ANNUALLY, AN ESTIMATED 11 MILLION INDIVIDUALS worldwide and 400,000 in the United States experience a burn injury.¹ In the past decade, the mortality rate in the United States was 3.3%. Survival rates have improved over the past few decades because of increased understanding of the cellular and systemic response to burns, advances in critical and surgical care, and prevention efforts in work, home, and recreational activities. Currently, the median lethal dose (LD-50) are burns which affect 70% total body surface area (TBSA).² Burn injury is one of the leading causes of disability worldwide (as measured by disability-adjusted life years), and particularly affects low- and middle-income countries.¹ Burn injuries present a unique constellation of rehabilitation issues, which include hypertrophic scarring, contractures, pain, and mobility impairments. Other complications include neuropathies, temperature regulation dysfunction, pruritis, bony abnormalities, psychological impairments, and community integration deficits.

Of the 450,000 burn injuries in the United States that receive medical treatment each year, 40,000 require hospitalization. Approximately 75% of hospitalized burn patients are treated at specialty burn centers.³ The survival rate for those treated at a burn center is 96.6%.³ Higher mortality is associated with older age, inhalation injury, and burn size. The mortality rate for burns outside of the United States is higher at 4.8% and varies by geography.^2,4 In the 2014 National Burn Repository report, which collected and analyzed available US hospital data between 2004 and 2013, the distribution of burn etiologies were: 43% from fire/flame, 34% from scald, 9% from hot object contact, 4% from electric, and 3% from chemicals. The etiology frequencies were similar in all age groups except in children less than 5 years, where scalds and contact burns were the most common etiologies.²

The majority of burn injuries occur in men (69%). The average age of the burn population is 32 years. Children younger than 16 years comprised 29% of burn cases and adults older than 60 years comprised 13% of burn cases. Approximately 73% of the burn injuries were reported to occur at home and 71% were reported to be accidental. The large majority of burn injuries (78%) had a TBSA burn less than 20%. In the United States, burns are most common in Caucasians (58.9%), followed by Blacks (19.7%), Hispanics (14.0%), Asians (2.4%), and Native Americans (0.8%).²

Burn injuries result in unique physiologic changes at the cellular, local, and systemic levels. This is a robust area of current investigation; nonetheless, general knowledge of burn physiology helps one understand the principles of burn care.

Local Response to Burns

There are three locally affected zones after burn injury, originally described in 1947 as: (1) the zone of coagulation, (2) zone of stasis, and (3) zone of hyperemia. The zone of coagulation contains permanently damaged tissue that is often at the center of burn injury. The zone of stasis has reduced perfusion; however, the tissue in this zone is salvageable within a few days after injury if properly managed by a skilled burn team, and this area is often the target of burn care management. The zone of hyperemia, which is the most peripheral by comparison, has increased perfusion from vasodilation and inflammation.^5–7

Contact with temperatures greater than 40°C results in protein denaturation, resulting in tissue damage on contact; overall tissue damage is dependent on temperature and duration of exposure.^7–9 Further damage results from enzymatic and free radical activation. At the cellular level, there are a number of complex physiologic changes that occur after a burn injury. Vasoconstriction initially occurs followed by vasodilation. Locally, histamine release contributes to increased vascular leakage into the extravascular space; additionally, serotonin, prostaglandins, thromboxane, kinins, catecholamines, bradykinin, nitric acid, TNF-α, interleukins, and other inflammatory mediators are released and contribute to the injury cascade at the site of injury.⁷ The neutrophils that migrate to the wound site are primed and produce reactive oxygen species in burned tissue; reactive nitrogen species also contribute to oxidative free radical damage.^9,10 Complement and coagulation systems are activated along with neutrophils, increasing free oxygen radicals at the site of injury and thrombosis.^8,9 These processes are accompanied by the cytokine-mediated systemic inflammatory response.

Systemic Response to Burns

In addition to the local effects, burn injuries create a systemic inflammatory response through the release of cytokines. This process begins immediately after injury and can persist for weeks and sometimes months after injury in larger burns (i.e., TBSA greater than 30%). The released cytokines produce a number of effects, including cardiovascular, respiratory, metabolic, and immunologic changes.⁶ Following a significant burn injury, oxygen consumption, cardiac output, and glucose tolerance are lowered, resulting in shock. At day 5 post-injury, these factors plateau, and for the next year, a hypermetabolic, catabolic state exists for burns greater than 30% TBSA.¹¹ During burn shock, patients require a large amount of volume for adequate perfusion of end organs due to increased capillary perfusion, leakage of intravascular volume into extravascular space, and insensible fluid losses due to loss of skin barrier.

After shock has been managed with fluid resuscitation and vasopressor medications as needed, a number of metabolic changes persist. Proinflammatory cytokines, such as IL-6, IL-8, IL-1β, IL-13, GM-CSF, IL-5, and IL-7 are increased during the first week after burn injury. To counteract the proinflammatory state, anti-inflammatory cytokines, including IL-10, IL-12, G-CSF, IL-17, IL-4, and IFN-γ are also elevated.¹² The persistent hypermetabolic state results in increased protein catabolism with subsequent reduced body weight, lean body mass, and bone mineral content; additionally, insulin resistance, reduced hormone levels (GH, IGF-I, T4), and increased cortisol and liver size are noted.¹³ While these physiologic changes can persist for a year or more, many of these changes improve by 24 months after injury.¹⁴

In the initial days and weeks following burn injury, many of the physiological changes are managed clinically. Maintenance of nutritional support is important to prevent wasting. A warm environment at 28 to 33°C reduces energy loss due to insensible losses. Addressing hormonal and catecholamine changes with pharmaceuticals is important; oxandrolone, a testosterone analog, helps mitigate the catabolic effects and propranolol improves tachycardia.^11,15 Oxandrolone has been found to improve lean body mass, strength and bone mineral densities¹⁵ and propranolol has been found to reverse muscle-protein catabolism.¹⁶ For patients with inhalation injury, mechanical ventilation is often required; inhalation injury is an independent risk factor for mortality.¹⁷

Burns are classified according to etiology as well as depth and size of injury. These factors play a role in assessing the severity of burn (Fig. 87–1).

Etiology

The etiologies of burn are thermal, electrical, chemical, and radiation. Thermal injuries involve the transfer of heat to the skin and underlying tissue. The types of thermal injuries are scald, flame, and contact. Wet heat causes significant injury due to the higher conduction of water compared to air and can injure deeper structures.^6,18 Radiation burns occur after close proximity to a radioactive source and can appear days later in a physical appearance similar to a thermal burn.¹⁹

Contact with an electrical current causes electrical burns, particularly when a current passes through the skin from an entry point to an exit point. The severity of the burn injury is based on the voltage. Domestic electric burns are currents of low voltage, whereas high-tension electric currents have a voltage greater than or equal to 1,000 V. High-tension burns involve extensive tissue and organ damage, and voltage greater than 70,000 V is fatal. Flash injury, alternatively, is caused by exposure to a high-voltage current arc without a current actually passing through the body; superficial burns typically result. With electric burns, cardiac health is of primary concern and amputation is common.⁶

Contact with acidic or alkali chemicals causes chemical burn injury; failure to remove the chemical causes continued injury to the skin tissue. Alkali chemicals, such as cement, typically cause worse burn injury compared to acidic chemicals. Some chemicals require specific management, such as neutralization.⁶

Staging Burns

Burn injuries are staged in a number of ways based on depth and percent of total body surface area involved. Each of these factors contributes to the characterization of the burn and recovery process.¹⁸ Burn injury is an evolving process, particularly in the initial days after injury; as a result, the classification of burn depth and size may change after initial assessment.⁷

The depth of the burn previously was described as a first, second, third, or fourth degree based on amount of skin and subcutaneous tissue penetration (Figs. 87–2 and 87–3). More accurately, this terminology has been replaced by describing the anatomic involvement, of which there are four descriptors as noted in Table 87–1.^7,18

There are three scales traditionally used to estimate the size of injury: Wallace rule of nines, palmar surface, and Lund and Browder. The Wallace rule of nines has been used as a brief bedside assessment for determining the TBSA involved in both the adult and pediatric population, taking into account the proportion of a child’s head and legs compared to those of an adult. However, while this scale can be used as an estimate, it is often not accurate and requires further investigation. The second scale used to estimate burn size uses the palmar surface of the patient, which is almost 1% of the TBSA and works well to estimate small burns. The most accurate scale for measuring burn size is the Lund and Browder chart (Fig. 87–4).^20,21

