1. Description of the problem
Major burns can be devastating injuries. They have historically been defined as >20% total body surface area (TBSA), as this level of tissue destruction is associated with increased capillary leak and release of inflammatory cytokines, which can result in hypovolemia and shock without appropriate and timely intervention. It is also the %TBSA at which most guided fluid resuscitation strategies/formulas are instituted.
There are multiple etiologies or mechanisms of burn injury, including thermal, electrical, or chemical injury, as well as the vesiculobullous diseases. In 1950, a 45% TBSA burn correlated to 50% mortality (LD50) in 21-year-old males; according to the 2010 National Burn Repository Annual Report, the LD50 for this age group now correlates to an 80% TBSA burn. This drastic change in burn survival is a direct result of improved resuscitative and surgical approaches to major burns.
The acute care provider must take a comprehensive team-based approach to managing major burns. This includes a thorough initial assessment and diagnosis, timely resuscitation, knowledge of appropriate transfer criteria, early surgical care and wound coverage, rehabilitation, and continuous reassessment.
2. Emergency Management
The initial assessment and emergency management of major burns follows the same principles as those commonly used in advanced cardiac and trauma life support, the ABCDEs.
An assessment for potential airway compromise. Look for evidence of inhalation injury, oropharyngeal burns or mucosal injury; initiate cervical spine precautions if there is concern for trauma in the initial injury; and use appropriate airway management techniques. Indications for intubation are: (1) oropharyngeal swelling, (2) erythema, (3) hoarseness, (4) stridor, or (5) tachypnea/dyspnea.
Respiratory compromise secondary to major burn injuries is common. Mechanisms for this include: (1) inhalation injury, (2) chemical irritation, (3) bronchospasm, (4) restrictive chest wall eschars, and (5) traumatic pulmonary injury from blasts or secondary falls.
Burn shock occurs with >20% TBSA burns – see the “Burn Shock” chapter for comprehensive coverage of burn shock.
Appropriate intravenous (IV) access is needed; a minimum of two large-bore IVs should be placed. Burn site and increasing peripheral edema may limit peripheral IV access, in which case central venous access through unaffected skin is preferable for significant resuscitation.
Check pulses routinely throughout the initial resuscitation – extremity eschars, especially when circumferential, may lead to compartment syndrome and place peripheral perfusion at risk. Assessment for the need for escharotomies should be done early, knowing that as resuscitation progresses, the affected tissue below the eschars will become edematous. This is also important when assessing circumferential burns of the abdomen and chest – restricted ventilation and abdominal compartment syndrome are not uncommon.
Major burn injuries can lead to sizable fluid shifts and require large amounts of resuscitation. The initial presentation, though, is rarely one of hypovolemia. If significant hypovolemia or hemodynamic instability is present, delayed presentation of the burn should be considered, but other potential sources (e.g. cardiogenic, acute blood loss, etc.) should be ruled out.
A thorough neurologic assessment, including mental status exam, Glasgow Coma Scale score calculation, and evidence of focal neurologic injury is standard. Carbon monoxide poisoning can present with confusion, disorientation, drowsiness and agitation, as can hypoxia. Associated trauma from falls and blasts resulting in spinal fractures and head injuries can occur.
Remove all clothing, obtain a brief estimation of burn depth and %TBSA of burned tissue, and rule out any concomitant injuries, including any sources of blood loss. Do so in an expeditious manner, being cognizant of the patient’s temperature status – all burn patients are at high risk for hypothermia, especially with prolonged evaporative, convective, and conductive heat loss exposures.
The secondary survey includes a thorough history and physical exam, which can provide additional information about other injuries incurred during the incident, as well as continuing the assessment of burn depth, %TBSA, and performing diagnostic tests/imaging.
Thorough History and Mechanism
Diagnosis of a major burn must be done in correlation with a thorough history of the events leading up to the injury, including knowledge of the mechanism, its qualitative specifics (e.g. type of liquid in a scald injury, or level of voltage in an electrical injury), as well as the timing of the burn. Much of this information should be ascertained during the primary survey, as this may be the only opportune time prior to other interventions (e.g. intubation, surgery, etc.) that may render the patient incapable of conveying a history.
Once emergency management has been instituted, appropriate fluid resuscitation must be started.
Calculating the %TBSA of the burn is necessary for guided fluid resuscitation. The most commonly used tools for estimating %TBSA are illustrated in the Lund-Brower chart (Figure 1) and the Rule of Nines chart (Figure 2).
