Evaluation and Management of Burn Injuries

EXECUTIVE SUMMARY

• Healthcare providers should avoid unnecessary tracheal intubation and use strict criteria for intubating patients with burn injuries, including facial burns, hoarse voice, soot in the mouth, or upper airway edema. Additional features, such as singed nasal vibrissae, bronchorrhea, and sooty sputum, should prompt healthcare providers to secure the patient’s airway. Airway assessment should be repeated frequently, since inhalation injury may not be readily apparent on initial evaluation.
• Any absolute compartment pressure greater than 30 mmHg or a diastolic blood pressure minus compartment pressure less than 30 mmHg indicates compartment syndrome, warranting escharotomy by a trained provider.
• Burn patients are vulnerable to what is known as the “lethal triad” of coagulopathy, acidosis, and hypothermia. Initial hematologic studies should be obtained, including a complete blood count, prothrombin time, activated partial thromboplastin time, and thromboelastography tests.
• A serum lactate level of 10 mmol/L in fire victims is a sensitive and specific indicator of cyanide poisoning.
• Current indications for intubation are full-thickness burns to the face or perioral region, circumferential neck burns, acute respiratory distress, progressive hoarseness, air hunger, respiratory depression, altered mental status, or supraglottic edema on bronchoscopy. Additionally, consider total body surface area (TBSA) as another criterion. There is no standardized cut-off for %TBSA. However, Advanced Burn Life Support recommends intubation in patients with > 30% TBSA burns.
• Although hypovolemia contributes to mortality in the early phases of burn shock, over-resuscitation can lead to increased edema formation and increased burn depth and coagulation zone.

Although burn injuries are seen less frequently then they used to be, it is still critical for the acute care provider to stay current on best practices for the care of the burn patient. The authors provide an update on the evaluation and management of burn injuries.

— Ann M. Dietrich, MD, Editor

Introduction

According to the International Society of Burn Injuries, a burn is an injury to the skin or organic tissue caused by thermal or acute trauma. A burn injury results from the heat of hot liquids, solids, or fire, but can also be from friction, cold, heat, radiation, chemical, or electric sources.¹ A complex pathophysiological process occurs in patients with severe burns that encompass > 20% total body surface area (TBSA), affecting multiple organ systems and requiring early and aggressive interventions to reduce morbidity and mortality. Given the decreasing incidence of burn injuries over the past three decades, clinicians are exposed to these types of injuries less frequently. Therefore, it is more important than ever to stay up to date on current recommendations for the acute care of burn patients. The management of burn patients is a long-term process that continues beyond the burn wounds themselves. It encompasses the injury’s systemic, social, and psychological consequences, which can negatively affect long-term mortality and morbidity.² This article aims to provide the clinician with the current recommendations on the initial management of the burn patient in the acute period after injury in the emergency department (ED).

Epidemiology

In the past few decades, there have been significant improvements in the outcomes for burn patients.³ As of 2016, almost 97% of those treated in burn centers survive.⁴ The incidence of burn injury has decreased significantly over the past three decades, from 215 to 101 per 100,000 when comparing data from 1990 vs. 2019.^1,5 However, despite the decreasing incidence, burns still comprise more than 400,000 ED visits per year and continue to be one of the leading causes of unintentional death in the United States.¹ Gender and age significantly influence incidence, since males are 1.5 times more likely to experience burns than the general population, and patients 20-29 years of age represent the majority of burn patients.^4-6 The majority of burns are due to flames (41%) and scalds (31%), with chemical (3.5%) and electrical injuries (3.6%) occurring much less often.⁷

The majority (~67%) of burns are minor and occupy < 10% of TBSA.⁸ Along with TBSA and smoke inhalation injury, age is one of the three most powerful predictors of outcome following thermal injury.⁷ Burn injury is the fifth most common cause of nonfatal injury in childhood, and children younger than 16 years of age represent 26% of all admissions to burn center hospitals.^8,9 Children in lower-income families with lower parental education and living in rural areas are at the highest risk.¹⁰

The proportion of elderly people affected by burns is similar to the general population, and mortality increases with age. Adults older than 60 years of age frequently lose independence and rely on skilled care after a burn injury.^2,8

Etiology

Many aspects of acute burn care have changed over the decades. Still, proportionally, most burn injuries healthcare providers encounter are the result of thermal burns. As of 2019, thermal burns accounted for 71% of all burn cases in the United States.⁷ In 2019, fires caused 3,515 deaths and 16,600 injuries in the United States, with risk factors for both fatal and nonfatal house fire injuries including young or old age, male gender, non-white race, low income, disability, smoking, and alcohol use.^11,12 Mainly for these reasons, children younger than 5 years of age and adults older than 65 years of age accounted for 45% of home fire deaths, and one-third to one-half of fatalities in house fires involved recent ingestion of alcohol.^13-16

A recent study identified statistically significant downward trends for both the rate of residential fire death (an average annual decrease of 2.2% to 2.6%) and the rate of residential fire death attributed to smoking (an average annual reduction of 3.5%).¹⁷ Many fatalities in enclosed fires die at the scene. In addition to inhalation injuries, which result from chemical or thermal irritation to the trachea and/or bronchi, the rapid depletion of oxygen in the interior of a building may cause asphyxia, along with carbon monoxide (CO) and cyanide (CN) poisoning in these patients.

Slightly less common than thermal burns from flames are scalds, chemical burns, electrical burns, or lightning injuries. Scalds account for 33% of the burns in any age group, but they are seen much more frequently in young children, particularly those younger than 4 years of age, where they account for up to 60% of admissions.^18-20 Annually, around the Fourth of July holiday, it is estimated that 1.86-5.82 firework-related burns per 100,000 persons occur in the United States, with the majority occurring in boys 10-14 years of age and with injuries found most commonly occurring on the hands, head, and eyes.^21-23

Many occupations may put patients at risk for burns as well. Most electrical burns in the occupational setting occur among electricians and power line workers. Special consideration must be taken since high-voltage burns result in severe muscle necrosis and require aggressive and early interventions. Those involved in manufacturing plants and fertilizing are at risk for chemical burns that occur when powerful acids or bases come into contact with skin, which, in addition to standard burn care, may require additional steps in management.²⁴ Burns from lightning can be severe but are rare, and deadly lightning strikes occur fewer than 30 times per year in the United States.²⁵

Only approximately 4% of those treated in specialized burn treatment centers die from burn injury or associated complications.^26,27 Burn center survivors with > 20% TBSA burn injuries tend to be younger with fewer comorbidities and, thus, have a better five-year survival than those with < 20% TBSA.²⁸ However, despite the appropriate resuscitation in the acute setting, burn patients still are at high risk for sepsis, acute respiratory failure, multisystem organ failure, and many other severe complications.²⁹ Two-thirds of the elderly living independently before their burn injury require a skilled nursing facility after hospitalization for burn care.³⁰ Recent studies identified the profound emotional, psychological, and spiritual impact of burns and how coping skills, family, community support, and general psychological health influence recovery from burn injuries more than burn care.³¹

Pathophysiology

All burn injuries involve tissue destruction caused by energy transfer, with different burns resulting in different pathophysiological responses. Flame burns cause immediate deep burns, whereas scalds initially appear more superficial. Thermal injury can occur with heat or cold. Frostbite causes direct cellular injury from crystallization of water in tissue and indirect injury from ischemia and reperfusion. Alkaline chemicals cause colliquative necrosis, and acidic burns cause coagulation necrosis. Furthermore, electrical injuries cause more deep tissue damage than what is visible on the skin.³²

The depth and severity of burns can vary based on the age of the patient and the anatomical location of the burn. The thickness of the skin varies by age, increasing from 5 to 50 years of age and thinning after age 65 years. Skin is thickest on the palms, soles, and upper back.³³ It is essential to identify the depth of burns because even partial-thickness burns disrupt the skin’s ability to prevent evaporative water loss, protect against environmental insults, control body temperature, and allow for sensation and excretion.