Initial Treatment

Initial management after burn injury is basic life support protocols, including assessment of airway, breathing, and circulation, in addition to removal of the inciting event (such as removing burned clothing to stop the burning process). Burn patients are kept warm to prevent fluid and heat loss and visible wounds are covered to prevent bacterial colonization. Application of water to wounds is used to reduce pain and remove chemicals from the skin or eyes. Attention to the circumstances of the burn injury is important to help identify potential complications, such as inhalation injury.^9,22,23 Tetanus prophylaxis is provided.²³

Patients with burns greater than 15% to 20% TBSA are recommended to undergo aggressive fluid resuscitation. While a number of different formulas exist to calculate the total amount of fluid required, the most commonly used formula is the Parkland protocol (Table 87–2). Of the total calculated amount of fluid, 50% is given in the first 8 hours, and the remainder is given in the following 16 hours. However, recent critiques of this strategy demonstrate that the formula can cause over-resuscitation, which is associated with worse outcomes. To insure adequate hydration, end-organ perfusion, and oxygenation, urine output is monitored (goal: 1.0 mL/kg/h or 30–50 cc/h). Patients are monitored closely and fluid adjustments are made as necessary as fluid requirements may change with deeper injuries and inhalation injury. On a case-by-case basis, immediate surgery may be necessary to prevent further injury. For example, circumferential burns injury often requires urgent debridement, escharotomy, or fasciotomy to prevent ischemia to the affected limb (see Fig. 87–5).⁹

Long-Term Treatment

Hospitalized burn patients require careful monitoring for optimal treatment. Central line catheters may be needed for hemodynamic monitoring, urinary catheters may be needed for assessment of output, and nasogastric tubes may be required for enteral feeding.²⁴ Additional fluid resuscitation may be necessary after the initial 24 hours, as reduced cardiac output is a common phenomenon in the early post-burn injury phase.²⁵

Patients should be washed with nonalcoholic-based solutions to fully evaluate the size and depth of injury. Superficial and superficial partial-thickness burns may require debridement; topical antimicrobial agents maintain a sterile, supportive healing environment. A number of topical agents and dressing products are available and may be tailored to optimize wound healing.^22,23 Deep partial and full-thickness burns typically require debridement, or removal of nonviable tissue, and grafting. Debridement allows optimal wound healing, prevention of bacterial invasion, and provides an appropriate wound bed for grafting.

Grafting serves many purposes. In order for a graft to be successful, the wound bed must be clean and healthy.²³ There are different types of grafts used. Allografts, including xenografts and cadaveric grafts, are used to temporarily cover the wound bed in larger burns to allow the bed to begin healing while preventing fluid loss and infection.^9,24,26 Bioengineered skin substitutes are also used for temporary wound coverage and their role as long-term skin substitutes is an active area of research.^9,24,26,27 A recent review found that Biobrane® and TransCyte® were more effective than silver sulfadiazine for partial-thickness burns affecting less than 15% of TBSA, whereas allogenic cultured skin and Apligraf® with autograft were effective for TBSA of 20% to 50%.²⁶ Autografts are the gold standard but are fragile and at risk for failure.^9,24,26,27 Split-thickness autografts are meshed to cover greater surface area but are cosmetically not as desirable as full-thickness autografts.^9,24

In addition, careful attention to nutritional status is needed to optimize healing, especially for larger burns that experience a hypermetabolic state. Gastric feeding to maintain caloric balance is recommended within the first 24 hours after injury. Nutritional requirements are calculated by indirect calorimetry and goals include nonprotein kilocalorie-to-nitrogen ratio of 100:1 and 2 grams of protein/kg/day. Careful monitoring of weight, prealbumin, and albumin levels is performed to assess for malnutrition. Both malnutrition and anemia contribute to poor wound healing.^9,23,28 The most common acute care burn complications include pneumonia, cellulitis, and urinary tract infections; patients are monitored for wound infection and septicemia.^2,23 Other common complications include functional impairments such as hypertrophic scarring, contractures, pain, debility, and gait abnormalities, which are discussed in detail below. In addition, other functional complications may include dysphagia, neuropathy, pruritis, body temperature dysregulation, heterotopic ossification, anxiety, post-traumatic stress, depression, as well as challenges in community reintegration.²⁹

Hypertrophic Scarring

Scarring after burn injury impacts function, quality of life, and symptoms. Hypertrophic scarring is characterized by rigid, raised, erythematous tissue after a burn injury that, unlike keloid scarring, is within the border of the original wound.^30–32 Hypertrophic scarring results from a disorganized active proliferative phase involving increased collagen deposition during wound healing and an imbalance between matrix formation and remodeling (Fig. 87–6).^33–35