Damage control in the injured patient

Abstract

The damage control concept is an essential component in the management of severely injured patients. The principles in sequence are as follows: (1) abbreviated surgical procedures limited to haemorrhage and contamination control; (2) correction of physiological derangements; (3) definitive surgical procedures. Although originally described in the management of major abdominal injuries, the concept has been extended to include thoracic, vascular, orthopedic, and neurosurgical procedures, as well as anesthesia and resuscitative strategies.

INTRODUCTION

“Damage control” has become an essential component of modern trauma care. This fundamental concept has a military origin. The United States Navy considers proficiency in basic damage control skills as part of basic seamanship. The stated objectives of shipboard damage control are as follows:

1. Take all practicable preliminary measures to prevent damage

2. Minimize and localize damage as it occurs

3. Accomplish emergency repairs as quickly as possible, restore equipment to operation, and care for the injured personnel.[1]

These objectives and the overriding principle of performing the minimum repairs necessary to maintain ship worthiness have been adapted to the care of severely injured patients. The most pervasive concept in trauma care over the last 2 decades has been the adoption of damage control principles.[2]

Damage control is a fundamental shift from the traditional surgical focus of anatomical restoration to that of physiological restoration. Pringle perhaps ushered the damage control concept by advocating temporary inflow occlusion and perihepatic packing for liver hemorrhage in 1908.[3] In 1982, Kashuk et al.[4] described the development of the “vicious cycle” of hypothermia, coagulopathy, and acidosis in major abdominal vascular injuries [Figure 1]. Stone et al. described truncating the operative procedure at the first indication of major coagulopathy in the following year.[5] As originally described, the damage control concept consists of 3 separate components.[2] Initially, the patient undergoes resuscitative, abbreviated surgery, where control of hemorrhage and contamination is rapidly obtained and definitive repairs deferred. The patient is then transported to the Intensive Care Unit (ICU) where active rewarming, correction of coagulopathy and acidosis occurs. Once normal physiology is restored, definitive surgical management is completed.

Figure 1.

The “Vicious Cycle” from Kashuk et al.[4]

THE LETHAL TRIAD

Independently, hypothermia, coagulopathy, and acidosis have been demonstrated to worsen the outcome of severely injured patients. If not corrected, each component can further perpetuate the vicious cycle, resulting in certain death.

Hypothermia results as an imbalance between heat loss and the body's ability to generate and maintain metabolic energy.[6] Clinically significant hypothermia occurs when the core temperature is <35ºC[7] ; 21% of all severely injured patients and up to 46% of all trauma patients requiring laparotomy are hypothermic.[8,9] In 1987, Jurkovich et al. demonstrated a 100% mortality in those severely injured patients undergoing laparotomy, who had a core temperature of <32ºC.[10] Hypothermia is associated with an increase in sympathetic drive with resulting peripheral vasoconstriction, end-organ hypoperfusion, and metabolic acidosis from anaerobic respiration.[11] In addition, hypothermia may exacerbate coagulopathy by causing dysfunction of the intrinsic and extrinsic coagulation pathways,[12] as well as platelet activity.[13,14]

Coagulopathy occurs due to a variety of mechanisms. Traditionally, the causes of coagulopathy in severely injured patients have been attributed to acidosis, hypothermia, consumption of clotting factors, and hemodilution. However, this theory has been challenged by recent data suggesting that acute coagulopathy in trauma is due to hypoperfusion rather than the aforementioned causes.[15–17] Brohi and colleagues have suggested that hypoperfusion leads to activation of protein C and systemic hyperfibrinolysis.[18,19]

Acidosis is a result of tissue hypoperfusion and subsequent switch from aerobic to anaerobic respiration. The adverse effects of acidosis on cardiac function were documented in physiological studies over 40 years ago.[20,21] In addition, impairment of oxygen utilization and coagulation dysfunction are associated with the acidotic state.[22–24]

IDENTIFYING THE “DAMAGE CONTROL” PATIENT

The damage control approach is only suitable for select group of patients. In Rotondo et al's original series, only patients with major vascular injury and 2 or more visceral injuries showed a survival benefit with a damage control approach.[2] Thus, only those with a severe injury pattern, whose physiologic reserve is insufficient to tolerate a prolonged, definitive operative procedure, should be subjected to a damage control approach. Asensio et al.[25] identified pre-operating room characteristics predictive of “exsanguinating syndrome,” in which a damage control approach would be appropriate [Box 1]. There is a 98% probability of developing life-threatening coagulopathy if the Injury Severity Score is >25, systolic blood pressure < 70 mmHg, pH < 7.1, and temperature < 34ºC.[26] Moore et al.[26] outlined indications for abbreviating the laparotomy [Box 2]. If the physiological boundaries have been breached, operative interventions must be abbreviated. Hirshberg and Mattox[27] furthermore recommend that “injury pattern recognition” guide the experienced surgeon toward an abbreviated operation.