In addition to the visible tissue injury, large surface area burns also cause plasma extravasation into the burn wound and surrounding tissues.³² When the burn reaches 20% to 30% TBSA, a broad spectrum of local and systemic homeostatic disorders and inflammation occur due to the plasma extravasation.³³ The inflammation and hemostatic disorders drive a distributive shock with intravascular hypovolemia, hormonal alterations, acid-base disturbances, hemodynamic change, and hematologic derangements. The inflammatory response has substantial effects on the microcirculation and the function of the heart and lungs.³⁴ The hypovolemia and depressed cardiac function within the first 24-48 hours because of inflammation and oxidative stress create decreased plasma volume, cardiac output, and urine output, and increased systemic vascular resistance resulting in reduced peripheral blood flow.^32,33

Because of the disruption in barrier function, moderate to extensive burns can have a significant free water deficit.³⁵ The large volumes of resuscitation required to maintain vascular volume cause edema because the rate of fluid filtered out of the microvessels exceeds the flow in the lymph vessels. The edema formation often follows a biphasic pattern, where an immediate and rapid increase in the water content of burn tissue develops in the first hour after burn injury.³³ The second phase is a more gradual influx of fluid into the burned skin and surrounding tissue in the first 12-24 hours after the injury.^33,36

After the initial resuscitation of the burn injury, the continued systemic inflammation, absence of barrier function, and inhalation injuries often predispose patients to severe infections leading to sepsis. Sepsis is the leading cause of death in patients with severe burns.³⁶ Additionally, after an initial hypometabolic state for 72-96 hours, a hypermetabolic state is observed for up to 36 months. The hypermetabolic state is caused by elevated catecholamines and glucocorticoids. These elevated hormones increase blood pressure, cause peripheral insulin resistance, and break down glycogen, protein, and lipids, resulting in increased body temperature, energy expenditure, and muscle wasting.³²

Frostbite is tissue damage caused by a cold injury resulting from exposure to intense cold, typically below the freezing point.³⁷ The process of tissue damage occurs in four overlapping stages: prefreeze, freeze-thaw, vascular stasis, and late ischemic.³⁸ The prefreeze phase involves tissue cooling with vasoconstriction and ischemia. Crystals form in the freeze-thaw stage, causing tissue damage and cell death.³⁸ After this thawing begins, ischemia, reperfusion injury, and inflammatory responses follow. When the vascular stasis phase occurs, the vessels fluctuate between constriction and dilation, and blood may leak or coagulate at this stage. Furthermore, the late ischemic phase results from progressive tissue ischemia, infarction, and inflammatory mediated injury. The destruction of the microcirculation is the main factor leading to cell death.³⁸

Chemical burns result from exposure of the mucosa or skin to corrosive agents.³³ Chemical burns account for approximately 10.7% of all burn injuries and 30% of deaths resulting from burns.³⁹ Chemical burns often result from pH variations (acidic or alkaline), which cause the denaturation of crucial structural and functional proteins. Alkaline materials often cause a more severe injury than acidic compounds. Acidic compounds cause coagulation necrosis with precipitation of proteins, whereas alkali materials cause liquefaction necrosis, allowing the material to penetrate deeper into the injured tissue.⁴⁰ The concentration, quantity, manner, duration of contact, extent of penetration, chemical mechanism of action, and physical state of the material (liquid, solid, gas) determine the severity of the chemical burn.

Electrical burns cause injury by the direct action of electrical forces on proteins, cell membranes, and tissue injury mediated by heat generation.⁴¹ The voltage, current, type of current (alternating current [AC] or direct current [DC]), path of the current, duration of contact, resistance at the point of contact, and individual susceptibility determine the severity of the injury. Domestic wiring in the United States operates on AC at 120 V. Thus, most electrical burns in U.S. EDs are low-voltage injuries.⁴¹ The organs and tissues most affected are a by-product of the pathway of current and resistance of the tissues. Therefore, more thermal damage occurs to high-resistance tissues (i.e., bone, tendon, and fat) than tissues with low resistance (i.e., nerve, blood vessels, and muscle) that are good conductors. The skin has intermediate resistance.

Lightning is the second leading cause of weather-related death in much of the world.^42-44 In contrast to domestic or industrial electric burns, and despite the millions of volts of electricity involved in lightning strikes, the injuries seen are highly varied from minimal cutaneous burns to severe, high-voltage burns. The pathognomonic sign of a lightning strike is known as Lichtenberg figures, an erythematous, fern-like branching pattern on the skin resulting from extravasation of blood in the subcutaneous tissues, appearing within an hour of injury, and fading rapidly.⁴²

Inhalation injuries are caused by exposure to heat, particulate matter, irritants, and toxic gases in fires. After inhalation injury, the main pathophysiologic changes include increased bronchial blood flow causing edema, increased mucus secretion, and eventually hypoxic vasoconstriction. Collectively these changes lead to airway obstruction, with thick casts formed from epithelial debris, fibrin clots, and mucus.⁴⁵ Even if treated early and aggressively, this inflammatory response may result in acute respiratory distress syndrome (ARDS) in up to one-third of patients and predisposes them to the development of bacterial pneumonia.⁴⁶

Inhalation injuries subdivide into supraglottic, subglottic, and systemic. Supraglottic injuries are most common because of the glottis’s protective effect, which closes to prevent heat from reaching subglottic structures. The resulting edema can cause airway obstruction, which may develop quickly during resuscitation.⁴⁵ Subglottic injuries are mostly chemically derived. The damaged endothelial cells create edema of the small airways, decrease alveolar surfactant activity, cause mucosal sloughing with fibrinous exudation into the airways, bronchospasm, and eventually airflow obstruction and atelectasis.

