Introduction to Burns

Original Editor - Carin Hunter based on the course by [TUTOR LINK/ PhysioPlus ReLab]
Top Contributors - Carin Hunter and Jess Bell

What is a Burn?[edit | edit source]

A burn is an injury to the skin or other organic tissue primarily caused by exposure to heat or other causative agents (radiation, electricity, chemicals).[1] According to WHO, it is a global public health problem, accounting for an estimated 180,000 deaths annually.[2] It is among the leading causes of disability in low and middle-income countries and almost two-thirds occur in the WHO African and South-East Asia regions.[2] Burns do not only affect the skin, they can have other effects on the tissue, organ and system networks such as smoke inhalation, as well as psychological effects. Burns affect all genders although females have slightly higher rates of death from burns compared to males. They also affect all age groups and are the fifth most common cause of non-fatal childhood injuries.[2]

Types of Burns[edit | edit source]

1. Thermal Burns[edit | edit source]

Thermal burn injuries are caused by exposure to an external heat source or hot liquids. An external heat source can be a hot solid object or even a cold object. Scalds are caused by wet substances, hot water, steam from hot water or cold water. The types of thermal burns are:

1.1 Flame Burns[edit | edit source]

Flame burns are caused by an exposure to an open fire. These are often associated with an inhalation injury and trauma. They tend to be mostly deep dermal or full-thickness burns. Flame burns are commonly found in adults, but they are also associated with abuse in children, domestic violence and certain rituals.

1.2 Contact Burns[edit | edit source]

Contact burns are caused by contact with an extremely hot object or surface, commonly seem with stoves, heaters and irons. Contact burns tend to be deep dermal or full-thickness burns. They are commonly seen in people with epilepsy, those who misuse addictive substances or in elderly people after a loss of consciousness.

1.3 Frostbite or Ice Burns[edit | edit source]

Frostbite occurs when the skin is exposed to cold, typically any temperature below -0.55C (31F), for an extended period of time. This causes the water in the cells of the skin and underlying tissue to freeze and crystalise. An individual can suffer an injury from this crystallisation or indirectly from the tissue becoming ischemic. Frostbite can affect any part of the body, but the extremities, such as the hands, feet, ears, nose and lips, are most likely to be affected. If frostbite penetrates the deeper skin layers, impacting tissue and bone, it can cause permanent damage.

An ice / snow burn is caused by ice or something very cold touching your skin for an extended period of time. Prolonged exposure to freezing temperatures, snow, or high-velocity winds can increase the chance of this type of burn. Ice burns are commonly caused by ice or cold packs being pressed directly against the skin when treating an injury or sore muscles.

1.4 Scalds[edit | edit source]

Scalds are caused by hot liquids. Commonly encountered liquids in this category are boiling water and cooking oil. Common mechanisms of injury include spilling of a hot drink or cooking oil or being exposed to hot bath water. Scalds tend to cause superficial to superficial partial burns. Scald burns cause about 70% of burns in children. They often occur in older adults as well.

2. Electrical Burns[edit | edit source]

An electrical burn is an injury caused by heat produced when an electrical current passes through a body. This can cause deep tissue injuries. The injury severity depends on many factors, the main ones being the pathway of the current, the resistance of the current in the tissues, and the strength and duration of the flow. AC (Alternating Current) and DC (Direct Current) are both potentially lethal and should not ever touched,[3] but they can present with different symptoms. In DC current burns, due to the nayure of the flow of current individuals often cannot pull themselves away, which increases the duration of the exposure to the current, whereas with AC current, indivuduals can let go during the "off" period but the voltage is often much higher.[4] Electrical burns are often associated with cardiac arrest, ventricular fibrillation, and tetanic muscle contractions.[1]

For more information, please see AC and DC Electric Shock Effects Compared

3. Chemical Burns[edit | edit source]

Chemical burns or caustic burns are injuries cause by the skin coming into direct contact with a chemical agent.[1] These can be strong acids, alkaline, or organic compounds. Chemical compounds can have different effects on human tissue depending on the following:

