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== Introduction ==
== Introduction ==
Burns is define as damage to some or all of the cells of the skin or other tissues primarily caused by thermal or other acute exposures such as heat, electrical discharge, friction, chemicals or radiation. But the majority of burn injuries are caused by heat from hot liquids, solids or fire (''Marc G. Jeschke1,2'' ✉'', Margriet E. van Baar3,4, Mashkoor A. Choudhry5, Kevin K. Chung6,'' ''Nicole S. Gibran7 and Sarvesh Logsetty. Burn Injury'').  Although all burn injuries involve tissue destruction due to energy transfer, different causes can be associated with different physiological and pathophysiological responses. For example, a flame or hot grease can cause an immediate deep burn, whereas scald injuries (that is, from hot liquids or steam) tend to appear more superficial initially, due to rapid dilution of the source and energy. Alongside injuries to the skin, burns can be accompanied by smoke inhalation on or other physical trauma to other organs. The injury affects not only the physical health but also the mental health and quality of life of the patient.  
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)<ref name=":0">Jeschke MG, Van Baar ME, Choudhry MA, Chung KK, Gibran NS, Logsetty S. Burn injury. Nat Rev Dis Primers. 2020;6(1):11.</ref><ref name=":1">World Health Organization. Burns. 2020. Available from: https://www.who.int/news-room/fact-sheets/detail/burns [Accessed 21st December 2020].</ref>. 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<ref name=":1" />.


Burns are a global public health problem, accounting for an estimated 180,000 deaths annually. The majority of these occur in low and middle-income countries and almost two-thirds occur in the WHO African and South-East Asia regions. In many high-income countries, burn death rates have been decreasing, and the rate of child deaths from burns is currently over 7 times higher in low and middle-income countries than in high-income countries (<nowiki>https://www.who.int/news-room/fact-sheets/detail/burns</nowiki>. Accessed 12/11/2020).
== Types of Burns ==
=== Electrical Burn  ===
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.<ref name=":0" /><ref>Lee RC. Injury by electrical forces: Pathophysiology, manifestations, and therapy.Curr. Probl. Surg. 1997:677-762</ref>


== Types of Burns ==
=== Thermal Burn ===
1. Electrical burn injury- Electric burn injury is caused by heat that is generated by the electrical energy as it passes through the body. It causes deep tissue damage that is greater than visible injury, and tissue damage in electrical injuries is correlated with the electric field strength (amperes and resistance of the tissue). The magnitude of the injury depends on the pathway of the current, the resistance to the current flow through the tissues, and the strength and duration of the current flow. ( Lee R.C. Injury by electrical forces: pathophysiology, manifestations, and therapy. Curr. Probl.Surg. 677-764. 1997). Alternating current is more dangerous than direct current and is often associated with cardiopulmonary arrest, ventricular fibrillation, and tetanic muscle contractions. Other significant injuries, such as long-bone or vertebral compression fractures, spinal cord injury, or traumatic brain injury, can occur if the victim falls on electrical contact. (pathology of physiotherapy.
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:


2. Thermal burn injury – Thermal injuries are categorized based on their aetiology and depth of injury. The depth of the thermal injury is related to contact temperature, duration of contact of the external source, and the thickness of the skin. Because the thermal conductivity of skin is low, most thermal burns involve the epidermis and part of the dermis. The most common thermal burns are associated with flames, Scalds (hot liquids), hot solid objects, steam, cold objects. They contribute to coagulation necrosis by inducing tissue damage through the transfer of energy.
* '''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<ref name=":2" />.
* Scalds- Scald burns injury results 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.
* '''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<ref name=":2" />.
* '''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<ref>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.</ref>.


* Flame- Flame comprise 50% of adult burns. They are often associated with inhalational injury and other concomitant trauma. Flame burns tend to be deep dermal or full-thickness.
=== Chemical Burn ===
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<ref name=":0" />.