Systemic effects of inhalation injury occur from toxicants and commonly from either hypoxia or hypercapnia.⁴⁵ After inhalation injury, the two major tissue asphyxiants are carbon monoxide (CO) and cyanide (CN).⁴⁵ CO is an odorless, colorless gas produced by the incomplete combustion of carbon-containing components.⁴⁶ CO preferentially binds to hemoglobin over oxygen with an affinity approximately > 200 times higher, resulting in decreased oxygen delivery. The brain and heart, where oxygen extraction is the highest, are the most vulnerable organs.⁴⁶ CN originates from the incomplete combustion of nitrogen-containing polymers, particularly those in plastics and other household products.⁴⁶ Similar to CO, CN impairs oxygen use and causes profound lactic acidosis. CO and CN often occur together and synergistically worsen oxygen delivery and utilization.⁴⁶

Clinical Features and Initial Assessment

Most burns seen and assessed in EDs, trauma centers, and burn centers are thermal burns. After receiving a thorough handoff and transition of care from emergency medical services, including information on the source of fire and the combustion products generated, the burn resuscitation begins with airway evaluation. Recent studies found that using the more restrictive ABA criteria for intubation decisions rather than liberal criteria was more sensitive and specific in detecting inhalation injuries. Intubation occurred unnecessarily in almost 38% of patients before arrival.^47,48 Thus, healthcare providers should avoid unnecessary tracheal intubation and use strict criteria, such as facial burns, hoarse voice, soot in the mouth, or upper airway edema.^49-51 Additional features, such as singed nasal vibrissae, bronchorrhea, and sooty sputum, should prompt healthcare providers to secure the patient’s airway. Airway assessment should be repeated frequently, since inhalation injury may not be readily apparent on initial evaluation.^49,52

The healthcare provider should assess the patient’s breathing pattern in conjunction with the airway. A respiratory rate less than 10 breaths/minute or greater than 30 breaths/minute is a sign of impending respiratory failure. Although not widely accepted at this time, scales are under development to predict the likelihood of delayed airway obstruction for inhalation injury, with some scores, such as the delayed intubation after inhalation injury (PDI) score, showing promise.⁵² In the meantime, the impending loss of airway is unlikely in patients with an adequate gas exchange at the time of examination.⁴⁷ However, profound or unexpected anoxia should raise concern for CO and CN poisoning, since CO remains one of the most frequent immediate causes of death following smoke-induced inhalation injury, especially in enclosed space fires. Also, accessory muscle demonstrating supraclavicular, intercostal, or sternal retractions, grunting, and nasal flaring all are indicators of increased work of breathing. Circumferential thoracic burns may compromise the mechanics of breathing.

Following breathing, the assessment of circulatory status should include skin color, peripheral pulses, and capillary refill. Heart rate and blood pressure can confirm adequate organ perfusion. Anxiety and pain may increase the heart rate in addition to hypovolemia. Additionally, hypotension in the acute phase immediately following a burn should raise concern for hemorrhagic shock, since concomitant traumatic injuries are common, especially with electrical burns. All extremities require pulse assessments with a heightened concern for compartment syndrome from deep or circumferential burns. Note that pulselessness occurs late in this process, and compartment damage may occur even in the presence of pulses.⁵³ Invasive blood pressure measurements can assist in diagnosing compartment syndrome. Escharotomies are the treatment of choice when this pathophysiology is present.⁵³ Failure to perform an escharotomy when indicated may lead to muscle necrosis and potentially amputations.

When the provider assesses disability using the Glasgow Coma Scale, the acute phase of a burn injury should not manifest any altered level of consciousness, even with severe burns. Consider other processes, such as trauma, CO, CN, or hypoxia, if the patient has an altered mental status. Acute CO poisoning may cause headache, syncope, confusion, or coma.³⁴ The classic cherry red oral mucosa is a rare finding in live patients. In elderly individuals, consider the additional factor of medical conditions and medications.

Next, fully expose the patient, remove all clothing, and thoroughly examine the patient. Additionally, remove all jewelry because of the risk of compromising blood flow as edema develops. Continually monitor for hypothermia.⁵² Provide careful attention regarding circumferential burns, evaluating for signs of compartment syndrome (i.e., pain, pallor, paresthesia, paralysis, pulseless, poikilothermia, and pain on passive extension).^40,53 If the patient cannot participate in the exam, measure compartment pressures. Any absolute compartment pressure greater than 30 mmHg or a diastolic blood pressure minus compartment pressure less than 30 mmHg indicates compartment syndrome warranting escharotomy by a trained provider.^34,40

TBSA assessment is required. This evaluation typically is completed in two steps: assessing the burn depth and the TBSA. The burn depth has critical implications in treatment, and TBSA is a good indicator of prognosis and governs fluid resuscitation.⁵¹ Recently, burn wound depth nomenclature has changed from first-degree through third-degree burns based on anatomical levels and tissues affected. Now, the two-level nomenclature is more focused on treatment strategies.³² Partial-thickness burns require conservative treatment, and full-thickness burns require surgical excision and transplant/grafting.³² Superficial burns involve only the epidermis and usually are erythematous and painful but do not contain blisters (e.g., a sunburn). Superficial burns are not part of the TBSA. A superficial partial-thickness burn involves the superficial dermis and typically involves blisters. The blisters leave a pink, wet, and sensitive region prone to bleeding when removed. Deep partial-thickness burns extend to the reticular dermis and demonstrate blistering but appear mottled and white with slow blanching and have diminished sensitivity to pinprick. Full-thickness wounds involve the entire dermis and underlying tissue and appear charred, leathery, firm, and are insensitive to touch.^32,34

This step is vital to assess the TBSA affected by partial-thickness and full-thickness burns, since the results dictate the starting point for resuscitation.³⁴ TBSA determination is under continual refinement led by international research with new and emerging methods involving 3D mapping and ultrasound, among others, to determine the burn size. Multiple contemporary methods exist, such as the patient’s palm, the rule of nines, and the Lund-Browder chart, which have poor accuracy.⁵² The patient’s body mass index, race, age, and sex standards contribute to TBSA misestimation.⁵⁴ It is essential to calculate an accurate estimate, since overestimation correlates with inappropriate fluid resuscitation, burn transfers, and poor outcomes.^54-56

Studies demonstrate overestimating burn severity and TBSA in children results in excessive fluid resuscitation before transfer to a burn center.⁵⁵ Children require special consideration because they have an increased body surface area in the head and neck, with a smaller surface area in the lower extremities. Infants have 21% of the TBSA in the head and neck and 13% in each leg, which incrementally approaches the adult proportions with increasing age. The Berkow formula can accurately determine the burn size in children.⁵⁷

Thermal injuries from cold also can cause severe injuries. Homelessness, alcohol consumption, inadequate clothing, wet clothing, and tight, constricting clothing are substantial predisposing factors for developing frostbite.³⁸ Frostbite ranges from freezing the uppermost layers of skin, termed “frostnip,” to severe frostbite, which affects deeper tissues, such as muscles and bones, known as true frostbite. With frostnip, there is a rapid resolution of symptoms with no long-term sequelae, whereas even a benign presentation of frostbite may lead to critical limb ischemia.³⁸ Acute compartment syndrome, though rare, may occur with frostbite.⁵⁸ The injury severity relates to the duration of exposure and the temperature in contact with the skin. The typical areas affected include ears, nose, cheeks, and penis.⁴¹ The initial appearance may be deceptive, since hyperemia is present in frostbite and frostnip. The patient may note insensitivity of the affected part initially and pallor. However, severe pain occurs during and immediately after the rewarming process. Blebs may become apparent after 12-24 hours. (See Figure 1.) Assessment of the severity may allow for better management of the injury since an accurate prognosis may not be possible for weeks to months until the injury fully evolves.

