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Emergency care of moderate and severe thermal burns in adults
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Emergency care of moderate and severe thermal burns in adults
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Dec 2016. | This topic last updated: Jan 18, 2017.

INTRODUCTION — Burns are a leading cause of accidental injury and death in the United States and worldwide [1-5]. Each year approximately one million people in the United States seek medical care for burns, approximately one-third of these in the emergency department (ED) [1,4-6]. Although the vast majority of injuries do not require hospitalization, severe burns can lead to significant morbidity and death.

The initial assessment and management of the patient with moderate and severe thermal burns will be reviewed here. Details of burn classification, burn management in children, treatment of minor burns, and other issues related to burn management are discussed separately. (See "Classification of burns" and "Emergency care of moderate and severe thermal burns in children" and "Overview and management strategies for the combined burn trauma patient" and "Overview of the management of the severely burned patient" and "Burn pain: Principles of pharmacologic and nonpharmacologic management" and "Treatment of minor thermal burns" and "Inhalation injury from heat, smoke, or chemical irritants".)

CLASSIFICATION OF BURNS — The American Burn Association (ABA) has classified thermal burns into minor, moderate, and major, largely based upon burn depth and size (table 1 and table 2 and figure 1). The treatment and prognosis of burn victims correlates with this classification. Therefore it is important that clinicians properly characterize the size and severity of their patients' burns. Reassessment of thermal burn size and depth is important, particularly early in the management of patients with severe injuries, as the extent of injury often increases. The classification of burns is reviewed in the tables above and discussed in detail separately. (See "Classification of burns".)


Initial interventions — Assessment and initial treatment of severe burns is performed simultaneously with trauma resuscitation (algorithm 1). Initial management focuses on stabilizing the airway, breathing, and circulation (ABC's). The primary evaluation includes assessing for evidence of respiratory distress and smoke inhalation injury, evaluating cardiovascular status, looking for other injuries, and determining the depth and extent of burns. (See 'Classification of burns' above.)

Hot and burned clothing and debris is removed (caretakers should take precautions to avoid injuring themselves when removing such material). Early transfer to a burn center should be arranged when injuries meet the criteria for major burns (table 1). Burn patients may sustain single or multisystem trauma and should be evaluated accordingly. (See "Initial management of trauma in adults".)

History — Paramedics, other victims, or the patient may be able to provide important information such as what burned (eg, chemicals, plastics, textiles), the location of the fire (eg, enclosed or open space), whether an explosion occurred (possibly causing a blast injury), whether the patient used alcohol or drugs, and whether there was associated trauma (eg, from falling debris). The AMPLE trauma history should be obtained, if possible (Allergies, Medications, Past medical history, Last meal, Events).

Airway management

Assessment and approach — Despite advances in ventilatory management, inhalation injury remains a leading cause of death in adult burn victims [1,4,5]. The risk of inhalation injury increases with the extent of the burn and is present in two-thirds of patients with burns greater than 70 percent of the total body surface area (TBSA) [7]. While assessing the airway, clinicians should immobilize the patient's cervical spine as appropriate.

It is critical to maintain the airway and provide supplemental oxygen in patients with major burns [8]. Upper airway edema following a burn-related injury can occur rapidly. Among patients who manifest signs of smoke inhalation, a sizable percentage develop complete airway obstruction and there is no clinical means to determine which patients will do so [9]. Fluid resuscitation can exacerbate laryngeal swelling, increasing the difficulty of tracheal intubation. Therefore, intubation should not be delayed if severe inhalation injury or respiratory distress is present or anticipated. Intubation prior to transport is prudent for many patients who require transfer to a burn center. Succinylcholine may be used as part of a rapid sequence intubation during the first 72 hours following a severe burn, but not thereafter because of the risk of severe hyperkalemia. A significant percentage of intubated burn patients will develop acute respiratory distress syndrome (ARDS). (See "Emergency airway management in the adult with direct airway trauma" and "Rapid sequence intubation for adults outside the operating room" and "Neuromuscular blocking agents (NMBA) for rapid sequence intubation in adults outside the operating room", section on 'Succinylcholine' and "Acute respiratory distress syndrome: Clinical features and diagnosis in adults".)

Common signs of significant smoke inhalation injury and the potential need for intubation include:

Persistent cough, stridor, or wheezing


Deep facial or circumferential neck burns

Nares with inflammation or singed hair

Carbonaceous sputum or burnt matter in the mouth or nose

Blistering or edema of the oropharynx

Depressed mental status, including evidence of drug or alcohol use

Respiratory distress

Hypoxia or hypercapnia

Elevated carbon monoxide and/or cyanide levels

Injury from the inhalation of hot gases generally occurs above the vocal cords and can cause significant edema. (See "Inhalation injury from heat, smoke, or chemical irritants".)

Flash burns often harm the face but rarely involve the airway, unlike severe burns from prolonged heat exposure associated with smoke inhalation.

Diagnostic tests and monitoring — Although initial results may be misleadingly normal, studies to assess pulmonary function should be obtained in patients at risk for inhalation injury [9]. These include an arterial blood gas (ABG) and a chest x-ray. Serial peak expiratory flow rates (PEFR), if obtainable, in addition to repeat ABGs, can provide evidence of declining pulmonary function, and are particularly useful early in a patient’s course. These studies can be repeated whenever findings from repeat examinations, pulse oximetry, or capnography suggest a decline in clinical status. (See "Simple and mixed acid-base disorders".)

Monitoring of end-tidal CO2 (EtCO2) using capnometry or capnography can provide useful information about respiratory status, adequacy of resuscitation, and potential cyanide toxicity, and should be initiated if feasible. A serum lactate concentration should also be obtained if cyanide poisoning is a concern. If available, fiberoptic laryngoscopy and bronchoscopy can assess the extent of airway injury and assist with intubation [9]. An electrocardiogram (ECG) is obtained to asses for cardiac dysfunction. (See "Carbon dioxide monitoring (capnography)" and "Inhalation injury from heat, smoke, or chemical irritants".)

Carbon monoxide and cyanide — The potential for carbon monoxide poisoning mandates that a carboxyhemoglobin level be obtained in all patients with moderate or severe burns. Standard pulse oximetry is NOT reliable with significant carbon monoxide toxicity. A standard arterial blood gas reports the concentration of oxygen dissolved in blood and cannot be used to establish or rule out the diagnosis of carbon monoxide or cyanide poisoning. (See "Carbon monoxide poisoning", section on 'Diagnosis'.)