* Contact- In order to get a burn from direct contact, the object touched must either have been extremely hot or the contact was long. These types of burns are commonly seen in people with epilepsy or those who misuse alcohol or drugs. They are also seen in elderly people after a loss of consciousness; such a presentation requires a full investigation as to the cause of the blackout. Contact burns tend to be deep dermal or full-thickness.
=== Radiation Burn ===
Hettiaratchy S., Dziewulski P. Pathophysiology and types of burns. BMJ . 2004. 1427-1429
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<ref name=":0" />.
* Frostbite is caused by a number of mechanisms including direct cellular injury from crystallization of water in tissue and indirect injury from ischaemia and reperfusion. These mechanisms lead not only to skin necrosis but also to deep tissue damage dame particular cause of a burn injury determines the treatment approach. . Nguyen C.M, Chandler R, Ratanshi I. and Logsetty, S. Handbook of Burns Vol 1 (eds Jeschke M.G., Kamolz  L.P., Sjoberg F, Wolf S.E) 529-547. (Springer, 2020), uptodate :
3. Chemical burn injury- Chemical burn injury is caused by tisssue contact with or ingestion, inhalation, or injection of strong acids, alkaline, or organic compounds.  Chemical agents can cause a varetys of caustic reactions, including alteration of pH, disruption of cellular membranes, and direct toxic effects on metabolic processes. In addition to the duration of exposure, the nature of the agent will determine injury severity. 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.


4.  Radiation- Radiation burns are the least common burn injury and they are caused by esposure to a radioactive source. This types of injuries have associated with the use of ionizing radiation in industry, with therapeutic radiation sources in medicine or in individuals who work in the nuclear industry. Radiofrequency energy or ionizing radiation can cause damage to skin and tissues. The most common type of radiation burn is the sunburn, this is caused by a prolonged exposure to UV rays. Radiation burns are often associated with cancer due to the ability of ionizing radiation to interact with and damage DNA. The clinical results of ionizing radiation depend on the dose, time of exposure, and type of particle that determines the depth of exposure. Depending on the photon energy, radiation can cause very deep internal burns.  (See "Clinical manifestations, evaluation, and diagnosis of acute radiation exposure".) burn.
== Classifications of Burns ==
Burns can be classified according to their severity, depth,<ref name=":0" /> and size of the burn.


== Classifications of burns ==
=== Classification by Depth ===
A burn injury can be classify according to its severity, its depth and size. According to the depth, it can be classified in:
'''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.
# Superficial thickness (first degree)- They are burns that affects only the uppermost layer of the skin (epidermis only); the skin becomes red, they do not blister but are painful, dry, and blanch with pressure. Over the next two to three days the pain and erythema subside, and by approximately day 4, the injured epithelium peels away from the newly healed epidermis. Such injuries are generally healed in six days without scarring. This process is commonly seen with sunburns.
# Partial-thickness (second degree)- Partial-thickness burns involve the epidermis and portions of the dermis. They are characterized as either superficial or deep.
* Superficial partial-thickness (formerly known as 2A burns)-  These burns characteristically form blisters within 24 hours between the epidermis and dermis. They are painful, red, and weeping and blanch with pressure Burns that initially appear to be only epidermal in depth may be determined to be partial thickness 12 to 24 hours later. These burns generally heal in 7 to 21 days; scarring is unusual, although pigment changes may occur. A layer of fibrinous exudates and necrotic debris may accumulate on the surface, which may predispose the burn wound to heavy bacterial colonization and delayed healing. These burns typically heal without functional impairment or hypertrophic scarring.
* Deep partial-thickness – These burns extend into the deeper dermis and are characteristically different from superficial partial-thickness burns. Deep burns damage hair follicles and glandular tissue. They are painful to pressure only, almost always blister (easily unroofed), are wet or waxy dry, and have variable mottled colourization from patchy cheesy white to red. They do not blanch with pressure. If the infection is prevented and wounds are allowed to heal spontaneously without grafting, they will heal in two to nine weeks. These burns invariably cause hypertrophic scarring. If they involve a joint, joint dysfunction is expected even with aggressive physical therapy. A deep partial-thickness burn that fails to heal in two weeks is functionally and cosmetically equivalent to a full-thickness burn. Differentiation from full-thickness burns is often difficult.
3.  Full thickness (third degree)- A full-thickness (third-degree) burn extends through the full dermis and often injures the underlying subcutaneous tissue. They are usually anesthetic or hypo-aesthetic. Skin appearance can vary from waxy white to leathery gray to charred and black. The skin is dry and inelastic and does not blanch with pressure. Burn eschar, the dead and denatured dermis, is usually intact. The eschar can compromise the viability of a limb or torso if circumferential. Large areas require skin grafting and their is high risk of infection. It is not typically painful owing to damage to the nerve endings, hairs can easily be pulled from hair follicles, and requires protection from becoming infected and, unless very small, surgical management. Small areas will heal with substantial scar or contracture.


4. Subdermal or Fourth degree- fourth-degree burn involves injury to deeper tissues, such as muscle or bone, is often blackened and frequently leads to loss of the burned part.
'''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.


