Last updated:
January 17, 2026
Overview
A burn is defined as the response of the skin, mucous membrane, and subcutaneous tissues to thermal and other few non-thermal injuries. Treatment of burns is complex (hence the need for specialised burn centres), and depends on the site of burn, the severity, mechanism, and comorbid conditions.
Important information to ask for in a patient with burn injuries
| Component | Description |
|---|---|
| Mechanism of burn | How, when and in what circumstances were they burned? A superficial burn that is ten days old, infected and deepened may need admission and debridement while a more recent superficial burn could be managed outpatient |
| Size | How big is the burn? |
| Depth | How deep is the burn? |
| Site | Where is the burn? |
| Inhalation | Could there have been smoke inhalation? |
| Other injuries | Are there other associated injuries? The could include inhalation injury (smoke at the scene) or C-spine fracture (car accident) |
| First aid | Have they received first aid or other treatment? Cool water applied after a burn can reduce the depth of injury. The burn might be deep if no first aid was given |
- Findings that are consistent with non-accidental injury (including burns)
- The explanation of injury does not fit the physical exam findings
- Inconsistency or change with repeated explanations of the injury
- Caregiver seems angry or avoids discussion when the medical professional seeks further details regarding the injury
- Description of events of injury is not consistent with the developmental age of the child e.g. an explanation that involves crawling or walking if a child is not able to do so
- History of abuse of other children or the child being treated
- Specific patterns of burn injury that are suspicious for non-accidental injury
- Burns to the face, head, buttock, perineum, and genitalia
- Obvious patterns from objects e.g. cigarettes, iron, light bulb, hot plate, knife, grid, fork
- Symmetrical burns of uniform depth
- Other signs of physical abuse e.g. bruises of varied ages and in areas not typical for bruising, old fractures
Pathophysiology of burns
Physiological response to burns
| Stage | Process |
|---|---|
| Stage I | Emergent |
| Stage II | Fluid-shift |
| Stage III | Hypermetabolism |
| Stage IV | Resolution |
Local effects of burns
Burns cause local damage by coagulation necrosis from the direct transfer of energy. Other types of burns e.g. chemical and electrical burns directly damage the cell membrane. Adequate resuscitation and good wound care can prevent the progression of a superficial to a deeper burn. Inappropriate resuscitation and infection can worsen the depth of a burn wound, causing a burn that would heal without needing a skin graft to ultimately require grafting.
Jackson’s zones of tissue damage following a burn injury
| Zone | Description | Nota bene |
|---|---|---|
| Zone of coagulation | Most severely burned tissue, usually in the center of the wound. Represents an area of irreversible tissue loss due to protein denaturation and coagulation necrosis | Damage is irreversible |
| Zone of stasis | Immediately surrounds the zone of coagulation and represents the zone of reduced tissue perfusion due increased vascular permeability and vascular damage worsened by Thromboxane A2 which causes vasoconstriction and is present in high amounts in burn wounds | Damage is reversible. Susceptible to further injury and can progress to coagulation necrosis |
| Zone of hperemia | Represents an area of increased tissue perfusion, vasodilation, and microvascular permeability and edema | Changes are reversible and the area is prone to recovery unless there is prolonged hypotension or infection |
Systemic effects of burns
- Metabolic changes
- Cardiac output initially decreases. However, in the first 5 days cardiac output increases to nearly 1.5 times normal resulting in myocardial oxygen consumption that can exceed that of marathon runners
- Hyperglycemia due to increased gluconeogenesis, glycogenolysis, and reduced insulin sensitivity.
