Sepsis is an independent risk factor for mortality following thermal injury, especially when multiorgan system failure is present. Open wounds, injured lungs, central venous catheters and urinary catheters place the burn patient at increased risk of infection and sepsis, in that order. Signs of systemic inflammatory syndrome (SIRS) are all normal findings induced by burn injury, leading to diagnostic uncertainty. Laboratory markers including peripheral white blood cell (WBC) levels, procalcitonin, C-reactive protein, human leukocyte antigen D-related (DR) expression and others have been proposed as early indicators of sepsis in the burn patient, all with mixed results. Absolute values and trends in WBC, neutrophil percentage and body temperature are unable to predict bloodstream infection in the burn patient. The promise of early markers is to provide earlier diagnosis and treatment of infection. Although controversial, the use of procalcitonin levels has been advocated due to its sensitivity, specificity and mortality correlation in patients with burns having sepsis. However there is insufficient evidence to support the use of procalcitonin as a single diagnostic marker for sepsis in patients with burn injury.
The largest entrance of infection in burns is the breakdown of the skin barrier. The monitoring of wounds and the use of topical and surgical therapies is the first line for prevention of burn wound infection.
Ventilator associated pneumonia (VAP) in severe burn patients is associated with increased mortality but the diagnosis of VAP is nebulous. Due to severe underlying inflammatory pulmonary pathology, accurate clinical diagnosis of VAP can be very difficult in burn patients and infiltrates may be due to noncardiogenic pulmonary edema (ie, ARDS) from SIRS. The emergence of multidrug resistant bacteria is a major problem as is the use of prolonged antibiotherapy.
Bloodstream and urinary tract infections are also of concern. Timing of central access exchange in the patient with burns is determined by the risk of colonization, need for placement through burned versus unburned tissue, and physician preference. The use of peripherally inserted central catheters lines may not decrease the risk of central-line-related bloodstream infections.3 Prompt removal of all indwelling catheters when no longer warranted provides the best balance between benefit and risk in the patient with burns. Blood and urinary tract infections are treated with removal of the catheter whenever possible and appropriately tailored antibiotic therapy. The use of systemic antibiotic prophylaxis has not been shown to decrease wound infection or any others in the burned patient and may promote infection with multidrug resistant organisms and fungal infections. Protocols vary in when surveillance cultures of burn wounds are performed. Burn wounds often become colonized but may or may not be causing sepsis. Systemic antibiotics are added to standard local wound care if infection is suspected (see Sec. “Wound Care”).
Acute infective endocarditis has a low prevalence in burn patients, but adds considerable morbidity and mortality. A common pathogen is Staphylococcus aureus and persistent bacteremia should prompt investigation for endocarditis. Other less frequent infections in burn patients include parotitis, sinusitis, chondritis of the ear and ocular infections.
Although wound sepsis in burns has steadily decreased, it remains a factor that adds morbidity and mortality. Cleansing and debridement of the wound is accomplished with mild soap and water or with chlorhexadine/normal saline washes. Most burn experts recommend debridement of all blisters larger than 0.5 cm to reduce the risk of bacterial colonization or infection. Burn wounds become colonized in the first few hours with gram-positive bacteria including S aureus and epidermidis, and by 5 days are predominantly colonized with gut flora such as Pseudomonas aeruginosa, Enterobacter cloacae, and Escherichia coli.
Health care workers must be vigilant in hand washing and maintenance of a clean environment around the wounds for prevention of cross-contamination in these immunocompromised patients. Culture swabs of all wound beds should be obtained upon admission and repeated serially to monitor for changes in colonization or if there is a clinical suspicion of wound sepsis. Quantitative cultures of the burn to diagnose wound invasion are best obtained by tissue biopsy, either in the operating room or at bedside. Bacterial colonization of burn wounds does not require systemic antibiotics but should be managed with early debridement and/or excision, together with appropriate topical and/or biologic dressings.
Cleansing and debridement is followed by application of a topical antimicrobial agent intended to control colonization, not sterilize the burn wound. Several layers of absorptive gauze and Kerlix cover the wound to decrease evaporative water losses. Minor burns can be managed with biologic dressings, silver-coated dressings, or tribiotic ointment covered with nonadherent gauze. Commonly utilized topical agents include silver sulfadiazine (silvadene), mafenide acetate (sulfamylon), and silver nitrate. Silvadene continues to demonstrate effective control of burn wound colonization, while remaining inexpensive and easy to apply. However, eschar penetration is minimal and complications related to leukopenia and hemolysis have been reported. Mafenide acetate cream (sulfamylon) is painful when applied to superficial partial thickness burns. Eschar penetration is greatest with sulfamylon, making it the topical agent of choice in burns where the eschar will not be excised immediately or when control of P aeruginosa is required. Metabolic acidosis may occur, as sulfamylon is a carbonic anhydrase inhibitor. Silver nitrate 0.5% solution has fallen out of favor due to electrolyte abnormalities and poor tissue penetration but may be used as a reasonably effective agent for treatment of gram-negative or fungal colonization. Other alternatives for topical treatment are available especially when patients are allergic to sulfas, such as bacitracin, neosporin, mupirocin (mainly gram-positive coverage), and polymyxin B.
Complications directly related to topical agents, frequent dressing changes often result in traumatized epithelialization and delayed wound healing. Silvadene has been shown to delay wound healing due to a direct toxic effect on keratinocytes. To avoid this silver impregnated dressings have been developed to provide antimicrobial coverage, adequate humidity, and decreased trauma, all with less frequent dressing changes. Biosynthetic products designed as epidermal substitutes are also used, allowing for faster reepithelialization, although their use is limited due to increased infection.