Although superficial and superficial partial-thickness burns usually heal without surgical intervention, more severe burns usually heal without surgical intervention, more severe burns need careful management, which includes topical antimicrobial dressings and/or surgery.
'''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.


Acording to size: Burn size is determined by one of two techniques: the rule of nine, the Lund-Browder method, and the Palmar surface.  
'''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.


''The Rule of Nine''- The Rule of Nines, also known as the Wallace Rule of Nines, is a tool used by trauma and emergency medicine providers to assess the total body surface area (TBSA) involved in burn patients.  Measurement of the initial burn surface area is important in estimating fluid resuscitation requirements since patients with severe burns will have massive fluid losses due to the removal of the skin barrier. This tool is only utilized for second-degree and third-degree burns (also referred to as partial thickness and full thickness burns) and aids the provider in quick assessment to determine the severity and intravenous fluid needs. The Rule of Nines estimation of body surface area burned is based on assigning percentages to different body areas. The entire head is estimated as 9% (4.5% for anterior and posterior). The entire trunk is estimated at 36% and can be further broken down into 18% for anterior compnents and 18% for the back. The anterior aspect of the trunk can further be divided into chest (9%) and abdomen (9%). The upper extremities total 18% and thus 9% for each upper extremity. Each upper extremity can further be divided into anterior (4.5%) and posterior (4.5%). The lower extremities are estimated at 36%, 18% for each lower extremity. Again this can be further divided into 9% for the anterior and 9% for the posterior aspect. The groin is estimated at 1%<ref>Cheah AKW, Kangkorn T, Tan EH, Loo ML, Chong SJ. The validation study on a three-dimensional burn estimation smart-phone application: accurate, free and fast? Burns Trauma. 2018;6:7.</ref><ref>Moore RA, Waheed A, Burns B. Rule of Nines. [Updated 2020 Jul 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: <nowiki>https://www.ncbi.nlm.nih.gov/books/NBK513287/</nowiki></ref>.
'''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.<ref name=":3" /><ref>Karami R, Abu-Sittah G, Ibrahim A. Burn Escharotomy. InOperative Dictations in Plastic and Reconstructive Surgery 2017 (pp. 191-193). Springer, Cham.</ref> Full-thickness burns cannot heal without surgery.


''Lund-Browder method''- Lund-Browder method is used instead of Rule of Nine for assessing the total surface area affected in children. Different percentages are used because the ratio of the combined surface area of the head and neck to the surface area of the limbs is typically larger in children than that of an adult. This chart, if used correctly, is the most accurate method. It compensates for the variation in body shape with age and therefore can give an accurate assessment of burns area in children<ref>Hettiaratchy S, Papini R. Initial management of a major burn: II--assessment and resuscitation. BMJ. 2004 Jul 10;329(7457):101-3. </ref>.
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.<ref name=":3">Zhang L, Labib A, Hughes PG. Escharotomy. InStatPearls [Internet] 2021 Oct 27. StatPearls Publishing.</ref>


''Palmar surface''—The surface area of a patient's palm (including fingers) is roughly 0.8% of total body surface area. Palmar surface are can be used to estimate relatively small burns (< 15% of total surface area) or very large burns (> 85%, when unburnt skin is counted). For medium sized burns, it is inaccurate.
'''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.


== Pathophysiology of burns ==
=== Classification by Size ===
Burn injuries result in both local and system responses.
Burn size is determined by one of the three techniques: The Rule of Nine, The Lund-Browder Method, The Palmar Surface.


=== Local response ===
'''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<ref>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].</ref>. 
Immediately after injury, the burn wound can be divided into three zones:  


1.      Zone of cagulation: This occurs at the point of maximum damage. In this zone there is irreversible tissue loss due to coagulation of the constituent proteins.
{| class="wikitable"
|Body Part
|Percentage
|-
|Head and Neck
|9%
|-
|Anterior Trunk
|18%
|-
|Posterior Trunk
|18%
|-
|Lower Extremity
|18% each
|-
|Upper Extremity
|9% each
|-
|Groin
|1%
|}


2.      Zone of stasis or zone of ischaemia:The surrounding zone of stasis is characterized by decreased tissue perfusion that is potentially salvageable. It lies adjacent to the zone of coagulation, this area is subject to a moderate degree of damage associated with vascular leakage, elevated concentrations of vasoconstrictors as well as local inflammatory reactions resulting in compromised tissue perfusion. The main aim of burns resurcitation is to increase tissue perfusion here and prevent any damage becoming irreversible. Additional insults such as prolonged hypotension, infection, or oedema can convert this zone into an area of complete tissue loss.
'''Lund-Browder Method''' - This method is used instead of the rule of nine method for assessing the total surface area affected in children<ref>Murari A, Singh KN. Lund and Browder chart-modified versus original: a comparative study. Acute Crit Care. 2019;34(4):276-281. </ref>. 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.  


