Burns Overview

Introduction[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][2]. According to WHO, it is a  global public health problem, accounting for an estimated 180,000 deaths annually. 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. 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]

Electrical Burn[edit | edit source]

Electrical burn injury is caused by heat that is generated when the electrical energy passes through the body causing deep tissue injury. The magnitude of the injury depends on the pathway of the current, the resistance of the current flow through the tissues, the strength, and the duration of the current flow. The different types of current causes various degrees of injury. For example, an alternating current is more dangerous than a direct current and it is often associated with cardiac arrest, ventricular fibrillation, and tetanic muscle contractions.[1][3]

Thermal Burn[edit | edit source]

Thermal burn injuries are caused by external heat sources (hot or cold), scalds (hot liquids), as a result of energy transfer, hot solid objects, steam and cold objects.

The types of thermal burns are:

  • Scalds - Scald burns result in about 70% of burns in children. They also often occur in elderly people. The common mechanisms are spilling hot drinks or liquids or being exposed to hot bathing water. Scalds tend to cause superficial to superficial partial burns[4].
  • Flame - Flame burns are often associated with inhalation injury and trauma. They comprise 50% of adult burns and tend to be mostly deep dermal or full-thickness burns[4].
  • Contact Burns - These types of burns are commonly seen in people with epilepsy or those who misuse alcohol or drugs or in elderly people after a loss of consciousness. Contact burns tend to be deep dermal or full-thickness burns. They occur after contact with an extremely hot object or surface.
  • Frostbite - Occurs when the skin is exposed to cold for a long time, causing the freezing of the skin or other underlying tissue. It is due to direct cellular injury from the crystallisation of water in tissue and indirect injury from ischemia[5].

Chemical Burn[edit | edit source]

A chemical burn injury is caused by tissue contact with chemical agents such as strong acids, alkaline, or organic compounds. Chemical agents depending on the duration of exposure and the nature of the agent have different effects on the skin. For example, contact with acid causes coagulation necrosis of the tissue (whereby the architecture of the dead tissue can be preserved), while alkaline burns generate liquefaction necrosis (whereby the tissue is transformed into a liquid, viscous mass). Systemic absorption of some chemicals is life-threatening, and local damage can include the full thickness of skin and underlying tissues[1].

Radiation Burn[edit | edit source]

Radiation burn is damage to the skin or other biological tissue and organs due to prolonged exposure to radiation. It is the least common burn injury and the most common type of radiation burn is the sunburn caused by prolonged exposure to Ultraviolet rays (UV). Other causes are associated with the use of ionising radiation in industry, high exposure to radiotherapy e.g. X-ray, and nuclear energy. Radiation burns are often associated with cancer due to the ability of ionising radiation to interact with and damage DNA[1].

Classifications of Burns[edit | edit source]

Burns can be classified according to their severity, depth,[1] and size of the burn.

Classification by Depth[edit | edit source]

Superficial-thickness or first-degree burns - Superficial thickness burns are burns that affect the epidermis only and are characterised by redness, pain, dryness, and with no blisters. Mild sunburn is an example of a superficial thickness burn.

Partial-thickness or second-degree burns - These burns involve the epidermis and a portion of the dermis. Partial-thickness burns are often broken down into two types, superficial partial-thickness burns and deep partial-thickness burns.

Superficial partial-thickness burns - Partial-thickness burns involve the epidermis and part for the dermis layer of the skin. Superficial partial-thickness burns extend through the epidermis down into the papillary, or superficial, a layer of the dermis. The injured site become erythematous because the dermal tissue has become inflamed. When pressure is applied to the reddened area. The area will blanch, but will demonstrate rapid capillary refill upon release of the pressure.

Deep partial-thickness burns- These burns extend deeper into the dermis and cause damage to the hair follicle and glandular tissue. They are painful to pressure, form blisters, are wet, waxy, or dry, and may appear ivory or pearly white.