Hyperbaric oxygen treatment may be needed if carbon monoxide levels are high, or if treatment for cyanide poisoning with methemoglobin is necessary but places the patient at risk for severe hypoxemia. Efforts to transport the patient for hyperbaric treatment must not detract from airway management and fluid resuscitation, the most important components of initial burn resuscitation. Treatment with high flow oxygen alone effectively removes carbon monoxide and the benefits of hyperbaric treatment remain a source of controversy. (See "Carbon monoxide poisoning", section on 'Hyperbaric oxygen'.)

Clinicians should consider the possibility of cyanide toxicity and keep a low threshold for initiating treatment. Complicating the diagnosis is the depressed level of consciousness of many severe burn victims, which may be caused by carbon monoxide, traumatic shock, or head injury, in addition to potential cyanide toxicity. A serum lactate measurement and end-tidal CO2 (EtCO2) monitoring may provide useful information when determining management of these patients and should be performed if cyanide poisoning is a possibility. Cyanide toxicity poisons mitochondria forcing cells to use anaerobic metabolism. This results in a lactic acidosis and a compensatory drop in EtCO2. (See "Cyanide poisoning", section on 'Diagnosis'.)

We suggest treatment for cyanide toxicity to be initiated in severe burn victims with an unexplained lactic acidosis or a low or declining EtCO2 level. If these measurements are unavailable, we suggest treatment be initiated in any patient demonstrating a depressed level of consciousness, cardiac arrest, or cardiac decompensation. Particularly with severe burn victims, we strongly prefer hydroxocobalamin to alternative cyanide antidotes. (See "Cyanide poisoning", section on 'Management'.)

Treatments — Supplemental oxygen and airway protection are the cornerstones of treatment for inhalation injury. Patients with severe burns often require tracheal intubation. (See 'Assessment and approach' above.)

Bronchodilators (eg, albuterol) can be useful when bronchospasm is present. Corticosteroids, however, have been associated with an increased risk of bacterial infection and should not be used [9].

Although fluid resuscitation is critically important in managing patients with significant burns, fluid status should be closely monitored in order to avoid overhydration and possible exacerbation of pulmonary edema. Some researchers have questioned the association between fluid resuscitation volumes and pulmonary edema [10]. (See 'Fluid resuscitation' below.)

Should mechanical ventilation be necessary, institution of low tidal volume ventilation to minimize airway pressures reduces the incidence of ventilator-associated lung injury and improves outcome [11]. Clinician tolerance of some degree of respiratory acidosis (so-called permissive hypercapnia) may be required to achieve lower airway pressures. Other ventilatory strategies, such as high frequency percussive ventilation and high-frequency oscillatory ventilation may be useful, but are not well studied in burn patients [11-14]. (See "Mechanical ventilation of adults in acute respiratory distress syndrome" and "High-frequency ventilation in adults".)

Treatments that may be helpful but need further study include inhaled nitric oxide to treat hypoxic vasoconstriction and aerosolized heparin and N-acetylcysteine (NAC) to remove bronchopulmonary casts [15-17]. As an example, in a small single-center, nonrandomized trial, pediatric burn victims with inhalation injury (confirmed by bronchoscopy) treated with aerosolized heparin and NAC experienced reduced reintubation rates, prevalence of atelectasis, and mortality compared with historical controls [18]. (See "Overview of the management of the severely burned patient" and "Overview and management strategies for the combined burn trauma patient".)

Fluid resuscitation

Approach to resuscitation — Burn shock during the initial 24 to 48 hours following major burns is characterized by myocardial depression and increased capillary permeability resulting in large fluid shifts and depletion of intravascular volume [19-21]. Rapid, aggressive fluid resuscitation to reconstitute intravascular volume and thereby maintain end-organ perfusion is crucial. Delays in fluid resuscitation and inadequate resuscitation are associated with increased mortality [22-24]. Arterial lines are often used to monitor blood pressure; urine output is used to determine the adequacy of fluid resuscitation (see 'Monitoring fluid status' below).

Over-resuscitation can be problematic and has been associated with multiple morbidities, including acute respiratory distress syndrome, pneumonia, multiorgan failure, and abdominal, extremity, and orbital compartment syndromes [25-27]. A survey of burn centers reported that initial fluid resuscitation exceeded recommended amounts in 58 percent of patients [11]. This reinforces the importance of calculating fluid resuscitation needs carefully and of continually adjusting resuscitation efforts according to the physiologic response. (See "Abdominal compartment syndrome in adults" and "Acute compartment syndrome of the extremities".)

According to the American Burn Association's practice guidelines, any patient with greater than 15 percent total body surface area (TBSA) nonsuperficial burns should receive formal fluid resuscitation [19]. Patients with major burns should have two large-bore intravenous (IV) lines placed through unburned skin, if possible, and may require central venous access. IV lines can be placed through burned tissue if necessary to avoid delays in resuscitation. The classification of burns is described in the accompanying figures and discussed in detail separately (figure 1 and table 2). (See "Classification of burns".)

Fluid selection — Fluid resuscitation of the patient with moderate or severe burns consists of an IV crystalloid solution. The ideal solution has not been determined, but lactated Ringer's solution (LR) is typically given; it contains physiologic concentrations of major electrolytes, and lactate may reduce the incidence of hyperchloremic acidosis that may occur with administration of extremely large volumes of isotonic saline (ie, 0.9 percent sodium chloride). Hartmann’s solution, another isotonic solution that differs slightly from LR in its concentrations of lactate and electrolytes, is also used. In animal models of burn injury, use of a combined solution of LR and ethyl pyruvate (an oxygen radical scavenger) for resuscitation was associated with increased survival, but this treatment has yet to be studied in humans [28].

The use of colloids or hypertonic saline for initial resuscitation is controversial. Colloids (eg, albumin solution, dextran) are significantly more expensive and, according to a meta-analysis of 21 trials involving 1385 critically ill patients, do not improve survival when compared with crystalloids, and are therefore not recommended [29]. The use of hypertonic saline as a resuscitation fluid does not appear to provide better outcomes than isotonic solutions and has been associated with increased rates of renal failure and death in one retrospective observational study [30,31].

Following initial resuscitation efforts, IV fluids are given to meet baseline fluid needs and maintain urine output. Any change to the infusion rate is made as gradually as possible [32]. Should urine output fall below 0.5 mL/kg per hour or other clinical parameters suggest inadequate resuscitation, additional fluid is infused. In such a circumstance, a bolus of IV crystalloid (approximately 500 to 1000 mL) is given and the infusion of crystalloid increased by approximately 20 to 30 percent. While adequate fluid resuscitation is crucial, care should be taken not to over-resuscitate.

