Summary
Burns are injuries to tissue caused by heat, chemicals, electricity, friction, and/or radiation. The two factors that influence the severity of a burn are its depth and the total body surface area (TBSA) involved. The current classification of burns is based on burn depth and recognizes four degrees: first degree (superficial), second degree (superficial partial-thickness and deep partial-thickness), third degree (full-thickness), and fourth degree (deeper-injury burn). The TBSA is calculated using Lund-Browder charts. Massive tissue necrosis, which occurs with severe burns, may result in sepsis, shock, and sequential organ failure (see “SOFA score” for details). Patients with severe burns may require intubation, supplemental oxygen, and resuscitation with IV fluids. Various formulas exist to calculate initial fluid requirement, but fluids should be adjusted to maintain clinical stability and appropriate urine output. Blood oxygen, arterial blood gas, electrolyte, and creatinine levels should be monitored closely in patients with third- and fourth-degree burns. In circumferential burns around limbs, peripheral pulses and capillary refill can be used to assess perfusion. Escharotomy should be performed to treat compartment syndrome and prevent acute limb ischemia. First- and second-degree burns can be treated with antiseptic ointment and dressings. Treatment of third- and fourth-degree burns involves debridement of necrotic tissue followed by skin graft or a tissue transfer via flap reconstruction. Burn wounds easily become infected, and large, severe burns are often fatal. The most common causes of death due to burns are shock, sepsis, and respiratory failure.
Etiology
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Thermal burns (most common) [1]
- Flame burns: fire
- Contact burns: hot surfaces
- Scalding: hot liquids or steam
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Nonthermal burns [2]
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Chemical burns
- Acids such as sulfuric acid (e.g., in lead acid batteries), nitric acid (e.g., explosives and polymer industry), hydrofluoric acid (e.g., in cleaning products for electronics), phenol, and acetic acid
- Alkalis such as anhydrous ammonia (e.g., in fertilizers), calcium oxide (e.g., in cement), sodium hydroxide, and potassium hydroxide
- Miscellaneous: white phosphorus (e.g., in fireworks), metals (e.g., sodium, potassium, lithium), bleaching agents (e.g., hydrogen peroxide, hypochlorite), vesicants (e.g., mustard gas), hydrocarbons (e.g., gasoline, diesel fuel)
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Electrical burns
- Low-voltage sources: electrical cords, outlets in households
- High-voltage sources: power lines, lightning
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Radiation burns
- Electromagnetic waves
- UV radiation (e.g., from sunlight, phototherapy)
- X-rays, gamma rays (e.g., from radiotherapy, radiodiagnostic procedures, nuclear accidents)
- Infrared waves (e.g., from warming lamps), microwaves
- High-energy particles (e.g., from radiotherapy, nuclear accidents): alpha particles, beta particles, high-energy neutrons
- Electromagnetic waves
- Friction burns: skin injury caused by abrasion against a hard surface (esp. at high speeds) and the heat generated by the resulting friction (e.g., from skidding across the street due to a motorcycle accident)
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Chemical burns
Although most burn injuries are unintentional, intentional injury must always be suspected in vulnerable populations, such as children and older adults.
Classification
Depth of burns [3]
The measurement of burn depth is based on the skin layer involved.
Overview of burn depth | ||||||
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Degree of burns | Affected tissue layers | Clinical features | Prognosis | |||
Pain | Wound blanching on pressure | Appearance | ||||
1st-degree burn (superficial burn) |
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2nd-degree burn (partial thickness burn) | 2a (superficial partial thickness burn) |
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2b (deep partial thickness burn) |
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3rd-degree burn (full thickness burn) |
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4th-degree burn (deeper injury burn) |
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In deep partial-thickness burns pain may be absent as a result of damage to sensory nerve endings.
Assessment of burn surface area involvement [3]
Total body surface area (TBSA) is the total area of skin involved in an injury (e.g., burn) or disease (e.g., psoriasis). TBSA is calculated using tools such as the Lund-Browder chart and the rule of nines to assess the severity of the skin condition.
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Rule of nines
- A clinical tool used to rapidly assess the extent of body surface area affected by burns in adults
- Divides the adult body's surface into 11 regions (head/neck, 2x anterior trunk, 2x posterior trunk, each arm, 2x each leg), each of which comprises ∼ 9% of the total body surface. or plus 1% for the genital/perineal region
- The rule of nines does not accurately account for pediatric proportions in children.
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Lund-Browder chart
- A set of charts that take into account the different proportions of children and adults (children have proportionally up to 20% larger heads and up to 13% smaller legs) to more precisely estimate the burn surface area involved.