  • The strength or concentration of the chemical
  • The site of contact (eye, skin, mucous membrane)
  • Ingestion or inhalation
  • Skin integrity
  • Volume of substance
  • Duration of exposure
  • Chemical process
    • Acids can causes "coagulation necrosis" of the tissue
    • Alkaline burns can cause "liquefaction necrosis"

4. Radiation Burns[edit | edit source]

A radiation burn is damage due to prolonged exposure to radiation. The most common type of radiation burn is sunburn caused by prolonged exposure to ultraviolet rays (UV). High exposure to radiotherapy can also cause erythema, known as radiation burns. These are often associated with cancer due to the ability of ionising radiation to interact with and damage DNA.[1]

5. Inhalation Burns/Injury[edit | edit source]

Inhalation injury refers to pulmonary injury resulting from inhalation of smoke or chemical products of combustion.[5] Inhalation injury results in direct cellular damage, alterations in regional blood circulation and perfusion, obstruction of the airways, and the release of pro-inflammatory cytokine and toxin release.[6][7] Inhalation injuries also cause reduced functionality of mucociliary clearance and weakening of alveolar macrophages.[8] This injury can be split into three categories:

5.1 Heat Injury to the Upper Airway[edit | edit source]

The greatest complication of a heat injury to the upper airway is an obstruction due to extensive swelling of the tongue, epiglottis, and aryepiglottic folds. The burns do not commonly extend into the lower airway as the larynx reflexively closes and the heat dissipates as air is not a good heat conductor. Swelling can take a few hours to develop. Thus, it is recommended to regularly assess the airway as an initial evaluation often changes as fluid resuscitation commences.

5.2 Chemical Injury to the Lower Airways[edit | edit source]

Combustion of materials leads to the the production of toxic materials to the respiratory tract. This may cause local chemical irritation in the respiratory tract.[5]

Common conditions:

  • Smoke produces toxins that may damage both the airway epithelial cells and capillary endothelial cells which can cause acute respiratory distress syndrome[9][10][11]
  • Burning rubber and plastic produces sulfur dioxide, nitrogen dioxide, ammonia and chlorine which effect the respiratory airways and alveoli
  • Burning laminated furniture may contain glues that may release cyanide gas during combustion
  • Burning cotton or wool produces aldehydes which are toxic to the human body[12]
Agent Characteristics Effects Source of Exposure
Ammonia Highly water soluble; colourless; sharp, pungent odour Highly irritating to eyes and upper airways; upper airway obstruction, such as laryngeal oedema, bronchospasm and noncardiogenic pulmonary edema may occur Agriculture (mostly fertilisers); plastics, pesticides, explosives and detergents manufacture; refrigerants, home cleaning products
Hydrogen chloride Highly water soluble; colourless to slightly yellow; pungent odour Laryngeal oedema, tracheobronchitis Dyes, fertilisers, textiles, rubber manufacture; metal ore refining; meat wrappers
Hydrogen sulfide Slightly water soluble; colourless; rotten egg odour (sewer or swamp gas) Airway irritant and chemical asphyxiant Decaying organic matter, in sewer and barns; petroleum refining, viscose rayon, rubber and mining industries; hot-asphalt paving
Hydrogen fluoride Highly water soluble; colourless; pungent odour; corrosive Chemical pneumonitis; can cause clinically important hypocalcemia Phosphate fertiliser, metal refining and etching, glass and ceramic etching, microelectronic, masonry, pharmaceuticals, chemical manufacture; rust removal agents
Sulfur dioxide Highly water soluble; colourless; pungent odour Bronchoconstriction, airway oedema, asthma, bacterial pneumonitis, bronchiolitis obliterans Airway pollution, burning of oil and coal,smelting, power plants, wineries, paper manufacture, chemical manufacture, food preparation
Chlorine Intermediate water solubility; greenish yellow noncombustible gas Tracheobronchitis, acute respiratory distress syndrome Household cleaners (household accidents involving the inappropriate mixing of hypochlorite cleaning solutions with acidic agents), paper production, sewage treatment, swimming pool maintenance, chemical manufacture, disinfection, chemical warfare
Oxides of nitrogen Low water solubility; nearly colourless; a sharp sweet smelling (nitric oxide), strong harsh odour (nitrogen dioxide) Bronchoconstriction, airway oedema, asthma, bronchiolitis obliterans Agriculture (Silo filler’s disease); manufacture of dyes, lacquers and fertiliser; firefighters; welding, air pollution, hockey rinks
Phosgene Low water solubility; colourless; musty odour at room temperature Mild upper airway irritation, noncardiogenic pulmonary oedema Firefighters, welding, paint strippers, chemical warfare; Phosgene is used an intermediate in the manufacture of dyes, insecticides, plastics and pharmaceuticals; household substances such as solvents, paint removers and dry cleaning fluid can produce phosgene when exposed to heat or fire

