The skin is an essential component of the nonspecific immune system, protecting the host from potential pathogens in the environment. Breaches in this protective barrier thus represent a form of immunocompromise that predisposes a patient to infection. Thermal burns may cause massive destruction of the integument as well as derangements in humoral and cellular immunity, permitting the development of infection caused by environmental opportunists and components of the host's skin flora.
Over the last decade, the estimated incidence of burn injuries in the United States has declined steadily; however, >1 million burn injuries are brought to medical attention each year. Although many burn injuries are minor and require little or no intervention, 50,000 persons are hospitalized for these injuries, 60% of whom require intensive care in a specialized burn center and 20,000 of whom have major burns involving at least 25% of the total body surface area. The majority of burn patients are men. Infants account for ~10% of all reported cases. Scalds, structural fires, and flammable liquids and gases are the major causes of burns, but electrical, chemical, and smoking-related sources are also important. Burns predispose to infection by damaging the protective barrier function of the skin, thus facilitating the entry of pathogenic microorganisms, and by inducing systemic immunosuppression. It is therefore unsurprising that multiorgan failure and infectious complications are the major causes of morbidity and death in serious burn injuries. As many as 10,000 patients in the United States die of burn-related infections each year, and 6 of the top 10 complications recently identified by the American Burn Association's 10-year review are infectious. These 10 most common complications are pneumonia (4.6%), septicemia (2.7%), cellulitis/traumatic injury (2.6%), respiratory failure (2.5%), wound infection (2.2%), other infection (2.0%), renal failure (1.5%), line infection (1.4%), acute respiratory distress syndrome (1.2%), and arrhythmia (1.0) (www.ameriburn.org/2007NBRAnnualReport.pdf).
Loss of the cutaneous barrier facilitates entry of the patient's own flora and of organisms from the hospital environment into a burn wound. Initially, the wound is colonized with gram-positive bacteria from the surrounding tissue, but the number of bacteria grows rapidly beneath the burn eschar, reaching ~8.4 × 103 cfu/g on day 4 after the burn. The avascularity of the eschar, along with the impairment of local immune responses, favors further bacterial colonization and proliferation. By day 7, the wound is colonized with other microbes, including gram-positive bacteria, gram-negative bacteria, and yeasts derived from the gastrointestinal and upper respiratory flora. Invasive infection'localized and/or systemic—occurs when these bacteria penetrate viable tissue. In addition, a role for biofilms has been recognized in experimental animal models of burn-wound infection. (Biofilms are surface-associated communities of bacteria, often embedded in a matrix, that allow the microbes to persist and to resist the effects of host immunity and antimicrobial agents.)
Streptococci and staphylococci were the predominant causes of burn-wound infection in the preantibiotic era and are still important pathogens. With the advent of antimicrobial agents, Pseudomonas aeruginosa became a major problem in burn-wound management. Less common anaerobic bacteria typically are found in infections from electrical burns or when open wound dressings are used. The widespread use of topical and more effective antimicrobial drugs has resulted in a decline in bacterial wound infections and the emergence of fungi (particularly Candida albicans, Aspergillus species, and the agents of mucormycosis) as increasingly important pathogens in burn-wound patients. Herpes simplex virus has been found in burn wounds, especially those on the neck and face and those associated with inhalation injury. Autopsy reports on patients with severe thermal burns over the last decade have identified an association of P. aeruginosa, Escherichia coli, Klebsiella pneumoniae, and Staphylococcus aureus with death; this association is independent of the percentage of the total body surface area covered by burns, the percentage of burns that are full-thickness (as opposed to partial-thickness), inhalation injury, and day of death after a burn. In addition, members of the Acinetobacter calcoaceticus-baumannii complex are among the most common pathogens at some burn centers.
The cascade of events that follows a severe burn injury and that leads to multiorgan system failure and death is thought to represent a two-step process; i.e., the burn injury itself, with ensuing hypovolemia and tissue hypoxia, is followed by invasive infection arising from large amounts of devitalized tissue. The frequency of infection parallels the extent and severity of the burn injury. Severe burn injuries cause a state of immunosuppression that affects innate and adaptive immune responses. The substantial impact of immunocompromise on infection is due to effects on both the cellular and the humoral arms of the immune system. For example, decreases in the number and activity of circulating helper T cells, increases in the number and activity of suppressor T cells, decreases in production and release of monocytes and macrophages, and diminution in levels of immunoglobulin follow major burns. Neutrophil and complement functions also have been shown to be impaired after burns. The increased levels of multiple cytokines detected in burn patients are compatible with the widely held belief that the inflammatory response becomes dysregulated in these individuals; bacterial cell products play a potent role in inducing proinflammatory mediators that contribute to this uncontrolled systemic inflammatory response. Increased permeability of the gut wall to bacteria and their components (e.g., endotoxin) also contributes to immune dysregulation and sepsis. Thus, a burn patient is predisposed to infection at remote sites (see below) as well as at the sites of burn injury. Another contributor to secondary immunosuppression after burn injuries is the endocrine system; increasing levels of vasopressin, aldosterone, cortisol, glucagon, growth hormone, catecholamines, and other hormones that directly affect lymphocyte proliferation, secretion of proinflammatory cytokines, natural killer cell activity, and suppressor T cells are seen.
Since clinical indications of wound infection are difficult to interpret, wounds must be monitored carefully for changes that may reflect infection. A margin of erythema frequently surrounds the sites of burns and by itself is ...