Figure 1. Frostbite
Source: Wikimedia Commons. https://commons.wikimedia.org/wiki/File:Frostbitten_hands.jpg

Electrical burns, including oral commissure burns and lightning and ocular burns, are a less common type of burn. Evaluating patients with high-voltage electrical injuries > 1,000 V should prompt unique considerations. There is a much higher likelihood of traumatic brain, intra-abdominal, and extremity injuries resulting from the electrical source throwing the patient. Spine fractures increase because of tetany and require complete immobilization until a spinal evaluation is performed.⁴⁰ Electrical injuries typically have a small TBSA with an average of 14%. However, estimating TBSA may be difficult because it is hard to ascertain deep tissue damage initially.⁵² Unlike compartment syndrome from burns caused by flame, in which the constricting tissue is the burn eschar, the fascia is the constricting tissue in patients with electrical injuries. The muscle swells after being heated by the current running through the bone, resulting in increased fascial compartment pressures. Signs of compartment syndrome from electrical injury are similar to those of other causes of compartment syndrome, with pain on passive extension as the most telling sign. Additional symptoms include pain out of proportion to examination, paresthesia, and pulselessness.⁴⁰

The etiology of oral commissure burn injury results from a child chewing on the end of a power cord. The burn often is unilateral, involving the lateral commissure, tongue, and alveolar ridge. Systemic manifestations are uncommon. Injury to the labial artery is not always immediately apparent because of vascular spasm, thrombosis, and the overlying eschar. Severe bleeding can occur later.⁵⁹

Ocular injuries occur in 7% of work-related injuries in the United States. As many as 20% of chemical injuries could lead to significant visual deficits, with alkali burns causing more severe ocular injuries compared to acidic solutions. The type of solution, concentration, pH, duration of exposure, and degree of penetration determine the extent of the damage. Therefore, obtain a full ocular assessment and thorough history. A patient can have decreased vision, eye pain, blepharospasm, conjunctivitis, and photophobia. In severe alkali burns, the globe may appear white as a result of ischemia of the conjunctiva and scleral blood vessels.⁴⁰ (See Figure 2.)

Figure 2. Chemical Eye Injury
Source: Wikimedia Commons. https://commons.wikimedia.org/wiki/File:Chemical_burn_injury..jpg

The unidirectional, massive current impulse from lightning produces unpredictable and variable features compared to more common electrical injuries.⁶⁰ Death usually occurs immediately following a lightning strike, but delayed cardiopulmonary arrest is possible. Initial stabilization of patients who have sustained lightning injuries should involve Advanced Trauma Life Support (ATLS), Advanced Cardiac Life Support (ACLS), and Advanced Burn Life Support (ABLS) principles, emphasizing total spinal immobilization and subsequent basic burn care and electrical injury management principles. Clinical features of lightning strikes include cardiac arrhythmias, muscle injury, central nervous system abnormalities (such as traumatic and hypoxic brain injury), loss of consciousness, confusion, amnesia, headaches, spinal cord injuries, paresthesias, weakness, otologic and ophthalmic findings, and the particular feature of transient fern-like patterns on the skin called Lichtenberg figures.⁶¹

Diagnostics

As stated previously, all burn patients are trauma patients, especially in the case of high-voltage electrical injuries. Point-of-care ultrasound should be performed and include a focused assessment with sonography in trauma (FAST) exam and evaluate the patient’s inferior vena cava to determine fluid status.⁶² All areas of concern discovered on primary or secondary surveys should prompt the appropriate imaging studies.⁶³

Burn patients are vulnerable to what is known as the “lethal triad” of coagulopathy, acidosis, and hypothermia.⁶⁴ Initial hematologic studies should be obtained, including a complete blood count, prothrombin time (PT), activated partial thromboplastin time (aPTT), and thromboelastography (TEG) tests. An increase in hematocrit or hemoglobin likely indicates a worsening plasma volume deficit. It also provides a baseline assessment for providers expecting surgical blood loss, critical illness anemia, and dilutional anemia due to fluid resuscitation.⁶⁵ A large percentage of patients with significant burns will develop coagulopathy during admission. Acute coagulopathy is an independent risk factor for in-hospital mortality even before fluid resuscitation.^66,67 Severe burn injuries also are prone to significant coagulopathy secondary to the hyperinflammatory nature of the burn injury.⁶⁶ In addition to PT, aPTT and TEG also may be useful to guide resuscitation and use of blood products, if necessary.⁶⁵

Draw an arterial blood gas (ABG) and chemistry panel to assess the presence of metabolic and respiratory acidosis. Within the first 48 hours of burn injury, acute kidney injury typically results from uncontrolled shock, under-resuscitation, and inflammatory processes. Rhabdomyolysis releases myoglobin (MB) from muscle cells, which blocks the renal tubules, causing constriction of the afferent arterioles and the release of free radicals, and further exacerbates acute kidney injury. Rhabdomyolysis may result from direct thermal injury or compartment syndrome within the first 24 hours and can be discovered by drawing a serum creatinine kinase and assessing for urine myoglobin. MB levels > 100 mg/dL create a dark, tea-colored urine.⁶⁷

Obtain an initial chest X-ray in all patients suspected of inhalation injury, despite the low sensitivity for parenchymal injury after smoke inhalation.⁴⁶ Another diagnostic option is a chest computed tomography (CT) that may reveal subtle differences in structural changes impairing pulmonary function.⁴⁶ One study used admission chest CT to measure bronchial wall thickness in suspected inhalation injury and found a correlation with the total number of ventilator days, intensive care unit days, and pneumonia.⁶⁸ Flexible fiberoptic bronchoscopy is the gold standard for diagnosing inhalation injury.^41,69 Bronchoscopy allows for direct visualization of the injured tissue and aids in diagnosing patients who would benefit from intubation. Bronchoscopic evidence of inhalation injury includes soot deposits, erythema, edema, mucosal blisters and erosions, hemorrhage, and bronchorrhea. The severity of the bronchoscopy findings correlates with mortality.^69,70

Carboxyhemoglobin (COHb) levels detect carbon monoxide poisoning. Use an ABG and pulse co-oximetry to measure the COHb level. There is a high correlation between arterial and venous COHb levels. Thus, if an ABG is unavailable, a venous blood gas will suffice.³⁴ The COHb level is not an absolute indicator of clinical severity, nor is rapid clearance of an elevated COHb level correlated with clinical improvement.⁷¹ A typical ratio of COHb to hemoglobin is up to 9% in smokers and 5% in nonsmokers. When interpreting COHb levels, consider time and duration of exposure, time from exposure to presentation, treatment, and clinical symptoms. Draw a chemistry panel to evaluate renal dysfunction or electrolyte abnormalities, since these are the most common laboratory abnormalities in burns.

