Unit
- Thermal injury mechanism: Heat causes protein denaturation and cell death in the skin and underlying tissues. The depth of injury depends on temperature, duration of contact, and tissue conductivity. First-degree burns affect only the epidermis; second-degree extend into the dermis; third-degree involve full-thickness destruction.
- Zone of coagulation: The central area of irreversible tissue damage where blood flow ceases and cells die immediately. Necrotic tissue must be debrided to prevent infection and promote healing. This zone is surrounded by zones of stasis and hyperemia.
- Zone of stasis: Adjacent to coagulation, this region has compromised blood flow and is at risk of irreversible injury without proper resuscitation and management. Interventions aim to preserve this zone to minimize burn size progression.
- Zone of hyperemia: The outermost area with increased blood flow due to inflammation. Tissue here is viable and typically recovers fully within days. This zone contributes to systemic inflammatory response syndrome (SIRS) in large burns.
- Systemic inflammatory response: Burns over 20% total body surface area (TBSA) trigger a cascade of cytokines and inflammatory mediators. This can lead to capillary leak, hypovolemia, and multi-organ dysfunction if not controlled.
- Cardiovascular changes: Within hours, myocardial contractility decreases and systemic vascular resistance increases. Fluid resuscitation must match the altered hemodynamics. Burn shock is a combination of hypovolemic and distributive shock.
- Metabolic response: Burn injury causes a hypermetabolic state that can persist for months. Energy expenditure doubles, leading to protein catabolism and muscle wasting. Early nutritional support is critical to attenuate this response.
- Immunosuppression: Disruption of skin barrier and systemic inflammation impair immune function, increasing infection risk. Wound colonization and sepsis are common causes of morbidity and mortality in burn patients.
- Inhalation injury: Smoke inhalation damages the airway and lung parenchyma, often complicating burn management. Carbon monoxide poisoning and upper airway edema require early intubation and oxygen therapy. Bronchoscopy confirms diagnosis, and aggressive pulmonary toilet is essential to prevent pneumonia.
- Fluid resuscitation formulas: The Parkland formula (4 mL/kg/%TBSA lactated Ringer's in 24 hours) guides initial volume replacement. Half is given in the first 8 hours, the rest over 16 hours. Urine output of 30-50 mL/hour in adults is the primary endpoint to avoid overresuscitation and compartment syndromes.
- Wound care and grafting: Early debridement removes nonviable tissue and reduces infection risk. Temporary biologic dressings (e.g., allograft, xenograft) protect the wound bed. Autografting with split-thickness skin grafts provides definitive coverage; meshing allows expansion for large defects.
- Pain management: Burn pain is intense and requires multimodal analgesia. Opioids are mainstay for procedural and background pain, often administered via patient-controlled analgesia. Adjuncts like ketamine, benzodiazepines, and nonpharmacologic methods (distraction, hypnosis) help reduce opioid requirements and anxiety.
Terminology
- Total Body Surface Area (TBSA)
- Percentage of skin surface affected by burns; used for severity classification and resuscitation formulas.
- Eschar
- Thick, coagulated necrotic tissue that forms in full-thickness burns; may require escharotomy to relieve pressure.
- Burn shock
- Hypovolemic and distributive shock phase within the first 48 hours after major burn injury.
Quick Revision
- Burn depth is classified into first, second, and third degree based on layers affected.
- The zone of stasis is salvageable with proper resuscitation; zone of coagulation is non-viable.
- Large burns (>20% TBSA) cause systemic inflammation, cardiovascular depression, and hypermetabolism.
- Immunosuppression and infection risk are major clinical concerns in burn management.