Full-thickness or third-degree burns - These burns extend through the full dermis and often affect the underlying subcutaneous tissue. Skin appearance can vary from waxy white to leathery grey to charred and black. The skin is dry and inelastic and does not blanch to pressure, it is not typically painful due to the damage to the nerve endings. The dead and the denatured skin (eschar) are removed to aid healing, and scarring is usually severe in a surgical procedure known as escharotomy, which involves incising through sections of burnt skin to release the eschar and its constrictive effects, restore distal circulation, and enable appropriate ventilation.[6][7] Full-thickness burns cannot heal without surgery.

If the burn is circumferential, either on the limbs or trunk, this will result in a tourniquet or splinting effect, causing defects in limb circulation. In addition, this will probably decrease respiratory muscle movement. This occurs because the damaged tissue has become inelastic due to eschar formation. As a result, it should be treated to prevent its complications, such as distal ischemia, compartment syndrome, respiratory failure, tissue necrosis, or death.[6]

Subdermal or fourth-degree burns - These involve injury to the deeper tissues, such as muscle or bone. They are often blackened and it frequently leads to loss of the burned part.

Classification by Size[edit | edit source]

Burn size is determined by one of the three techniques: The Rule of Nine, The Lund-Browder Method, The Palmar Surface.

The Rule of Nine- This method is also known as the Wallace Rule of Nines because it is named after Dr Alexander Wallace the surgeon who first publish the method. The Rule of Nine is used to estimate the total body surface area (TBSA) involved in burn patients and also used to estimate fluid resuscitation required by a burns patient. The body surface estimation is by assigning percentages to different body areas[8].

Body Part Percentage
Head and Neck 9%
Anterior Trunk 18%
Posterior Trunk 18%
Lower Extremity 18% each
Upper Extremity 9% each
Groin 1%

Lund-Browder Method - This method is used instead of the rule of nine method for assessing the total surface area affected in children[9]. Different percentages are used because the ratio of the combined surface area of the head and neck compared to the surface area of the limbs is typically larger in children than in adults.

Palmar Surface Method - The palmar surface can be used to estimate relatively small burns or large burns. But for medium size burns, it is inaccurate. The surface area of a patient’s palm including the fingers is used to calculate the TBSA.

Pathophysiology of Burns[edit | edit source]

A burns injury depending on the severity of the injury can result in both local and debilitating systemic effects on all other organs and systems distant to the burn area.

Local Effect[edit | edit source]

This occurs immediately after the injury and the burn wound can be divided into three zones[10][4].

  • Zone of coagulation: This occurs at the point of maximum damage and this zone is characterised by irreversible tissue damage due to coagulation of the constituent proteins that occurs as a result of the insult.
  • Zone of stasis or zone of ischemia: This zone lies adjacent to the zone of coagulation and it is subject to a moderate degree of damage associated with vascular leakage, elevated concentration of vasoconstrictors, and local inflammatory reactions resulting in compromised tissue perfusion. But the integrity of the tissue in this zone can be saved with proper wound care
  • Zone of hyperemia: This is the outermost zone. It is characterised by the eased blood supply and inflammatory vasodilation. The tissue here will recover unless there is severe sepsis or prolong hypoperfusion.


Systemic Response[edit | edit source]

In severe burn injury, >30% TBSA complex reaction occurs both from the burn area and in the area distant to the burn. Cytokines, chemokines and other inflammatory mediators are released in excess resulting in extensive inflammatory reactions within a few hours of injury[12]. The initial response depending on the size of the burn injury is similar to the inflammation that is triggered after tissue destruction such as trauma or major surgery[13]. Different factors contribute to the magnitude of the host response, they include: burn severity (percentage TBSA and burn depth), burn cause, inhalation injury, exposure to toxins, other traumatic injuries, and patient-related factors such as age, pre-existing chronic medical conditions, drug or alcohol intoxication, and timing of presentation to medical aid[1]. This inflammatory response leads to rapid oedema formation which is caused by increased microvascular permeability, increased hydrostatic microvascular pressure, vasodilation, and increased extravascular osmotic activity. These reactions are due to the direct heat effect on the microvasculature and to the chemical mediators of inflammation. Vasodilation and increased venous permeability at the early stage of the injury are caused by the release of histamine. Also, prostaglandin is released by damage to the cell membranes which causes the release of oxygen-free radicals released from polymorphonuclear leucocytes which activate the enzymes catalyzing the hydrolysis of prostaglandin precursor. These hemodynamic changes lead to continuous loss of fluid from the blood circulation causing increased haematocrit levels and a rapid fall in plasma volume, leading to a decrease in cardiac output and hypoperfusion on the cellular level. Burn shock occurs if fluid loss is not adequately restored[14].