Evaluate CN toxicity by assessing for the presence of a base deficit and elevated lactic acid levels. CN has a very short half-life, and serum levels are not reliable. For this reason, when serum levels are measured, the levels often are falsely low. In addition, not all facilities have CN testing readily available. Serum lactate levels increase proportionally with CN poisoning. A serum lactate level of 10 mmol/L in fire victims is a sensitive and specific indicator of CN poisoning.⁴⁶ An electrocardiogram (ECG) may provide clues to CN toxicity with an ST-elevation myocardial injury pattern or various arrhythmias from electrolyte abnormalities.

Management

As stated in the previous section, the initial management of a burn patient should be as with any other trauma patient, starting with ATLS and ABLS protocols, especially given that many burns have concurrent traumatic injuries. Consider inhalation injuries, particularly when assessing airway, breathing, and disability. Discover inhalation injuries early and act upon them quickly. There is no consensus on diagnostic criteria for inhalation injury in the clinical setting. Most often, the diagnosis is a subjective judgment. Note that intubation is not without risks. A study published in 2010 at a large burn center revealed that out of 879 intubation burn victims, more than 50% did not require intubation, as evidenced by their prompt extubation after admission.⁴¹

Current indications for intubation are full-thickness burns to the face or perioral region, circumferential neck burns, acute respiratory distress, progressive hoarseness, air hunger, respiratory depression, altered mental status, or supraglottic edema on bronchoscopy. Additionally, consider TBSA as another criterion. There is no standardized cut-off for %TBSA. However, ABLS recommends intubation in patients with > 30% TBSA burns.⁴¹ The ABLS recommendation stems from the generalized inflammatory response with resulting soft tissue edema from the extensive volume fluid resuscitation leading to airway edema and the levels of analgesia and sedation required to manage pain in patients with > 30% TBSA.⁴¹ Use an endotracheal tube (ETT) > 7.5 mm. Ensure airway adjuncts, such as bougie, laryngeal-mask airway, video laryngoscopy, and fiberoptic equipment, are readily available. Burns involving the head and neck may make intubation difficult, and in these circumstances, flexible fiberoptic bronchoscopy for awake intubation is the safest.⁴⁶

There is no consensus for initial ventilator settings. However, in a study published in 2021, patients with ARDS had a decreased severity and rapid resolution within the first week by implementing a high positive end-expiratory pressure (PEEP) strategy in mechanically ventilated burn patients.⁷² Additionally, permissive hypercapnia aids in lung-protective strategies by allowing lower tidal volumes (4-6 mL/kg ideal body weight) and lower airway pressures (< 30 cm H₂O) to decrease iatrogenic lung injury and barotrauma.⁴¹ Studies have found that the use of adjuncts, such as nebulized heparin or saline and humidified oxygen, can prevent airway obstruction from the thick casts formed by sloughed epithelium, mucous, and developing pseudomembranes.^41,73 Prophylactic antibiotics and steroids are not helpful.⁷³

CO and CN synergistically create increased tissue hypoxia, acidosis, and decreased cerebral oxygen consumption and metabolism. Initiate treatment for both in any patient with severe inhalation injury, unexplained hypotension, altered mental status, elevated lactic acid, or high mixed venous CO₂.^73,74 Initiate 100% oxygen by nonrebreather in all patients with suspected CO exposure. After consultation with a local hyperbaric oxygen therapy center, a medical toxicologist, or a regional poison center, initiate hyperbaric oxygen therapy if appropriate.⁷⁵ The half-life of COHb on room air at normal atmospheric pressure ranges from four hours on room air vs. < 60 minutes on 100% O₂ at atmospheric pressure.^24,73 Administer first-line treatment of hydroxocobalamin if cyanide poisoning is suspected.^73,76 Second-line therapies include sodium nitrite with sodium thiosulfate, being cautious of the side effects of hypotension and methemoglobinemia.⁷⁵

Burns that involve > 20% TBSA can cause shock. Fluid resuscitation is one of the vital lifesaving interventions in the early management of burn patients. Crystalloids are used for fluid resuscitation in the United States to counteract the intravascular hypovolemia of burn shock. Lactated Ringer’s solution is the most commonly used crystalloid in U.S. medical centers. Clinical trials of normal saline vs. plasma-lyte vs. lactated Ringer’s in non-burn patients have been contradictory.⁴⁶

Recent studies demonstrate that more restrictive fluid resuscitation may lead to better outcomes.⁷⁷ Even prior to determining TBSA, the ABA recommends initiating fluids for visibly large burns with two large bore venous catheters and initiating fluids at a rate of 500 mL per hour of lactated Ringer’s for those older than 14 years of age.⁷⁸ The three most commonly used formulas to help guide resuscitation are the ATLS guidelines, Parkland formula, and modified Brooke formula. There is no clear evidence of which formula has better outcomes. Thus, there is no official standard of care.⁷⁹ For all three formulas, half of the crystalloid volume is infused during the first eight hours post-burn and the remaining half is infused over the following 16 hours.³⁴ As opposed to the widely accepted Parkland formula, which recommends 4 mL × weight in kg × % TBSA (up to 50%) as the total volume of crystalloid required for resuscitation, both the modified Brooke formula and the ATLS guidelines recommend 2 mL × weight in kg × %TBSA, which should be used to help guide infusion rates and prevent over-resuscitation. Finally, studies such as that performed by Chung and colleagues brought forward what they call a “rule of tens” for adult patients in which the initial fluid rate equals the TBSA × 10, which provides an infusion rate between the Parkland and Brooke estimations for almost 90% of patients.⁴¹

The resuscitation of children uses separate formulas, including the Brooke formula of 3 mL/kg per TBSA of lactated Ringer’s for the first 24 hours, with half given over the first eight hours. The Shriners Cincinnati and Galveston formulas adjust to account for pediatric patients’ larger body surface area-to-weight ratio. They suggest upward of 3 mL/kg of body surface area, plus maintenance fluids, plus evaporative losses.⁴¹ In addition, children also are given 5% dextrose in half normal saline at a maintenance rate.^74,80

Although hypovolemia contributes to mortality in the early phases of burn shock, over-resuscitation can lead to increased edema formation and increased burn depth and coagulation zone. Fluid creep also can lead to pulmonary edema and abdominal compartment syndrome (ACS). ACS has a mortality of more than 80% in burn patients.^32,79 Early goal-directed therapy is of utmost importance in burn patients with > 20% TBSA by monitoring vital signs, urine output, serum lactate, base deficit, and inferior vena cava measurement by bedside ultrasound. Recommended urine output is 30 mL/h to 50 mL/h in adults and 1.0 mL/kg per hour to 2.0 mL/kg per hour in infants. High-dose vitamin C correlates with a decreased 24-hour fluid requirement, weight gain in edema in one study, and is an adjunct.⁸¹