If adequate resuscitation has been achieved and the patient is stabilized, the crystalloid solution can be changed to 5 percent dextrose in one-half isotonic saline (ie, 0.45 percent sodium chloride) with 20 mEq of potassium chloride per liter given at a maintenance rate to keep urine output at or above 0.5 mL/kg per hour. Clinicians should continue to monitor the patient's fluid status closely.

Enteral resuscitation may be a useful treatment for burn shock patients when intravenous therapy is unavailable, such as with large scale disasters. The World Health Organization (WHO) Oral Rehydration Solution (ORS) has been used successfully to resuscitate animals with 40 percent TBSA burns [33]. No human studies have been performed to validate this approach. Information about how to make ORS can be found on the WHO website (www.who.int/en/).

Estimating initial fluid requirements — No formula provides a precise method for determining the burn victim's fluid requirements; the formulas described here provide only a starting point and guide to initial fluid resuscitation [34]. Such factors as patient age, severity of burn, associated injury, and comorbidities can substantially alter the actual fluid requirements of individual patients. As an example, patients with inhalation injury require greater resuscitation volumes than those without [35,36]. Therefore, adjustments to estimate fluid needs must be made based upon a burn patient's physiologic response to resuscitation. (See 'Monitoring fluid status' below.)

Either the Parkland or the modified Brooke formula is a reasonable starting point for determining fluid requirements in adult patients. The Parkland (also known as Baxter) formula is the most widely used guide to initial resuscitation fluid needs in the burn patient, although some studies have questioned its accuracy [37,38]. According to this formula, the fluid requirement during the initial 24 hours of treatment is 4 mL/kg of body weight for each percent of TBSA burned, given IV (calculator 1) [19]. Superficial burns are excluded from this calculation. One-half of the calculated fluid need is given in the first eight hours, and the remaining half is given over the subsequent 16 hours. The rate of infusion for intravenous resuscitation fluid should be as constant as possible; sharp decreases in infusion rates can lead to vascular collapse and an increase in edema [32].

In addition to calculators (like the one above), a nomogram has been developed to help clinicians rapidly determine fluid requirements according to the Parkland formula [39]. A table with the nomogram and instructions for its use is provided (figure 2).

One alternative to Parkland is the modified Brooke formula, according to which the fluid requirement during the initial 24 hours of treatment is 2 mL/kg of body weight for each percent of TBSA burned, given IV. According to one retrospective review, use of the modified Brooke formula may reduce the total volume used in fluid resuscitation without causing harm [40].

Another alternative method for estimating initial fluid requirements in adults with severe burns is the Rule of Tens [41,42]. This simple method involves two or three steps, depending on patient size:

Estimate burn area (TBSA) to the nearest 10 percent.

Multiply the percent TBSA x 10 – The result gives the initial fluid rate in mL/hour for adults weighing 40 to 80 kg.

For patients who weigh more than 80 kg, increase the rate by 100 mL/hour for every additional 10 kg of body weight.

Children require maintenance fluid in addition to calculated fluid resuscitation volumes, and also need dextrose in the resuscitation fluid. The Galveston formula may allow for more accurate calculation of the initial fluid resuscitation children require. It is discussed separately. (See "Emergency care of moderate and severe thermal burns in children", section on 'Fluid resuscitation'.)

Monitoring fluid status — Confirming the adequacy of resuscitation is more important than strict adherence to Parkland or any fluid resuscitation formula. Monitoring urine output using an indwelling bladder catheter (eg, Foley catheter) is a readily available means of assessing fluid resuscitation. Hourly urine output should be maintained at 0.5 mL/kg in adults. Patients with minimal or no urine output after sustaining severe burns, despite appropriate fluid resuscitation, generally do not survive.

Clinical signs of volume status, such as heart rate, blood pressure, pulse pressure, distal pulses, capillary refill, and color and turgor of uninjured skin are monitored every hour for the first 24 hours. Inadequate fluid resuscitation is the most common cause of diminished distal pulses in the newly burned patient [22].

Another potential cause of diminished pulses is peripheral edema, which develops in many severe burn patients due to the large fluid volumes needed for resuscitation. As edema increases, elevated compartment pressures can compromise distal circulation and may require escharotomy. (See 'Escharotomy' below.)

Specific laboratory measurements such as mixed venous blood gas and serum lactate concentration are additional important guides to the adequacy of resuscitation [38]. A decrease in mixed venous oxygen saturation and an increase in serum lactate suggest inadequate end-organ perfusion (elevated serum lactate can also occur with carbon monoxide or cyanide poisoning). (See "Carbon monoxide poisoning" and "Cyanide poisoning".)

If available, invasive monitoring, such as central venous pressure, may be useful for monitoring fluid resuscitation, but it is generally not used in acute burn management. The American Thoracic Society (ATS) consensus conference report for the detection, correction, and prevention of tissue hypoxia, as well as other ATS guidelines, can be accessed through the ATS web site at www.thoracic.org/statements.

Care should be taken not to give excess IV fluid beyond what is needed as this may exacerbate pulmonary edema, a common problem among burn victims. However, some researchers have questioned the association between fluid resuscitation volumes and pulmonary edema [10]. (See "Treatment of severe hypovolemia or hypovolemic shock in adults".)

New technologies to guide fluid resuscitation are being developed, but require further study before widespread implementation can be recommended [43-46]. Esophageal echo-Doppler and cardiac output monitoring are being studied with the goal of developing less invasive means of assessing the adequacy of fluid resuscitation in patients with severe burns. Other approaches being studied include Doppler ultrasound measurement of renal perfusion and computer-guided infusions based upon urine output.

Blood transfusion — Although evidence is limited, blood transfusions have been associated with increased mortality in patients with severe thermal burns, and we suggest that aggressive transfusion be avoided [47-49]. For patients not at significant risk for an acute coronary syndrome (ACS), we suggest transfusing patients with two units of packed red blood cells only if the hemoglobin falls below 8 g/dL; for patients at risk for ACS, we suggest a transfusion threshold of 10 g/dL. Transfusion of the trauma patient with severe hemorrhage is discussed separately. (See "Initial evaluation and management of shock in adult trauma", section on 'Transfusion of blood products'.)

Hemoconcentration occurs during the first several hours immediately following a severe burn and transfusions are generally unnecessary. Thereafter, bone marrow function is depressed and transfusions may be needed. Erythropoietin has not been shown to prevent anemia or decrease transfusion requirements and is not in general use at burn centers [11].

