Burns Overview

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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.

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 (https://www.who.int/news-room/fact-sheets/detail/burns. Accessed 12/11/2020).

Types of Burns

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.

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 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 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.

• 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.

Hettiaratchy S., Dziewulski P. Pathophysiology and types of burns. BMJ . 2004. 1427-1429

• 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

A burn injury can be classify according to its severity, its depth and size. According to the depth, it can be classified in:

1. 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.
2. 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.

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.

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

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%.

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.

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.

Pathophysiology of burns

Burn injuries result in both local and system responses.

 Local response

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.

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.

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.

Systemic response

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.

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.

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.

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.

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.

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.

Effect on the respiratory system- Inflammatory mediators cause bronchoconstriction, in severe burns, and adult respiratory distress syndrome can occur.

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 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.

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 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.

Immunological changes- Non-specific down regulation of the immune response occurs, affecting both cell mediated and humoral pathways.

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