Box 1.

Preoperative indications for damage control from Asensio et al.[25]

Box 2.

Indications for abbreviated celiotomy from Moore et al.[26]

Although originally described for those patients requiring abdominal operative interventions, the same criteria for damage control apply for other body regions. Damage control principles have been described for thoracic, vascular, neurosurgical, and orthopedic injuries, as well as trauma anesthesia.[28–41] For example, in orthopedic procedures, severe associated head injury and/or pulmonary contusion have been suggested as indications for damage control surgery.[42–44]

DAMAGE CONTROL SEQUENCE AND INTERVENTIONS

Damage control principles are applicable in all initial phases of care of the severely injured patient [Figure 2]. Temporary and definitive interventions at each phase are summarized in Table 1.

Figure 2.

Damage control sequence

Table 1.

Summary of damage control and defi nitive interventions

Prehospital and Emergency Department damage control interventions are aimed toward temporarily stopping hemorrhage and maintaining minimum perfusion until definitive hemorrhage control can be achieved. Rapid transport of the patient from the scene to early surgical care has enabled the survival of many injured patients, who previously had a significant risk of dying in the prehospital phase. Many advancements in prehospital transport have been made during military conflicts. The injury to admission interval was reduced from 12-18 h in World War II to 1.2–5 h for the Vietnam war, with a corresponding decrease in mortality from 9.5% to 2.3%. This was in part due to the improved aeromedical evacuation of injured soldiers.[45,46] The US Army has adopted a staged approach to battlefield treatment, where damage control principles are practiced by Forward Surgical Teams and/or at the Combat Support Hospital.[47]

Most prehospital temporary hemostatic maneuvers also have a military origin. Tourniquet use has been demonstrated to be effective and life-saving during recent military conflicts in Iraq and Afghanistan.[48–51] Tourniquets must be applied correctly, as inappropriately applied devices cause an increase in bleeding due to occlusion of low-pressure venous outflow and inadequate occlusion of arterial inflow.[52]

Topical hemostatic agents for external bleeding include dry fibrin sealant dressings, chitosan dressings, and mineral zeolite. These agents have been used again in military conflicts with success for mainly large soft tissue injuries with small vessel bleeding.[53,54]

The concept of “permissive hypotension” was originally noted by Cannon et al. [55] and subsequently shown by Bickell et al.[56] to be beneficial in patients with penetrating injuries to the torso. Early hemostatic resuscitation has also been described as “damage control resuscitation.” The concept behind this strategy is that early replacement of blood, plasma, and platelets will prevent spiralling into the vicious cycle due to excessive infusion of crystalloid solution. The military experience in Iraq indicated a physiological improvement in those injured soldiers resuscitated with a 1:1:1 ratio of Packed Red Blood Cells toFresh Frozen Plasma and Platelets, respectively.[57–60] Emerging data suggest that this strategy may likewise improve survival in severely injured civilian trauma patients,[61–63] but awaits confirmation in prospective trials.

Within the operating room, damage control concepts apply to both anesthesia and surgery. Damage control anesthesia aims to rapidly establish a definitive airway, maintain oxygenation, prevent hypothermia, initiate correction of coagulopathy, and maintain permissive hypotension until definitive hemorrhage control has been obtained[28,29] [Table 2].

Table 2.

Anesthetic resuscitation goals during and after damage control surgery (from Dutton et al.[29])

Abdominal damage control entails rapid celiotomy, control of hemorrhage, limiting contamination, and temporary abdominal closure.[2,6,11] Surgical bleeding may be controlled by a combination of packing, direct arterial ligation, vascular clamping in situ, splenectomy, and nephrectomy, whereas contamination is limited by rapid stapled resections, temporary hollow viscus closures and pancreatic drainage.[2,11,25–27,64–67] Temporary abdominal closure is most commonly achieved with a vacuum-assisted dressing.[68,69] Alternative methods of temporary closure include towel clip or running nylon skin closure, Bogota bag, or silo closure. Removal of packs, thorough re-exploration, complete vascular repair, establishment of gastrointestinal continuity or stoma formation, and fascial closure are carried out in the definitive phase.[25,27]

Thoracic injuries present a unique challenge, as structures within the chest are not easily controlled with temporary maneuvers. Rapid and definitive control of hemorrhage and air leaks is required. Packing is limited to the apices and cardiophrenic angles, but lung injuries can be rapidly controlled with nonanatomic, stapled wedge resections.[30] Pulmonary tractotomy can achieve rapid hemorrhage control in penetrating lung injury.[37,70] Esophageal injuries are best treated by diversion and wide drainage.[30] Temporary closure can be achieved by simple mass closure or vacuum-assisted dressings.[11,30] Definitive procedures at re-operation include removal of packs, thorough exploration for air leaks, and chest wall closure.