Table showing some chemical irritants causing acute inhalation injury: their effects and sources of exposure. Table from Acute Inhalation Injury[13]

5.3 Systemic Toxicity due to Carbon Monoxide or Cyanide Exposure[edit | edit source]

Carbon monoxide (CO) is produced during a fire, when any carbon-based product is not completely burned. When inhaled, CO binds with haemoglobin in the blood stream and reduces the oxygen delivery.[14] Diagnosis entails an accurate history, changes in mental status and high carboxyhaemoglobin levels. Occasionally patients may require mechanical ventilation and treatment of shock.

Common symptoms can include:[15]

  • Headaches
  • Nausea and vomiting
  • Dizziness
  • Exhaustion
  • Changes in mental state
  • Chest pain
  • Difficulty breathing
  • Myocardial ischaemia
  • Poisoning can lead to a brain injury with associated neurological problems. Symptoms include:
    • Cognitive sequelae
    • Anxiety and depression
    • Persistent headaches, dizziness
    • Sleep problems
    • Motor weakness
    • Vestibular and balance problems
    • Gaze abnormalities
    • Peripheral neuropathies
    • Hearing loss
    • Tinnitus
    • Parkinsonian-like symptoms

Cyanide is often a byproduct of burning household materials. Cyanide intoxication is often found in conjunction with a CO inhalation injury. Cyanide intoxication lowers the lethal threshold of both cyanide and CO.[16] Diagnosis entails an accurate history, changes in mental status, carboxyhaemoglobin concentrations higher than 10%[17][18][10] and high lactate levels.[14]

For more information, please see Inhalation Injury

6. Friction Burn[edit | edit source]

A friction burn is an abrasion that occurs when the skin rubs against another surface. A friction burn is not a true burn. However, because friction can generate heat, in extreme cases, a patient will present with burns to the outer layer of the skin. Common causes are rope burn, rug burn, chafing or skinning.

Burn Classification[edit | edit source]

Burns can be classified according to their severity or depth.[1] The characteristics of a burn can vary in amount of pain and colour of burn, depending on its depth. Always be the on the look out for signs of inhalation burns, which are common in burns around the mouth or nose. Burns may have many complications and can cause shortness of breath, hoarseness of the voice, and stridor (noisy breathing due to airflow obstruction) or wheezing. Common symptoms are itchiness, as this is a sign of the healing process, and numbness or tingling following an electrical injury. Burns can have a large impact on an individual's mental health and this should always be taken into consideration.

Classification by Depth[edit | edit source]

Type Layers Involved Signs and Symptoms Healing Time Prognosis and Complications
First-Degree / Superficial Epidermis Red



No blisters

5–10 days Heals well. Repeated sunburns increase the risk of skin cancer later in life.
Second-Degree / Superficial Partial Thickness Epidermis and can extend into the superficial dermis Redness with a clear blister. Blanches with pressure, but shows rapid capillary refill when released.

Generally moist

Very painful

2–3 weeks Local infection (cellulitis) but no scarring typically
Second-Degree / Deep Partial Thickness Extends into deep (reticular) dermis

Often causes damage to the hair follicle and glandular tissue

Appears yellow or white.

Less blanching than superficial.

Very painful to pressure and uncomfortable

Blisters are common

Often moist and waxy

Occasionally dry and may appear ivory or pearly white

3–8 weeks Scarring, contractures (may require excision and skin grafting)
Third-Degree / Full Thickness Extends through entire dermis and can often affect the underlying subcutaneous tissue Appearance can vary from waxy white, leathery grey or charred black.