Besides burn shock, the burn injury can result in other types of injury which include inhalation injury. Inhalation injury is caused by heat or inhalation of smoke or chemical products of combustion leading to various degrees of damage. Usually, it is present in conjunction with the burn and can range from a minor injury to a severe injury. Inhalation injury can be divided into three types: systemic toxicity due to products of combustion (carbon monoxide (CO) and cyanide poisoning); upper airway thermal injury; and lower (bronchi and distal) airway chemical injury. Patients can sustain all of these in a closed-space fire. CO poisoning, more accurately categorised as a systemic intoxication, is easily diagnosed from the serum carboxyhaemoglobin level determined as part of the arterial blood gas measurement at hospital admission[1].

In addition to the effects above, a severe burn injury has an effect on different organs and systems in the body. The effects include:

Effect on the Cardiovascular System[edit | edit source]

The initial response to a severe burn injury is characterised by hypovolemia and reduced venous return. This concomitantly leads to a decrease in cardiac output, increased heart rate, and peripheral resistance. In addition to the cardiac dysfunction, pulmonary resistance increases causing an increase in right and left-ventricular work-load[15][16].

Effect on the Respiratory System[edit | edit source]

Following smoke inhalation, inflammatory mediators are released in the lungs leading to bronchoconstriction and adult respiratory distress syndrome[4].

Effect on the Renal System[edit | edit source]

The renal system is affected following alterations in the cardiovascular system. Renal blood flow and glomerular filtration rate are reduced secondary to hypovolemia, diminished cardiac output, and the effects of angiotensin, vasopressin and aldosterone. These alterations are usually translated in the form of oliguria as an early sign of renal compromise. Failure to promptly and adequately manage these cases may lead to acute tubular necrosis, renal failure, and mortality.

Effect on the Liver[edit | edit source]

There is substantial depletion of the hepatic proteins, alterations in serum levels of triglycerides and free fatty acids are highlighted, both of which are significantly increased secondary to a decrease in fat transporter proteins rendering the liver susceptible for fatty infiltration and hepatomegaly with resultant increased risk of sepsis and burn mortality.

Effects on Gastrointestinal System/Metabolism[edit | edit source]

The basal metabolic rate increases up to three times its original rate. This coupled with splanchnic hypoperfusion, necessitates early and aggressive enteral feeding to decrease catabolism and maintain gut integrity. It causes mucosal atrophy, reduced absorptive capacity, and increased surface permeability.

Effect on the Endocrine System[edit | edit source]

The stress hormones i.e. catecholamine, glucagon and cortisol among other hormones are actively involved at the onset of burns injuries. These hormones display an exponential increase in their levels; sometimes reaching 10 fold their normal values. The significance of such an upsurge resides in its influence on the cardiovascular system and the resultant fluid shifts that follow these changes. The stress hormones are thereby considered as the initiators of the hypermetabolic-catabolic and proteolytic-response.

Burn Prevention[edit | edit source]

Recommendations from the World Health Organization for individuals, communities and public health officials on how to reduce burn risk[17].

  • Enclose fires and limit the height of open flames in domestic environments.
  • Promote safer cookstoves and less hazardous fuels, and educate regarding loose clothing.
  • Apply safety regulations to housing designs and materials, and encourage home inspections.
  • Improve the design of cookstoves, particularly about stability and prevention of access by children.
  • Lower the temperature in hot water taps.
  • Promote fire safety education and the use of smoke detectors, fire sprinklers, and fire-escape systems in homes.
  • Promote the introduction of and compliance with industrial safety regulations, and the use of fire-retardant fabrics for children’s sleepwear.
  • Avoid smoking in bed and encourage the use of child-resistant lighters.
  • Promote legislation mandating the production of fire-safe cigarettes.
  • Improve the treatment of epilepsy, particularly in developing countries.
  • Encourage further development of burn-care systems, including the training of health-care providers in the appropriate triage and management of people with burns.
  • Support the development and distribution of fire-retardant aprons to be used while cooking around an open flame or kerosene stove.