Damage control principles for vascular trauma hinges on 2 categories of vascular repairs: simple and complex.[31] Complex repairs include vascular reconstructions, such as patch angioplasty, –end anastomosis and graft interposition, which are time consuming and not ideal in the hypothermic, coagulopathic patient. Simple techniques include lateral repair, ligation,[71] and temporary shunt.[39,41,67,72,73] Fasciotomy is advisable to prevent compartment syndrome.[31,74] Once appropriate physiology has been restored, definitive vascular reconstruction can be achieved before delayed closure of fasciotomy wounds.[11,31]

Since the 1980s, “early total care” has been the standard of care for orthopedic injuries following Bone's landmark paper[75] demonstrating an increase in pulmonary complications with delayed femoral fracture repair. However, an increasing understanding of the inflammatory process and effects of orthopedic intervention, otherwise known as the “second hit,” led to the concept of damage control orthopedics.[43,44] Temporary external fixation or traction for long-bone fractures and minimally invasive pelvic stabilization for pelvic fractures are the initial orthopedic interventions.[34,40] Definitive open reduction internal fixation should take place after resuscitation. Some data suggest that definitive fixation should occur within 24 h of injury or after 5 days to avoid pulmonary complications.[76]

The critical component of head injury management is prevention of secondary brain injury.[77,78] Optimizing the general condition of the patient is essential in optimizing outcomes from head injury. Damage control neurosurgery involves rapid arrest of intracranial bleeding, the evacuation of intracranial hematomas and the early debridement of compound wounds to the skull.[32] Craniectomy may be beneficial for cerebral edema, however, dural closure should be attempted to prevent intracranial infection. The extent of debridement, however, remains a controversial issue, as aggressive debridement of brain tissue, bone and missile fragments, may at times worsen neurologic deficits.[79,80] Bone defects are repaired once the brain swelling subsides.

After the initial damage control surgery, secondary resuscitation takes place in the ICU. The aims as previously stated are to rewarm the patient and correct acidosis and coagulopathy. Rewarming to a temperature of 37°C can be achieved by warming the ICU room, removing any wet sheets or clothing, covering the patient with warm blankets and applying a forced air-warming device.[81,82] Intravenous fluid warmers have improved the resuscitation of major trauma patients.[83,84] Extracorporeal warming techniques are sometimes required for profound hypothermia.[85] Initial coagulation targets should include INR < 1.2, fibrinogen >100 mg/dL, platelets > 100,000/mm³.[81,82] In addition, Vitamin K and calcium should also be administered. Although activated factor VII was a promising adjunct in the arrest of nonsurgical sources of hemorrhage, recent trials failed to show a mortality benefit.[86,87] Acidosis is usually corrected once the patient is adequately warmed and resuscitated. Hemodynamic and invasive monitoring can aid goal-directed resuscitation.[81,82]

OUTCOMES AND COMPLICATIONS FROM DAMAGE CONTROL SURGERY

A review by Rotondo et al.[88] identified an overall 50% mortality and 40% morbidity in 961 damage control patients. The early reports of damage control surgery demonstrated a significant improvement in mortality when comparing patients undergoing abbreviated procedures to those patients undergoing conventional surgery.[2,5] More recent series have confirmed a survival benefit with the damage control approach.[89,90] It is important to note that these comparisons apply to damage control laparotomy; mortality outcomes have not yet been demonstrated in other damage control procedures.

Complications from damage control laparotomy include intra-abdominal abscess formation (0%–83%), enteric fistula (2%–25%), dehiscence (9%–25%), abdominal compartment syndrome (2%–25%), and inability to reapproximate the fascia edges (10–40%).[2,5,26,27,64,66,68,69,89,91,92] Orthopedic external fixation may increase pin-site infection and damage control vascular procedures may increase graft infections.[31,34]

CONCLUSION

It is essential that trauma providers be au-fait with the principles of damage control for they are clearly life-saving in many patients with multisystem trauma. The damage control concept originated over 100 years ago, and has since grown to encompass all phases of the initial care of the severely injured patient. By learning from the accumulated experience, outcomes and complications of damage control, modern surgeons can apply this strategy following a rationalized approach.[93] Nowadays, damage control principles are also applied for non-trauma care, including the treatment of abdominal compartment syndrome and intra-abdominal sepsis.[94,95] Ongoing and future developments will continue to define the most appropriate patients that may benefit from damage control.