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Burns are injuries of skin or other tissue caused by thermal, radiation, chemical, or electrical contact. Burns are classified by depth (superficial and deep partial-thickness, and full-thickness) and percentage of total body surface area (TBSA) involved. Complications and associated problems include hypovolemic shock, inhalation injury, infection, scarring, and contractures. Patients with large burns (> 20% TBSA) require fluid resuscitation. Treatments for burn wounds includes topical antibacterials, regular cleaning, elevation, and sometimes skin grafting. Intensive rehabilitation, consisting of range-of-motion exercises and splinting, is often necessary.
Burns cause about 3000 deaths/yr in the US and about 2 million physician visits.
Thermal burns may result from any external heat source (flame, hot liquids, hot solid objects, or, occasionally, steam). Fires may also result in toxic smoke inhalation (see also Carbon Monoxide Poisoning ).
Radiation burns most commonly result from prolonged exposure to solar ultraviolet radiation ( sunburn) but may result from prolonged or intense exposure to other sources of ultraviolet radiation (eg, tanning beds) or from exposure to sources of x-ray or other nonsolar radiation (see Radiation Exposure and Contamination).
Chemical burns may result from strong acids, strong alkalis (eg, lye, cement), phenols, cresols, mustard gas, phosphorus, and certain petroleum products (eg, gasoline, paint thinner). Skin and deeper tissue necrosis caused by these agents may progress over several hours.
Electrical burns result from heat generation and electroporation of cell membranes associated with massive current of electrons. Electrical burns often cause extensive deep tissue damage to electrically conductive tissues, such as muscles, nerves, and blood vessels, despite minimal apparent cutaneous injury.
Events associated with a burn (eg, jumping from a burning building, being struck by debris, motor vehicle crash) may cause other injuries. Abuse should be considered in young children and elderly patients with burns.
Burns and smoke inhalation often occur together but may occur separately. When smoke is inhaled, toxic products of combustion injure airway tissues. Hot smoke usually burns only the pharynx because the incoming gas cools quickly. An exception is steam, which carries much more heat energy than smoke and thus can also burn the lower airways (below the glottis). Many toxic chemicals produced in routine house fires (eg, hydrogen chloride, phosgene, sulfur dioxide, toxic aldehydes, ammonia) cause chemical burns. Some toxic products of combustion, such as carbon monoxide or cyanide, impair cellular respiration systemically.
Upper airway injury usually causes symptoms within minutes but occasionally over several hours; upper airway edema may cause stridor. Lower airway injury may also occur with upper airway injury and usually causes symptoms (eg, oxygenation problems highlighted by increasing oxygen requirements or decreases in lung compliance) 24 h or later.
Smoke inhalation is suspected in patients with respiratory symptoms, a history of confinement in a burning environment, or carbonaceous sputum. Perioral burns and singed nasal hair may also be clues.
Diagnosis of upper airway injury is by endoscopy (laryngoscopy or bronchoscopy) that is adequate to see the upper airways and trachea and shows edema, tissue damage, or soot in the airways; however, injury occasionally develops after an initial normal study. Endoscopy is done as soon as possible, usually with a flexible fiberoptic scope, typically after or simultaneously with endotracheal intubation in patients with significant findings. Diagnosis of lower airway injury is by chest x-ray and oximetry or ABGs; abnormalities may develop early or only days later. Cyanide and carbon monoxide toxicity should be considered; carboxyhemoglobin levels are measured in patients with significant smoke inhalation.
All patients at risk of smoke inhalation injury are given 100% oxygen by face mask initially. Patients with airway obstruction or respiratory distress require endotracheal intubation or another artificial airway and mechanical ventilation. Patients with edema or significant soot in the upper airways require intubation as soon as possible because the airway becomes more difficult to intubate as edema increases. Bronchoscopy is usually done at the same time as intubation. Patients with lower airway injury may require supplemental oxygen, bronchodilators, and other supportive measures.
Burns cause protein denaturation and thus coagulative necrosis. Around the coagulated tissue, platelets aggregate, vessels constrict, and marginally perfused tissue (known as the zone of stasis) can extend around the injury. In the zone of stasis, tissue is hyperemic and inflamed.
Damage to the normal epidermal barrier allows bacterial invasion and external fluid loss; damaged tissues often become edematous, further enhancing volume loss. Heat loss can be significant because thermoregulation of the damaged dermis is absent, particularly in wounds that are exposed.
First-degree burns are limited to the epidermis.
Partial-thickness (also called 2nd-degree) burns involve part of the dermis and can be superficial or deep.
Superficial partial-thickness burns involve the papillary (more superficial) dermis. These burns heal within 1 to 2 wk, and scarring is usually minimal. Healing occurs from epidermal cells lining sweat gland ducts and hair follicles; these cells grow to the surface, then migrate across the surface to meet cells from neighboring glands and follicles.
Deep partial-thickness burns involve the deeper dermis and take ≥ 2 wk to heal. Healing occurs only from hair follicles, and scarring is common and may be severe.
Full-thickness (3rd-degree) burns extend through the entire dermis and into the underlying fat. Healing occurs only from the periphery; these burns, unless small, require excision and skin grafting.
Burns cause both systemic and local complications. The major factors contributing to systemic complications are breakdown of skin integrity and fluid loss. Local complications include eschars and contractures and scarring.
The greater the percentage of TBSA involved, the greater the risk of developing systemic complications. Risk factors for severe systemic complications and mortality include all of the following:
The most common systemic complications are hypovolemia and infection.
Hypovolemia, causing hypoperfusion of burned tissue and sometimes shock, can result from fluid losses due to burns that are deep or that involve large parts of the body surface; whole-body edema from escape of intravascular volume into the interstitium and cells also develops. Hypoperfusion of burned tissue also may result from direct damage to blood vessels or from vasoconstriction secondary to hypovolemia.
Infection, even in small burns, is a common cause of sepsis and mortality, as well as local complications. Impaired host defenses and devitalized tissue enhance bacterial invasion and growth. The most common pathogens are streptococci and staphylococci during the first few days and gram-negative bacteria after 5 to 7 days; however, flora are almost always mixed.
Metabolic abnormalities may include hypoalbuminemia that is partly due to hemodilution (secondary to replacement fluids) and partly due to protein loss into the extravascular space through damaged capillaries. Dilutional electrolyte deficiencies can develop; they include hypomagnesemia, hypophosphatemia, and hypokalemia. Metabolic acidosis may result from shock. Rhabdomyolysis or hemolysis can result from deep thermal or electrical burns of muscle or from muscle ischemia due to constricting eschars. Rhabdomyolysis causing myoglobinuria or hemolysis causing hemoglobinuria can lead to acute tubular necrosis and acute kidney injury.
Hypothermia may result from large volumes of cool IV fluids and extensive exposure of body surfaces to a cool emergency department environment, particularly in patients with extensive burns.
Ileus is common after extensive burns.
Eschar is stiff, dead tissue caused by deep burns. A circumferential eschar, which completely encircles a limb (or sometimes the neck or torso), is potentially constricting. A constricting eschar limits tissue expansion in response to edema; instead, tissue pressure increases, eventually causing local ischemia. The ischemia threatens viability of limbs and digits distal to the eschar, and an eschar around the neck or thorax can compromise ventilation.
Scarring and contractures result from healing of deep burns. Depending on the extent of the scar, contracture deformities can appear at the joints. If the burn is located near joints (particularly in the hands), in the feet, or in the perineum, function can be severely impaired. Infection can increase scarring. Keloids form in some patients with burns, especially in patients with darker skin.
Wound symptoms and signs depend on burn depth:
First-degree burns: These burns are red, blanch markedly and widely with light pressure, and are painful and tender. Vesicles or bullae do not develop.
Superficial partial-thickness burns: These burns blanch with pressure and are painful and tender. Vesicles or bullae develop within 24 h. The bases of vesicles and bullae are pink and subsequently develop a fibrinous exudate.
Deep partial-thickness burns: These burns may be white, red, or mottled red and white. They do not blanch and are less painful and tender than more superficial burns. A pinprick is often interpreted as pressure rather than sharp. Vesicles or bullae may develop; these burns are usually dry.
Full-thickness burns: These burns may be white and pliable, black and charred, brown and leathery, or bright red because of fixed Hb in the subdermal region. Pale full-thickness burns may simulate normal skin except the skin does not blanch to pressure. Full-thickness burns are usually anesthetic or hypoesthetic. Hairs can be pulled easily from their follicles. Vesicles and bullae usually do not develop. Sometimes features that differentiate full thickness from deep partial thickness burns take 24 to 48 hours to develop.
Location and depth of burned areas are recorded on a burn diagram. Burns with an appearance compatible with both deep partial-thickness and full-thickness are presumed to be full-thickness.
The percentage of TBSA involved is calculated; only partial-thickness and full-thickness burns are included in this calculation (1). For adults, the percentage TBSA for parts of the body is estimated by the rule of nines ( see Figure: (A) Rule of nines (for adults) and (B) Lund-Browder chart (for children) for estimating extent of burns.); for smaller scattered burns, estimates can be based on the size of the patient’s entire opened hand (not the palm only), which is about 1% of TBSA. Children have proportionally larger heads and smaller lower extremities, so the percentage TBSA is more accurately estimated using the Lund-Browder chart (see Figure: (A) Rule of nines (for adults) and (B) Lund-Browder chart (for children) for estimating extent of burns.).
In hospitalized patients, Hb and Hct, serum electrolytes, BUN, creatinine, albumin, protein, phosphate, and ionized calcium should be measured. ECG, urinalysis for myoglobin, and a chest x-ray are also required. Myoglobinuria (suggesting hemolysis or rhabdomyolysis) is suggested by urine that is grossly dark or that tests positive for blood on dipstick in the absence of microscopic RBCs. These tests are repeated as needed. Muscle compartments are evaluated in patients with myoglobinuria.
Infection is suggested by wound exudate, impaired wound healing, or systemic evidence of infection (eg, feeding intolerance, decrease in platelet count, increase in serum glucose level). Fever and WBC count elevation are common in burns without infection and therefore are unreliable signs of developing sepsis. If the diagnosis is unclear, infection can be confirmed by biopsy; cultures from the wound surface or exudate are unreliable.
Treatment begins in the prehospital setting. The first priorities are the same as for any injured patient: ABC (airway, breathing, and circulation). An airway is provided, ventilation is supported, and possible associated smoke inhalation is treated with 100% oxygen. Ongoing burning is extinguished, and smoldering and hot material is removed. All clothing is removed. Chemicals, except powders, are flushed with water; powders should be brushed off before wetting. Burns caused by acids, alkalis, or organic compounds (eg, phenols, cresols, petrochemicals) are flushed with copious amounts of water continuing for at least 20 min after nothing of the original solution seems to remain.
IV fluids are given to patients in shock or with burns > 10% TBSA. A 14- to 16-gauge venous cannula is placed in 1 or 2 peripheral veins through unburned skin if possible. Venous cutdown, which has a high risk of infection, is avoided.
Initial fluid volume is guided by treatment of clinically evident shock (1). If shock is absent, fluid administration aims to replace the predicted deficit and supply maintenance fluids. The Parkland formula (4 mL/kg) × % TBSA burned (second-degree and third-degree burns) is used to estimate fluid volume needs in the first 24 h after the burn (not after presentation to the hospital) and determines the rate of IV fluid administration. Half the calculated amount is given over the first 8 h; the remainder is given over the next 16 h. Fluid is given as lactated Ringer's solution because large amounts of normal saline could result in hyperchloremic acidosis.
For example, in a 100-kg man with a 50% TBSA burn, fluid volume by the Parkland formula would be
Half of the volume, 10 L, is given in the first 8 h after injury as a constant infusion, and the remaining 10 L is given over the following 16 h. In practice, this formula is only a starting point, and infusion rates are adjusted based on clinical response. Urine output, typically measured with an indwelling catheter, is the usual indicator of clinical response; the goal is to maintain output between 30 and 50 mL/h in adults and between 0.5 and 1.0 mL/kg/h in children. When giving typical large volumes of fluid, it is also important to avoid fluid overload and consequent heart failure and compartment syndrome. Clinical parameters, including urine output and signs of shock or heart failure, are recorded at least hourly on a flow chart.
Some clinicians give colloid, usually albumin, after 12 h to patients who have larger burns, are very young or very old, or have heart disease and require large fluid volumes.
If urine output is inadequate despite administration of a large volume of crystalloid, consultation with a burn center is necessary. Such patients may respond to an infusion of colloid or other measures. Patients with inadequate urine output despite administration of a large volume of crystalloid are at risk of resuscitation complications including compartment syndromes of the abdomen and extremities.
For patients of any age with rhabdomyolysis, fluid should be given to maintain urine output between 0.5 and 1 mL/kg/h. Some authorities recommend alkalinizing the urine by adding 50 mEq NaHCO3 (one 50-mL ampule of 8.4% solution) to a liter of IV fluid.
After adequate analgesia, the wound is cleaned with soap and water, and all loose debris is removed. Water should be room temperature or warmer to avoid inducing hypothermia. Ruptured blisters, except for small ones on palms, fingers, and soles, are debrided. Unruptured blisters can sometimes be left intact, but should be treated by application of a topical antimicrobial. In patients who are to be transferred to a burn center, clean dry dressings can be applied (burn creams may interfere with burn wound assessment at the receiving facility), and patients are kept warm and relatively comfortable with IV opioids.
After the wound is cleaned and is assessed by the final treatment provider, burns can be treated topically. For shallow partial-thickness burns, topical treatment alone is usually adequate. All deep partial-thickness burns and full-thickness burns should ultimately be treated with excision and grafting, but in the interim, topical treatments are appropriate.
Topical treatment may be with antimicrobial salves (eg, 1% silver sulfadiazine), commercial dressings incorporating silver (eg, sustained-release nanocrystalline silver dressings), or biosynthetic wound dressings (also called artificial skin products). Topical salves must be changed daily, and silver sulfadiazine may induce transient leukopenia. Some (but not all) silver-impregnated dressings must be kept moist but can be changed as infrequently as every 7 days (to minimize pain associated with repeated wound care). Artificial skin products are not changed routinely but can result in underlying purulence necessitating removal, particularly when wounds are deep. Burned extremities should be elevated.
A tetanus toxoid booster (0.5 mL sc or IM) is given to patients with all but minor burns who have been previously fully vaccinated and who have not received a booster within the past 5 yr. Patients whose booster was more remote or who had not received a full vaccine series are given tetanus immune globulin 250 units IM and concomitant active vaccination (see Tetanus : Prevention).
Escharotomy (incision of the eschar) of constricting eschars may be necessary to allow adequate expansion of the thorax or perfusion of an extremity. However, constricting eschars rarely threaten extremity viability during the first few hours, so if transfer to a burn center can occur within that time, escharotomy can typically be deferred until then.
Hypothermia is treated (see Hypothermia : Treatment), and pain is relieved. Opioids (eg, morphine) should always be given IV, and large doses may be needed for adequate pain control. Treatment of electrolyte deficits may require supplemental calcium (Ca), magnesium (Mg), potassium (K), or phosphate (PO4).
Nutritional support is indicated for patients with burns > 20% TBSA or preexisting undernutrition. Support with a feeding tube begins as soon as possible. Parenteral support is rarely necessary.
After initial treatment and stabilization, the need for hospitalization is assessed. Inpatient treatment, optimally at a burn center, is strongly suggested for
In addition, hospitalization may be necessary if
Many experts recommend that all burns, except for 1st-degree burns < 1% TBSA, be treated by experienced physicians and that brief inpatient care be strongly considered for all burns > 2% TBSA. Maintaining adequate analgesia and exercise can be difficult for many patients and caregivers.
Prophylactic systemic antibiotics are not given.
Initial empiric antibiotic treatment for apparent infection during the first 5 days should target staphylococci and streptococci (eg, with vancomycin for inpatients). Infections that develop after 5 days are treated with broad-spectrum antibiotics that are effective against gram-positive and gram-negative bacteria. Antibiotic selection is subsequently adjusted based on culture and sensitivity results.
Surgery is indicated for burns that are not expected to heal within 2 wk, including most deep partial-thickness burns and all full-thickness burns. Eschars are removed as soon as possible, ideally within 3 days to prevent sepsis and facilitate early wound grafting, which shortens hospitalization and improves the functional result. If burns are extensive and life threatening, the largest eschars are removed first to close as much burn area as early as possible.
After excision, grafting proceeds ideally using partial-thickness autografts (the patient’s skin), which are permanent (2). Autografts can be transplanted as sheets (solid pieces of skin) or meshed grafts (sheets of donor skin that are stretched to cover a larger area by making multiple, regularly spaced, small incisions). Meshed grafts are used in areas where appearance is less of a concern when burns are > 20% TBSA and donor skin is scarce. Meshed grafts heal with an uneven gridlike appearance, sometimes with excessive hypertrophic scarring.
When burns are > 40% TBSA and the supply of autograft material appears insufficient, an artificial dermal regeneration template can be used as temporary coverage (2). Allografts (viable skin usually from cadaver donors) or xenografts (eg, pig skin) can also be used temporarily; they are rejected, sometimes within 10 to 14 days. Both types of temporary coverage must ultimately be replaced with autografts.
Fasciotomy is done when edema within a muscle compartment elevates compartment pressure > 30 mm Hg.
Physical and occupational therapy are begun at admission to help minimize scarring and contractures, particularly for body surfaces with high skin tension and frequent movement (eg, face, hands), and to optimize function. Active and passive range-of-motion exercises become easier as the initial edema subsides; they are done once or twice daily. After grafting, exercises are usually suspended for 3 days, then resumed. Extremities affected by deep partial-thickness burns or full-thickness burns are splinted in functional positions as soon as possible and kept splinted continuously (except during exercise) until the graft has been placed, healing has occurred, or both.
Outpatient treatment includes keeping burns clean and, to the extent possible, keeping the affected body part elevated. Dressings should be changed daily for burns treated with topical salves. The salve is applied and then covered with a dry nonadherent gauze dressing and compression wraps. Silver dressings should be changed every 3 to 7 days. Dressing change simply involves removing the older dressing and replacing it with new one. Biosynthetic wound dressings should not be changed in the absence of purulence. Biosynthetic dressings should simply be covered with dry gauze, which is changed daily.
Outpatient follow-up visits are scheduled as needed depending on burn severity (eg, for very minor burns, initial visit within 24 h, then subsequent visits every 5 to 7 days). Visits include debridement if indicated, reassessment of burn depth, and evaluation of the need for physical therapy and grafting. Patients should return earlier if they note signs of infection, such as increasing redness extending from the wound edges, increasing purulence and pain, or a change in the appearance of the wound with development of black or red spots. Should these signs occur, medical evaluation should ensue urgently. Outpatient treatment is acceptable for minor burn-wound cellulitis in healthy patients aged 2 to 60 yr; hospitalization is indicated for other infections.
Pham TN, Cancio CL, Gibran NS. American Burn Association practice guidelines burn shock resuscitation. J Burn Care Res J 29(1):257-266, 2008. doi: 10.1097/BCR.0b013e31815f3876.
Kagan RJ, Peck MD, Ahrenholz DH, et al. Surgical management of the burn wound and use of skin substitutes: an expert panel white paper. J Burn Care Res 34:e60–79. doi: 10.1097/BCR.0b013e31827039a6.
Clues to burn depth include presence of vesicles or bullae (suggesting a partial-thickness burn); and decreased sensation, dry leathery eschar, hypoesthesia, and ability to easily pull hairs (suggesting a full-thickness burn).
If burns are > 10% TBSA, give IV lactated Ringer's solution at an initial rate guided by the Parkland formula (4 mL × wgt (kg) × %TBSA burned during the 1st 24 h after the burn) and adjusted based on hourly urine output.
For eschars that are circumferential or constricting, consider escharotomy.
Supportive measures include adequate analgesia and, if burns are > 20% TBSA, early nutritional support.
Strongly consider hospitalization if burns involve the hands, feet, or perineum (partial-thickness or deeper); are > 5% TBSA (partial-thickness or deeper); are > 1% TBSA (full-thickness); or if patients are > 60 or < 2 yr or are unlikely to fully adhere to home care measures.
Treat surgically if an eschar is present, compartmental pressure is > 30 mm Hg, or, usually, if burns are full or deep partial-thickness.
For infections, apply topical antimicrobials (for prevention); routinely inspect burns (for early diagnosis); and use systemic antibiotics, change topical treatment as needed, and occasionally excise the infected area (for treatment).
Begin physical and occupational therapy early to minimize scarring and contractures.
Drug NameSelect Trade
morphineDURAMORPH PF, MS CONTIN
sulfadiazineNo US brand name
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