Infections Related to Burns

In 2019, unintentional injury was the leading cause of death in children aged 1–18 years of age in the US, accounting for approximately one-third of all deaths. Of these deaths, burns were the seventh leading cause in children <1 year, the fifth leading cause in children 1–4 years of age, and the third leading cause in children 5–9 years old. Overall, the population incidence of nonfatal burn injury in the age group of 1–19 years was 103.1 per 100,000 in 2019. Children <4 years and Black/African American children are at the greatest risk for fire and burn-related injury and death. Most of these injuries are preventable. Most young children suffer scald burns caused by hot liquids and steam. Older children are more likely to sustain contact burns caused by direct contact with fire. On occasion, burn injuries can result from medical therapies, such as therapeutic application of heat, ignition of flammable medications (rubbing alcohol and hot oils), or burns from hot-air vaporizers. Total medical cost of unintentional fire/burn-related deaths and injuries among US children <19 years of age exceeds $395 million. Total charges of pediatric admissions for unintentional fire/burn injuries average $19,064 per case.

The survival of children with burns depends on the following factors: (1) age, (2) the percentage of total body surface area (TBSA) burned, (3) the depth of the burn injury, (4) the type of burn, and (5) management. Young children, particularly those <2 years, have a lower survival rate for the same TBSA burned than older children and adults. Advances in burn care (improvements in resuscitation, intensive care, and care of the burn wound) have narrowed the gap in survival for small children. Currently, the extent of burn associated with a 50% survival in patients >1 year is a TBSA of about 90%, with nearly equal mortality among patients with burns up to 60% and a tremendous rise in mortality rate for those with larger burns. Inhalation injury contributes significantly to mortality among children with burns. Data suggest that the major causes of death in burned children are multiorgan system failure with or without sepsis, followed by anoxic brain injury. ^, The enormous progress in burn survival and therapy is attributable to the following factors: care of patients in centers specializing in the treatment of burns; knowledge of the pathophysiology of shock and aggressive treatment of patients with fluid resuscitation and other adjunctive therapies; recognition of the importance of the caloric requirement of the burned patient and its role in wound healing; and advances in the care of the burn wound itself, especially early debridement and excision of the wound, use of topical antimicrobial agents, judicious use of antibiotics systemically, and improved grafting materials and techniques.

TBSA can be estimated either from the Lund and Browder chart or using the size of the patient’s palm, which is roughly 1% of the TBSA at any age, as a measure. The depth of burn injury is determined by the extent of damage to tissues and is classified by degrees: a first-degree burn involves the epidermis only and is painful, red, and dry, resembling a sunburn; a second-degree burn involves the dermis, is severely painful, usually is erythematous and is moist, weeps, and may have blisters and bullae; a third-degree burn involves the subcutaneous tissue and is usually white or waxy-appearing, dry, avascular, and painless. Depth is alternatively classified as either partial thickness, involving the epidermis or superficial dermis, or full-thickness, involving the deep dermis and subcutaneous tissue. The larger the percentage of TBSA involved and the deeper the burn, the higher the mortality, both immediately after the injury (primarily from shock or occasionally from other associated injuries) and after successful resuscitation (from infectious complications). The type of burn is also important; scald burn is less commonly fatal than flame burn, especially if the latter is associated with pulmonary injury.

Children with burns >30% TBSA, flame and inhalation injuries, and full-thickness burns are at highest risk for infectious complications. Burn victims are susceptible to a wide variety of infections associated with relative immunosuppression and complications of intensive care. Virtually any organ can become the target of an infection in such patients. The most common infections in burned children are burn wound and catheter-associated infections. Infections related to intravascular and urinary catheters and endotracheal tubes are discussed in Chapter 100 . Infection of the burn wound occurs with greatest frequency in burned children. Burn wound septicemia is associated with at least an 80% mortality rate in children.

Diagnosis of infectious complications in a burn victim is challenging. Although fever and elevated peripheral white blood cell count with a left shift are usual indicators of infection, their positive predictive value for infectious complications in burn victims is very low because they occur commonly in uninfected burned children whose wounds by skin or graft are uncovered. Neither height of fever (frequently >39°C) nor response to antipyretic therapy is a reliable indicator of infection. Peak fever in burned children without infection usually occurs on the second day after the burn, with a second peak around the sixth and seventh days. Fever is probably the result of an increase in metabolic rate and an alteration of hypothalamic temperature regulation. Fever usually subsides without specific therapy, coincident with re-epithelialization of the burn wound or successful grafting of all open areas. Thus, fever alone in the burned child is not a reliable indicator of need to investigate for infection or prescribe antibiotic therapy.

Hypothermia is usually a more reliable indicator of infection, although children with burns affecting a high percentage of TBSA who are left uncovered for prolonged periods during dressing changes can have hypothermia that requires external warming. Hypotension due to fluid shifts is common early in the postburn period and usually can be differentiated from infectious causes because of rapid improvement with fluid resuscitation.

Several inflammatory mediators have been evaluated in attempts to distinguish infection from the normal response to thermal injury. They include tumor necrosis factor (TNF), interleukin-1β (IL-1β), ^, IL-6, ^, IL-8, ^, procalcitonin, and C-reactive protein. Levels of mediators in burned patients are higher than those in healthy children, probably owing to pro-inflammatory response to thermal injury. Although several studies have shown significant differences in levels of these inflammatory mediators between burned patients with septicemia and those with uncomplicated thermal injury, ^{, ,} none is highly discriminatory. However, changes in serial C-reactive protein levels can occur during septicemia an average of 2.3 days earlier than a decrease in platelet count or clinical manifestations.

Thus, the diagnosis of infectious complications is made through evaluation of all clinical signs, examination of the burn wound and all catheter sites, and consideration of supporting laboratory evidence and results of culture of blood, urine, or quantitative burn wound biopsy specimens.