The Lund-Browder chart is beneficial in institutions that admit burn patients of all ages, and gives a more accurate estimation of burn size, as a patient’s size and proportions grow and differ with age.
The Rule of Nines chart is very easy to remember, but has been shown to have greater variability than other techniques and tends to overestimate burn size. Overestimation of burn size may cause unintended over-resuscitation, which can lead to excessive edema, ARDS, abdominal compartment syndrome or extension of burn depth. It is not accurate in the assessment of pediatric burn injuries.
Estimation of Burn Depth
Estimation of burn depth is not required for immediate resuscitation needs, but is very important when planning future surgical intervention. Burns are dynamic wounds, and depth can vary depending on time of exposure, contact temperature, skin thickness, and adequacy of resuscitation. Although precise burn depth estimation can be impossible with larger complex injuries, this dynamic nature warrants constant reassessment of the wounds throughout the initial resuscitation process.
The traditional classification system describes burns as the “degree” of involvement (e.g. first-degree, second-degree, etc.). The newer classification system focuses on a description of the layers of tissue affected, which can then be applied to surgical decision-making. Below is an outline of the commonly used classification systems:
Superficial Partial Thickness (Second-Degree)
Deep Partial Thickness (Second-Degree)
Deep Full-Thickness (Fourth-Degree)
Various modalities for burn depth estimation, besides clinical acumen, have been developed over the years, including radioactive isotopes, photometry, vital dyes, Doppler and echo ultrasound, and nuclear imaging, but their accuracy has been somewhat lacking. Novel technology, laser Doppler imaging, is noninvasive and simple to use, has decreased time to estimation in comparison with clinical judgment, and has a prediction accuracy approaching 100% in small studies, but knowledge of the technology’s limitations and further research is warranted.
Inhalation injury refers to the inhalation of hot gases and potentially toxic fumes, usually in association with a burn injury. This injury disproportionately increases morbidity and mortality, and is associated with a >40% increase in resuscitative fluid requirements.
Although there are currently no standardized diagnostic criteria or grading systems, the following important warning signs and risk factors can help predict the presence of inhalation injury:
a history of smoke or fireexposure in an enclosed space
singed nose or facial hairs
stridor, hoarseness, dyspnea,voice change
loss of consciousness
bronchoscopic evidence ofsoot in airways, mucosal ulceration, erythema (considered confirmatory)
Acute airway obstruction occurs in >20% of patients with inhalation injury. The clinical manifestations of inhalation injury are variable, as is the timing of airway compromise. Stridor upon presentation should be an immediate indication for intubation. Delayed pulmonary and systemic implications of this type of injury include increased systemic capillary leak, bronchospasm, bronchorrhea, mucosal sloughing, alveolar flooding, reduced ciliary clearance and surfactant function, bronchial debris obstruction, and complete airway obstruction from upper airway edema. These delayed complications should warrant continued reassessment of airway patency within the first 24 hours.
Carbon Monoxide Poisoning
Carbon monoxide (CO) poisoning is common in patients with inhalation injury from an enclosed space fire exposure. Carbon monoxide binds to deoxyhemoglobin with an affinity >200 times that of oxygen, forming carboxyhemoglobin (COHb), which in turn shifts the oxyhemoglobin curve to the left, decreasing the effective tissue oxygen delivery. It can also disrupt the cytochrome oxidase pathway, causing intra- and extracellular hypoxia. Non-smokers have COHb levels as high as 3 percent at baseline, whereas heavy smokers can exhibit levels as high as 15 percent. Signs and symptoms of CO poisoning include:
10-20% COHb – headache, malaise
20-30% COHb – drowsiness, lethargy, nausea and vomiting
30-40% COHb – confusion, agitation, dizziness
40-50% COHb – ataxia, coma, respiratory depression
50% or greater – myocardial infarction, imminent death
Once the initial clinical assessment and stabilization has been performed, the following are suggested diagnostic tests to obtain:
Laboratory – complete bloodcount; basic metabolic panel; coagulation screen; type andscreen/cross-match; carboxyhemoglobin; cardiac enzymes (suspected electrical injury); arterial blood gas (especially in inhalation injury); serum lactate; urine myoglobin (suspected rhabdomyolysis)
Procedures – ECG; bronchoscopy (inhalation injury)
Imaging – chest x-ray; CT scan for assessment of concomitant injuries.
