Unit
- Thermal injury cascade: When skin is exposed to temperatures above 44°C (111°F), protein denaturation begins, triggering a complex inflammatory response. Local tissue damage releases mediators such as histamine, prostaglandins, and cytokines, increasing capillary permeability and causing edema. This zone of stasis can progress to necrosis without proper resuscitation.
- Zones of injury: The classic model describes three concentric areas: the zone of coagulation (irreversible tissue death), the zone of stasis (compromised but potentially salvageable), and the zone of hyperemia (increased blood flow with minimal damage). Management focuses on preventing stasis conversion to coagulation.
- Systemic inflammatory response: Extensive burns (>20% total body surface area, TBSA) trigger a systemic response that affects multiple organ systems. The release of inflammatory mediators can lead to capillary leak syndrome, hypovolemic shock, and immunosuppression, requiring careful fluid management and monitoring.
- Metabolic changes: Severe burns induce a hypermetabolic state characterized by increased energy expenditure, protein catabolism, and insulin resistance. This response can persist for months, necessitating nutritional support with high protein intake and close monitoring of glucose levels.
- Fluid shift and edema: Increased capillary permeability causes fluid to shift from intravascular to interstitial spaces, leading to hypovolemia and edema formation. Escharotomy may be needed if edema compromises circulation in circumferential burns of the extremities or chest.
- Immune system compromise: Burn injury disrupts skin barrier function and depresses both innate and adaptive immunity. Patients are at high risk for wound infections, pneumonia, and sepsis. Topical antimicrobials and strict infection control are standard preventive measures.
- Cardiovascular response: Early after injury, cardiac output decreases due to hypovolemia. After resuscitation, a hyperdynamic state emerges with increased heart rate and cardiac output. Blood pressure may remain low despite fluid administration due to decreased systemic vascular resistance.
- Renal and gastrointestinal effects: Reduced renal blood flow can cause acute kidney injury if fluid resuscitation is inadequate. The gastrointestinal tract may suffer from splanchnic vasoconstriction, increasing the risk of stress ulcers and ileus. Enteral nutrition should be started early to maintain gut integrity.
- Inhalation injury: Burn patients with inhalation injury often present with facial burns, carbonaceous sputum, and hoarseness. Airway edema can progress rapidly, and early intubation is indicated. Pulmonary damage includes mucosal inflammation, bronchospasm, and impaired surfactant function, leading to ventilation-perfusion mismatch. Oxygen therapy and bronchoscopy assist in management.
- Endocrine derangements: Severe burns alter the hypothalamic-pituitary-adrenal axis, increasing cortisol and catecholamine levels. This stress response contributes to hyperglycemia, lipolysis, and protein wasting. Adrenal insufficiency may occur in some patients, requiring careful monitoring and possible replacement therapy. Insulin resistance is common and must be managed aggressively.
- Hematologic changes: Burn injury can cause hemoconcentration early due to plasma loss, followed by dilutional anemia after resuscitation. Coagulation abnormalities, including thrombocytopenia and disseminated intravascular coagulation, may develop. Transfusion thresholds and coagulation factor replacement should be guided by serial laboratory assessments to avoid complications.
- Neurologic and psychological effects: Burn patients often experience pain, anxiety, and delirium during acute care. Cerebral edema can occur from fluid shifts, and seizures may develop from metabolic disturbances. Long-term psychological sequelae include post-traumatic stress disorder, depression, and body image issues. Early psychiatric consultation and adequate analgesia are essential.
Terminology
- Zone of coagulation
- The central area of irreversible tissue damage due to direct heat exposure; necrotic tissue must be debrided or excised.
- Zone of stasis
- The surrounding area with reduced blood flow and potential viability; it can be salvaged with appropriate resuscitation and wound care.
- Zone of hyperemia
- The outermost area of increased blood flow and inflammatory response; usually heals spontaneously without intervention.
- Eschar
- Thick, dry, necrotic tissue resulting from a full-thickness burn; may require escharotomy if it constricts surrounding structures.
Quick Revision
- Burn pathophysiology involves a thermal injury cascade with three zones of injury.
- Systemic effects include SIRS, hypermetabolism, fluid shifts, and immune compromise.
- Fluid resuscitation and early nutrition are critical to prevent complications.
- Understanding these mechanisms guides management decisions in burn care.