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Sheehy's Emergency Nursing, 6th ed.

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CHAPTER 26 – Burns

Cheryl Wraa

Burn trauma continues to be an immense challenge to caregivers in the emergency department (ED), playing a critical rolein the care of the burn patient. Every year in the United States an estimated 500,000 patients are treated in the ED for burninjury. Of these, approximately 4000 die with the majority of deaths, approximately 3500, due to residential fires. The majorityof deaths, approximately 75%, occur at the scene or during initial transport. Admissions to the hospital due to burn injurynumber approximately 40,000 annually in the United States with more then 60% being admitted to hospitals with specializedburn centers. Decreases of burn incidence and hospitalization are attributed to fire and burn prevention education,regulation of consumer products, and implementation of occupational safety standards. The recent decline in mortality isattributed to early excision and closure of the burn wound. Other factors contributing to the decline are management of burnpatients in specialty burn units, improved resuscitation, control of infection, and support of the hypermetabolic response. Asignificant portion of morbidity and mortality associated with burn injuries is due to associated injuries. Pulmonary pathologyfrom inhalation injury is the major cause of burn trauma death, with the majority of deaths at the extremes of age. Burn injuryand deaths associated with fires are the third leading cause of accidental death in children between the ages of 1 and 14years.

More than 90% of all burns are considered preventable. Education, particularly in the school-age population, combined withlegislative efforts is helping decrease the number of burn injuries. The American Burn Association has developed effectivepublic education programs. Legislation has been enacted that requires smoke alarms and sprinkler systems in publicbuildings, hotels, apartments, and new homes. For the caregiver an accurate classification of injury, timely intervention, andrapid transport to an appropriate burn facility significantly reduces burn injury mortality and morbidity.

ETIOLOGY

Not all burns are caused by fire. Tissue damage may be secondary to chemicals, hot liquids, tar, electricity, lightning, orfrostbite. The location and duration of exposure to the source affects outcome, regardless of the specific source of burninjury. Specific mechanisms of burn injury are described in the following sections.

Thermal Burns

Thermal injuries represent the majority of all burns. They may result from flame, flash, steam, or scalding liquid. Figure 26-1presents example of one cause of burn injury.

FIGURE 26-1 Burn injuries occur as a result of exposure to flame and smoke. (Courtesy Tacoma FireDepartment, Tacoma, Wash.)

Scald Burns

Scalds from hot liquids are the most common cause of all burns. Exposure to water at 140° F (60° C) for 3 seconds cancause a deep partial-thickness or full-thickness burn. If water is 156° F (69° C), the same type of burn occurs in only 1second. As a comparison, fresh brewed coffee is about 180° F (82° C). Tap water scalds occur within seconds and oftenhappen during routine activities, involve large body surface area (BSA) burns, and are the most common source of scald-related deaths. Soups and sauces, which are a thicker consistency, remain in contact longer with the skin and causedeeper burns. Other liquids that cause scalds are cooking oil and grease. When used for cooking, oil and grease may reach400° F (204° C). Immersion burns are usually deep and severe because of prolonged contact with a scalding liquid.

Specific groups of patients at risk for scald burns include those with preinjury comorbidities such as neurologic impairment,diabetes, and the extremes of ages. Adults older than 60 years disproportionately suffer burns from hot liquids. The fact

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that older patients are at high risk for burn injury and experience worse prognoses than younger patients is welldocumented. This has been attributed to their compromised physical health status with chronic, debilitating conditions thatincrease the risk, exacerbate the extent of the injury, and impair recovery.

Flame Burns

Burns from flames are the next most common cause of burns. Fortunately, the number of house fires has decreased withincreased use of smoke detectors. Most flame burns are caused by careless smoking, motor vehicle crashes, and clothingignited from stoves or space heaters. Flame burns that occur outdoors are usually secondary to misuse of cooking stovesfueled by white gasoline, lanterns in tents, smoking in a sleeping bag, and gasoline or kerosene used in a charcoal fire.

Flash Burns

Explosions of natural gas, propane, gasoline, or other flammable liquids cause flash burns—the third most common type ofthermal burn. The explosion causes intense heat for a very brief time. Flash burns are usually partial thickness, althoughdepth is dependent on the amount and kind of fuel that explodes. Flash burns can be large and are often associated withsignificant thermal damage to the upper airway.

