Evaluation of the Burn Wound: Management Decisions

Introduction

Advances in the resuscitation of burn patients have greatly improved survival so that death from burn shock has become uncommon. In the 21st century, prompt functional recovery for the burn patient hinges on proper early management of the burn wound. The greatest advance in burn care to date has been the institution of early surgical burn wound excision with an immediate or delayed wound closure strategy individualized to each patient. For years, burns were treated by daily washing, removal of loose dead tissue, and application of some sort of topical nostrum until wounds healed or granulated. Superficial dermal burns healed within 2 weeks, and deep dermal burns healed over many weeks if infection could be prevented. Full-thickness burns lost their eschar in 2–6 weeks by bacterial enzyme production and daily bedside debridement; split-thickness skin grafts were applied usually 3–8 weeks after injury. A 50% graft survival rate was acceptable, and repeated grafting eventually closed the wound. The prolonged and intense inflammatory response led to hypertrophic scars, contractures, and considerable physical and psychological disability.

Burns that heal within 3 weeks generally do so without significant hypertrophic scarring or functional impairment, although long-term pigmentation is unpredictable. Burns needing longer than 3 weeks to heal often result in unsightly hypertrophic scars and functional impairment. State-of-the-art burn care now involves early excision and grafting. The challenge is to define “early.” Knowing which burn wounds benefit from early excision and grafting requires understanding of skin biology and pathophysiological changes caused by thermal injury. In spite of ongoing efforts to objectively assess wound depth, the standard technique for determining burn depth in the 21st century remains clinical assessment of the wound by a burn specialist.

Pathophysiology of the Burn Wound

Pathophysiological Changes of Thermal Injury

Applied heat at the cellular level causes denaturation of proteins and loss of plasma membrane integrity. Temperature and duration of contact have a synergistic effect; cell necrosis occurs after 1s of exposure at 156°F (69°C), or after 1h at 113°F (45°C). Following a burn, necrosis occurs at the center of the injury and becomes progressively less severe at the periphery. Jackson's description in 1953 of the three zones of injury remains our conceptual understanding of the burn wound ( Fig. 10.1 ). The zone of coagulation at the center of the wound has no remaining viable cells. A mix of viable and nonviable cells, capillary vasoconstriction, and ischemia characterizes the surrounding zone of stasis; this “at-risk” zone may convert to necrosis in the presence of hypoperfusion, desiccation, edema, or infection. Approximately half of the cells in the zone of stasis undergo apoptosis or necrosis as a result of oxidative stress, ongoing inflammation, and decreased blood flow due to microthrombosis. Systemic factors such as advanced age, diabetes, and other chronic illnesses increase risk for “conversion.” Efforts to enhance wound healing have focused on prevention of necrosis in the zone of stasis since medical care has little impact on the outcome of the zone of coagulation. Protection of this sensitive area is achieved with adequate fluid resuscitation, avoidance of vasoconstriction and edema, and prevention of infection. Optimal wound care consists of nondesiccating dressings, topical antimicrobials, and regular monitoring of the wound. At the periphery of the burn wound, the zone of hyperemia contains viable cells with vasodilation mediated by local inflammatory mediators. Tissue in this zone usually recovers unless complicated by infection or hypoperfusion.

Interest in cooling of the wound to minimize the extent of injury can be traced to antiquity but, firm evidence of its efficacy is lacking. Cooling immediately after injury should not supersede other priorities in the evaluation of the injured patient. The optimal temperature and duration of cooling is unknown but excessive or prolonged cooling may be harmful in that it promotes vasoconstriction and systemic hypothermia. Current guidelines of the American Burn Association recommend limiting cooling to 30 min in the management of minor burns. Modalities to improve dermal perfusion and block injury from released inflammatory mediators have also garnered much interest. Whereas beneficial effects of many pharmacologic agents such as heparin, steroidal and nonsteroidal anti-inflammatory agents, thromboxane inhibitors, and epidermal growth factor have been reported, all remain investigational since none has demonstrated clinical validity.