José Manuel Collado Delfa

Abstract

Burns are one of the most devastating traumatic injuries, mainly affecting the most vulnerable population groups (children, women, and elderly) living in the poorest social conditions. Thermal injuries occur by an increase in temperature able to cause tissue damage. The most frequent etiologic agent is fire/flames, closely followed by scalds. Aside from local destruction (coagulative necrosis), when burn injuries involve > 20% of the total body surface area the systemic inflammatory response puts life at risk: the shock in the acute phase and the sepsis for the rest of the evolution are the leading causes of death. Inhalation injury in the context of a fire/flame burn dramatically worsens the prognosis. Primary assessment of the burned patient must follow the Advanced Trauma Life Support guidelines, and major burns demand transfer to a burn unit. Accurate diagnosis of burn depth is the main challenge because early and definitive coverage with skin grafts remains the gold standard definitive treatment.

Other traumatic agents, such as electricity, chemicals, and cold, can also cause tissue damage that resembles a thermal injury. Although an increase in temperature may coexist in some circumstances, the main injurious mechanisms of these other agents are different, and they are classified as nonthermal injuries.

Keywords: burn, chemical injury, cold injury, electrical injury, nonthermal injury, thermal injury

Thermal injury can be defined as a traumatic injury caused by a temperature increase beyond a threshold able to cause tissue damage. Etiologic factors are contact with hot elements (solids, liquids or scalds, gases), thermal radiation (fire/flames, sun, infrared lamps, etc.), and mechanical friction.

Other nonthermal traumatic agents, such as electricity, chemicals, and cold, can also cause tissue damage with an appearance and behavior reminiscent of a burn injury; however, they have a singular pathophysiology, clinical presentation, and treatment.

According to the latest estimates, 973 million people suffered some kind of traumatic injury that required medical care in 2013. Of these, 31 million were injured by fire/flames, heat, and hot substances (337 injured/100,000 inhabitants), resulting in 12.3 million years of disability-adjusted life years (DALYs). Even though the global rate of DALYs has fallen by 33% since 1990, in regions like sub-Saharan Africa, Oceania, eastern Europe, and the Caribbean this figure remains relatively unchanged.

The population distribution of thermal injuries is one of the most unjust among traumatic injuries, with the most vulnerable population groups being children, the elderly, and women. Over 95% of deaths from fire/flames burns are concentrated in lowand middle-income countries, and in high-income countries, they affect the poorest social sectors.

According to the 2015 National Burn Repository of the American Burn Association the most frequent etiologic burn agent is fire/flames (43%), followed by scalds (34%), contact with hot objects (9%), electrical injuries (4%), and chemical injuries (3%). While electrical and chemical etiologies occur mainly in work-related industrial settings, the rest of the agents are more common outside the workplace. Of note, high-voltage electrical injuries have been related to illegal sales of copper in times of economic crisis.

Most adults suffer burns by fire/flames followed by scalds, men commonly at the workplace and in outdoor accidents, whereas women and the elderly usually at home. Children sustain burns mainly by scalds at home, followed by contact with hot objects in younger than 2 years and fire/flames in older than 2 years.

Cold injuries are a well-documented problem in countries with extreme temperatures and frequent among military personnel during wartime, alpinists, and the homeless, and following occupational accidents with refrigerants and propellants (Freon gas, liquid nitrogen, carbon dioxide).

About 3–10% of burn injuries are intentional in the context of suicide and aggression. Suicide has an overall mortality rate of 65% worldwide, with flame and chemicals being the most frequent causal agents. Risk factors include psychiatric conditions, drug addictions, and gender violence. Children < 2 years are at greater risk of aggression, mainly by immersion in hot liquids and contact with cigarettes or hot objects.

Total days of acute hospital stay approximately equals the burn size expressed as the percent of total body surface area (TBSA), except in the group with burns 50–80% TBSA where hospital stay increases. Fire/flame burns have the highest complication and mortality rates, followed by electrical injuries. Regardless of the cause, the maximal rate of complications occurs in infants and the elderly and increases progressively with age. Associated inhalation injury increases mortality, though it is less evident for burns > 60% TBSA because these already bear a poor prognosis.

Although most burn injuries are not fatal, those who survive do so with varying functional and aesthetic sequelae, which may cause psychological distress and generate a cascade of personal, family, social, and labor repercussions.

Finally, prevention through strategies like regulation of electrical systems, smoke detectors, temperature limiters in running water heaters, and use of fireproof clothes and construction materials have proven effective in reducing morbidity, mortality, and the economic burden of burns in developed countries.

Temperature is a measurement of the average kinetic energy resulting from the random movement of molecules constituting a physical element. In theory, temperature can range from absolute zero (no molecular movement) to infinite.