- Most accurate method for both adults and children
Body surface area estimation | |||
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Segment | Adult | Small child | Infant |
Head | 9% | 16% | 18% |
Trunk | 36% (4 x 9%) | ||
Arms | 18% (2 x 9%) | ||
Thighs | 18% (2 x 9%) | 14.5% | 13.5% |
Lower legs and feet | 18% (2 x 9%) | 14.5% | 13.5% |
Genital region | 1% |
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Palmar method
- A method of calculating TBSA using the palm as a unit of measurement to account for different proportions.
- Least reliable method
1st-degree burns are not included when calculating the total body surface area affected by burns.
Burn severity [4][5]
Burn severity is assessed based on burn depth, TBSA, location, and cause.
Classification of burn severity | ||
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Criteria | Management | |
Minor burn |
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Moderate burn |
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Major burn |
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Pathophysiology
Thermal burns
Local effects
- Local changes at the burn site (Jackson model of the burn wound) [1]
- Zone of coagulation: a central zone of irreversible, coagulative necrosis
- Zone of stasis: surrounds the central zone of coagulation and is comprised of damaged but viable tissue with decreased perfusion
- Zone of hyperemia: surrounds the zone of stasis and is characterized by inflammation and increased blood flow
- Bacterial colonization of the burn site
- Almost all burn wounds are colonized by bacteria.
- Common pathogens that infect burn wounds include MRSA, Pseudomonas, Klebsiella, Acinetobacter, and Candida.
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Eschars: a skin lesion characterized by dried, necrotic skin tissue
- Can cause constrictive effects
- Circumferential eschars (burns that fully encircle the chest, neck, abdomen, and/or an extremity) → loss of skin elasticity → impaired blood flow and/or compartment syndrome (caused by an accumulation of fluids) → acute ischemia distal to the eschar
- Significant eschar on chest or neck → restriction of chest excursion → asphyxia
Inadequate resuscitation and/or wound care may result in irreversible damage to the zone of stasis and increased burn depth.
Systemic effects [6]
Burns involving > 30% of the body surface area and third- or fourth-degree burns are likely to have systemic effects.
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Release of cytokines and other inflammatory mediators → systemic inflammatory response syndrome
- Increased vascular permeability → extravasation of protein and fluid from the intravascular compartment into interstitial tissue → generalized edema, acute respiratory distress syndrome, and hypovolemic shock with paralytic ileus
- Disseminated intravascular coagulation (DIC)
- Evaporative fluid loss → hypothermia, dehydration
- Hemolysis, muscle damage → hemoglobinuria and/or myoglobinuria → acute tubular necrosis
- Immunosuppression
Nonthermal burns [7]
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Chemical burns [8]
- Acid exposure → coagulative necrosis → limited depth of tissue damage
- Alkali exposure → cell membrane fatty acid saponification and protein complex formation → liquefactive necrosis → deeper penetration of the agent → increased risk of systemic poisoning
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Electrical burns [9]
- Electrical current enters the body (entry point) → tissue resistance converts electrical energy to heat → direct heat damage → current exits the body (exit point)
- Low-voltage electricity (< 1000 V): entry and exit points are typically close together → burns at the site of contact
- High-voltage electricity (≥ 1000 V): entry and exit sites are far away from each other → extensive deep-tissue and/or organ damage despite little or no apparent skin injury → high risk of rhabdomyolysis, compartment syndrome, and vascular thrombosis
- See also “Electrical and lightning injuries.”
- Electrical current enters the body (entry point) → tissue resistance converts electrical energy to heat → direct heat damage → current exits the body (exit point)
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Radiation burns [10]
- UV waves, x-ray waves, gamma waves, alpha particles, beta particles → DNA damage (directly or indirectly via free radical formation) → cell apoptosis
- See also “Radiation injury.”
Alkali burns cause significantly more tissue damage and have a higher risk of systemic toxicity than acid burns. Local tissue damage from alkalis can continue for up to 2–3 days after exposure.
Diagnostics
Burn severity is based on clinical history and physical examination, but further testing may be necessary to monitor for complications and guide therapy.
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Pulse oximetry
- To monitor for hypoxemia
- In circumferential limb wounds, assess perfusion via pulse oximetry (> 90% indicates adequate perfusion), capillary refill, and peripheral pulses to monitor for ischemia and compartment syndrome.
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Blood tests
- Blood gas analysis: to monitor for hypoxemia, metabolic, and/or respiratory acidosis
- Serum electrolytes: to monitor for hyperkalemia and hyponatremia in the acute phase and hypernatremia in the post-acute phase [11]
- BUN/creatinine: to monitor for acute renal injury
- Hemoglobin, hematocrit : to monitor for hemolysis
- Serum protein and albumin levels: to monitor for hypoalbuminemia in the acute phase
- Wound swab and blood cultures: in suspected wound infection or sepsis
Treatment
Minor burns [12]
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Management of the burn area
- Remove clothing, dirt, and debris.