There are multiple etiologies/mechanisms of burn injury:
Contact – direct contact, commonly of longer duration, with a hot surface (e.g.stove, flat iron, industrial accidents); these can cover the entire spectrum of burn depth.
Scalds – exposure to hot liquids or gases; commonly superficial burns.
Flame – exposure to a fire, often involving inhalational injury; commonly causing partial- and full-thickness burns.
Flash – a more brief exposure to heat, whether it be a short blast, or close proximity to a high-voltage arc; commonly partial-thickness burns.
Low-voltage(<1000V) – domestic injuries; concern for cardiac arrhythmias if the source is alternating current; commonly causing partial- and full-thickness burns at entry and exit sites.
High-voltage(>1000V) – occupational injuries; can result in extensive soft tissue damage and limb loss; concern for rhabdomyolysis.
Voltages >70,000V can be fatal.
Can be caused by household products, but are usually the result of industrial accidents.
Copious irrigation and complete removal of the chemical is key; litmus paper testing can confirm removal.
A continuum of disorders mostly in the pediatric population involving epidermal detachment; similar resuscitation and complications as the burn population.
Toxic epidermal necrolysis
Staphylococcal scalded skin syndrome
Non-Accidental Burn Injury
The 2009 National Burn Repository reported a 10-year review of more than 90,000 patients: 1.6% of injuries were secondary to suspected abuse or assault, 1.2% were self-inflicted injuries, and 1.2% were suspected child abuse. 3-20% of all pediatric child abuse cases involve burn injuries. Child abuse cases, in particular, can become emotionally charged situations, and it is important to take an objective systematic approach towards its investigation. Obtain a thorough history, including a social history, document the pattern of injury and whether it matches the history, and obtain a skeletal radiographic survey. The following is a list of common risk factors and patterns indicative of likely abuse:
contact wounds with obvious sources (e.g. cigarettes, irons, etc.)
splash burns (more common in adult abuse)
glove or stocking distribution
restraint injuries or other traumatic injuries indicative of abuse (multiple bruises, old fractures on radiography, etc.)
infants and school-aged children, as well as elderly and dependent adults.
poor hygiene, missed immunizations
single or adolescent parent
poor parent-child bonding
parental/caretaker apathy, lack of concern
child has lethargy, apathy, little emotion
delayed presentation to the emergency department
inconsistency in the history
Once there is suspicion of abuse, notification of child protective services or the police will initiate an appropriate investigation.
4. Specific Treatment
Once fluid resuscitation has begun, the burn wound invariably develops edema. The eschar of a full-thickness burn can become an inelastic tourniquet, especially if it is circumferential – this swelling can affect peripheral perfusion, chest wall excursion and ventilation, as well as abdominal perfusion, leading to abdominal compartment syndrome.
Indications for Escharotomy
absence of peripheral Doppler pulses.
signs and symptoms of nerve compression.
extremity compartment pressures >40 mmHg (consideration should be given to those >25 mmHg).
evidence of pulmonary or hemodynamic compromise with thoracic burns.
abdominal pressures >25 mmHg or evidence of abdominal compartment syndrome.
prophylactic escharotomiesfor obvious circumferential full-thickness burns in concordance withclinical judgment.
An escharotomy is an urgent procedure, best performed by experienced personnel in an operating room environment, to ensure appropriate hemostasis and sterility. The incision is made through the burned tissue to the underlying unburned viable tissue only. The incisions follow the long axis of the extremity in the mid-medial and mid-lateral lines. Thoracic escharotomies are performed to provide mobility to the chest wall, and decompressive laparotomy may be warranted in those individuals with evidence of abdominal compartment syndrome.
Rhabdomyolysis is another concern when faced with potential compartment syndromes. The presence of urine myoglobin and oliguria can aid in the diagnosis. Appropriate hydration and removal of compressive sources are the therapy of choice.
In those patients with confirmed injury, close observation and supportive care are the most effective management. In those patients requiring intubation and mechanical ventilation, ventilatory strategies avoiding acute lung injury are key, as is aggressive pulmonary toilet, and prevention of ventilator-associated pneumonia. The use of adjuvant therapy to reduce inflammation and free radical formation in inhalation injury has been widely studied. In the past few years, the use of inhaled heparin/N-acetylcysteine has been examined. It has shown some benefit on mortality in the pediatric population, as well as improving oxygenation in the first 72 hours, but it has made little difference in other clinical outcomes. Most of the significant upper airway edema will resolve within the first 72 hours of injury and, in the absence of any significant lower airway injury/compromise, this can lead to fairly rapid ventilatory liberation.