Immediate burn care and cooling — Any hot or burned clothing, jewelry, and obvious debris should immediately be removed to prevent further injury and to enable accurate assessment of the extent of burns (caretakers should take precautions to avoid injuring themselves when removing such material).

Burned areas should be cooled immediately using cool water or saline soaked gauze. For small and moderate sized burns, cooling can minimize the zone of injury. Multiple studies have investigated optimal burn cooling, with durations from 15 minutes to three hours [50-52]. We generally apply saline-soaked gauzes, at a temperature of approximately 12ºC, for 15 to 30 minutes. Cooling tissue to around 12ºC (54ºF) during the first several hours after injury effectively decreases pain from burns; ice and freezing should be avoided to prevent frostbite, systemic hypothermia, and extension of burn injury.

Core body temperature is continuously monitored while cooling is performed to help prevent hypothermia, especially when dealing with burns greater than 10 percent TBSA; body temperature below 35ºC (95ºF) should be avoided [53,54]. Warmed intravenous fluids can be used to maintain core body temperature. (See 'Fluid resuscitation' above and "Accidental hypothermia in adults".)

Pain and anxiety management — Partial-thickness burns in particular can be excruciatingly painful. Intravenous (IV) morphine has been the mainstay of pain management for patients with significant burns. These patients may require extremely large doses of IV morphine or other opioids. It is reasonable to give patients with significant burns benzodiazepines given the anxiety associated with these injuries. The treatment of pain and anxiety in critically ill and burn patients is discussed in detail separately. (See "Burn pain: Principles of pharmacologic and nonpharmacologic management" and "Pain control in the critically ill adult patient".)

SECONDARY SURVEY AND MANAGEMENT — After the primary survey and initial resuscitation measures are performed, a detailed secondary survey, including a thorough physical examination and the management steps listed below, should be undertaken. Injuries commonly missed in the secondary survey include corneal abrasions and perineal wounds. The secondary survey is discussed in greater detail separately. (See "Initial management of trauma in adults", section on 'Secondary evaluation'.)

Laboratory studies and monitoring — Ongoing pulse oximetry and cardiac monitoring are performed for all patients with significant thermal burns. Routine laboratory studies obtained in such patients generally include: complete blood count, electrolytes, blood urea nitrogen, creatinine, glucose, venous blood gas (VBG), and carboxyhemoglobin. Arterial blood gas (ABG), chest radiograph, and an electrocardiogram (ECG) are obtained in any patient at risk for inhalation injury. A cyanide level may be helpful, particularly in the setting of unexplained severe lactic acidosis. (See "Cyanide poisoning" and "Inhalation injury from heat, smoke, or chemical irritants".)

A blood type and cross-match is obtained for any victim of significant trauma in anticipation of the need for transfusion. Other laboratory studies that may be useful in assessing muscle, cardiac, or end-organ injury include urine myoglobin, serum creatine kinase, and serum lactate. The VBG is a useful tool for assessing shock and the adequacy of resuscitation [55]. Findings from VBG analysis, including base deficit, correlate with ABGs [56]. (See "Initial management of trauma in adults" and "Clinical manifestations and diagnosis of rhabdomyolysis" and "Prevention and treatment of heme pigment-induced acute kidney injury (acute renal failure)".)

Chemoprophylaxis — Patients with extensive burns are considered to be immunosuppressed on the basis of altered neutrophil activity, T lymphocyte dysfunction, and imbalance in the production of cytokines [57-59]. Bacterial colonization of the burn eschar site can result. The burn also destroys the physical barrier to tissue invasion, which permits spread of the bacteria to the dermis and through the lymphatics along fibrous septae. Once invasion occurs, organisms can proliferate, especially in necrotic tissue, and can invade blood vessels producing a secondary bacteremia. Therefore, prophylaxis against infection with topical antibiotics is given to all patients with nonsuperficial burns.

Tetanus — Tetanus immunization should be updated if necessary for any burns deeper than superficial-thickness. Tetanus immune globulin should be given to patients who have not received a complete primary immunization (table 3) [60]. (See "Tetanus-diphtheria toxoid vaccination in adults" and "Tetanus".)

Antibiotics — Topical antibiotics are applied to all nonsuperficial burns. If the patient is immediately transferred to a burn center, burns are covered with clean, dry dressings and antibiotics are applied at the burn center. Treatment can be started in the ED if, for example, delays in transferring the patient to a burn center are anticipated. The best treatment of blistered burns is unclear. We apply topical antibiotics to partial thickness burns with intact blisters. Topical chemoprophylaxis is typically continued until wound epithelialization is complete. Prophylactic intravenous antibiotics are not typically given [61,62].

Selection of the topical antibiotic should be made in consultation with the burn center or admitting team, if treatment is begun in the ED. Classically, silver sulfadiazine (SSD) is used to prevent infection; it should be avoided near the eyes or mouth in those with sulfonamide hypersensitivity and in pregnant women, newborns, and nursing mothers. Bacitracin is a good alternative topical antibiotic in these individuals. Triple antibiotics (eg, polymyxin B, neomycin) can also be used. Because of decreased cost, many favor bacitracin. Topical antibiotic treatment is discussed in detail separately. (See "Local treatment of burns: Topical antimicrobial agents and dressings", section on 'Topical antimicrobial agents'.)

Wound management — Burn wounds should be cleaned. Embedded bits of clothing or other materials are removed by copious irrigation. Tar and asphalt can be removed with a mixture of cool water and mineral oil but should not be debrided. Copious amounts of polymyxin-B bacitracin zinc ointment (polysporin) applied for several days will emulsify residual tar. Management of tar and asphalt is discussed separately. (See "Topical chemical burns", section on 'Tar and asphalt'.)

Some providers clean burns using skin disinfectants (eg, Hibiclens, Betadine), but such disinfectants can inhibit the healing process and are discouraged. There is growing support for washing the wound using only mild soap and water [2,63-66]. The cleaning and debridement of burn wounds are discussed separately. (See "Local treatment of burns: Topical antimicrobial agents and dressings", section on 'Cleansing and debridement'.)

In addition to IV opioids, local or regional anesthesia can be used prior to wound care in patients with excruciating pain. However, injection directly into the wound or topical application should be avoided [51]. (See 'Pain and anxiety management' above.)

Ruptured blisters should be removed, but the management of clean, intact blisters is controversial. Needle aspiration of blisters should never be performed as this increases the risk of infection. Burn blisters are discussed separately. (See "Local treatment of burns: Topical antimicrobial agents and dressings", section on 'Burn blisters'.)

Wound dressings — Patients rapidly transferred to a burn center can be wrapped in a clean dry sheet and do not require any additional dressing. Otherwise, all partial and full-thickness burns should have dressings.

A fine, nonadherent, mesh gauze (eg, Telfa®) typically is applied, after the burn is cleansed and a thin layer of topical antibiotic is applied. Circulatory impairment is minimized by applying this nonadherent dressing in successive strips rather than wrapping it around the wound [67]. The dressing is held in place using either a tubular net bandage or gauze wraps lightly applied. The following video clips show a basic burn dressing being applied in the operating room: (movie 1).

Deep wounds may require biologic or biosynthetic dressings or bismuth-impregnated petroleum gauze. Burn dressings are discussed separately. (See "Local treatment of burns: Topical antimicrobial agents and dressings", section on 'Dressings'.)  

Escharotomy — With deep dermal and full thickness burns, the dermis can become stiff and unyielding, and this tissue is referred to as an eschar (picture 1). Incision of an eschar (ie, escharotomy) may be necessary to preserve respiratory function or prevent ischemia [19,68,69]. Ideally, escharotomy is performed by a physician experienced with the procedure to avoid damage to underlying structures, but on rare occasions a clinician caring for a patient with severe burns who lacks such experience may need to perform the procedure, possibly prior to transferring the patient to a burn center or higher level of care [70]. Drawings showing the approximate lines of incision used for escharotomy are provided (figure 3 and figure 4 and figure 5).

Escharotomy of the neck or chest may be required if mechanical constriction from eschar prevents adequate chest excursion and compromises respiration. An adequate chest escharotomy should lead to clinically meaningful improvements in respiration (picture 2).

Patients with circumferential abdominal burns can occasionally develop intra-abdominal hypertension, possibly leading to abdominal compartment syndrome. These conditions are best treated in a designated burn center. (See "Abdominal compartment syndrome in adults".)

Decompressive escharotomy of an extremity may be required for circumferential full-thickness burns, if eschar and underlying edema cause distal ischemia (picture 3 and picture 1). Although a number of parameters exist to guide the timing of extremity escharotomies, most often the decision is made clinically based upon the presence of constrictive wounds and compromised distal perfusion. Constrictive swelling does not occur until fluid resuscitation is underway (typically a minimum of three to four hours is needed), and escharotomy is rarely required in the immediate aftermath of a burn. If transfer of a patient with severe or circumferential burns is delayed, extremities should be reassessed to determine whether escharotomies are needed prior to departure to ensure continued distal perfusion. Assessment of distal perfusion may include examination of capillary refill, distal pulses (by palpation or Doppler ultrasound), skin temperature, tissue pliability, and pulse oximetry. Pulse oximetry above 90 percent suggests there is adequate distal perfusion and no need for escharotomy [71].  

Escharotomy incisions may be performed with coagulation electrocautery, which causes less bleeding, or a scalpel. Extremity incisions should extend through the eschar to the fatty tissue just beneath, but no further; fascia should be left intact. Adequate incisions should improve distal circulation. If perfusion fails to improve after the procedure, the clinician should reassess the escharotomy depth and location, and any incisions deemed insufficiently deep should be re-incised. If the escharotomy is adequate but perfusion remains poor, elevated compartment pressures may be contributing and should be measured. Guidance from a burn surgeon by phone can be helpful.

Clinicians should keep in mind the distinction between escharotomy, an incision through the eschar only, and fasciotomy, which involves incisions through all involved fascial layers and is performed to treat acute compartment syndrome (ACS) of the extremities. Patients with significant burns may develop ACS, requiring fasciotomy, which is discussed separately. Potential complications from extremity escharotomies include bleeding and injury of the brachial artery, saphenous vein, ulnar nerve at the elbow, superficial peroneal nerve at the knee, and the neurovascular bundles and extensors of the digits [72]. (See "Acute compartment syndrome of the extremities" and "Lower extremity fasciotomy techniques".)

Gastrointestinal interventions — Shock from thermal burn injuries results in mesenteric vasoconstriction predisposing to gastric distension, ulceration (so-called Curling's ulcer), and aspiration. Therefore, a nasogastric tube should be placed in patients with moderate or severe burns >20 percent TBSA [22]. High-risk patients receive medication to reduce gastric acid secretion, but this is usually initiated after admission. (See "Stress ulcer prophylaxis in the intensive care unit".)

Although generally not begun in the emergency department, early enteral feedings (ie, within 24 hours of injury) to meet basic patient energy needs attenuate the catabolic response to burns and are associated with improved outcomes [19,73,74]. Overfeeding does not help to maintain lean body mass and is associated with fatty liver so is to be avoided [75]. (See "Nutrition support in critically ill patients: Enteral nutrition".)

Modulating the catabolic response — Major burns cause a hypermetabolic state that is associated with a number of harmful physiologic derangements including immunosuppression, impaired wound healing, muscle catabolism, and hepatic dysfunction. A number of treatments are used to attenuate this hypermetabolic state. These treatments are generally initiated in the intensive care unit but may be started in the emergency department in close coordination with the burn team that will be assuming care of the patient. (See "Hypermetabolic response to severe burn injury".)

DISPOSITION — Patients who meet the American Burn Association's (ABA) criteria for major burns should be transferred to a burn center (table 1). Patients with moderate burns should be admitted for intravenous hydration and surgical care of their wounds.

Because of the initial difficulties in differentiating deep partial-thickness burns from full-thickness burns, clinicians should have a low threshold for consulting surgery for any patient with what appears to be a deep partial-thickness burn affecting more than 3 percent TBSA (total percentage of body surface area). An algorithm assisting with identifying and managing ambulatory burn patients is provided (algorithm 1). General guidelines for hospitalization include the following:

Admit patients suspected of inhalation injury for observation; fiberoptic bronchoscopy or xenon ventilation perfusion scanning is useful if the diagnosis is in doubt [7,51,76,77]. Pulmonary dysfunction causes more than 75 percent of fire-related deaths [1,4,5]. Initial evaluations may be normal in patients with inhalation injury who subsequently develop severe respiratory distress. Check for carbon monoxide poisoning; treatment with hyperbaric oxygen may be necessary [78]. Consider cyanide poisoning and provide presumptive treatment when indicated. (See 'Airway management' above and 'Carbon monoxide and cyanide' above and "Inhalation injury from heat, smoke, or chemical irritants".)

Admit patients with moderate to severe burns (table 1).

Admit patients with circumferential partial or full-thickness burns.

Patients at greater risk for development of infection of nonsuperficial wounds, such as diabetics and the elderly, generally should be hospitalized.

Patients with a high voltage injury who have an abnormal electrocardiogram (nonspecific ST-T wave changes most commonly) are at increased risk for cardiac arrhythmias and should be observed until the ECG normalizes [51,64]. (See "Environmental and weapon-related electrical injuries".)


Mortality — The chance of survival after a severe burn increased steadily in the second half of the 20th century due to a number of therapeutic developments, including vigorous fluid resuscitation, early excision of burn wounds, advances in critical care and nutrition, topical antibiotic use, and the evolution of specialized burn centers [79]. Even among patients hospitalized for burns, survival exceeds 95 percent [80,81].

A number of studies have investigated the variables associated with increased mortality in burn patients. In one retrospective review of 1665 patients admitted to a tertiary care hospital (mean burn size 14 ±20 percent TBSA, mean age 21± 20 years), three risk factors for death were identified [80]:

Age greater than 60 years

Nonsuperficial burns covering over 40 percent TBSA

Inhalation injury

The authors developed a mortality formula that predicts a 0.3, 3, 33, or 90 percent mortality depending upon whether zero, one, two, or three risk factors are present.

This study was criticized for having too few patients with three risk factors to make an accurate mortality estimate, and for having a high incidence of do not resuscitate orders among the sicker patients [79]. In addition, mortality estimates by others who used this model have not coincided with those predicted [82]. Nevertheless, the formula appears to provide a reasonable approximation of the risk of death in patients with severe burns.

Patient autonomy and aggressiveness of care — Although well beyond the scope of this review, the issue of patient autonomy in the setting of severe thermal injury warrants mention. Victims of severe burns face a prolonged, frequently painful period of treatment, during much of which their ability to communicate their desires will be impaired by the effects of and treatments for their injuries. Therefore, at the start of their initial resuscitation, during which many patients are lucid, it is reasonable to ask what types of care they wish and do not wish to receive [83]. (See "Advance care planning and advance directives" and "Ethical issues in palliative care" and "Ethical considerations in effective pain management at the end of life".)

SUMMARY AND RECOMMENDATIONS — Patients with severe thermal burns are at significant risk of death and major morbidity. Proper management during their initial resuscitation reduces such risk (algorithm 1). Below are listed critical points in the initial management of patients with severe thermal injury.

Airway, breathing, and circulation – Perform a primary trauma survey with appropriate management (algorithm 1). Look for evidence of respiratory distress and smoke inhalation injury, a common cause of death in the acute burn victim. Initial assessment may reveal no evidence of injury, but laryngeal edema can develop suddenly and unexpectedly. Aggressive airway management with early intubation is warranted if there is evidence of inhalation injury. Signs and symptoms of inhalation injury are described above. Obtain a chest x-ray, arterial blood gas, and electrocardiogram in all patients at risk for respiratory problems. (See 'Airway management' above and 'Laboratory studies and monitoring' above.)

Burn depth and size determine fluid resuscitation and the need for transfer (table 1). They must be accurately assessed. (See "Classification of burns".)

Burn shock – Vascular collapse from burn shock is a critical component of the pathophysiologic response to severe burns. Rapid, aggressive fluid resuscitation to reconstitute intravascular volume and maintain end-organ perfusion is crucial. Fluid requirements are based initially upon a formula (eg, Parkland) and subsequently upon patient response to the initial IV fluids. (See 'Fluid resuscitation' above.)

Initial, estimated fluid requirements – We suggest using lactated ringers for fluid resuscitation (Grade 2C). The Parkland-Baxter formula can be used to calculate initial fluid needs. According to this formula, the fluid requirement during the initial 24 hours of treatment is 4 mL/kg of body weight for each percent of TBSA burned, given IV (calculator 1). Superficial burns are excluded from this calculation. One-half of the calculated fluid need is given in the first eight hours, and the remaining half is given over the subsequent 16 hours. The rate of infusion for IV resuscitation fluid should be as constant as possible; rapid declines in infusion rates can lead to vascular collapse and an increase in edema. (See 'Estimating initial fluid requirements' above.)

Monitoring fluid status – Monitor urine output using an indwelling bladder catheter (eg, Foley catheter). Hourly urine output should be maintained at 0.5 mL/kg in adults. Clinical signs of volume status, such as heart rate, blood pressure, pulse pressure, distal pulses, capillary refill, and color and turgor of uninjured skin are monitored every hour for the first 24 hours. Inadequate fluid resuscitation is the most common cause of diminished distal pulses in the newly burned patient. A decrease in mixed venous oxygen saturation and an increase in serum lactate suggest inadequate end-organ perfusion. (See 'Monitoring fluid status' above.)

Carbon monoxide and cyanide – Burn patients may be exposed to carbon monoxide, requiring immediate treatment with high-flow oxygen (and possibly hyperbaric oxygen), and cyanide, requiring antidotal therapy. (See 'Carbon monoxide and cyanide' above.)

Wound care – Cool and clean wounds, but avoid inducing hypothermia in this process. Mild soap and water is suitable. Monitor the patient's core temperature continually. Remove any jewelry and any hot or burned clothing and obvious debris not densely adherent to the skin. Irrigation with cool water may be used. Topical antibiotics are applied to all nonsuperficial burns. If the patient is immediately transferred to a burn center, burns are covered with clean, dry dressings and antibiotics are applied at the burn center. There is no role for prophylactic IV antibiotics. (See 'Wound management' above.)

Pain control and additional interventions – Give opioids (eg, morphine) to treat pain and give tetanus prophylaxis. Extremely high doses of opioids may be required. Benzodiazepines can help relieve anxiety. (See 'Chemoprophylaxis' above.)

Coordination with burn team – Emergency clinicians should coordinate patient care closely with either the admitting or, in the case of transfer, with the accepting burn team. A number of additional medications may be of benefit, but most are begun after the patient has left the emergency department (ED). We institute glycemic control using an insulin drip as early as possible. Additional treatments to minimize the catabolic response should be initiated in close consultation with the burn team that will assume care of the patient. (See 'Modulating the catabolic response' above and 'Gastrointestinal interventions' above.)

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  1. Brigham PA, McLoughlin E. Burn incidence and medical care use in the United States: estimates, trends, and data sources. J Burn Care Rehabil 1996; 17:95.
  2. Mertens DM, Jenkins ME, Warden GD. Outpatient burn management. Nurs Clin North Am 1997; 32:343.
  3. Wasiak J, Spinks A, Ashby K, et al. The epidemiology of burn injuries in an Australian setting, 2000-2006. Burns 2009; 35:1124.
  4. Gomez R, Murray CK, Hospenthal DR, et al. Causes of mortality by autopsy findings of combat casualties and civilian patients admitted to a burn unit. J Am Coll Surg 2009; 208:348.
  5. Bloemsma GC, Dokter J, Boxma H, Oen IM. Mortality and causes of death in a burn centre. Burns 2008; 34:1103.
  6. www.ameriburn.org/resources_factsheet.php (Accessed on September 02, 2005).
  7. Monafo WW. Initial management of burns. N Engl J Med 1996; 335:1581.
  8. Cancio LC. Airway management and smoke inhalation injury in the burn patient. Clin Plast Surg 2009; 36:555.
  9. Miller K, Chang A. Acute inhalation injury. Emerg Med Clin North Am 2003; 21:533.
  10. Holm C, Tegeler J, Mayr M, et al. Effect of crystalloid resuscitation and inhalation injury on extravascular lung water: clinical implications. Chest 2002; 121:1956.
  11. Ipaktchi K, Arbabi S. Advances in burn critical care. Crit Care Med 2006; 34:S239.
  12. Cioffi WG Jr, Rue LW 3rd, Graves TA, et al. Prophylactic use of high-frequency percussive ventilation in patients with inhalation injury. Ann Surg 1991; 213:575.
  13. Cartotto R, Ellis S, Smith T. Use of high-frequency oscillatory ventilation in burn patients. Crit Care Med 2005; 33:S175.
  14. Chung KK, Wolf SE, Renz EM, et al. High-frequency percussive ventilation and low tidal volume ventilation in burns: a randomized controlled trial. Crit Care Med 2010; 38:1970.
  15. Sheridan RL, Hurford WE, Kacmarek RM, et al. Inhaled nitric oxide in burn patients with respiratory failure. J Trauma 1997; 42:629.
  16. Desai MH, Mlcak R, Richardson J, et al. Reduction in mortality in pediatric patients with inhalation injury with aerosolized heparin/N-acetylcystine [correction of acetylcystine] therapy. J Burn Care Rehabil 1998; 19:210.
  17. Toon MH, Maybauer MO, Greenwood JE, et al. Management of acute smoke inhalation injury. Crit Care Resusc 2010; 12:53.
  18. Murakami K, McGuire R, Cox RA, et al. Heparin nebulization attenuates acute lung injury in sepsis following smoke inhalation in sheep. Shock 2002; 18:236.
  19. Saffle, JR. Practice guidelines for burn care. J Burn Care 2001; 22(Suppl):i.
  20. Hettiaratchy S, Dziewulski P. ABC of burns: pathophysiology and types of burns. BMJ 2004; 328:1427.
  21. Evers LH, Bhavsar D, Mailänder P. The biology of burn injury. Exp Dermatol 2010; 19:777.
  22. Ramzy PI, Barret JP, Herndon DN. Thermal injury. Crit Care Clin 1999; 15:333.
  23. Wolf SE, Rose JK, Desai MH, et al. Mortality determinants in massive pediatric burns. An analysis of 103 children with > or = 80% TBSA burns (> or = 70% full-thickness). Ann Surg 1997; 225:554.
  24. Holm C, Melcer B, Hörbrand F, et al. The relationship between oxygen delivery and oxygen consumption during fluid resuscitation of burn-related shock. J Burn Care Rehabil 2000; 21:147.
  25. Klein MB, Hayden D, Elson C, et al. The association between fluid administration and outcome following major burn: a multicenter study. Ann Surg 2007; 245:622.
  26. Dulhunty JM, Boots RJ, Rudd MJ, et al. Increased fluid resuscitation can lead to adverse outcomes in major-burn injured patients, but low mortality is achievable. Burns 2008; 34:1090.
  27. Sullivan SR, Ahmadi AJ, Singh CN, et al. Elevated orbital pressure: another untoward effect of massive resuscitation after burn injury. J Trauma 2006; 60:72.
  28. Fink MP. Ethyl pyruvate. Curr Opin Anaesthesiol 2008; 21:160.
  29. Perel P, Roberts I. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2012; :CD000567.
  30. Bunn F, Roberts I, Tasker R, Akpa E. Hypertonic versus near isotonic crystalloid for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2004; :CD002045.
  31. Huang PP, Stucky FS, Dimick AR, et al. Hypertonic sodium resuscitation is associated with renal failure and death. Ann Surg 1995; 221:543.
  32. Gueugniaud PY, Carsin H, Bertin-Maghit M, Petit P. Current advances in the initial management of major thermal burns. Intensive Care Med 2000; 26:848.
  33. Michell MW, Oliveira HM, Kinsky MP, et al. Enteral resuscitation of burn shock using World Health Organization oral rehydration solution: a potential solution for mass casualty care. J Burn Care Res 2006; 27:819.
  34. Blumetti J, Hunt JL, Arnoldo BD, et al. The Parkland formula under fire: is the criticism justified? J Burn Care Res 2008; 29:180.
  35. Dai NT, Chen TM, Cheng TY, et al. The comparison of early fluid therapy in extensive flame burns between inhalation and noninhalation injuries. Burns 1998; 24:671.
  36. Navar PD, Saffle JR, Warden GD. Effect of inhalation injury on fluid resuscitation requirements after thermal injury. Am J Surg 1985; 150:716.
  37. Holm C, Mayr M, Tegeler J, et al. A clinical randomized study on the effects of invasive monitoring on burn shock resuscitation. Burns 2004; 30:798.
  38. Holm C, Melcer B, Hörbrand F, et al. Haemodynamic and oxygen transport responses in survivors and non-survivors following thermal injury. Burns 2000; 26:25.
  39. Theron A, Bodger O, Williams D. Comparison of three techniques using the Parkland Formula to aid fluid resuscitation in adult burns. Emerg Med J 2014; 31:730.
  40. Chung KK, Wolf SE, Cancio LC, et al. Resuscitation of severely burned military casualties: fluid begets more fluid. J Trauma 2009; 67:231.
  41. Chung KK, Salinas J, Renz EM, et al. Simple derivation of the initial fluid rate for the resuscitation of severely burned adult combat casualties: in silico validation of the rule of 10. J Trauma 2010; 69 Suppl 1:S49.