Recent surveys identified that the United States has a shortage of practicing burn physicians; thus, if a burn patient develops compartment syndrome, nonburn physicians will need to be trained in escharotomies.⁸² All deep circumferential burns to the extremities can cause neurovascular compromise. An indication for emergency escharotomy/fasciotomy occurs when the patient has circumferential deep burns affecting the extremities or chest wall. When compartment syndrome involves the chest wall, ventilation issues occur because of decreased chest wall compliance. Losing pulses is a late finding in compartment syndrome affecting extremities.⁸³ Incisions for escharotomies of the extremities occur along the medial and lateral lines, with the extremity held in the anatomical position. Incisions for hand escharotomies occur along the second and fourth metacarpals. Do not perform incisions along the ulnar aspect of the thumb and the radial aspect of the index finger to avoid injuring the neurovascular bundle.⁸⁴

Hypothermia is a component of the lethal triad. Cooling the burn wounds may prevent further tissue damage and is effective if carried out within 20 minutes. Current recommendations are to use cold, running tap water on the burn. Do not use ice.⁸⁵ Do not delay definitive care to dress burn wounds. After the initial resuscitation and disposition have been established, dress the burn wounds with an antimicrobial agent because of the breach in the skin’s barrier and natural defense against common pathogens. For partial-thickness burns, the goal of topical agents is to reduce environmental factors causing pain and provide a hospitable environment for wound healing. Such choices include bacitracin, polymyxin B, mupirocin, mafenide acetate, silver-containing topical agents, and more. Deep burns commonly require silver-containing agents that penetrate the eschar and provide higher protection from infection if placed within 48 hours of the burn.^85,86

High-voltage electrical injuries (i.e., > 1,000 V) have a higher likelihood of traumatic injuries and severely damaged muscles. Therefore, have a low threshold for surgical consultation in patients with any signs of compartment syndrome. The fasciotomy rates and amputation of extremities are higher in high-voltage injuries (25%) than in low-voltage injuries (5%). In addition, there is an increased risk of rhabdomyolysis and myoglobinuria causing renal injury due to either direct muscle injury or resulting from compartment syndrome. Estimating TBSA is more difficult in these patients because deep burns are hard to identify and quantify. Thus, fluid resuscitation for electric burns is double the standard, with urine output goals of 50-100 mL/hr. Cardiac arrhythmias, such as ventricular fibrillation and asystole, also are common. Therefore, place the patient on continuous telemetry for at least 24 hours.^32,40

Chemical burns are a rare circumstance during which airway, breathing, and circulation are not prioritized first. Decontamination is the most critical first step, which includes removing the offending agent from contact with the patient, removing clothing, and often providing copious irrigation. Irrigation begins with the eyes and face, preventing further inhalation or ingestion of the toxin. Irrigation of the patient involves a large-volume shower or decontamination station with appropriate drains to avoid additional exposure to the chemicals. Immediate and copious irrigation reduces the extent and depth of the injury. The use of neutralizing agents is controversial because they can produce exothermic and thermal reactions that worsen the injury. Hydrofluoric acid burns are the exception, for which calcium gluconate is used for irrigation. After irrigation, manage wounds with the same principles of burn care.⁴⁰

Thoroughly irrigate corneal injuries because it is difficult to ascertain whether the cause was thermal or gaseous material. Continue frequent and copious eye irrigation if a chemical eye injury is known. Evert and examine the upper and lower eyelids. Alkali injuries may require irrigation for several hours. During irrigation, test the wound pH after waiting for two to five minutes from stopping irrigation, preventing false results. Morgan lenses are a helpful adjunct for eye irrigation.⁸⁵ Orbital compartment syndrome can develop in the first 24-96 hours following large-volume resuscitation or from full-thickness burns to the periorbital skin.⁸⁶ Monitor intraocular pressures in suspected orbital compartment syndromes. Levels > 30 mmHg indicate the need for compartment release with lateral canthotomy.^41,77

For initial management of a patient with suspected frostbite, remove jewelry. The injured areas often are insensate and need protection from trauma. Rewarming in the field should not be pursued until the affected tissue can remain thawed, and there is no risk of refreezing, since refreezing directly affects morbidity. Also, systemic hypothermia may be present and requires treatment before frostbite, since this results in peripheral vasoconstriction, which may exacerbate the frostbite injury.

It is important to remember that frostbite injuries can be extremely painful, and an appropriate level of analgesia should be provided prior to manipulation. Traditional recommendations include placing the affected area in a water bath with a temperature of 40-42°C. The duration of re-warming is approximately 30 minutes or until the return of sensation and flushing at the most distal aspect of the affected region.

Unroofing the blisters remains a controversial topic, with insufficient data to make recommendations. Clear or cloudy blisters may contain prostaglandins and thromboxanes, causing further damage to the underlying tissue and requiring drainage of the blister. Hemorrhagic blisters are thought to extend into the vascular plexus and may signify more profound damage. Hemorrhagic blisters typically are not drained. After rewarming, currently recommended therapies include ibuprofen twice daily to inhibit harmful prostaglandins, aloe vera, and tissue plasminogen activator (tPA) if used within 24 hours of thaw. tPA has demonstrated improvement in digit salvage. Unless the patient is exhibiting signs of sepsis, amputation should be delayed after frostbite, since complete demarcation may not occur for one to three months.^25,37,38,41

Disposition

Identifying burn patients appropriate for transfer to a burn facility correlates with improved morbidity and mortality. Additionally, consider the need for specialists, including nephrology for renal replacement therapy, ophthalmology for eye injuries, and trauma surgery or orthopedic surgery for traumatic injuries. The American Burn Association has referral guidelines indicating those patients who require transfer to a burn center.

If the patient requires a transfer, it is crucial to communicate effectively between the transferring unit and the burn center. Review the ABCs of the trauma resuscitation with the accepting provider, including the most recent vital signs and significant physical exam findings.

Stabilize the patient before transportation. A patient with a severe burn requires a minimum of two intravenous catheters, preferably in an unburned upper extremity, a Foley catheter in place, and a nasogastric tube for decompression preventing distention from a gastric ileus. The patient also should have a rectal temperature probe to maintain body temperature between 38°C and 39°C with assistance from active and passive rewarming agents. After addressing any wounds requiring escharotomies, open chest wounds, and any active bleeding, wound management before transport is limited to applying clean, non-adherent dressings. Many burn centers recommend placing a clean, dry sheet over the burns. More definitive wound management with topical antimicrobial agents or biologic dressings should occur after the disposition is made and the patient is transported to a burn center.⁴¹

Summary

After receiving a thorough history from emergency personnel regarding type and duration of exposure, treat all burn patients as trauma patients, with ATLS or ABLS protocols evaluating and securing ABCDEs (airway, breathing, circulation, disability, exposure) during the initial phase of resuscitation. Consider additional traumatic injuries, inhalation injuries, and eye injuries, since these are subtle and may be missed. Have a high suspicion for compartment syndrome in heavily burned patients and evaluate for circumferential burns. The cause of a burn injury determines the treatment approach. The depth of the wound and TBSA are paramount to the fluid resuscitation protocol, the decision to transfer, the morbidity and mortality of the injury, and the need for long-term care. See Table 1 for a review of key aspects of the initial burn resuscitation and the American Burn Association’s recommendations for transfer to a burn center.

