Management of the Difficult Abdomen and Damage Control Surgery

Jay S. Jenoff

Patrick Kim

Massive hemorrhage remains the second leading cause of injury-related, prehospital mortality, surpassed only by central nervous system injury.¹ Early trauma mortality is most frequently due to uncontrolled bleeding.² The evolution of care of the most severely injured patients has led to a step-wise approach of stabilization, resuscitation, and delayed definitive repair.³ Patient evaluation and treatment at both the prehospital scene as well as in the emergency department have been shortened in these patients. This population, identified as suffering the “lethal triad” of ongoing acidosis, hypothermia, and coagulopathy, are being expedited both into and out of the operating room (OR). This process, termed damage control surgery by Rotondo et al., addresses immediately life-threatening hemorrhage and contamination at initial contact. This is followed by aggressive correction of metabolic derangement, with specific attention to the “triad” mentioned in the preceding text.

As the principles of trauma surgery have developed, damage control techniques have been applied to truncal injury in both the thoracic as well as the abdominal cavities. Vascular compromise in the extremities has also been addressed in this manner, with operative management aimed at early reperfusion followed by delayed, definitive repair. This chapter will describe the techniques and sequence of the damage control, as named by Rotondo and Schwab in 1993, along with the resulting sequelae of this process.⁴

Traditionally, the phrase damage control is a naval term describing efforts to preserve a ship with extensive penetrating damage to its hull. The aim is to keep the vessel afloat and maintain overall mission integrity. Techniques would involve procedures to occlude gaps in the ship’s body, the closing of compartmentalized watertight doors to limit the spread of damage, and local extinguishing of fires. Such procedures would keep the ship righted, buying time for definitive repair.⁵

In the care of the trauma patient, similar principles are applied. Early identification of appropriate patients allows limitation of pre-OR (prehospital scene, emergency department) resuscitation, expediting the patient to laparotomy. The initial goals are limited to control of hemorrhage through temporary intra-abdominal packing and largevessel ligation, along with containment of contamination. This process is abbreviated to return the patient to the intensive care unit (ICU) setting for aggressive resuscitation aimed at rapid return to physiologic and metabolic normalcy. On successful resuscitation, the patient is returned to the OR for definitive repair of their injuries. If feasible, abdominal wall closure is performed at this time. For
some, this may be done in a delayed manner, involving planned hernia repair up to a year from initial injury. Overall, this approach provides a strategy to combat the physiologic and metabolic mortality, which often follows successful technical intervention in the trauma patient.

HISTORY

Damage control techniques date back to the early 20th century.⁶ In 1908, Pringle described intra-abdominal packing for hepatic hemorrhage.⁷ Halsted went on to expand on this concept, placing protective rubber sheets between the packs and the liver parenchyma.⁸ As the science of surgery progressed over the next few decades, these techniques were largely abandoned, with primary repair of injuries becoming the mainstay of treatment. This dominated surgical technique from the end of World War II and continued for the next 30 years.⁹

Interest in abbreviated laparotomy reemerged in 1976 when Lucas and Ledgerwood published a prospective study of hepatic packing at the Detroit General Hospital.¹⁰ This was followed by Calne et al. who reported a similar experience in 1979.¹¹ In 1981, Feliciano et al. described a population exhibiting acidosis, hypothermia, and coagulopathy, and published a 90% survival rate in ten of these patients who underwent intra-abdominal packing for liver trauma.¹² In 1983, Stone et al. broadened and organized the process of damage control surgery. These techniques were not limited to hepatic trauma. The initial laparotomy was limited and coagulopathy corrected. On return of hemodynamic stability, operative intervention for definitive repair was pursued. Of note, 11 of 17 patients believed to possess lethal coagulopathy went on to survive their injuries.¹³

This approach to the traumatically injured patient would continue to grow over the next decade, and in 1993 Rotondo and Schwab coined the phrase “damage control.” In detail, they standardized the three stages on which damage control surgery is based presently. Their initial study showed a 58% overall survival, which increased to 77% in selected population (major vascular injury with two or more visceral injuries).⁴ The three stages were described as mentioned in the subsequent text.

