr, Juan A. Asensio, Tamer Karsidag, Luis Manuel García-Núñez, Patrizio Petrone, Amanda J. Morehouse, Alexander D. Vara, John S. Weston, Donald Robinson, Edward Lineen, Allan Capin

Exsanguination has been defined as an extreme form of hemorrhage with ongoing bleeding that, if not surgically controlled, will lead to death. Therefore, the speed by which the exsanguinating trauma patient moves from the prehospital, emergency department, operating room, and intensive care unit is important to survival. Certain conditions and complexes of injuries require damage control to prevent exsanguination. This chapter will describe validated indicators that can be used both preoperatively and intraoperatively to improve outcomes. This chapter will also outline current guidelines for the institution of damage control in trauma patients. Emphasis is placed on the current indications for damage control as defined by key studies. Awareness of these guidelines can improve outcomes after major intra-abdominal injuries and hemorrhage and also assist in the management of one of the well-known sequelae of damage control, the post-traumatic open abdomen.

HISTORY

Bailout/damage control surgery following trauma has developed as a major advance in surgical practice in the last 20 years. The principles of damage control surgery defied the traditional surgical teaching of definitive operative intervention and were slow to be adopted. Currently, techniques developed by trauma surgeons known as damage control surgery have been successfully used 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 was first to describe the “bailout” approach of staged surgical procedures for severely injured patients. This approach emerged after his observation that early death following trauma was associated with severe metabolic and physiologic derangements following severe exsanguinating injuries. Following massive transfusion exceeding two blood volumes in trauma and emergency surgery, severe physiologic derangement ensued and mortality 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 approach, now called “damage control,” describes it as multiphasic, where 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 ECG 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. Low temperature also impairs the host’s immunologic function. Hypothermia is aggravated by 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.

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%–40% of platelets remain in circulation. The prothrombin time (PT), partial prothrombin 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 and cardiac output. 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.

MODELS FOR DAMAGE CONTROL

Stone’s original work in 1983 only provided the intraoperative observation of coagulopathy as an indication for “bailout.” In this study, 17 patients underwent the “bailout” procedure, which included an initial laparotomy, followed by packing in patients with an observed clinical coagulopathy, and then completion of the surgical procedure once the coagulopathy was improved. This resulted in 11 survivors with a mortality rate of 35%. Subsequently, Rotondo et al. described the multiphase approach to the management of exsanguinating patients sustaining abdominal injury, but did not define any objective parameters during the intraoperative phase of damage control. The authors reported a survival rate of 77% in a very small subgroup of patients with major vascular injury and two or more physical injuries. Burch et al. proposed a model based on core temperature 32° C or less, pH 7.09 or less, and pRBC transfusion of more than 22 units that could predict 48-hour survival; the authors also described the “lethal triad.” In a study based on 39 patients, Sharp et al. defined a temperature 33° C or less, pH 7.18 or less, PT 16 seconds or higher, PTT 50 seconds or higher, and more than 10 units of pRBCs transfused as objective parameters to indicate the need for early packing.

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