REFERENCES

1. Crowe CS, Massenburg BB, Morrison SD, et al. Trends of burn injury in the United States. Ann Surg 2019;270:944-953.
2. Mason SA, Nathens AB, Byrne JP, et al. Increased rate of long-term mortality among burn survivors: A population-based matched cohort study. Ann Surg 2019;269:1192-1199.
3. Brigham PA, McLoughlin E. Burn incidence and medical care use in the United States: Estimates, trends, and data sources. J Burn Care Rehabil 1996;17:95-107.
4. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics. National Hospital Ambulatory Medical Care Survey: 2018 Emergency Department Summary Tables. October 2021.
5. National Center for Injury Prevention and Control, NEISS All Injury Program operated by the Consumer Product Safety Commission for numbers of injuries. Bureau of Census for population estimates.
6. American Burn Association. Burn Injury Fact Sheet. Published February 2018. https://ameriburn.org/wp-content/uploads/2017/12/nbaw-factsheet_121417-1.pdf
7. American Burn Association. National Burn Repository 2019 Update. Report of data from 2009-2018. Ameriburn.org
8. National Burn Repository 2017 Update: Report of data from 2008-2017. Chicago: American Burn Association.
9. World Health Organization. Burns. Published March 6, 2018. https://www.who.int/news-room/fact-sheets/detail/burns
10. Padalko A, Cristall N, Gawaziuk JP, Logsetty S. Social complexity and risk for pediatric burn injury: A systematic review. J Burn Care Res 2019;40:478-499.
11. U.S. Fire Administration. U.S. fire deaths, fire death rates, and risk of dying in a fire. Published Nov. 15, 2021. https://www.usfa.fema.gov/data/statistics/fire_death_rates.html
12. Warda L, Tenenbein M, Moffatt ME. House fire injury prevention update. Part I. A review of risk factors for fatal and non-fatal house fire injury. Inj Prev 1999;5:145-150.
13. McGwin G Jr, Chapman V, Rousculp M, et al. The epidemiology of fire-related deaths in Alabama, 1992-1997. J Burn Care Rehabil 2000;21:75-83.
14. Gerson L, Wingard D. Fire deaths and drinking: Data from the Ontario Fire Reporting System. Am J Drug Alcohol Abuse 1979;6:125-133.
15. Squires T, Busuttil A. Alcohol and house fire fatalities in Scotland, 1980-1990. Med Sci Law 1997;37:321-325.
16. Phelan T. National Fire Protection Association (NFPA) 1600, 2007, and 2010. In: Encyclopedia of Crisis Management. SAGE Publications, Inc. http://dx.doi.org/10.4135/9781452275956.n220
17. Kegler SR, Dellinger AM, Ballesteros MF, Tsai J. Decreasing residential fire death rates and the association with the prevalence of adult cigarette smoking — United States, 1999-2015. J Safety Res 2018;67:197-201.
18. Brigham PA, McLoughlin E. Burn incidence and medical care use in the United States: Estimates, trends, and data sources. J Burn Care Rehabil 1996;17:95-107.
19. Ahuja RB, Bhattacharya S, Rai A. Changing trends of an endemic trauma. Burns 2009;35:650-656.
20. Peck MD, Shankar V, Bangdiwala SI. Trends in injury-related deaths before and after dissolution of the Union of Soviet Socialist Republics. Int J Inj Contr Saf Promot 2007;14:139-151.
21. Billock RM, Chounthirath T, Smith GA. Pediatric firework-related injuries presenting to United States emergency departments, 1990-2014. Clin Pediatr 2017;56:535-544.
22. McFarland LV, Harris JR, Kobayashi JM, Dicker RC. Risk factors for fireworks-related injury in Washington State. JAMA 1984;251:3251-3254.
23. Berger LR, Kalishman S, Rivara FP. Injuries from fireworks. Pediatrics 1985;75:877-882.
24. Jeschke MG, Kamolz L-P, Sjöberg F, Wolf SE. Handbook of Burns, 2nd ed. Vol 1. 2020. Springer 2020.
25. Roeder PG. The Ties that bind: Aid, trade, and political compliance in Soviet-Third World relations. International Studies Quarterly 1985;29:191.
26. Miller SF, Bessey PQ, Schurr MJ, et al. National Burn Repository 2005: A ten-year review. J Burn Care Res 2006;27:411-436.
27. Saffle JR, Davis B, Williams P. Recent outcomes in the treatment of burn injury in the United States: A report from the American Burn Association Patient Registry. J Burn Care Rehabil 1995;16:219-232.
28. Santos JV, Oliveira A, Costa-Pereira A, et al. Burden of burns in Portugal, 2000-2013: A clinical and economic analysis of 26,447 hospitalisations. Burns 2016;42:891-900.
29. Nielson CB, Duethman NC, Howard JM, et al. Burns. J Burn Care Res 2017;38:e469-e481.
30. Alden NE, Bessey PQ, Rabbitts A, et al. Tap water scalds among seniors and the elderly: Socio-economics and implications for prevention. Burns 2007;33:666-669.
31. Blakeney P, Meyer W, Moore P, et al. Social competence and behavioral problems of pediatric survivors of burns. J Burn Care Rehabil 1993;14:65-72.
32. Jeschke MG, van Baar ME, Choudhry MA, et al. Burn injury. Nat Rev Dis Primers 2020;6:11.
33. Rae L, Fidler P, Gibran N. The physiologic basis of burn shock and the need for aggressive fluid resuscitation. Crit Care Clin 2016;32:491-505.
34. Stapczynski JS, Ma OJ, Tintinalli JE, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill Education/Medical; 2019.
35. Nielson CB, Duethman NC, Howard JM, et al. Burns. J Burn Care Res 2017;38:e469-e481.
36. El Khatib A, Jeschke MG. Contemporary aspects of burn care. Medicina 2021;57:386.
37. Basit H, Wallen TJ, Dudley C. Frostbite. In: StatPearls. StatPearls Publishing. July 2021.
38. McIntosh SE, Freer L, Grissom CK, et al. Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Frostbite: 2019 Update. Wilderness Environ Med 2019;30:S19-S32.
39. Yano K, Hata Y, Matsuka K, et al. Effects of washing with a neutralizing agent on alkaline skin injuries in an experimental model. Burns 1994;20:36-39.
40. Friedstat J, Brown DA, Levi B. Chemical, electrical, and radiation injuries. Clin Plast Surg 2017;44:657-669.
41. Herndon D. Total Burn Care. 5th ed. Elsevier; 2018.
42. Ritenour AE, Morton MJ, McManus JG, et al. Lightning injury: A review. Burns 2008;34:585-594.
43. Holle RL. Recent studies of lightning safety and demographics. 22nd International Lightning Detection Conference; 4th International Lightning Meteorology Conference; 2012. https://www.vaisala.com/sites/default/files/documents/Recent%20Studies%20of%20Lightning%20Safety%20and%20Demographics.pdf
44. Cherington M, Walker J, Boyson M, et al. Closing the gap on the actual numbers of lightning casualties and deaths. 11th Conference on Applied Climatology, Dallas, TX, American Meteorological Society.
