What is the pathophysiology of burn injury?

Pathophysiology of Burn Injury

Burn injury involves a complex pathophysiological process characterized by local tissue damage and systemic inflammatory responses that can lead to multiple organ dysfunction, with severity determined by burn depth, size, and location.

Local Tissue Response

The local pathophysiological changes in burn injury include:

• Tissue Damage: Burns cause loss of epidermis and dermis, with injuries potentially extending deeply into soft tissue, reaching underlying muscle and bone 1
• Edema Formation: Profound local edema develops, increasing the risk for compartment syndrome 1
• Barrier Disruption: Thermal injury disrupts the skin barrier, making the wound susceptible to infection due to impaired local immune response 2
• Wound Progression: Burns follow a dynamic process where initial injury may expand in the hours and days following the insult 3

Systemic Response

Burns trigger a significant systemic response, particularly in severe cases:

• Inflammatory Cascade: Burns initiate a severe and prolonged inflammatory response with release of inflammatory mediators including TNF-alpha, IL-1beta, IL-6, and IL-2 4
• Hypermetabolic State: Early initiation of nutritional support (within 6-12 hours) is critical as it attenuates the neuro-hormonal stress response and hypermetabolic state that follows burn injury 1
• Immune Dysfunction: The immune system becomes dysregulated, with both hyperinflammatory and immunosuppressive phases occurring 5
• Distributive Shock: Major burns can lead to cardiovascular collapse and electrolyte derangements from fluid shifts 1

Organ System Effects

The systemic inflammatory response following burns can affect multiple organ systems:

• Cardiovascular: Myocardial depression, increased vascular permeability, and hypovolemia 5
• Pulmonary: Respiratory distress and potential acute respiratory distress syndrome 1
• Renal: Acute kidney injury from hypovolemia and inflammatory mediators 1
• Gastrointestinal: Intestinal barrier dysfunction, bacterial translocation, and ileus 5
• Hematologic: Coagulation abnormalities and increased risk of thrombosis 1

Burn Depth Classification and Pathophysiology

Burns are classified by depth, which determines healing potential:

• Superficial burns: Involve only epidermis with minimal systemic effects
• Superficial partial-thickness: Damage to epidermis and upper dermis
• Deep partial-thickness: Destruction extends into deeper dermis
• Full-thickness burns: Complete destruction of epidermis and dermis, requiring surgical intervention 3

Infection Risk and Wound Colonization

Infection is a major complication and leading cause of death in burn patients:

• Colonization Timeline: Gram-negative bacteria typically colonize burn wounds within a week of injury 2
• Bioburden: Debridement of necrotic tissue is essential to reduce bacterial load and prevent invasive infection 2
• Systemic Spread: Burn wound infections can progress to sepsis, defined as "severe organ dysfunction attributed to host's disordered response to infection" 6

Long-term Consequences

Burns have significant long-term pathophysiological effects:

• Scarring and Contractures: Abnormal collagen deposition and remodeling
• Psychological Impact: Burns affect not only physical health but also mental health and quality of life 5
• Chronic Inflammation: Persistent inflammatory state can continue long after initial injury 5

Clinical Implications

Understanding burn pathophysiology guides clinical management:

• Fluid Resuscitation: Critical to address hypovolemia and prevent shock
• Wound Management: Early debridement and appropriate dressings to minimize infection risk 2
• Nutritional Support: Early nutritional intervention (within 12 hours) to counter hypermetabolic state 1
• Thromboprophylaxis: Routine thromboprophylaxis is recommended in the initial phase due to hypercoagulable state 1

The complex pathophysiology of burn injury requires a comprehensive approach to management that addresses both local wound care and systemic manifestations to improve outcomes and reduce morbidity and mortality.