  42. Bacomo FK, Chung KK. A primer on burn resuscitation. J Emerg Trauma Shock 2011; 4:109.
  43. Namias N. Advances in burn care. Curr Opin Crit Care 2007; 13:405.
  44. Wang GY, Ma B, Tang HT, et al. Esophageal echo-Doppler monitoring in burn shock resuscitation: are hemodynamic variables the critical standard guiding fluid therapy? J Trauma 2008; 65:1396.
  45. Reid RD, Jayamaha J. The use of a cardiac output monitor to guide the initial fluid resuscitation in a patient with burns. Emerg Med J 2007; 24:e32.
  46. Salinas J, Chung KK, Mann EA, et al. Computerized decision support system improves fluid resuscitation following severe burns: an original study. Crit Care Med 2011; 39:2031.
  47. Kwan P, Gomez M, Cartotto R. Safe and successful restriction of transfusion in burn patients. J Burn Care Res 2006; 27:826.
  48. Palmieri TL, Caruso DM, Foster KN, et al. Effect of blood transfusion on outcome after major burn injury: a multicenter study. Crit Care Med 2006; 34:1602.
  49. Higgins S, Fowler R, Callum J, Cartotto R. Transfusion-related acute lung injury in patients with burns. J Burn Care Res 2007; 28:56.
  50. Pushkar NS, Sandorminsky BP. Cold treatment of burns. Burns Incl Therm Inj 1982; 9:101.
  51. Hartford, CE. Care of outpatient burns. In: Total Burn Care, Herndon, D (Eds), WB Saunders, Philadelphia 1996. p.71.
  52. Allwood JS. The primary care management of burns. Nurse Pract 1995; 20:74, 77.
  53. Purdue GF, Layton TR, Copeland CE. Cold injury complicating burn therapy. J Trauma 1985; 25:167.
  54. Singer AJ, Taira BR, Thode HC Jr, et al. The association between hypothermia, prehospital cooling, and mortality in burn victims. Acad Emerg Med 2010; 17:456.
  55. Baron BJ, Barrett D, Stavile KL, et al. Correlation of arterial and venous base deficits during the initial assessment of trauma patients [abstract]. Acad Emerg Med 2000; 7:567.
  56. Evron S, Tress V, Ezri T, et al. The importance of blood sampling site for determination of hemoglobin and biochemistry values in major abdominal and orthopedic surgery. J Clin Anesth 2007; 19:92.
  57. Bjerknes R, Vindenes H, Laerum OD. Altered neutrophil functions in patients with large burns. Blood Cells 1990; 16:127.
  58. Schwacha MG, Ayala A, Chaudry IH. Insights into the role of gammadelta T lymphocytes in the immunopathogenic response to thermal injury. J Leukoc Biol 2000; 67:644.
  59. Peter FW, Schuschke DA, Barker JH, et al. The effect of severe burn injury on proinflammatory cytokines and leukocyte behavior: its modulation with granulocyte colony-stimulating factor. Burns 1999; 25:477.
  60. Karyoute SM, Badran IZ. Tetanus following a burn injury. Burns Incl Therm Inj 1988; 14:241.
  61. Avni T, Levcovich A, Ad-El DD, et al. Prophylactic antibiotics for burns patients: systematic review and meta-analysis. BMJ 2010; 340:c241.
  62. Barajas-Nava LA, López-Alcalde J, Roqué i Figuls M, et al. Antibiotic prophylaxis for preventing burn wound infection. Cochrane Database Syst Rev 2013; :CD008738.
  63. Baxter CR. Management of burn wounds. Dermatol Clin 1993; 11:709.
  64. Waitzman AA, Neligan PC. How to manage burns in primary care. Can Fam Physician 1993; 39:2394.
  65. Hill MG, Bowen CC. The treatment of minor burns in rural Alabama emergency departments. J Emerg Nurs 1996; 22:570.
  66. Greenhalgh DG. The healing of burn wounds. Dermatol Nurs 1996; 8:13.
  67. Martinez S. Ambulatory management of burns in children. J Pediatr Health Care 1992; 6:32.
  68. Orgill DP, Piccolo N. Escharotomy and decompressive therapies in burns. J Burn Care Res 2009; 30:759.
  69. White CE, Renz EM. Advances in surgical care: management of severe burn injury. Crit Care Med 2008; 36:S318.
  70. Kupas DF, Miller DD. Out-of-hospital chest escharotomy: a case series and procedure review. Prehosp Emerg Care 2010; 14:349.
  71. Piccolo NS, Piccolo MS, Piccolo PD, et al. Escharotomies, fasciotomies and carpal tunnel release in burn patients--review of the literature and presentation of an algorithm for surgical decision making. Handchir Mikrochir Plast Chir 2007; 39:161.
  72. Sheridan RL, Tompkins RG. What's new in burns and metabolism. J Am Coll Surg 2004; 198:243.
  73. Mosier MJ, Pham TN, Klein MB, et al. Early enteral nutrition in burns: compliance with guidelines and associated outcomes in a multicenter study. J Burn Care Res 2011; 32:104.
  74. Wasiak J, Cleland H, Jeffery R. Early versus late enteral nutritional support in adults with burn injury: a systematic review. J Hum Nutr Diet 2007; 20:75.
  75. Hart DW, Wolf SE, Herndon DN, et al. Energy expenditure and caloric balance after burn: increased feeding leads to fat rather than lean mass accretion. Ann Surg 2002; 235:152.
  76. Peate WF. Outpatient management of burns. Am Fam Physician 1992; 45:1321.
  77. Moylan JA. Supportive therapy in burn care. Smoke inhalation. Diagnostic techniques and steroids. J Trauma 1979; 19:917.
  78. Heimbach DM, Waeckerle JF. Inhalation injuries. Ann Emerg Med 1988; 17:1316.
  79. Saffle JR. Predicting outcomes of burns. N Engl J Med 1998; 338:387.
  80. Ryan CM, Schoenfeld DA, Thorpe WP, et al. Objective estimates of the probability of death from burn injuries. N Engl J Med 1998; 338:362.
  81. Saffle JR, Davis B, Williams P. Recent outcomes in the treatment of burn injury in the United States: a report from the American Burn Association Patient Registry. J Burn Care Rehabil 1995; 16:219.
  82. Choinière M, Dumont M, Papillon J, Garrel DR. Prediction of death in patients with burns. Lancet 1999; 353:2211.
  83. Imbus SH, Zawacki BE. Autonomy for burned patients when survival is unprecedented. N Engl J Med 1977; 297:308.
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