3.      Zone of hyperaemia: This is the outermost zone and tissue perfusion is increased. The tissue here will invariably recover unless there is severe sepsis or prolonged hypoperfusion. This zone is characterized by increased blood supply with healthy tissues under no major jeopardy or demise. The outermost region of the wound is characterized by increased inflammatory vasodilation.
'''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.


=== Systemic response ===
== Pathophysiology of Burns ==
Burns exceeding 30% of total body surfase area (TBSA) result in considerable hypovolemia coupled with formation and release of inflammatory mediators with subsequent systemic effect, namely a distinctive cardiovascular dysfunction known as burn shock. Burn shock is a complex process of circulatory and microcirculatory impairment as well as oedema generation in both traumatized and non-traumatized tissues. Even with timely and adequate fluid support, this pathophysiologic state remains incompletely reversible. In fact, burn shock involves an anomalous condition of inadequate tissue perfusion with resultant insufficient oxygen and nutrient delivery as well as failure to remove waste products from tissues.
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.


Despite proper fluid resuscitation and adequate preload, pulmonary and systemic vascular resistances are increased and myocardial depression follows.This, in turn, will stimulate further exacerbation of the inflammatory response and contribute to the risk of organ failure. A typical immediate response after a thermal insult is plasma extravasation followed by a sequence of hemodynamic events.The most common hemodynamic changes include diminished plasma volume, cardiac output, and urine output as well as increased systemic vascular resistance with resultant reduced peripheral blood flow. Unlike in hemorrhage, burn insults are associated with an increase in heamoglobin and hematocrit.
=== Local Effect ===
This occurs immediately after the injury and the burn wound can be divided into three zones<ref>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.</ref><ref name=":2" />.
* 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.


Odema formation is another characteristic reaction of burn injuries. As the ratio fluid filtered out of microvesels to fluid entering them becomes more than 1, oedeama is developed. The process of oedma formation is biphasic. Initiated in the first hour following burn trauma, the primary phase witnesses an abruupt increase in the water content of traumatized tissues. The second phase involves a more gradual increase in fluid flux of both burned and intact skin and soft tissues 12-24 hours post-burn. Whether fluid resuscitation is provided or not determines the amount of oedema development. Following burn-induced plasma extravasation, addiitional extravasation occurs following resuscitation since fluid support increases blood flow and capillary pressure. On the other hand, the oedema remanins self-limited when no fluid is administered. In addition to the trauma type and extent, type and amount of administered fluid also play a key role in determining the volume of oedema.
* 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


In response to burn injury, alterations in metabolic pathways and pro-inflammatory cytokines promote the shift of muscle protein metabolism into a faster rate of degradation than synthesis. Significant net protein loss becomes evident in the form of negative whole-body and cross-leg nitrogen balance. Accelerated protein degradation contributes to a remarkable decrease in lean body mass and muscle wasting associated with a decrease in strength and delay in rehabilitation.
* 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.
{{#ev:youtube|j4v7PFw5wA0}}<ref>Amando Hasudungan. Burns (DETAILED) Overview - Types, Pathophysiology, TBSA. Available from: https://www.youtube.com/watch?v=j4v7PFw5wA0 [last accessed 30/12/2020]</ref>
=== Systemic Response ===
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<ref>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.</ref>. 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<ref>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. </ref>. 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<ref name=":0" />. 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|Burn shock]] occurs if fluid loss is not adequately restored<ref>Arturson G. Pathophysiology of the burn wound. Ann Chir Gynaecol.1980;69(5):178-90.
</ref>.  


Energy substrate metabolism is also modified as a result of the metabolic changes seen in severe burns.Glucose is consumed through anaerobic  pathways with resultant high lactate production. Patients with severe burns experience increased glucose production, particularly from alamine. Amino acids become the main fuel for glucose generation through gluconeogensis, leaving very few of them involved in their original function as building blocks of body protein. Nitrogen excretion, primarily inurea, increases and the body becomes short of protein storage. Persistent hyperglycemia experienced in burn patient is explained vy and increase in gluconeogenic substrates, attention of suppressive effect of insulin on hepatic glucose release, ehanced hepatic glycogenolysis,and impaired glucose disposal. Glycogenolysis enhancement in burns, is secondary to the direct effect of sympathetic stimulation as well as catecholamine.
Besides [[Burn Shock|burn shock]], the burn injury can result in other types of injury which include [[Inhalation Injury|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<ref name=":0" />.