Carbon Monoxide Poisoning
The current recommendations for therapy include removal from the source and supplemental oxygen. The half-life of COHb is approximately 2-4 hours while exposed to room air; applying 100% oxygen can decrease this to 20-30 minutes; hyperbaric oxygen, although very effective and having been shown to provide some acute as well as long-term benefits, is lacking appropriate guidelines for use and is commonly impractical and unavailable. Patients with COHb levels >25% should invariably be intubated and ventilated with 100% oxygen.
Cyanide poisoning is commonly a concern, especially in patients with suspected inhalation injury or with significant exposure to products of combustion of synthetic polymers and household materials. It will commonly present as a metabolic acidosis. There are several treatment options, including a cyanide antidote kit (amyl nitrate perles, sodium nitrite, and sodium thiosulfate) or a cyanokit (hydroxycobalamin). Although prophylactic administration occurs, it should be reserved until other sources of metabolic acidosis have been ruled out, such as under-resuscitation or the more common carbon monoxide poisoning.
Effective fluid resuscitation is one of the cornerstones of modern burn care. Patients with burns >20% should undergo guided fluid resuscitation based on body size and %TBSA. Most burn centers follow a variant of the Parkland resuscitation formula (now also known as the Consensus formula) and strive to maintain a minimum perfusion pressure (MAP > 65 mmHg) and a minimum urine output of 0.5-1 mL/kg/hr.
See the “Burn Shock” chapter.
Burn Wound Dressings and Topical Antimicrobials
Treatment of burns begins with hydrotherapy. The wounds are washed with warm water and chlorhexidine and debrided of any necrotic or loose tissue, and blisters are deroofed. Topical antimicrobials and occlusive dressings, such as cling or mesh gauze, and a compressive elastic wrap in the case of extremity burns, are applied. This is done to prevent any further progression of tissue damage or desiccation. Common topical antimicrobials are as follows:
Silver sulfadiazine (SSD)
Cerium plus SSD
Xeroform (Bismuth petroleum)
Early Excision, Coverage and Grafting
For deeper burns, ones that are unlikely to heal on their own, early excision has been shown to decrease morbidity and mortality, bacterial colonization, and hospital length of stay. According to the American Burn Association White Paper, surgical excision should ideally take place within the first post-burn week. Tangential or fascial excisions are acceptable techniques, and single- or multi-stage graftings can be used to cover the wounds. Common temporary dressings placed after excision, while awaiting an appropriate granulation bed, are:
Allograft – cadaver graft
AlloDerm – an acellulardermal matrix
Integra – a bilayer dermalanalogue that promotes regeneration
Biobrane – a biosyntheticmesh
Xenograft – pig skin
Cultured keratinocytes -cultured epithelial autograft
Excision and grafting should be done by an experienced burn surgeon. Regional burn centers provide the personnel and expertise needed to manage major burn wounds; care should be transferred appropriately.
American Burn Association Burn Center Referral Criteria
Second- and third-degree burns on >10% TBSA in patients <10 or >50 years of age
Second- and third-degree burns on >20% TBSA in other age groups
Second- and third-degree burns involving the face, hands, feet, genitalia, perineum, and major joints
Third-degree burns on >5% TBSA
Electrical burns, including lightning injury
Burn injury in patients with pre-existing medical disorders that could complicate management, prolong recovery or affect mortality
Any patient with burns and concomitant trauma (such as fracture) in which the burn injury poses the greatest risk of morbidity or mortality
Hospitals without qualified personnel or equipment for the care of children should transfer children to a burn center with these capabilities.
Burn injury in patients who will require special social/emotional and/or long-term rehabilitative support, including cases involving suspected child abuse and substance abuse
5. Disease monitoring, follow-up and disposition
Considerations After Emergency Management
Adequacy of Resuscitation
Fluid resuscitation is the cornerstone of acute therapy for major burns. Maintaining an adequate fluid balance requires an intimate knowledge of the pathophysiology and natural history of major burns. The “Burn Shock” chapter provides a thorough description of the strategies that have been developed to provide adequate resuscitation to patients with major burns, as well as the monitoring required as the wounds and systemic responses evolve.
Burn injuries induce a hypermetabolic response, which can increase the basal metabolic rate by more than 100%. Patients with major burns are at risk of developing protein calorie malnutrition with associated poor wound healing, immune suppression and infection; most require supplementation despite robust oral intake. Enteral feeding can be started as early as 12 hours post-burn, and has been linked to reduced wound infection risk, enhanced wound healing and shorter hospital length of stay in both adult and pediatric populations. Other therapies proposed for reducing the catabolism of burn injuries include anabolic steroids such as oxandrolone, and the beta blocker propranolol.
Rehabilitation starts the day of the injury and can continue for years. Initially, edema management and functional range-of-motion techniques are used while the patient is still recovering from the acute injury. Improvement of breathing mechanics is the focus in those with inhalational injury or significant chest wall burns. Extremity burns commonly require splinting to prevent deformation and development of contractures. Pressure garments are used several days after grafting; they not only help reduce edema but also can be beneficial in the prevention of hypertrophic scar formation as wound healing progresses. Other techniques used to reduce scar formation include massage, moisturizing creams, and formed moulds. It is important to remember that burns are not only physically demanding, but psychologically as well, especially as the patient is reintroduced into a body image-focused society.
Outpatient follow-up after hospital discharge commonly occurs to reassess for pain control, contracture and scar formation, infection, as well as to assess the patient’s functional status and to continue education.
An initial understanding of the local histologic response that occurs after a burn injury is imperative. The three zones of a burn as described by Jackson in 1953 are:
Zone of coagulation
Zone of stasis
Zone of hyperemia
These wounds are dynamic and can convert to irreversibly damaged tissue in the presence of poor perfusion, excessive edema, tissue desiccation, tissue shearing, and infection. Efforts must be made to prevent this conversion and loss of the zone of stasis.
For a description of the systemic effects of burns and pathophysiology at the cellular level, see the “Burn Shock” chapter.
Burns are a major problem in the developed and developing world. They are common, they are devastating both physically and psychologically, and they span the entire age spectrum. A 10-year review from the National Burn Repository published in 2010 showed 148,419 acute burn admissions to U.S. burn centers. Of these admissions, 70% were male, with a mean age of 32 years, 17% were <5 years of age and 12% were >60 years of age. Only 36.7% of patients had a major burn (> 20%TBSA), and inhalational injury was reported in 5.9% of patients. Flame and scald burns accounted for 72% of total cases. 66% of burn injuries occur in the home, with only 14.6% being work-related. The average length of hospital stay declined over the past 10 years from 11 to 9 days, and can be predicted as 1 day for every %TBSA burned.
Survival has remained at 95%, with deaths from burn injury increased at the extremes of age, increasing burn size, and the presence of inhalational injury. The leading cause of death was multiple organ failure complicated by pneumonia, wound infection and cellulitis. Risk factors for mortality include age >60 years, TBSA burn >40% and inhalational injury, with a predicted mortality of 0.3%, 3%, 33% or 90% depending on whether 0, 1, 2 or 3 risk factors were present respectively. Inhalational injury has a disproportionate effect on mortality following burns, with an increase in mortality to 30% as opposed to 5% for the group as a whole.
The strongest predictor of discharge disposition and functional independence is TBSA of the burn. Only 27.6% of patients were discharged directly home if they had a burn injury with a TBSA >30.75%. If TBSA > 37.5% was combined with age >57.5 years, patients were far less likely to return home directly from the hospital (47.5%), versus 90% for patients <57.5 years with a <37.5% burn.
Special considerations for nursing and allied health professionals.
What's the evidence?
Hettiaratchy, S, Papini, R. “ABC of burns”. BMJ. vol. 328. 2004. pp. 1555-1557.
Pham, TN, Cancio, LC, Gibran, NS. “American Burn Association Practice Guidelines: Burn Shock Resuscitation”. J Burn care Res. vol. 29. 2008. pp. 257-265.
Lawton, G, Dheansa, B. “The management of major burns – a surgical perspective”. Current Anaesthesia & Critical Care xxx. 2008. pp. 1-7.
Sheridan, RL. “Burns”. Critical Care Medicine. vol. 30. 2002. pp. S500-514.
Bessey, PQ, Jeng, JC. “National Burn Repository 2010 Annual Report”. . 2010. pp. 1-127.
Lund, CC, Browder, NC. “Estimation of areas of burns”. Surg Gyn Obst. vol. 79. 1944. pp. 352-8.
Wachtel, TL, Berry, CC, Wachtel, EE. “The inter-rater reliability of estimating the size of burns from various burn area chart drawings”. Burns. vol. 26. 2000. pp. 156-70.
Kagan, RJ, Peck, MD, Ahrenholz, DH. “Surgical Management of the Burn Wound and Use of Skin Substitutes”. . 2009. pp. 1-50.
Mertens, DM, Jenkins, ME, Warden, GD. “Outpatient burn management”. Nurs Clin North Am. vol. 32. 1997. pp. 343
Jaskille, AD, Shupp, JW, Jordan, MH. “Critical Review of burn depth assessment techniques: Part I. Historical Review”. J Burn Care Res. vol. 30. 2009. pp. 937-47.
Jaskille, AD, Ramella-Roman, JC, Shupp, JW. “Critical Review of burn depth assessment techniques: Part II. Review of Laser Doppler Technology”. J Burn Care Res. vol. 31. 2010. pp. 151-7.
Latenser, BA. “Critical Care of the burn patient: The first 48 hours”. Crit Care Med. vol. 37. 2009. pp. 2819-2826.
Woodson, LC. “Diagnosis and Grading of Inhalation Injury”. J Burn Care Res. vol. 30. 2009. pp. 143-5.
Weaver, LK. “Carbon Monoxide Poisoning”. N Engl J Med. vol. 360. 2009. pp. 1217-25.
Hatzifotis, M, Williams, A, Muller, M. “Hydrofluoric acid burns”. Burns. vol. 30. 2004. pp. 156-9.
Dries, D. “Management of burn injuries – recent developments in resuscitation, infection control and outcomes research”. Scand J Trauma, Resuscitation and Emergency Medicine. vol. 17. 2009. pp. 14-27.
Greenwood, JE, Dunn, KW, Davenport, PJ. “Experience with severe extensive blistering skin disease in a paediatric burns unit”. Burns. vol. 26. 2000. pp. 82-7.
Abood, GJ, Nickoloff, BJ, Gamelli, RL. “Treatment Strategies in Toxic Epidermal Necrolysis Syndrome: Where Are We At?”. J Burn Care Res. vol. 29. 2008. pp. 269-76.
Miller, SF, Jeng, JC, Bessey, PQ. “National Burn Repository 2009 Annual Report”. . 2009. pp. 1-132.
Peck, MD, Priolo-Kapel, D. “Child Abuse by Burning: A Review of the Literature and an Algorithm for Medical Investigations”. J Trauma. vol. 53. 2002. pp. 1013-22.
Orgill, DP, Piccolo, N. “Escharotomy and Decompressive Therapies in Burns”. J Burn Care Res. vol. 30. 2009. pp. 759-68.
Kealey, GP. “Carbon Monoxide Toxicity”. J Burn Care Res. vol. 30. 2009. pp. 146-7.
Barillo, DJ. “Diagnosis and Treatment of Cyanide Toxicity”. J Burn Care Res. vol. 30. 2009. pp. 148-52.
Palmieri, TL, Greenhalgh, DG. “Topical Treatment of Pediatric Patients with Burns: A Practical Guide”. Amer J Clin Derm. vol. 3. 2002. pp. 529-34.
Mosier, MJ, Pham, TN, Klein, MB. “Early Enteral Nutrition in Burns: Compliance With Guidelines and Assoicated Outcomes in Multicenter Study”. J Burn Care Res. vol. 32. 2010. pp. 1-6.
Garrel, DR, Davignon, I, Lopez, D. “Length of care in patients with severe burns with or without early enteral nutritional support”. J Burn Care Rehabil. vol. 12. 1991. pp. 85-90.
Jackson, DM. “The Diagnosis of the Depth of Burning”. Brit J Surg. vol. 40. 1953. pp. 588-96.
Saffle, JL. “The phenomenon of "fluid creep" in acute burn resuscitation”. J Burn Care Res. vol. 28. 2007. pp. 382-95.
Ryan, CM, Schoenfeld, DA, Thorpe, WP. “Objective estimates of the probability of death from burn injuries”. N Engl J Med. vol. 338. 1998. pp. 362-6.
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- 1. Description of the problem
- 2. Emergency Management
- 3. Diagnosis
- 4. Specific Treatment
- 5. Disease monitoring, follow-up and disposition
- Special considerations for nursing and allied health professionals.
- What's the evidence?