Conclusion[edit | edit source]

Burns injuries have physical, socio-economic, and psychological effects especially in cases of severe burns injuries. They impact not only the affected part of the body, but also the organs and systems of the body. They require an early and prompt response to reduce the effect of an injury. Besides this, they require an interdisciplinary approach to prevent the adverse effects of the injury.

References[edit | edit source]

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Jeschke MG, Van Baar ME, Choudhry MA, Chung KK, Gibran NS, Logsetty S. Burn injury. Nat Rev Dis Primers. 2020;6(1):11.
  2. 2.0 2.1 World Health Organization. Burns. 2020. Available from: https://www.who.int/news-room/fact-sheets/detail/burns [Accessed 21st December 2020].
  3. Lee RC. Injury by electrical forces: Pathophysiology, manifestations, and therapy.Curr. Probl. Surg. 1997:677-762
  4. 4.0 4.1 4.2 4.3 Hettiaratchy S, Dziewulski P. ABC of burns: pathophysiology and types of burns. BMJ. 2004;328(7453):1427-9.
  5. Nguyen, C. M., Chandler, R., Ratanshi, I. & Logsetty, S. In: Jeschke, MG, Kamolz LP, Sjöberg F. & Wolf SE. editor. Handbook of Burns Vol. 1. Springer, 2020:p529–547.
  6. 6.0 6.1 Zhang L, Labib A, Hughes PG. Escharotomy. InStatPearls [Internet] 2021 Oct 27. StatPearls Publishing.
  7. Karami R, Abu-Sittah G, Ibrahim A. Burn Escharotomy. InOperative Dictations in Plastic and Reconstructive Surgery 2017 (pp. 191-193). Springer, Cham.
  8. Moore RA, Waheed A, Burns B. Rule of Nines. StatPearls (Internet), 2020. Available from: https://www.ncbi.nlm.nih.gov/books/NBK513287/[Accessed 17th December 2020].
  9. Murari A, Singh KN. Lund and Browder chart-modified versus original: a comparative study. Acute Crit Care. 2019;34(4):276-281.
  10. Kaddoura I, Abu-Sittah G, Karamanoukian R, Papazian N. Burn injury: a review of pathophysiology and therapeutic modalities in major burns. Ann Burns Fire Disasters. 2017:30(2):95-102.
  11. Amando Hasudungan. Burns (DETAILED) Overview - Types, Pathophysiology, TBSA. Available from: https://www.youtube.com/watch?v=j4v7PFw5wA0 [last accessed 30/12/2020]
  12. Osuka A, Ogura H, Ueyama M, Shimazu T. & Lederer JA. Immune response to traumatic injury: harmony and discordance of immune system homeostasis. Acute Med. Surg. 2014;63–69.
  13. Abu-Sittah GS, Sarhane KA, Dibo SA, Ibrahim A. Cardiovascular dysfunction in burns: a review of the literature. Ann Burns Fire Disasters. 2012;25(1):26-37.
  14. Arturson G. Pathophysiology of the burn wound. Ann Chir Gynaecol.1980;69(5):178-90.
  15. Abu-Sittah GS, Sarhane KA, Dibo SA, Ibrahim A. Cardiovascular dysfunction in burns: a review of the literature. Ann Burns Fire Disasters. 2012;25(1):26-37.
  16. Williams FN, Herndon DN, Suman OE, Lee JO, Norbury WB, Branski LK, Mlcak RP, Jeschke MG. Changes in cardiac physiology after severe burn injury. J Burn Care Res. 2011;32(2):269-74.
  17. World Health Organization‎. A WHO plan for burn prevention and care. World Health Organization, 2018. Available from: https://apps.who.int/iris/bitstream/handle/10665/97852/9789241596299_eng.pdf?sequence=1&isAllowed=y [Accessed 27th December 2020].