- Protein breakdown resulting in loss of muscle mass and reduced strength
- 10% loss leads to immune dysfunction
- 20% loss leads to decreased wound healing
- 30% loss leads to an increased risk of pneumonia and pressure ulcers
- 40% loss leads to death
- Anorexia
- Pyrexia
- Stimulation of hepatic lipid synthesis
- Promotion of acute-phase protein synthesis
- Reduced albumin synthesis (a negative acute-phase protein
- Inflammation and oedema
- Third spacing due to increased capillary permeability (capillary leak). This leads to hypoperfusion
- Effects on cardiovascular system
- Cardiac output initially decreases but then increases over time
- Depressed cardiac output is due to decreased blood volume, increased blood viscosity due to fluid losses, and ventricular dysfunction
- Increased cardiac output is due to tachycardia (can be 160-170% higher than normal in paediatric patients)
- Cardiac output initially decreases but then increases over time
- Effects on the respiratory system
- Bronchoconstriction
- ARDS due to cytokine-mediated vascular and tissue damage
- Inhalational injury can directly damage the oro-tracheal-bronchial tissues, and increase the likelihood of ARDS
- Lung damage also predisposes to pneumonia
- Effects on the cardiovascular system
- Curling’s ulcer due to splanchnic hypoperfusion
- Splanchnic hypoperfusion leads to stress-induced gastric hypersecretion and mucosal damage)
- Mucosal atrophy (12-18 hours post-burn)
- Decreased absorption of glucose, amino acids, and fatty acids
- Increased intestinal permeability which promotes translocation of bacteria and fungi (can be reversed by early enteral feeding)
- Curling’s ulcer due to splanchnic hypoperfusion
- Effects on the renal system
- Acute renal failure due to thirds spacing, decreased blood volume, and reduced cardiac output
- Effects on the immune system
- Immunosuppression in burns > 20% TBSA (reduced production, function, and activation of neutrophils, macrophages, and B- and T-lymphocytes)
- Increased risk for pneumonia and wound infections
- Immunosuppression in burns > 20% TBSA (reduced production, function, and activation of neutrophils, macrophages, and B- and T-lymphocytes)
Types of burns according to mechanism
55% of burns are caused by flame and 40% are caused by scalds. Chemical and electrical burns comprise about 5%. Scalds are common in children. Electric and chemical burns are common in adults. Flame burns > scalds in adults.
| Burn | Description | Nota bene |
|---|---|---|
| Thermal burn | Flame burn | Responsible for 50% of burns in adults and the most common cause of admission and mortality due to associated inhalational injury, trauma, and carbon monoxide poisoning. Tends to be deep partial thickness and full thickness. Requires grafting |
| Scald | Burn caused by spilling or exposure to hot liquids. Common in children (70% in children under 5) and the elderly. More superficial than flame burns. Scalds from hot oil or fat are often deep and may need grafting | |
| Contact burn | Burn caused by prolonged direct contact with very hot or very cold objects. Common in patients with epilepsy, the elderly, or with alcohol abuse. Can arouse suspicion for non-accidental burns. Typically partial-thickness or full-thickness. Often need grating. | |
| Flash burn | Burn caused by hot gases or combustible liquid | |
| Frostbite | Occurs when skin is exposed to extreme cold | |
| Chemical burn | Exposure to extreme acids (Battery, HCL) or alkali (Drain cleaner, fertilizer) | Evolves over time. Alkaline burns are worse due to liquefaction. Acid burns produce coagulation necrosis. Formic acid can cause hemolysis and hemoglobinuria, hydrofluoric acid can cause hypocalcemia |
| Electrical burn | Electrical shock or lightning strike | Can cause deep tissue injury between the entry and exit points (muscles, heart, and nerves) and lead to serious complications. Voltage determines the extent of damage. Deep tissue injury is linked to cardiac arrhythmia, muscle necrosis and myoglobinuria |
| Respiratory (Inhalation) burn | Thermal (superheated air) or Chemical (smoke) inhalation | A major concern is respiratory compromise and CO exposure. Burning plastics can produce hydrogen cyanide |
| Circumferential burn | Burns on the chest wall that go around the entire circumference | Tourniqet effect – remove patient accessories ASAP as oedema can interrupt the vascular supply to the distal extremity. Can also interfere with breathing if on the chest wall. Indication for Escharotomy. |
| Radiation burn | Sunburn from UV radiation, X-rays and other imaging, Therapeutic radiation | |
| Friction burn | Heat causes mechanical disruption of tissue from contact with an abrasive or rough surface |
Complications of burns
Common causes of death in burns patients include shock, sepsis and respiratory failure
Effects of burns
- Acute (early) complications of burns (48-72h)
- Hypothermia
- Shock
- Sepsis (Common causative organisms include S.aureus (including MRSA), Enterococcus, and Pseudomonas)
- Respiratory failure (ARDS)
- Multi-organ failur (e.g. Renal failure)
- Sub-acute (intermediate) complications of burns
- DVT
- Post-burn hypermetabolism
- Malnutrition (hypoproteinemia)
- Curling ulcers
- Paralytic ileus
- Infection (wound infection, hypostatic pneumonia)
- Anemia
- Chronic complications of burns
- Hypertrophic scars
- Keloid formation
- Contractures
- Marjolin ulcer (Tx is wide excision or amputation)
- Psychological problems
- Complication of chemical burns
- Eyes: Cataracts or vision loss
- Esophagus: Strictures
- Systemic poisoning
- Complication of electrical burns
- Arrhythmia
- Myoglobinuria → Renal failure
- Rhabdomyolysis