Severe burns, such as full-thickness (third-degree) or large-area partial-thickness (second-degree) burns, initiate profound systemic changes that compromise the body’s entire defense structure. Consequently, infection stands as the leading cause of illness and death for patients who survive the initial trauma. This extreme vulnerability to pathogens results from the simultaneous failure of physical protection, the collapse of systemic immunity, and the unique characteristics of the wound itself.
Compromise of the Skin Barrier
The skin is the largest organ and serves as the primary physical shield, composed of the outer epidermis and the underlying dermis. This intact barrier prevents the entry of environmental microbes into sterile internal tissues. A severe burn instantly destroys this continuous, protective layer, creating a direct, open portal for bacteria and fungi.
The damage exposes the underlying subcutaneous tissue, transforming the internal environment from sterile to one exposed to external contamination. Microbes normally harmless on the skin surface gain unimpeded access to the deep, nutrient-rich tissues. This loss of physical containment is the primary reason for the rapid onset of infection risk.
Systemic Immunosuppression
The initial burn trauma triggers a massive, uncontrolled inflammatory response that evolves into profound immune dysfunction. This involves a surge of pro-inflammatory mediators (Systemic Inflammatory Response Syndrome, or SIRS) followed by a compensatory anti-inflammatory response (CARS). The patient enters a state of global immunosuppression, making them susceptible to infections far from the burn site.
Specific immune cells lose their ability to function correctly. Neutrophils, the first-responder white blood cells, are released in large numbers but are often immature and functionally impaired. Their ability to move toward infection sites (chemotaxis) is significantly reduced, failing to contain invading microbes.
The adaptive immune system is also suppressed, shifting T-helper cell function from the infection-fighting Th1 type to the Th2 type. This suppression includes decreased T-cell activity and impaired production of antibodies (IgM, IgA, and IgG), which are necessary for long-term defense. This immune paralysis prevents the body from mounting an effective, coordinated defense against any pathogen.
The Infectious Nature of the Burn Eschar
The dead, denatured tissue that forms over a deep burn is called eschar, and it presents an ideal breeding ground for microbial growth. Composed of coagulated protein and hydrated by seeping fluid, eschar is a rich culture medium for bacteria and fungi.
Crucially, the heat causes thermal thrombosis, destroying blood vessels within the eschar and the tissue beneath it. This avascular state creates a physical sanctuary for microbes, preventing circulating immune cells and systemically administered antibiotics from reaching the colonization site. The eschar acts as a physical shield, allowing pathogens to proliferate rapidly, which can lead to invasive burn wound infection and sepsis.
Pathogen Translocation and Medical Interventions
Infections in burn patients arise from two main categories: endogenous and exogenous sources.
Endogenous Sources
Endogenous infections often stem from the translocation of the patient’s own gut bacteria. The stress response following a severe burn causes significant changes in the gastrointestinal tract, including reduced blood flow and damage to the intestinal mucosal barrier. This damage allows bacteria, such as those from the Enterobacteriaceae family, to pass from the intestine into the bloodstream and internal organs, leading to systemic infection.
Exogenous Sources
Exogenous sources are typically nosocomial, or hospital-acquired, infections introduced by necessary medical procedures. Interventions breach residual barriers, creating direct entry points for environmental organisms. These organisms are frequently multi-drug-resistant, making them especially challenging to treat in an already immunocompromised patient. Interventions include:
- Central venous catheters.
- Urinary catheters.
- Mechanical ventilation for smoke inhalation injuries.