SURGICAL TECHNIQUES FOR THORACIC, ABDOMINAL, PELVIC, AND EXTREMITY DAMAGE CONTROL

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CHAPTER 60 SURGICAL TECHNIQUES FOR THORACIC, ABDOMINAL, PELVIC, AND EXTREMITY DAMAGE CONTROL

Injury severity and spectrums of injury have continually evolved, resulting in greater and different challenges for the modern trauma surgeon. High energy blunt trauma, with resultant multisystem organ injury, as well as increasingly sophisticated firearms with greater wounding capacity, has resulted in greater severity of injury. Despite the fact that these injury patterns are more likely to result in the death of a patient, improvements in prehospital transport and trauma resuscitation have allowed more moribund patients to reach the hospital alive but in extremis. Damage control surgery, addressing the life-threatening injuries immediately but delaying definitive repair until the metabolic and physiologic perturbations have been corrected, has evolved to address this population of patients.

Damage control has three separate and distinct phases of management. The first phase includes aggressive volume expansion, rapid control of hemorrhage, and the minimization of contamination, often associated with placement of packing to tamponade bleeding. Next, contamination from hollow viscus injuries is quickly obtained. Temporary wound management strategies are implemented. The second phase, which occurs in the intensive care unit (ICU), involves the aggressive rewarming of the hypothermic patient, with correction of coagulopathy, and ongoing resuscitation with crystalloids and blood. Once normal physiology has been re-established, the third phase involves definitive operative management of the patient’s injuries.

Indications for damage control strategy are multiple. The goal of the damage control procedure is to preserve life in the face of devastating injuries with profound hemorrhagic shock. As described by Moore et al., they include an inability to achieve hemostasis resulting from ongoing coagulopathy, a technically difficult or inaccessible major venous injury, a time-consuming procedure in the face of under-resuscitated shock, and a need to address other life-threatening injuries. These indications have been expanded to include hemodynamically unstable patients with high-energy blunt torso trauma or multiple penetrating injuries, or any trauma patient presenting in shock with hypothermia and coagulopathy (Table 1). Most commonly applied to the abdomen, damage control approaches have now been applied successfully to both devastating thoracic and orthopedic injuries.

Table 1 Indications for Damage Control Procedures

Adapted with permission from Rotondo MF, Zonies DH: The damage control sequence and underlying logic. Surg Clin North Am 77:761–777, 1997.

PREDISPOSING FACTORS

The goal of damage control procedures is the early termination of surgical intervention before the development of irreversible physiologic derangement. Uncontrolled hemorrhage results in global ischemic injury, while resuscitation subjects the patient to further injury resulting from the period of reperfusion. Inevitably the lethal triad of hypothermia, coagulopathy, and acidosis develops. While each of these complications is potentially life threatening in and of themselves, the combination of the three together results in an exponential increase in morbidity, contributing to a downward spiral that eventually results in the patient’s demise if not corrected. Damage control surgery, by abbreviating surgical intervention and returning the patient to the ICU for correction of the lethal triad, has resulted in improved mortality over time.

Hypothermia is defined as a core temperature of less than 35° C. The reasons for hypothermia after trauma include aggressive resuscitation with unwarmed fluids, exposure at the time of the primary and secondary survey with radiant heat loss to the environment, and evaporative loss from exposed peritoneal and pleural surfaces in the operating room. The incidence of clinical hypothermia after trauma laparotomy is 57%. Hypothermia has clearly been shown to increase mortality, increasing significantly in patients with a core temperature less than 34° C, and approaching 100% in patients with a core temperature less than 32° C.

Hypothermia has systemic effects, including negative impact on hemodynamics (decreased heart rate and cardiac output, increased systemic vascular resistance), renal function (decreased glomerular filtration rates), and central nervous system depression. Hypothermia also independently affects the coagulation cascade, as clot formation relies on a series of temperaturedependent enzymatic reactions. Studies have clearly demonstrated increases in prothrombin time (PT), thrombin time, and partial thromboplastin time (PTT). Hypothermia also affects platelet function, leading to sequestration in the portal circulation and prolonged bleeding times.

Metabolic acidosis occurs after hemorrhagic shock because of the switch from aerobic to anaerobic metabolism during periods of hypoperfusion. The detrimental effects of acidosis include depressed myocardial contractility and a diminished response to inotropic medications. Acidosis predisposes the myocardium to ventricular dysrhythmias and can worsen intracranial hypertension. Finally, acidosis has been shown to worsen coagulopathy by independently prolonging PTT and decreasing Factor V activity. Acidosis has been linked to the development of disseminated intravascular coagulation (DIC) and may exacerbate a consumptive coagulopathy.

Hypothermia, acidosis, and coagulopathy develop secondary to the dilutional effects when massive resuscitation initially is comprised of crystalloid and packed red blood cells without the addition of clotting factor replacement. Exposed tissue factor secondary to tissue injury also contributes to the development of coagulopathy through the activation of the clotting cascade and resultant consumption of clotting factors.

PHASE I: DAMAGE CONTROL OPERATION

Damage Control Laparotomy

Most damage control procedures are performed in the abdomen. In fact, the earliest descriptions of what subsequently became known as damage control surgery were in patients with major hepatic injuries, in whom the placement of perihepatic packing and staged operative management resulted in decreased morbidity and mortality. The most common injuries that trigger a damage control approach are major liver injuries and major vascular injuries.

The primary method of controlling hepatic hemorrhage is packing. The technique of pack placement is of the utmost importance and depends on the anatomic nature of the liver injury. Major hepatic lacerations require complete mobilization of the liver and inflow occlusion (the Pringle maneuver) to minimize blood loss. Direct ligation of bleeding vessels in the depth of the laceration is necessary to obtain surgical hemostasis. Once major vessel bleeding has been controlled, perihepatic packs should be placed anteriorly and posteriorly, compressing the liver between the two beds of packs and providing tamponade. In penetrating injuries, balloon tamponade of the missile tract, in conjunction with perihepatic packing, can be life saving.

There are several options available for the management of major vascular injuries. Some venous injuries will respond to packing. Ongoing bleeding, however, requires direct surgical intervention. Many abdominal vascular injuries can be managed with simple ligation of the bleeding vessel (Table 2). Ligation, however, is not tolerated in aortic or proximal superior mesenteric artery injuries, and is not technically feasible in retrohepatic caval injuries. These injuries are typically initially approached by an attempt at repair or the placement of a temporary intraluminal shunt, with planned repair at a second operation (phase 3). Commonly, Argyle carotid shunts and Javid shunts have been used for this purpose. Chest tubes may be used when larger conduits are necessary. The shunts should be secured using umbilical tapes, vessel loops, or suture, and do not require anticoagulation to maintain patency. Another technique for the management of exsanguinating vascular injury is the use of endoluminal balloon catheters to obtain proximal and distal control of hemorrhage. The catheters are inserted into the vessel at the site of injury, and the balloon inflated. This technique allows repair of the injured vessel in a relative dry operative field.

Table 2 Abdominal Vessel Ligation and Expected Complications

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Vessel Complication Recommendations
Celiac axis None  
Splenic artery None if the short gastric vessels are intact  
Common hepatic artery None if the portal vein is intact, possible gallbladder ischemia Cholecystectomy (may be done at second look)
Superior mesenteric artery Bowel ischemia Second-look procedure
Superior mesenteric vein Bowel ischemia Second-look procedure
Portal vein Bowel ischemia Second-look procedure
Suprarenal inferior vena cava Possible renal failure