Skin is dry, lacking in elasticity

No blanching

Not painful (nerve ending damage is common)

Stiff and white/brown. No blanching

Prolonged (months) and unfinished/incomplete Eschar, or the dead, denatured skin, is removed

Results in scarring, contractures and amputation (early excision recommended)

Cannot heal without surgery

Fourth-Degree Extends through entire skin, and into underlying fat, muscle and bone Black; charred with eschar


No elasticity


Does not heal; Requires excision Amputation, significant functional impairment and in some cases, death

Classification by Size[edit | edit source]

The Parkland Burn Formula is the most widely used formula to estimate the fluid resuscitation required by a burns patient on hospital admission, usually within the first 24 hours. When applying this formula, the first step is to calculate the percentage of body surface area (BSA) damaged, which is most commonly done by the "Wallace Rule of Nines".[19] When conducting a paediatric assessment, the Lund-Browder Method is commonly used, as children have a greater percentage surface area of their head and neck compared to an adult. The formula recommends 4 milliliters per kilogram of body weight in adults (3 milliliters per kilogram in children) per percentage burn of total body surface area (%TBSA) of crystalloid solution over the first 24 hours of care.[20]

4 mL/kg/%TBSA (3 mL/kg/%TBSA in children) = total amount of crystalloid fluid during first 24 hours

The latest research has indicated that while this method is still in use, the fluid levels should be constantly monitored, while assessing the urine output,[21] to prevent over-resuscitation or under-resuscitation.[22]

The Rule of Nine and Lund-Browder Method Percentages[edit | edit source]
Body Part Percentage for Rule of Nine Percentage for Lund-Browder Method
Head and Neck 9% 18%
Entire chest 9% 9%
Entire abdomen 9% 9%
Entire back 18% 18%
Lower Extremity 18% each 13.5%
Upper Extremity 9% each 9% each
Groin 1% 1%
Palmar Surface Method[edit | edit source]

The "Rule of Palm" or Palmar Surface Method can be used to estimate body surface area of a burn. This rule indicates that the palm of the patient, with the exclusion of the fingers and wrist, is approximately 1% of the patients body surface area. When a quick estimate is required, the percentage body surface area will be the number of the patient's own palm it would take to cover their injury. It is important to use the patient's palm and not the provider's palm.

Jacksons’ Burn Wound Model[edit | edit source]

Jacksons’ Burn Wound Model is a model used to understand the pathophysiology of a burn would. This model divides the wound into three zones.

  • Zone of Coagulation: This is the area central to the injury and is the area that experiences the greatest tissue damage.
  • Zone of Stasis or Zone of Ischaemia: This area is adjacent to the zone of coagulation and as the name suggests, it is a zone in which the there is slowing of circulating blood due to the damage. This zone can usually be saved with the correct wound care.
  • Zone of Hyperemia: This zone is circumferential and is characterised by the eased blood supply and inflammatory vasodilation. This tissue has a good recovery rate, as long as there are no complications, such as severe sepsis or prolonged hypo-perfusion.

For more information please see the article on A Systematic Review on Classification Identification and Healing Process of Burn Wound Healing[23]

This video describes the pathophysiology of Burns[24]

References[edit | edit source]