A rise in tissue temperature occurs when energy is transferred. Conceptually, the energy that originates from a thermal source is called heat, and the energy that originates from a nonthermal source is called work.

Heat can be transferred by conduction, convection, or radiation, with the first two involving direct physical contact with the energy source. In conduction, the energy source remains static, as when one is touching an incandescent material or dipping a hand in a bowl of hot water. In convection, the contact is established with a fluid in motion as with running water or steam causing a continuous turnover of molecules at the source–tissue interface, which prevents the system from reaching thermal equilibrium. Radiation requires no contact and can be emitted by any physical element with temperature other than absolute zero in the form of electromagnetic waves (0.1–100 μm). Examples include sunlight and infrared lamps. The surface of living organisms behaves as a dark body that easily absorbs radiation.

Work implies not only a physical force that causes displacement but also opposition forces that interfere with it. Friction is the opposition force involved in burns.

Energy transferred as heat or generating friction increases random molecular movement in tissue at the interaction point, elevating its temperature. The energy is then transmitted from the surface to the deep tissues by conduction. Biological tissues are poor conductors of heat; the less their water content, the poorer their conduction capacity.

The first signs of cellular injury begin to appear at temperatures > 45°C when proteins and nucleic acids denature, leading to metabolic and structural dysfunction. The most remarkable histological feature is cell edema due to failure of the sodium-potassium adenosine triphosphatase (Na⁺/K⁺-ATPase) pump. Denaturation may be slowly reversed by cooling down. With temperatures > 60 °C, proteins and nucleic acids precipitate and cells die. It is an irreversible phenomenon whose histological expression is the coagulative necrosis. Macroscopically, tissues appear desiccated and mummified with a yellow-gray or blackish hue (eschar tissue), whereas microscopically the original histological architecture remains identifiable. Burns destroy skin and its appendages, dermal vascular plexus, and sensitive cutaneous nerves impairing its protective function as a physical and biological barrier, as well as its other functions, such as thermoregulation, synthesis of vitamin D, and sensation, all of which are essential for our adaptation to the external environment and social interaction. Cell destruction releases electrolytes, enzymes, and other cytoplasmic proteins that serve as injury markers (K⁺, myoglobin, creatine phosphokinase [CPK], L-lactate dehydrogenase).

Jackson identified three zones of thermal injury: coagu lation, stasis, and hyperemia. In the coagulation zone, injury is maximal and irreversible, featuring coagulative necrosis. The stasis zone surrounds the area of coagulation and is characterized by protein denaturation, cell dysfunction, and blood stasis. The outermost is the hyperemia zone, which shows minimal cell injury and intense local vasodilation. It is important to note that final extension of the necrosis zone depends on the evolution over time of the other two zones. Additional cell death can be explained by the onset of immediate autophagy and delayed cellular apoptosis as well as by the addition of factors that hinder healing in the areas of stasis and hyperemia, such as hypoxemia, deficient blood supply, interstitial edema, desiccation, and local infection.

Local Changes

The repair of any wound, including burn wounds, comprises three successive and partially overlapping phases.

The inflammatory phase takes place during the first week and begins with the release of primary mediators of cellular origin (histamine, serotonin, platelet-activating factor, and arachidonic acid metabolites) and plasmatic origin (coagulation factors, complement and kynin pathways components). They cause changes in the local microcirculation with primary vasoconstriction followed by vasodilation, increased endothelial permeability with interstitial edema, circulatory stasis, and microthrombosis. These mediators also stimulate the homing of other inflammatory cells in charge of removing debris and releasing cytokines that modulate and amplify the inflammatory response as secondary mediators.

The proliferative phase starts approximately 4 days after injury and lasts 3 weeks. Key features of this phase include a high rate of collagen production by fibroblasts, formation of new blood vessels from preexisting ones (angiogenesis), and the start of epithelialization.

Systemic Changes

When burn injuries involve > 20% TBSA, the inflammatory response mediated by cytokines becomes systemic and may last for several months.

Acute Phase

The most prominent features of the acute phase are the abrupt increase in endothelial and cell membrane permeability and cellular dysfunction. The increase in permeability causes a rapid shift of protein-rich fluid into the interstitial space and subsequent interstitial and cellular edema. As a response to the hypovolemic shock, peripheral and splanchnic vasoconstriction occurs to ensure perfusion of vital organs.