45. Foncerrada G, Culnan DM, Capek KD, et al. Inhalation injury in the burned patient. Ann Plast Surg 2018;80(3 Suppl 2):S98-S105.
46. Otterness K, Ahn C. Emergency department management of smoke inhalation injury in adults. Emerg Med Pract 2018;20:1-24.
47. Cai AR, Hodgman EI, Kumar PB, et al. Evaluating pre burn center intubation practices: An update. J Burn Care Res 2017;38:e23-e29.
48. Vivó C, Galeiras R, del Caz MDP. Initial evaluation and management of the critical burn patient. Med Intensiva 2016;40:49-59.
49. Gigengack RK, Cleffken BI, Loer SA. Advances in airway management and mechanical ventilation in inhalation injury. Curr Opin Anaesthesiol 2020;33:774-780.
50. Dyson K, Baker P, Garcia N, et al. To intubate or not to intubate? Predictors of inhalation injury in burn‐injured patients before arrival at the burn centre. Emerg Med Australas 2020;33:262-269.
51. Jeschke MG, Kamolz L-P, Sjöberg F, Wolf SE. Handbook of Burns. 2nd ed. 2020.
52. Matsumura K, Yamamoto R, Kamagata T, et al. A novel scale for predicting delayed intubation in patients with inhalation injury. Burns 2020;46:1201-1207.
53. Coban YK. Rhabdomyolysis, compartment syndrome and thermal injury. World J Crit Care Med 2014;3:1.
54. Borhani-Khomani K, Partoft S, Holmgaard R. Assessment of burn size in obese adults; a literature review. J Plast Surg Hand Surg 2017;51:375-380.
55. Swords DS, Hadley ED, Swett KR, Pranikoff T. Total body surface area overestimation at referring institutions in children transferred to a burn center. Am Surg 2015;81:56-63.
56. Pham C, Collier Z, Gillenwater J. Changing the way we think about burn size estimation. J Burn Care Res 2019;40:1-11.
57. Mataro I, Lanza A, Di Franco S, et al. Releasing burn-induced compartment syndrome by enzymatic escharotomy-debridement: A case study. J Burn Care Res 2020;41:1097-1103.
58. Brandão RA, St. John JM, Langan TM, et al. Acute compartment syndrome of the foot due to frostbite: Literature review and case report. J Foot Ankle Surg 2018;57:382-387.
59. Koumbourlis AC. Electrical injuries. Crit Care Med 2002;30(Suppl):S424-S430.
60. Davis C, Engeln A, Johnson EL, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of lightning injuries: 2014 update. Wilderness Environ Med 2014;25(4Suppl):S86-S95.
61. Mutter E, Langley A. Cutaneous Lichtenberg figures from lightning strike. CMAJ 2019;191:E260.
62. Orso D, Paoli I, Piani T, et al. Accuracy of ultrasonographic measurements of inferior vena cava to determine fluid responsiveness: A systematic review and meta-analysis. J Intensive Care Med 2020;35:354-363.
63. Sherren PB, Hussey J, Martin R, et al. Lethal triad in severe burns. Burns 2014;40:1492-1496.
64. Sen S, Hsei L, Tran N, et al. Early clinical complete blood count changes in severe burn injuries. Burns 2019;45:97-102.
65. Sherren PB, Hussey J, Martin R, et al. Acute burn induced coagulopathy. Burns 2013;39:1157-1161.
66. Kaita Y, Nishimura H, Tanaka Y, et al. Effect of acute coagulopathy before fluid administration in mortality for burned patients. Burns 2021;47:805-811.
67. Coban YK. Rhabdomyolysis, compartment syndrome and thermal injury. World J Crit Care Med 2014;3:1.
68. Yamamura H, Kaga S, Kaneda K, Mizobata Y. Chest computed tomography performed on admission helps predict the severity of smoke-inhalation injury. Crit Care 2013;17:R95.
69. Walker PF, Buehner MF, Wood LA, et al. Diagnosis and management of inhalation injury: An updated review. Crit Care 2015;19:351.
70. Albright JM, Davis CS, Bird MD, et al. The acute pulmonary inflammatory response to the graded severity of smoke inhalation injury. Crit Care Med 2012;40:1113-1121.
71. Grieb G, Groger A, Bozkurt A, et al. The diversity of carbon monoxide intoxication: Medical courses can differ extremely—A case report. Inhal Toxicol 2008;20:911-915.
72. Perry T, Pinette W, Miner J, et al. Outcomes in ventilated burn patients with acute respiratory distress syndrome: An evaluation of early high-PEEP strategy using Berlin criteria. J Burn Care Res 2021;Sep 14. doi: 10.1093/jbcr/irab169. [Online ahead of print].
73. Deutsch CJ, Tan A, Smailes S, Dziewulski P. The diagnosis and management of inhalation injury: An evidence based approach. Burns 2018;44:1040-1051.
74. Palmieri TL. Pediatric burn resuscitation. Crit Care Clin 2016;32:547-559.
75. Gigengack RK, Cleffken BI, Loer SA. Advances in airway management and mechanical ventilation in inhalation injury. Curr Opin Anaesthesiol 2020;33:774-780.
76. Nguyen L, Afshari A, Kahn SA, et al. Utility and outcomes of hydroxocobalamin use in smoke inhalation patients. Burns 2017;43:107-113.
77. Daniels M, Fuchs PC, Lefering R, et al. Is the Parkland formula still the best method for determining the fluid resuscitation volume in adults for the first 24 hours after injury? — A retrospective analysis of burn patients in Germany. Burns 2021;47:914-921.
78. American Burn Association. Advanced Burn Life Support Course. Provider Manual 2018 Update. http://ameriburn.org/wp-content/uploads/2019/08/2018-abls-providermanual.pdf
79. Boehm D, Menke H. A history of fluid management—From “one size fits all” to an individualized fluid therapy in burn resuscitation. Medicina 2021;57:187.
80. Gillenwater J, Garner W. Acute fluid management of large burns: Pathophysiology, monitoring, and resuscitation. Clin Plast Surg 2017;44:495-503.
81. Rizzo JA, Rowan MP, Driscoll IR, et al. Vitamin C in burn resuscitation. Crit Care Clin 2016;32:539-546.
82. Butts CC, Holmes JH, Carter JE. Surgical escharotomy and decompressive therapies in burns. J Burn Care Res 2020;41:263-269.
83. Tolles J. Emergency department management of patients with thermal burns. Emerg Med Pract 2018;20:1-24.
84. de Barros MEPM, Coltro PS, Hetem CMC, et al. Revisiting escharotomy in patients with burns in extremities. J Burn Care Res 2017;38:e691-e698.
85. Roshangar L, Rad JS, Kheirjou R, et al. Burns: Review of molecular mechanisms and therapeutic approaches. Wounds 2019;31:308-315.
86. Wang Y, Beekman J, Hew J, et al. Burn injury: Challenges and advances in burn wound healing, infection, pain and scarring. Adv Drug Deliv Rev 2018;123:3-17.
87. American Burn Association. Burn center referral criteria. Advanced Burn Life Support. https://ameriburn.org/wp-content/uploads/2017/05/burncenterreferralcriteria.pdf