  1. 1.0 1.1 1.2 1.3 1.4 Jeschke MG, van Baar ME, Choudhry MA, Chung KK, Gibran NS, Logsetty S. Burn injury. Nature Reviews Disease Primers. 2020 Feb 13;6(1):1-25.
  2. 2.0 2.1 2.2 World Health Organization. Burns. 2020. Available from: [Accessed 29th May 2022].
  3. Dalziel CF. Effects of electric shock on man. IRE Transactions on Medical Electronics. 1956 Jul:44-62.
  4. Nowak K, Paduszyński K. Analysis of factors and hazards associated with electric shock. Prace Naukowe Politechniki Śląskiej. Elektryka. 2018.
  5. 5.0 5.1 Dries DJ, Endorf FW. Inhalation injury: epidemiology, pathology, treatment strategies. Scandinavian journal of trauma, resuscitation and emergency medicine. 2013 Dec;21(1):1-5.
  6. Reper P, Heijmans W. High-frequency percussive ventilation and initial biomarker levels of lung injury in patients with minor burns after smoke inhalation injury. Burns. 2015; 41:65–70. [PubMed: 24986596]
  7. Kadri SS, Miller AC, Hohmann S, Bonne S, Nielsen C, Wells C, Gruver C, Quraishi SA, Sun J, Cai R, Morris PE. Risk factors for in-hospital mortality in smoke inhalation-associated acute lung injury: data from 68 United States hospitals. Chest. 2016 Dec 1;150(6):1260-8.
  8. Al Ashry HS, Mansour G, Kalil AC, Walters RW, Vivekanandan R. Incidence of ventilator associated pneumonia in burn patients with inhalation injury treated with high frequency percussive ventilation versus volume control ventilation: A systematic review. Burns. 2016 Sep 1;42(6):1193-200.
  9. Trunkey DD. Inhalation injury. Surgical Clinics of North America. 1978 Jan 1;58(6):1133-40.
  10. 10.0 10.1 McCall JE, Cahill TJ. Respiratory care of the burn patient. Journal of Burn Care & Rehabilitation. 2005 May 1;26(3):200-6
  11. Shubert J, Sharma S. Inhalation injury. 2018
  12. Ahmed Laskar A, Younus H. Aldehyde toxicity and metabolism: the role of aldehyde dehydrogenases in detoxification, drug resistance and carcinogenesis. Drug metabolism reviews. 2019 Jan 2;51(1):42-64.
  13. Hasarı AI, Gorguner M, Akgun M. Acute inhalation injury. EAJM. 2010;42:28-35.
  14. 14.0 14.1 Culnan DM, Craft-Coffman B, Bitz GH, Capek KD, Tu Y, Lineaweaver WC, Kuhlmann-Capek MJ. Carbon monoxide and cyanide poisoning in the burned pregnant patient: an indication for hyperbaric oxygen therapy. Annals of plastic surgery. 2018 Mar;80(3 Suppl 2):S106.
  15. Weaver LK. Carbon monoxide poisoning. Undersea & hyperbaric medicine: journal of the Undersea and Hyperbaric Medical Society, Inc. 2020 Jan 1;47(1):151-69.
  16. Culnan DM, Craft-Coffman B, Bitz GH, Capek KD, Tu Y, Lineaweaver WC, Kuhlmann-Capek MJ. Carbon monoxide and cyanide poisoning in the burned pregnant patient: an indication for hyperbaric oxygen therapy. Annals of plastic surgery. 2018 Mar;80(3 Suppl 2):S106.
  17. Moore SJ, Ho K, Hume AS. Severe hypoxia produced by concomitant intoxication with sublethal doses of carbon monoxide and cyanide. Toxicology and applied pharmacology. 1991 Jul 1;109(3):412-20.
  18. Traber DL, Linares HA, Herndon DN, Prien T. The pathophysiology of inhalation injury—a review. Burns. 1988 Oct 1;14(5):357-64.
  19. Bereda G. Burn Classifications with Its Treatment and Parkland Formula Fluid Resuscitation for Burn Management: Perspectives. Clinical Medicine And Health Research Journal. 2022 May 12;2(3):136-41.
  20. Mehta M, Tudor GJ. Parkland formula. 2019
  21. Ahmed FE, Sayed AG, Gad AM, Saleh DM, Elbadawy AM. A Model for Validation of Parkland Formula for Resuscitation of Major Burn in Pediatrics. The Egyptian Journal of Plastic and Reconstructive Surgery. 2022 Apr 1;46(2):155-8.
  22. Ete G, Chaturvedi G, Barreto E, Paul M K. Effectiveness of Parkland formula in the estimation of resuscitation fluid volume in adult thermal burns. Chinese Journal of Traumatology. 2019 Apr 1;22(02):113-6.
  23. Abazari M, Ghaffari A, Rashidzadeh H, Badeleh SM, Maleki Y. A systematic review on classification, identification, and healing process of burn wound healing. The International Journal of Lower Extremity Wounds. 2022 Mar;21(1):18-30.
  24. Amando Hasudungan. Burns - Pathophysiology Available from: