Sandra L. Werner
THERMAL BURNS
EPIDEMIOLOGY
Approximately 500,000 Americans are treated for burns annually, and 40,000 are hospitalized. Most ED burn patients are treated and discharged. Of those patients requiring hospitalization, over 60% are admitted to one of the country’s 125 burn centers.
The risk of burns is highest in the 18- to 35-year-old age group. There is a male-female ratio of 2:1 for both injury and death. Scald injuries are more common in the pediatric and elderly populations.
The death rate in patients over 65 years of age is much higher than in the overall burn population.
The risk of death from a major burn is associated with increased burn size, increased age, concomitant inhalation injury, and female sex.
Significant advances in burn management have decreased the mortality rate for major thermal burns to 4%.
PATHOPHYSIOLOGY
Thermal injury results in local and systemic homeo-static derangements including disruption of cell membrane function, hormonal alterations, changes in tissue acid-base balance, as well as hemodynamic and hematologic affects, all of which contribute to burn shock.
Fluid and electrolyte abnormalities in burn shock are caused by dysfunction of the sodium pump and include a cellular influx of sodium and fluid, and extracellular migration of potassium.
Significant metabolic acidosis may be present in large burns. Patients with burns covering >60% total body surface area (TBSA) may have depression myocardial activity.
Hematologic derangements include an early increase in hematocrit and viscosity, followed by anemia in the later phases.
Thermal injury is progressive. Initial local effects include release of vasoactive substances, cellular dysfunction, and edema. The systemic response results in changes in the neurohormonal axis and alterations in all organ systems. The released neurohormonal and vasoactive substances act at the local level, causing progression of the burn wound.
A full-thickness burn has three zones:
Coagulation—tissue is irreversibly destroyed by thrombosis of blood vessels
Stasis—tissue is viable but there is stagnation of circulation
Hyperemia—tissue is viable and there is increased blood flow
Inadequate resuscitation results in increased tissue damage within the zone of stasis.
Prognosis of burn patients is most affected by the severity of the burn, presence of inhalation injury, associated injuries, patient’s age, preexisting conditions, and acute organ failure.
CLINICAL FEATURES
Burns are categorized by their size and depth. Burn size is calculated as the percentage of total body surface area (BSA) involved.
The most common method to estimate the percentage of BSA burned is the “rule of nines” (Fig. 127-1).
A more accurate tool to determine the percentage of BSA burned, especially in infants and children, is the Lund and Browder burn diagram (Fig. 127-2).
For smaller burns, the patient’s hand can be used as a “ruler” to estimate percent BSA. This area represents approximately 1% of the patient’s BSA.
Burn depth has historically been described in degrees: first, second, third, and fourth.
A more clinically relevant classification scheme categorizes burns as superficial partial-thickness, deep partial-thickness, and full-thickness. Table 127-1 summarizes the characteristics of each type of burn.
Inhalation injury occurs most frequently in closed-space fires and in patients with decreased cognition (intoxication, overdose, head injury).
Both the upper and the lower airway can be injured by heat, particulate matter, and toxic gases.
Thermal injury is usually limited to the upper airway and can result in acute airway compromise.
Particulate matter can reach the terminal bronchioles and cause bronchospasm and edema.
Clinical indicators of smoke inhalation injury include facial burns, singed nasal hair, soot in the upper airway, hoarseness, carbonaceous sputum, and wheezing.
Carbon monoxide poisoning should be suspected in all patients with smoke inhalation injury.
Consider hydrogen cyanide poisoning in fires involving nitrogen-containing polymer products such as wool, silk, polyurethane, and vinyl.
FIG. 127-1. Rule of nines to estimate the percentage of burn.
FIG. 127-2. Lund and Browder diagram to estimate the percentage of a burn.
TABLE 127-1 Burn Depth Features Classified by Degree of Burn
DIAGNOSIS AND DIFFERENTIAL
Burns are classified as major, moderate, or minor. Table 127-2 summarizes the American Burn Association (ABA) burn classifications and recommended patient dispositions.
Inhalation injury is diagnosed based on clinical history of an enclosed-space fire and presence of facial burns, singed nasal hairs, carbonaceous sputum, soot in the upper airway, and/or wheezing on examination.
The chest radiograph in smoke inhalation injury may be normal initially. Flexible fiberoptic bronchoscopy can confirm the diagnosis.
Obtain carboxyhemoglobin levels if carbon monoxide poisoning is suspected.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Management of patients with moderate to major burns is divided into three phases: prehospital care, ED resuscitation, and transfer to a burn center.
Prehospital care consists of stopping the burning process, establishing an airway, initiating fluid resuscitation, relieving pain, and protecting the burn wound.
In the ED, reevaluate the airway and administer 100% oxygen.
Intubate and ventilate the patient if indicated by the presence of oral/perioral burns, circumferential neck burns, stridor, depressed mental status, or respiratory distress. Obtain an ABG with co-oximetry and a CXR.
Establish at least two IV lines in unburned areas and initiate fluid resuscitation using the Parkland or similar burn formula.
The Parkland formula calls for Lactated Ringers, 4 mL/kg times the percentage of BSA burned, given over 24 hours. Give half the calculated amount in the first 8 hours post injury and the remainder over the next 16 hours.
The 24-hour time interval begins at the time the patient sustained the burn, not the time of resuscitation onset. The percentage BSA used in this calculation includes only second- and third-degree burns.
Further fluid resuscitation is guided by vital signs, cerebral and peripheral perfusion, and adequate urine output.
Evaluate and treat traumatic injures using standard trauma resuscitation guidelines (see Chapter 158, Trauma in Adults; Chapter 159, Trauma in Children; and Chapter 160, Geriatric Trauma).
After initiating resuscitation, address burn wounds. Apply cool compresses to small burns. Cover large burns with sterile, dry sheets, as saline-soaked sheets may cause hypothermia.
Administration of empiric intravenous antibiotics and application of topical antibiotics is not recommended.
Administer intravenous opiod analgesia early and titrate to relief of pain.
Treat inhalation injury with humidified oxygen, intubation and ventilation, bronchodilators, and pulmonary toilet. Treat severe carbon monoxide poisoning with hyperbaric oxygen therapy.
Perform escharotomy as indicated for circumferential burns of the neck, chest, or extremities.
Update tetanus prophylaxis, if needed. Give tetanus immune globulin to patients without primary immunization.
Hospitalize patients with moderate and major burns. The ABA’s criteria for burn center referral are listed in Table 127-3.
Minor burns can be treated on an outpatient basis. Table 127-4 summarizes the care of minor burns. Patients with minor burns may be discharged from the ED, provided close follow-up is available.
TABLE 127-2 Burn Depth Features: American Burn Association Burn Classification
TABLE 127-3 American Burn Association Burn Unit Referral Criteria
Third-degree burns in any age group
Electrical burns, including lightning injury
Chemical burns
Inhalation injury
Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality
Burn injury in any patients with concomitant trauma (such as fractures) in whom the burn injury poses the greatest risk of morbidity or mortality
Burn injury in children in hospitals without qualified personnel or equipment to care for children
Burn injury in patients who will require special social, emotional, or long-term rehabilitative intervention
Burn injury in children <10 y and adults >50 y of age
TABLE 127-4 ED Care of Minor Burns
CHEMICAL BURNS
EPIDEMIOLOGY
Chemical burn injuries account for 5% to 10% of burn center admissions.
Common household chemical burns are usually minor and are caused by lye (drain cleaner), halogenated hydrocarbons (paint removers), phenols (deodorizers, disinfectants), sodium hypochlorite (bleach), and sul-furic acid (toilet bowl cleaner).
Alkalis and acids are commonly used in numerous industrial processes including tanning, curing, extracting, and preserving.
White phosphorus has been used in military munitions and may be found in rodenticides, pesticides, and fireworks.
Body sites most often burned by chemicals are the face, eyes, and extremities.
Although chemical burns are smaller and have a lower mortality rate than thermal burns, wound healing and hospital length of stay are longer.
PATHOPHYSIOLOGY
Contact with chemical agents can result in burns, irritant contact dermatitis, allergic reaction, thermal injury, or systemic toxicity.
Skin damage by chemicals can be similar to thermal injury, ranging from superficial erythema to full-thickness loss. Chemical burns may initially appear deceptively mild, but progress to more extensive skin damage and systemic toxicity.
Factors that influence tissue damage include the quantity and strength/concentration of the agent, manner and duration of contact, phase of the agent, mechanism of action, and extent of penetration.
Factors that influence percutaneous absorption of chemicals include the body site exposed, integrity and condition of the skin, nature of the chemical, and occlusion of the exposed area.
The majority of chemical burns are caused by acids or alkalis. Alkalis usually produce far more tissue damage than acids.
Acids typically cause coagulation necrosis, which produces a leathery eschar that limits further damage.
Alkalis cause liquefaction necrosis, allowing deeper tissue damage to occur.
CLINICAL FEATURES
Skin damage from chemical burns depends on the type of agent, concentration, volume, and duration of exposure.
Hydrofluoric (HF) acid is a special case as it rapidly penetrates intact skin and causes progressive pain and deep tissue destruction without obvious superficial damage.
Chemical burns of the eye are true ocular emergencies.
Acid ocular burns quickly precipitate proteins in the superficial eye structures, resulting in a “ground glass” appearance.
Alkali ocular burns are more severe due to deeper, ongoing penetration. Severe chemosis, blanched conjunctiva, and an opacified cornea can occur. Blindness can result from retinal penetration with destruction of sensory elements.
Lacrimators (tear gas and pepper mace) cause ocular, mucous membrane, and pulmonary irritation.
DIAGNOSIS AND DIFFERENTIAL
Diagnosis is usually made by history of exposure to a chemical agent.
Chemical topical exposure should be considered in all cases of skin irritation/pain.
For ocular exposures, pH paper can help distinguish alkali from acid exposure.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
The first priority in treatment of chemical burns is to terminate the burning process.
Remove garments. Brush off dry chemical particles. Immediately irrigate the skin copiously with water.
Cover elemental metals (sodium, lithium, calcium, magnesium) with mineral oil because exposure to water may cause a severe exothermic reaction.
For ocular burns, begin irrigation with 1 to 2 L of normal saline. In patients with acid or alkali burns, continue irrigation until pH is normal.
Patients with alkali burns will require prolonged irrigation.
Visual acuity check and pH testing should follow, not precede, ocular irrigation.
Consult with an ophthalmologist.
Treatment for specific chemical burns is provided in Table 127-5.
Options for treating cutaneous HF acid burns are provided in Table 127-6. Consult with a plastic surgeon for patients with HF acid burns of the hands, feet, digits, or nails.
After initial decontamination, initiate IV fluid resuscitation, analgesia, and tetanus immuno-prophylaxis, and address systemic toxicity, as needed.
TABLE 127-5 Treatment of Select Chemical Burns
TABLE 127-6 Options for Treatment of Hydrofluoric Acid Skin Burns
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 210, “Thermal Burns,” by Lawrence R. Schwartz and Chenicheri Balakrishnan, and Chapter 211, “Chemical Burns,” by Fred R Harchelroad Jr. and David M. Rottinghaus.