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FUTURE DEVELOPMENTS Both basic science and clinical research efforts the past 30 years have changed the methods of fluid resuscitation, wound closure and nutritional support of the burned patient and significantly decreased the mortality and morbidity experienced by patients with severe thermal injuries. On-going research will significantly alter our ability to appropriately intervene into the various aspects of the 'burn syndrome'. The early vascular changes invoked by the burn injury may be modulated with the use of various thromboxane synthetase inhibitors, decreasing the incidence of tissue ischemia and progressive dermal necrosis. Inhalation injury, which continues to account for a significant number of burn-related deaths, may be treated with high-frequency 'jet' ventilation, synthetic surfactants, oxygen radical scavengers and mucolytic agents. These agents may also decrease the severity of ARDS in the burn population, which has replaced the 'shock lung syndrome' so frequently seen 20 years ago. Hypertonic saline resuscitation may hold promise for the treatment of burn injuries in the pre-morbidly compromised patient who is exquisitely sensitive to volume overload. Bacterial translocation, which is currently thought to be a major component of the infection/sepsis cycles of the burn patient, may be attenuated or ablated with early aggressive enteral nutrition, selective mesenteric vasodilators or prostaglandin inhibitors. Other infectious complications may be combated with monoclonal antibodies, future generations of antibiotics, pseudomonal 'vaccination' or selective endotoxin binding agents. Replacement of the destroyed cutaneous tissue may be performed completely in the laboratory, using new tissue culturing techniques of autologous or non-antigenic homologous cells. Artificial collagen matrices may also become available, providing a scaffolding for the in-growth of autologous fibroblasts and capillaries. Various endogenous human growth factors have recently been identified, isolated and spliced into bacterial hosts, making sufficient quantities available so that their application to wounds becomes feasible. The use of various pharmacologic agents to modulate the post-burn hypermetabolic response, such as beta blocking agents and human growth hormone, may decrease the amount of post-burn morbidity and promote the maintenance or rapid restoration of nutrient substrate hemostasis.
CONCLUSIONS Successful management of the acute burn patient requires prompt aggressive fluid resuscitation, metabolic/nutritional support, control of bacterial infection, anticipation and prevention of complications, timely closure of the burn wound, and early initiation of rehabilitation therapy. Burn shock must be adequately treated. Post-burn malnutrition must be prevented. In the post-burn stress response, all major organ systems are affected. Closure of the wound is essential for correction of the pathophysiologic post-burn derangements. In essence, management of the burn patient is a race against time, as rapidity of wound closure is inversely related to mortality. This race must be tempered, however, with thoughtful considerations of ultimate function, cosmesis, and quality of life.
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