- Cool with room-temperature or cool running water.
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Wound care
- Irrigation: cleaning the wound with mild soap and water
- Topical moisturizers (e.g., calamine lotion, aloe vera-based gels): symptom relief for 1st-degree burns
- Consider deroofing blisters. [12]
- Consider antiseptic ointments (e.g., silver sulfadiazine) or topical antibiotics (e.g., bacitracin) for 2nd-degree burns.
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Wound dressing: indicated in 2nd-degree burns
- Types of dressings (e.g., paraffin-impregnated gauze, hydrocolloid dressings, biosynthetic dressings)
- Wet-to-dry dressing: for infected wounds or wounds with devitalized tissue
- Pain management: oral NSAIDs, acetaminophen
- Prophylaxis: tetanus vaccination
Moderate and major burns [13]
Initial management
Immediate management of moderate and major burns should prioritize the ABCDE approach.
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Airway
- Intubation is indicated if an inhalation injury is suspected or if burns involve > 30% TBSA.
- Do not delay intubation if needed, as fluid resuscitation can increase laryngeal swelling.
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Breathing
- Administer 100% oxygen, if carbon monoxide poisoning is suspected.
- Escharotomy is indicated in circumferential burns of the trunk and neck
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Circulation: Fluid resuscitation with crystalloids is indicated to ensure sufficient perfusion in patients with major burns. [14]
- Lactated Ringer solution (LR) is preferred over hypertonic saline (HTS) because HTS may cause hyperchloremic metabolic acidosis.
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The volume for 24 hours of initial fluid therapy with LR is calculated using the Parkland formula: 4 mL x [% of TBSA affected by 2nd- and 3rd-degree burns] x weight (in kg).
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Because of the risk of serious complications from overresuscitation (e.g., pleural effusion and compartment syndrome), current ATLS and American Burn Association guidelines recommend adjusting the Parkland formula as follows:
- Individuals ≥ 14 years of age: half the volume calculated using the Parkland formula
- Individuals < 14 years of age who are ≥ 30 kg: initial fluid therapy with LR for a 24-hour period using 3 mL x [% of TBSA affected by 2nd- and 3rd-degree burns] × weight (in kg)
- Children < 30 kg: 24 hours of initial fluid therapy followed by 24 hours of maintenance fluid therapy with a glucose-containing solution is required.
- Half of the recommended fluid volume should be administered within the first 8 hours and the remaining half over the course of the next 16 hours.
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Because of the risk of serious complications from overresuscitation (e.g., pleural effusion and compartment syndrome), current ATLS and American Burn Association guidelines recommend adjusting the Parkland formula as follows:
- Combining crystalloids with colloids (e.g., albumin, plasma) or high-dose vitamin C can reduce fluid requirements.
- After initial stabilization, patients who require aggressive fluid resuscitation should undergo urethral catheterization to monitor urine output and adjust fluids accordingly.
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Management of the burn area
- Remove clothing, dirt, and debris.
- Cool the burnt area with room-temperature or cool running water or saline-soaked gauze, and cover the wound with a sterile dressing.
- Core body temperature should be monitored for hypothermia; if body temperature is < 35°C, warm IV fluids can be given.
- Cool with caution or not at all in patients with burns > 10% TBSA because of the high risk of hypothermia.
Because of the high risk of serious complications, the ATLS and American Burn Association recommend giving only half of the fluid resuscitation volume calculated using the Parkland formula in individuals ≥ 14 years. The volume is administered over 24 hours, with one half given in the first 8 hours and the remaining half over the next 16 hours.
Because fluid resuscitation can worsen laryngeal edema, intubation should be performed as early as possible, if necessary.
Do not use ice or ice water.
Subsequent management [13]
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Indications for treatment in a special burn unit
- 2nd-degree burns involving > 10% of TBSA or 3rd-degree burns involving > 5% of TBSA
- Inhalation injury
- Burns involving the hands, feet, genitalia, or major joints
- High-voltage electrical burns and chemical burns
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Wound care
- Early debridement of necrotic tissue [13]
- Wound dressing depends on specific burn characteristics. Options include:
- Free-skin grafts (split thickness or full thickness)
- Flap reconstruction with free or pedicled flaps [15]
- Topical antibiotics (e.g., silver sulfadiazine, bacitracin, neomycin)
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Nutritional support
- Enteral feeding via a nasogastric or nasoduodenal feeding tube is preferred over parenteral.
- Early initiation of nutritional support helps to control the hypermetabolic response.
- Pain management: NSAIDs, opioids
- Anxiety management: benzodiazepines
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Prophylaxis
- Proton pump inhibitors or H2 antagonists: curling ulcer prophylaxis (see “Stress ulcers” and “Stress ulcer prophylaxis”)
- Vaccination: tetanus prophylaxis
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Antibiotic therapy: Routine prophylactic systemic antibiotic therapy is not recommended.
- If infection or sepsis occur, treat empirically (e.g., with vancomycin) until MRSA can be ruled out.
- Treat for Pseudomonas (e.g. with cefepime) if suspected.
- Supportive measures: physical therapy
Specific considerations
Eschars
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Circumferential eschar: Perform a Doppler test and check capillary refill time, peripheral pulses, sensation, and pulse oximetry in the limb hourly for 24–48 hours to assess for vascular/respiratory compromise or compartment syndrome.
- No vascular/respiratory compromise or compartment syndrome
- Raise the legs or upper body
- Perform a range-of-motion exercises as tolerated
- Vascular/respiratory compromise or compartment syndrome
- Escharotomy: an incision of the burnt necrotic tissue to prevent constriction of the skin
- Fasciotomy is indicated if compartment syndrome develops.
- No vascular/respiratory compromise or compartment syndrome
- Chest/neck eschars: escharotomy in impending or active respiratory compromise
Chemical burns
- Immediate, copious irrigation of all areas of exposure with water
Burns from dry lime, phenols, and metals should not be irrigated.
Complications
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Shock, sepsis, and respiratory failure
- Most common causes of death from burns.
- Common causative organisms of sepsis include Staphylococcus aureus (including MRSA), Enterococcus (including VRE), and Pseudomonas.
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Circumferential burns may lead to:
- Compartment syndrome
- Acute limb ischemia (e.g., weak/absent pulse, paresthesia, pallor in the affected limb)
- Abdominal compartment syndrome
- Increased intraabdominal pressure (e.g., jugular venous distension, hypotension, tachycardia)
- Curling ulcers
- Keloid formation, contractures
- Marjolin ulcer
- Complications of chemical burns
- Cataracts or vision loss (if the burn involves the eyes)
- Esophageal strictures (if the burn involves the esophagus)
- Systemic poisoning
- Complications of electrical burns: arrhythmias
We list the most important complications. The selection is not exhaustive.
Inhalation injury
- Definition: damage to the respiratory tract that occurs due to the inhalation of hot smoke and/or noxious gases
- Etiology: inhalation of hot smoke, particles (< 1 μm diameter in size), and/or irritant/noxious gases (e.g., ammonia, chlorine)
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Diagnostics
- Inhalation injury should be suspected when any of the following are present:
- In suspected inhalation injury, the following tests should be performed:
- Bedside respiratory function tests to rule out airway obstruction
- Chest x-ray to rule out ARDS
- Carboxyhemoglobin levels
- End-tidal CO2 (ETCO2), serum lactate
- Flexible fiberoptic laryngoscopy: may show laryngeal edema
- Flexible fiberoptic bronchoscopy : may show mucosal erythema and edema, blistering, ulceration, and/or soot deposition
- Treatment: : intubation and high-flow oxygen therapy
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Complications
- Airway obstruction due to laryngeal edema
- Tracheobronchitis
- Pneumonitis
- ARDS
- Arsenic poisoning
- Carbon monoxide poisoning
- Cyanide poisoning
- Prognosis: Resolution often occurs spontaneously within 2–3 days.
Postburn hypermetabolism
- Definition: a metabolic phenomenon that can occur in patients with moderate to severe burn injuries characterized by an initial hypometabolic phase followed by a hypermetabolic state
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Pathophysiology: an increase in catecholamines, cortisol, and inflammatory cytokines → severe metabolic alterations
- Elevated resting energy expenditures
- Insulin resistance
- ↑ Gluconeogenesis
- ↑ Lipolysis
- Protein catabolism
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Clinical features
- Hypometabolic phase (ebb phase)
- Onset within 48 hours of the burn injury
- Decreased cardiac output, oxygen consumption, and metabolic rate
- Hypermetabolic phase (flow phase)
- Onset 5–7 days after the injury
- Can persist for up to ∼ 3 years
- Hyperdynamic circulation: ↑ blood pressure, ↑ heart rate
- Muscle wasting, protein loss
- Significant weight loss
- Hyperglycemia
- Increased body temperature
- Multiorgan dysfunction
- Hypometabolic phase (ebb phase)
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Management
- Early excision and grafting
- Analgesia
- Nutritional support
- Anabolic steroids
- Glycemic control with insulin
- Beta blockers (e.g., propranolol) to decrease resting metabolism
References:[16][17]