''Effect on the cardiovascular system''- Cardiac function is subject to several modifications starting at the time of injury. Before any plasma voume reduction is detected, receptors on thermally affected skin induce a neurogenic response intiating a rapid cardiac output depression. This is associated with an intial reduction followed by a remarkable increase in cardiac index starting onthe third day. As cardiac stress become massive, myocardial depression ensues. The persistent depression is caused by hypovolemia, high systemic vascular resistance, low venous return, and the effects of myocardial depressant substance. In addition, capillary permeability is increased, leading to loss of intravascular proteins and fluids into the interstitial compartment. Peripheral and splanchnic vasoconstriction occurs. Myocardial contractility is decreased. These change coupled with fluid loss from the burn woung, result in systemic hypotension and end organ hypoperfusion.
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 respiratory system''- Inflammatory mediators cause bronchoconstriction, in severe burns, and adult respiratory distress syndrome can occur.
==== Effect on the Cardiovascular System ====
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<ref>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. </ref><ref>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. </ref>.


''Effect on renal system''- The renal system is affected following alterations in the cardiovascular system. Renal blood flow and glomerular filtratin 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 og renal compromise. Failure to promptly and adequately manage these cases may lead to acute tubular necrosis, renal failure, and mortality.
==== Effect on the Respiratory System ====
''Following smoke inhalation, inflammatory mediators are released in the lungs leading to bronchoconstriction and adult respiratory distress syndrome<ref name=":2">Hettiaratchy S, Dziewulski P. ABC of burns: pathophysiology and types of burns. BMJ. 2004;328(7453):1427-9. </ref>.''


''Effect on the liver''- There is substantial depletion of the hepatic proteins , in additon, alterations in scrum 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.
==== Effect on the Renal System ====
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.


''Effects on gastrointestinal system/metabolism''- The basal metabolic rate increases up to three times its original rate. This coupled with splanchnic hypotperfusion, necessitates early and aggressive enteral feeding to decrease catabolism and maintain gut integrity. It causes mucosal atrophy, reduced absorptive capacity, and increased surface permeability. In proportion to burn size, apoptotic epithelial cell death occurs, stimulating bowel mucosa degeneration. Mucosal atrophy subsequently leads to several defects in the absorptive function of the digestive system, notably the uptake of glucose, amino acids as well as fatty acids.Brush border lipase activity is also disturbed. Increase in bowel permeability to macromolecuales is also noted following alterations in intestinal blood supply.
==== Effect on the Liver ====
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.


''Effect on the Endocrine system''- It is characterized by significant alterations in the hypothalamic-anterior-pituitary-peripheral-hormone axes, this response follows a biphasic pattern. The target-organ resistance is considered to be responsible for the low levels of effector hormones seen in the acute phase. In the long-term phase, on the other hand, decreased levels of target organ hormones are due to suppression at the leve of the hypothalamus. Among the hormones actively involved at the onset of injury are catecholamine, glucagon and cortisol, collectively labelled as stress hormones.These hormones display an exponential increase in their levels, somtimes reaching 10 fold their normal valuses. The significance of such an upsurge resides in its influence onthe cardiovascular system and the rusltant fluid shifts that follow these changes. The stress hormones are thereby considered as the initiators of the hypermetabolic-catabolica nd proteolytic-response.
===== Effects on Gastrointestinal System/Metabolism =====
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.


''Immunological changes''- Non-specific down regulation of the immune response occurs, affecting both cell mediated and humoral pathways.
==== Effect on the Endocrine System ====
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.


== Resources  ==
== Burn Prevention ==
*bulleted list
Recommendations from the World Health Organization for individuals, communities and public health officials on how to reduce [[Burn Prevention|burn risk]]<ref>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].</ref>.
*x
* Enclose fires and limit the height of open flames in domestic environments.
or
* 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.


#numbered list
== Conclusion ==
#x
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  ==
== References  ==


<references />
<references />
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[[Category:Burns]]

Latest revision as of 23:03, 13 December 2022

Original Editor - Olajumoke Ogunleye

Top Contributors - Olajumoke Ogunleye, Jess Bell, Carin Hunter, Ahmed M Diab, Naomi O'Reilly and Chelsea Mclene  

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.

[11]

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].
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