The origin of cellular dysfunction is multifactorial and not only explained by tissue hypoxia. There is a tendency toward hypothermia, and basal metabolism is depressed in the acute phase. In addition, there is low cardiac output secondary to a reduced preload and the negative effect of cytokines in heart contractility, with a characteristic poor response to vasoactive drugs (cardiogenic shock). Renal function is affected by reduced blood volume, and there is renal tubular dysfunction due to hypoperfusion and tubular obstruction by cell debris. Mesenteric hypoperfusion causes mucosal edema and paralytic ileus. Leukocytosis with neutrophilia is prominent due to intravascular displacement and depletion of bone marrow reserves. In addition, destruction of red blood cells within the cutaneous vascular plexus leads to anemia and coagulation. Coagulation is affected by the loss of coagulation factors to the interstitial space, direct platelet destruction by temperature, and consumption of both from intravascular thrombosis.

Subacute Phase (> 48–72 Hours)

Restoration of permeability follows a downwardsloping exponential curve. It is already evi dent at 8–12 hours and normalizes from 48 hours onward, allowing reversal of the hypovolemic shock and edema reabsorption with transient polyuria.

During this phase, the stress state from burn injury generates a nonspecific clinical picture known as the systemic inflammatory response syndrome (SIRS), which sets in motion a hypermetabolic, hyperdynamic, and inflammatory response.

The hypermetabolic response is aimed at generating enough energy to withstand the inflammatory response and cope with subsequent tissue repair. It correlates with burn size, doubling the basal metabolism with burns > 40% TBSA, and may take up to 2 years to return to preinjury values. Thyroid function is inhibited, and basal metabolism becomes regulated by stress response hormones (cortisol, catecholamines, and glucagon). Because the use of sugars and fats is partially blocked, proteins represent the primary source of energy in this phase. Although gluconeogenesis is stimulated and the release of insulin is increased, there is peripheral insulin resistance that limits cellular intake of glucose, leading to hyperglycemia. Fortunately, uptake of sugar by the central nervous system, red blood cells, and wound bed works independently of the action of insulin. Hyperinsulinism blocks ketogenesis from fatty acids, and hyperglycemia promotes their hepatic reesterification back into triglycerides. Because the synthesis of transport lipoproteins is also insufficient, triglycerides cannot return to the fatty tissue and thus remain in the liver (steatosis), producing hepatomegaly.

The generation of energy from protein breakdown has a severe impact, with skeletal muscle being the most affected tissue because of its high protein content. Additionally, there is a rearrangement of liver protein synthesis, with acute phase proteins taking over visceral ones. The net result is weight loss and reduction in lean body mass with weakened muscle (known as self-cannibalism), all of which compromise inflammatory response, wound healing, and growth of pediatric patients. Laboratory workup will show a low serum protein level, a negative nitrogen balance, increased blood and urine urea, elevated C-reactive protein, and reduction of protein synthesis markers (albumin, prealbumin, and transferrin).

In order to withstand the hypermetabolic response, a hyperdynamic state ensues, with in creased cardiac output, tachycardia, tachypnea, and peripheral vasodilation, the latter being more evident after the first week.

Although initially beneficial, a SIRS prolonged in time can overcome the compensatory mechanisms and cause multiple organ dysfunction syndrome (MODS) and death by exhaustion.

Inhalation injury is the leading cause of death during a fire, and a significant worsening factor when associated with a burn injury.

Local effects of inhalation are irritant (physical stimulus of mechanical receptors by solid particles in suspension), thermal (hot gases that burn the mucosal layer), and, most important, toxic, which is dependent on the chemical nature of combustion products. Irritant and toxic effects can freely affect the entire airway, whereas burns rarely cause injury beyond the glottis because the upper airway absorbs most of the heat of inspired air. The reflex response is immediate and involves sneezing, mucous hypersecretion, cough with carbonaceous sputum, and laryngeal and bronchial spasms. The clinical features of mucosal injury present later following a typical temporal sequence and are secondary to inflammation, loss of cilia function and alveolar surfactant, and necrosis. Edema develops within the first hours after injury and may be silent or present with hoarseness, dysphonia, and glottis obstruction. ARDS and atelectasis usually appear on day 3–5, followed by lower airway infection after the first week.

HCN in its pure state is a colorless liquid or gas. Its gaseous form is generated in large quantities by the combustion of nitrogen materials of domestic (plastic, wool, silk, polyurethane) or industrial origin. Its absorption is immediate and travels mainly bound to plasma proteins with a half-life of 4–8 hours. Most of it is cleared renally after being transformed into thiocyanide in the liver. HCN inhibits different metabolic pathways, such as the cytochrome C mitochondrial oxidase pathway. Its clinical features are also nonspecific, derived from cellular hypoxia, and include peripheral vasodilation, low blood pressure, and neurologic symptoms, such as headache, lethargy, and coma. Survivors may show permanent neurologic disabilities. The smell of sour almonds is noticeable in < 40% of patients.

Clinical Workup and Treatment of Inhalation Injury

Low values of oxygen saturation (SaO₂) and oxygen partial pressure (pO₂) are always present in severe cases of inhalation injury but their normal values do not rule out it. Among asphyxiant gases only CO diminishes the capacity of blood to transport O₂ but the usual pulse oximeters do not differentiate between carboxyhemoglobin (COHb) and oxyhemoglobin (O₂Hb), displaying a mistaken normal SaO₂.

Direct visualization of the mucosa using indirect laryngoscopy and bronchoscopy helps to identify local airway injuries and confirm a diagnosis of inhalation; however, in cases of pure intoxication with asphyxiant gases, the airway might be normal. Chest X-ray is of little use initially and only shows positive signs within a few days once respiratory complications appear. Chest computed tomography, radionuclide imaging with 133-xenon, and pulmonary function testing are not routinely used.

Diagnosis of CO intoxication requires COHb > 10% (normal values are< 5% in nonsmokers and 5–10% in smokers); however, if enough time has elapsed or oxygen has been applied to favor CO clearance, normal values may be observed. HCN plasma levels can also be measured but this test is not readily available and is time consuming, making it of little value in common clinical practice. If an anoxic encephalopathy is suspected, a full neurologic assessment is mandatory, and as soon as the patient’s state allows, a cranial computed tomographic (CT) scan should be performed.

Treatment should be aggressive and start immediately at the slightest suspicion. Although management of inhalation injury is mainly symptomatic, specific therapies exist for asphyxiant gas intoxication.

If CO intoxication is suspected, administering 100% O₂ reduces CO half-life to 80–100 minutes. In pregnant women O₂ therapy should continue for a period of time after COHb normalization due to the different fetal pathophysiology. Hyperbaric O₂ should be considered when COHb is > 20%, but its application in patients with severe burns is limited due to logistical difficulties.

Every burned patient should be considered a trauma patient and treated accordingly until proven otherwise. The burn can be a distracting factor that diverts the attention from other coexisting injuries that might result to be more deleterious.

Prehospital Care

Primary Assessment and Intubation Criteria

Primary assessment must identify and treat immediate life-threatening injuries, following the ABCDE algorithm of the Advanced Trauma Life Support guidelines.

Airway: Burns can block airway due to edema and/or laryngeal spasm. Orotracheal intubation (OTI) should be performed whenever a patent upper airway cannot be secured.

Breathing: It may be impaired by burns restricting ventilation (deep circumferential burns affecting the thorax and abdomen) and by inhalation injury. As a general rule, high flow (15 L/min), 100% oxygen should be administered, ideally with a reservoir mask, to ensure maximum fraction of inspired oxygen. If intoxication by asphyxiant gases is suspected act accordingly. Failure to maintain respiratory function requires OTI and mechanical ventilation.

Disability: A basic neurologic status assessment is performed including the Glasgow Coma Scale (GCS). Burn injuries rarely affect neurologic status, with the exception of asphyxiant gas intoxication. GCS ≤ 8 is an indication for OTI.

Exposure: All clothing and accessories should be removed. It allows primary assessment, eliminates any retained heat source, and prevents compartment syndrome as a consequence of subsequent edema. The patient should be covered immediately after to reduce the risk of hypothermia.

Secondary Assessment

Secondary assessment should be performed only on stable patients, with continuous monitoring of vital functions. The priority for unstable patients is their transport to a hospital facility.

Burns should be cooled down by means of irrigation or immersion in tap water or 0.9% NS at room temperature (12–18°C) for 15–20 minutes, which also provides an analgesic effect, though it is discouraged for adult burns > 15% TBSA and for children burns due to the risk of hypothermia. An alternative is hydrogel dressings, which provide a refreshing sensation without increasing the risk of hypothermia. Debridement of blisters and applying wound dressing that might interfere with definitive hospital assessment should be postponed. Burns should be covered with sterile drapes or clean dry linen to avoid contamination and reduce painful stimuli. Finally the patient should be covered with a thermal blanket, keeping affected areas elevated.

Superficial second-degree burns are the most painful. Topical treatment provides some analgesic effects, but it is often insufficient and systemic analgesia is necessary. When conventional analgesia is inadequate, intravenous opioids are the treatment of choice.

A strict indication for nothing by mouth should be made before hospital admittance. If paralytic ileus is suspected, gastric decompression should be considered especially when the patient is to be transported by means of unpressurized air cabins (helicopter).

Hospital Care

Initial Assessment

On arrival to the burn unit, the ABCDE algorithm is reassessed and continuing monitoring of vital signs is maintained. Intubation criteria should be reviewed and indirect laryngoscopy or bronchoscopy performed if airway injury is suspected.