experimentation, risk-taking, and employment.6 Intentional burns account for around 10% of all cases of

child abuse.7 Scalds from hot bath immersion are the most frequent cause of these cases. Other common

etiologies of intentional burns include contact with heated objects including cigarettes, irons, and heated

kitchen utensils.

Adults

In contrast to the pediatric population, flame burns are the most common cause of burns in adults and

the elderly. Flame burns account for 35% to 42% of hospital admissions in adults, while scald burns

account for 15% to 18% of hospital admissions related to burn injuries.3 Cigarette ignition of

upholstered furniture or bedding accounts for 47% of fires and alcohol appears to be a significant

contributor.8

Elderly

The elderly (defined by age greater than 65 years) suffer a disproportionately higher percentage of

hospitalizations due to burns in comparison to the general adult population. A 10-year analysis from

1995 to 2005 using data from the National Burn Repository showed that individuals over the age of 65

comprised 12% of all burn unit admissions and that the average age of those admitted was 76 ± 7

years.9 The most frequent cause of burns that led to death in elderly women was a result of clothing

ignition during cooking.10 Elderly burn patients treated for scald burns had relatively small burns

(<13% of total body surface area [TBSA]) but high mortality rates (30%).11–13 Overall, burns are the

fourth leading cause of mortality in the elderly population. Together, these results suggest that the

medical, economic, and social burdens of burn will likely increase as the general population continues to

age.

Race and Ethnicity

Differences also exist in the susceptibility to burns by race and ethnicity. Burns are the leading cause of

injury-related death in Black children between the ages of 1 and 9 and the rates are 2.7 times higher

than in White, Hispanic, and Asian/Pacific Islander children.14 Likewise, in adults, the rate of nonfatal

burns in Black Americans aged 35 to 39 years was 221 per 100,000 Blacks, which is remarkably higher

than the 135 per 100,000 Whites with burns in the same age group.3 The emergency room visit rate for

burns from 1993 to 2004 in the United States was 62% greater among Black Americans (340 per

100,000 Black Americans) than White Americans (210 per 100,000 White Americans).15 The ageadjusted death rate from burns of all causes in the United States in 2006 was highest in Blacks (2.4 per

100,000) and lowest in Asians (0.4 per 100,000), with Native Americans (1.5 per 100,000), White nonHispanics (1.1 per 100,000), and Hispanics (0.8 per 100,000) falling in between this range.3 These

trends can be translated to the elderly population, as the mortality rate for burn-related injuries in the

elderly was 4.6 times greater in Black Americans than in White Americans.16

There are also significant differences in the gender distribution of burns between age groups. Adult

men more frequently seek care in the emergency department (69%). This may be due to the increased

severity of their burns caused by industrial accidents, compared to women (31%).6 Elderly are also

more highly represented among older burn victims than in younger populations.17,18 The greater

preponderance of older women with burn injuries reflects the decrease in workplace-related injuries

among the geriatric population.

Socioeconomic Status

Socioeconomic status (SES) factors such as low household income, crowded household living conditions,

and unemployment also increase the risk of burns. In the metropolitan Oklahoma City, Oklahoma, the

overall fire-related hospitalization and death rate was 3.6 per 100,000.19 Stratification of the data based

on household income, property values, and quality of housing demonstrated that the injury rate in

lower SES was 15.3 per 100,000.20 The proportion of children in the lowest SES groups requiring

hospitalization for treatment in US burn centers is twice the proportion of all children in the general

population.3 Furthermore, the incidence of house fires was eight times greater in low income families

compared to high incomes.21 The higher incidence of house fires has been attributed to the frequent

absence of functioning smoke detectors.21 Together, these results highlight the increased need for

education and prevention campaigns for lower SES groups to reduce household fires and burn injuries.

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ETIOLOGY

Numerous modalities, including fire or flame, scalds, contact, electrical conduction, and chemicals can

produce burns. Between 2002 and 2011, 44% of burns were produced by fire or flame, 33% by scald,

9% by contact, 4% by electricity, 3% by chemical, and 7% defined as other.

