Infection remains the leading cause of death among patients who are hospitalized for burns or the wound cellulitis. The risk of burn wound infection is directly related to the extent of the burn and is related to impaired resistance resulting from disruption of the skin's mechanical integrity and generalized immune suppression. Burn wounds might be classified as wound cellulitis, which involves the unburned skin at the margin of the burn, or as an invasive wound infection, which is characterized by microbial invasion of viable tissue beneath the burn wound eschar. Bacterial burn wound infections and mortality from burn wound sepsis decrease with swift burn debridement and wound closure and the use of effective topical and systemic anti-microbial chemotherapies. Unfortunately, the number of invasive fungal burn wound infections has risen appreciably, likely because of excessive antimicrobial use. On the whole mortality rates from burn wound sepsis remain high.

Managing the wound cellulitis

Management of serious burn wounds is aimed at preventing the progression of injury by maintaining adequate tissue oxygenation through aggressive volume repletion and early removal of necrotic tissue followed by wound closure. Effective topical antimicrobial therapy and daily wound inspection are necessary to monitor for infection, which might cause conversion of partial-thickness burns to full-thickness injuries. Burn injury causes mechanical disruption to the skin, which permits environmental microbes to invade the deeper tissues. The common skin barrier to microbes is replaced by a moist, protein-rich, avascular eschar that fosters microbial growth. The avascularity of the eschar prevents migration of immune cells and restricts the distribution of systemically administered antibiotics. Furthermore, toxic intermediaries free by the eschar can impede the immune response.

Thermal injuries leading to the cellulitis

Thermal injury has a serious impact on the host's cellular and humoral immune systems. The degree of immune suppression is comparative to the duration and temperature of thermal exposure. The injury produces a loss of skin and subjacent tissue, resulting in an area of irreparable central coagulation necrosis surrounded by an area of pronounced inflammation and hyperemia. The presence of major thermal injury damages all circulating and stationary phagocytic cells, as well as bactericidal activity. Reduction of T-cell activity, decreases in inflammatory cytokine levels, and decreases in complement levels result in global impairment of host defenses. Although advances in local burn therapies, together with the judicious use of antimicrobials, undoubtedly have reduced infectious complications from large burns, secondary opportunistic infections with fungal pathogens have been noted in recent years. This especially is widespread in patients sustaining larger burns who receive multiple doses of broad-spectrum peri-operative antibiotics during wound debridement and/or antibiotics for infections at other sites.