Damage control stage one (DC I)—early laparotomy with control of hemorrhage and contamination followed by temporary abdominal closure.

Damage control stage two (DC II)—ICU resuscitation aimed at hemodynamic stabilization and correction of metabolic derangement.

Damage control stage three (DC III)—return to the OR for definitive repair with or without abdominal wall closure.

Johnson and Schwab defined a fourth stage, damage control Ground Zero (DC 0), in 2001. This stage begins in the prehospital setting and is aimed at identifying the select population that will benefit from damage control techniques, leading to limitation of preoperative resuscitation times.¹⁴

INDICATIONS FOR DAMAGE CONTROL

Over the last century, the indications for damage control have grown in number. Proper selection of appropriate patients is necessary, because just as failure to apply damage control principles may increase mortality, overuse will surely increase morbidity.

Rotondo et al. defined what they termed a maximal injury subset of patients who would benefit from damage control. These patients had a major vascular injury, two or more visceral injuries, and profound shock. Survival was 77% in these patients compared to 11% in those undergoing laparotomy with primary repair at initial surgery. In 1997, Rotondo and Zonies expanded on this by defining “key” factors in selecting the correct population for damage control.¹⁵

Moore et al. published their criteria for damage control in 1998. Their indications were similar and take into account available resources at the time of resuscitation.¹⁶

THE PHYSIOLOGY BEHIND DAMAGE CONTROL

With the improvement of transfusion services in trauma centers, blood banks developed the ability to rapidly provide the resources to meet massive transfusion requirements. However, patients ultimately succumbed to metabolic failure after bleeding was controlled and contamination eliminated. This “triad of death,” metabolic acidosis, hypothermia, and coagulopathy, created an ongoing physiologic derangement with one entity augmenting the other two.¹⁷ It is what Kashuk termed the bloody vicious cycle. It is these metabolic abnormalities that are the primary goal of the damage control two (DC II) phase of resuscitation.¹⁸ The physiology of these processes is described in the subsequent text.

Acidosis

Hypovolemic shock leads to tissue ischemia and conversion from aerobic to anaerobic metabolism. Lactate, the end product, leads to a profound metabolic acidosis. This state leads to uncoupling of β-adrenergic receptors leading to catecholamine resistance. The resultant depressed cardiac output, hypotension, and ventricular arrhythmias exacerbate the shock state and further lactic acid production. Concomitantly, acidosis worsens the existing coagulopathy.¹⁹

Abramson et al. correlated lactate clearance with postinjury mortality. Survival was 100% when the body was able to clear lactate with 24 hours, whereas it fell to 14% if clearance took 48 hours or greater.²⁰ Rapid correction of metabolic acidosis is pursued during the damage control sequence. Control of hemorrhage in DC I and aggressive restoration of euvolemia in DC II are mainstays of therapy. Although controversial, adjunctive measures such as pulmonary artery catheter placement with measurement of continuous cardiac output and mixed venous oxygen saturation are often employed. They allow optimization of fluid resuscitation and pharmacologic therapy to maximize oxygen delivery to tissues.

Hypothermia

Hypothermia, defined as a core body temperature <35°C, is present in two thirds of trauma patients admitted to a Level I trauma center.²¹ At 32°C, mortality is 100% in the trauma population. Cushman et al. found a 40-fold higher incidence of death in patients with a core temperature <35°C.²²

Hypothermia in trauma patients stems from many etiologies. Environmental exposure at the prehospital scene, in the trauma bay, and in the OR is a common cause. Hypovolemic shock and the resultant decrease in oxygen delivery and consumption impair the ability of the body to generate heat. Compounding this are intoxication and pharmacologic intervention such as neuromuscular blocking agents administered with anesthesia. Room temperature resuscitation fluids and cooled blood products can quickly lower body temperature. Efforts to reverse these processes and prevent further cooling include warming the environment, limiting exposure to only that which is necessary, and active warming strategies (intravenous [IV] fluid/blood product warmers, Bair Hugger/Arctic Sun warming devices, cavitary irrigation), and should be employed as indicated. In extreme circumstances, continuous venovenous hemodialysis and even cardiopulmonary bypass may be employed for rapid warming in the most severe of circumstances.

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