Burns are caused by contact of heat, cold, or chemicals with the cutaneous surface of the skin. The

depth of the burn injury is proportional to the temperature and duration of exposure. Burn depth is also

dependent on the body region due to differences in skin thickness and blood flow.

Scald burns are most commonly caused by water in the community. Once the water temperature

exceeds 156°F, only 1 second is needed for a full-thickness burn injury. The difference in contact time

underlines the importance of making sure hot water heaters are set at a low enough temperature to

minimize childhood bath and shower scald injuries (120°F). It takes 3 minutes for a burn to occur from

120°F whereas it takes only 1 second for a burn to occur from 156°F water.

Though water scalds do not always cause full-thickness injury due to the variation in temperature,

grease burns almost uniformly cause a deep partial- or full-thickness burn. Grease is usually 400°F and

thus even minimal exposure will cause significant thermal injury. Tar and asphalt also exceed 400°F to

500°F making them a high burn injury risk for industrial workers. Water and grease injury sites should

be cleansed with aqueous solutions. Tar, however, requires a petroleum-based solution to remove it

from the burn wound.

Flame Burns

Thermal injuries, caused by fire or flames, are the most common burn etiology reported over the past

decade.22 These injuries usually occur as a result of flammable liquids, motor vehicle crashes, cooking

fires, or if bedding/clothes ignite. Despite improved fire safety at home with smoke detectors as well as

improved safety at industrial sites, flame injuries are still relatively common and frequently cause

partial- and full-thickness burn injuries. Flame injuries are associated with the highest risk of death and

complications compared to all other burn etiologies. Flame burns most commonly occur at home (64%),

while work fires and recreational fire burns account for 12% and 6% of flame burns, respectively. When

evaluating thermal injuries, it is important to consider the possibility of smoke inhalation as its presence

significantly impacts the morbidity and mortality of patients with flame burns. Inhalation injury occurs

in 17% of patients with flame burns. The presence of smoke inhalation in burn patients is associated

with an overall mortality rate of 24%, compared to the mortality rate of 4% in patients without smoke

inhalation.

Contact Injuries

Contact burns occur as the result of direct contact with hot surfaces and material, most frequently glass,

metal, or plastic. The depth of the injury will depend on the heat of the material and the length of

contact. Frequent sites of injury include the palms of the hands as people, especially toddlers, often fall

with outstretched hands. Other commonly seen contact injuries are due to hot metal devices such as

space heaters, curling irons, or motorcycle exhaust systems.

Electrical Burns

Electrical injuries occur more frequently in adults than children since most result from occupational

exposure. As one of the most devastating and debilitating injuries cared for in burn centers, electrical

injuries comprise 4% of all reported etiologies. Patients who have high-voltage electrical injuries,

defined as greater than 1,000 V, are at elevated risk of spine fracture injury due to tetany and require

complete immobilization until vertebral injury is excluded. Providers must also evaluate patients with

high-voltage injuries for cardiac damage. Direct muscle injury from current flow may cause gross

myoglobinuria, requiring more aggressive fluid resuscitation.23 Patients with gross myoglobinuria often

require fasciotomy of affected limbs and a severe electrical injury often requires monitoring in the ICU.

Bone has the highest conductance and electricity flows along the skeleton cause significant muscle

necrosis adjacent to the bone. TBSA involved is not necessarily associated with prognosis and it does not

quantify damage to deep tissues in electrical injuries.

Thermal injuries occur as electricity can generate temperatures over 100°C. Electroporation occurs as

electrical force drives water into lipid membrane causing cell rupture. Tissue resistance in decreasing

order includes bone, fat, tendon, skin, muscle, vessel, and nerve. Bone heats to a high temperature and

burns surrounding structures such as muscle which is the reason why muscle swelling and compartment

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syndrome are common in high-voltage electrical injuries.

Alternating current causes tetanic muscle contraction and the “no let-go” phenomenon. This occurs

due to simultaneous contraction of (stronger) forearm flexors and (weaker) forearm extensors. Current

flow through tissue can cause burns at entrance/exit wounds and hidden injury to deep tissues. Current

will preferentially travel along low-resistance pathways. Current will pass through soft tissue, contact

high-resistance bone, and travel along bone until it exits to the ground. Vascular injury to nutrient

arteries and damage to intima and media can result in thrombosis.

Electrical exposure can cause significant injuries to other organ systems besides the skin and

musculoskeletal system. From a cardiac standpoint, arrhythmias are common at the scene (any voltage)

or in the hospital (high voltage ≥1,000). Heart rhythm should be monitored continuously for at least

24 hours if cardiac injury is suspected at the scene or if a high-voltage injury has occurred. Ventricular

fibrillation and asystole are the most common and Advanced Cardiac Life Support should be instituted

immediately. Coronary artery spasm and myocardial injury and infarction have also been described. A

normal cardiac rhythm on admission, however, means dysrhythmia is unlikely and thus 24-hour

monitoring is not needed.24 Additionally, injury to solid organs, acute bowel perforation, and gallstones

after myoglobinuria have been described. Myoglobinuria occurs due to the disruption of muscle cells.

Myoglobinuria from other causes requires increased fluid administration, however, burn resuscitation

usually provides adequate fluid. Cataracts are also a long-term adverse effect of electrical injury

necessitating ophthalmology evaluation and follow-up.

When taking the patient to the operating room for debridement and grafting of electrical injuries, the

physician should perform serial debridements and allow the tissue to completely declare itself. These

injuries will often evolve with progressive muscle necrosis over time, thus early grafting (within the

first week) often fails to fully close the burn wound. These injuries have similarities to crush injuries

and thus multiple trips to the operating room for debridement should not be viewed as failure.

Chemical Burns

General Approach to Chemical Burn Treatment

2 Healthcare providers should use personal protective equipment – always considering that the

chemicals are still present and must be neutralized or temporized. With few exceptions (see below), all

chemical burns should be copiously irrigated with water. Water dilutes but does not neutralize the

chemical and cools the injured area. Neutralization of the chemical is generally contraindicated because

neutralization may induce a hyperthermic reaction leading to further thermal injuries. Water irrigation,

however, is contraindicated or ineffective following exposure to elemental sodium, potassium, and

lithium (precipitates an explosion). Dry lime should be brushed off, not irrigated. Phenol is water

insoluble and should be wiped from the skin with polyethylene glycol-soaked sponges.

Types of Chemical Burns

Alkali causes liquefaction necrosis and protein denaturation and is found in oven and drain cleaning

products, fertilizers, and industrial cleaners. Alkali injuries extend deeper into tissues following

exposure and are especially disruptive to the eye. Acids cause damage tissue via coagulation necrosis

and protein precipitation. Acid burns tend to be self-limited secondary to pain as the patient will quickly

react to the offending agent. Organic compounds (phenol and petroleum) cause damage due to fat

solvent action (cell membrane solvent action) and systematic absorption with toxic effects on the liver

and kidneys. These agents can also cause significant erythema in the surrounding areas that can be

mistaken for cellulitis.

Specific Types of Chemical Burns

Hydrofluoric acid is a potent and corrosive acid used for rust removal, glass etching, and to clean

semiconductors. It is a weak acid but the fluoride ion is toxic as it leaches calcium from cells.

Hydrofluoric acid causes severe pain and local necrosis and should be treated with copious water

irrigation. The fluoride ion is neutralized with topical calcium gel (one ampule of calcium gluconate in

100-g lubricating jelly). If symptoms persist intra-arterial calcium infusion (10-mL calcium gluconate

diluted in 80 mL of saline, infused over 4 hours) and/or subeschar injection of dilute (10%) calcium

gluconate solution should be administered. Fluoride ion binds free serum calcium and thus it is crucial

to make sure to check the serum calcium and replace with intravenous (IV) calcium as needed.

Phenol is commonly used in disinfectants and chemical solvents, it is an acidic alcohol with poor

water solubility. Phenol causes protein disruption and denaturation resulting in coagulation necrosis.

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Systemically, phenol can cause cardiac arrhythmias and liver toxicity. Thus patients should have cardiac

and liver functions monitored. Additional adverse effects include renal injury and demyelination. Given

phenol’s anesthetic effect, pain is not a reliable indicator of injury. Treatment is copious water irrigation

and cleansing with 30% polyethylene glycol or ethyl alcohol.

Tar is used in the paving and roofing industry and can be heated to 260°C (∼500°F) prior to

application. Tar causes thermal injury and then solidifies as it cools, often becoming enmeshed with hair

and skin. Patients with tar injuries should be cooled with copious water irrigation to stop the burning

process. Tar removers promote micelle formation to break the tar – skin bond. Sterile surfactant

mixture (De-Solv-it or Shur-Clens) allows tar to be wiped away quickly. Wet dressings using polysorbate

(Tween 80) or Neomycin cream for 6 hours prior to tar removal can also be effective.

White phosphorus is used to manufacture military explosives, fireworks, and methamphetamine.

Obvious particles should be brushed off. Skin should be irrigated with 1% to 3% copper sulfate solution.

Copper sulfate stains the particles black for identification. Copper sulfate will also prevent ignition

when particles are submerged in water. After copper sulfate irrigation, the exposed area should be

placed in a water bath and the white phosphorous removed.

Anhydrous ammonia is an alkali used in fertilizer. Skin exposure is treated with irrigation and local

wound care. Exposure is associated with rapid airway edema, pulmonary edema, and pneumonia. It is

important to consider early intubation for airway protection in these cases.

Methamphetamine injuries have been on the rise. In addition to these compounds being highly

flammable, exposure to methamphetamines causes tachycardia (greater than expected with a similar

size burn), hyperthermia, agitation, and paranoia. Any suspicion of chemical injury to the globe should

be treated with prolonged irrigation with Morgan lenses. Eyelids may need to be forced open due to

edema or spasm. Utilize topical ophthalmic analgesic and consult an ophthalmologist.

Frostbite

Frostbite injuries frequently result in severe ischemic damage of distal extremities. Frostbite

classification is similar to that of burn injury with first degree demonstrating hyperemia and no blisters

with no tissue loss expected; second degree having blisters and edema but still no tissue loss; third

degree with hemorrhagic blisters, throbbing pain, and likely tissue loss; and fourth degree with mottled

or cyanotic skin, hemorrhagic blisters, and frozen deeper tissues.

3 Historically, these patients have been managed expectantly with long periods of observation

followed by amputation of devitalized tissue. Recent advances with interventional radiology,

thrombolytic therapy, and nuclear medicine have changed the treatment paradigm and protocol for

these patients (Algorithm 12-1). Current treatment paradigms for patients with frostbite include rapid

rewarming of affected area in 104°F to 108°F water bath, not radiant heat as well as ibuprofen 400 mg,

elevation of the limb, tetanus prophylaxis, and appropriate referral. If the patient has severe frostbite

within the last 24 hours, the patient should be transferred to a center with interventional radiology

expertise. Once they arrive, these patients should receive an arterial line (usually brachial or femoral)

and intra-arterial tPA which treat the microvascular thrombosis.25 Additionally, patients might benefit

from nitroglycerin to treat vasospasm. Patients should return to the interventional radiology suite after

12 hours to evaluate progress and potentially treat again. In general, tPA is stopped after 48 hours.

After 5 to 7 days, a nuclear bone scan can help assess the extent of deeper tissue necrosis as the more

superficial tissue will often appear worse than the actual extent of the injury.

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