Contact Burns

Contact with a hot object such as metal, plastic, glass, or hot coals results in contact burns. The burns are usually notextensive but tend to be deep. People involved in industrial accidents often have contact burns associated with crushinjuries from machine presses or hot, heavy objects. An increased incidence of contact burns has been seen in toddlerssecondary to the increased use of wood-burning stoves. The most common injury is to the palm when a child falls againstthe stove with hands outstretched.

Electrical Burns

As electricity passes through the body and meets resistance from body tissues, it is converted to heat in direct proportion toamperage and the body’s electrical resistance. It initially passes through the skin, causing an external burn at the entry andexit sites, with extensive damage internally between these sites. Nerves, blood vessels, and muscle are less resistant andmore easily damaged than bone or fat. The heart, lungs, and brain can sustain immediate damage. The nervous system isparticularly sensitive to electrical burns. Damage to the brain, spinal cord, and myelin-producing cells causes devastatingtransverse myelitis. Autonomic dysfunction can cause pupils to appear fixed and dilated, but this finding should not causeresuscitation efforts to stop. The smaller the body part through which the electricity passes, the more intense the heat andthe less it is dissipated. Consequently, extensive damage can occur in the fingers, hands, forearms, toes, feet, and lowerlegs. If the path is near or through the heart, damage to the heart’s electrical conduction system can cause spontaneousventricular fibrillation or other dysrhythmias. Papillary muscle damage may lead to sudden valvular incompetence andcardiac failure. Alternating current is more likely to induce ventricular fibrillation than direct current.

Most lightning injuries do not traverse the body but flow around it, creating a shock wave capable of causing fractures anddislocations. Close to two thirds of patients sustain a ruptured eardrum. About 70% of patients who survive a lightning strikecomplain of paresthesia or paralysis. Fortunately, both conditions are usually temporary.

Chemical Burns

Chemicals cause a denaturing of protein within the tissues or a desiccation of cells. Chemical concentration and duration ofexposure determine extent of the burn. Alkali products usually cause more tissue damage than acids. A wet chemicalshould be removed as soon as possible by flushing with copious amounts of water. Dry substances should be brushed offthe skin before the area is flushed. Care must be taken not to expose the caregiver to the chemical during this procedure. Allfluids used to decontaminate the patient should be contained; the fluid should not be allowed to drain into the generaldrainage system. Chemical burns can be deceiving as to depth; appearances can be similar in surface discoloration untiltissue begins to slough days later. Consequently, all chemical burns should be considered deep partial thickness or fullthickness until proven otherwise. After chemical removal, wounds are managed in the same manner as thermal burns.

Frostbite

Frostbite is actual freezing of tissue from exposure to freezing or below-freezing temperatures. In a cold environment thebody attempts to maintain heat by vasoconstriction of peripheral blood vessels to reduce heat exchange. The longer theperiod of exposure, the more peripheral blood flow is reduced. When extremities are left unprotected, intracellular andextracellular fluids can freeze, forming crystals that damage local tissues. Blood clots may form and impair circulation to thearea.

Signs, symptoms, and classification of frostbite are the same as thermal burns. The affected extremity should be rapidlyrewarmed using warm water. Use of excessive heat such as steam is dangerous and can cause unnecessary damage.Dress the rewarmed extremity and immobilize it with a padded splint. As with flame burns, frostbite can be very painful, sopain management is needed. For a more extensive review of frostbite, see Chapter 40.

Cold immersion of the foot or hand is a nonfreezing injury that occurs from chronic exposure to wet conditions attemperatures just above freezing. The extremity may appear black, but deep tissue destruction may not be present. Initiallythere is an alternating arterial vasospasm and vasodilation with the tissue first cold and numb, progressing to hyperemia in24 to 48 hours. As the injury progresses to hyperemia, the patient experiences intense burning sensation and dysesthesia.

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Tissue damage occurs with resultant edema, blistering, redness, ecchymosis, and ulcerations. Attention to hygiene willprevent local infection, cellulitis, or gangrene.

Patients who have exposure to chronic repetitive damp cold may develop chilblain, or pernio. This is a dermatologiccondition that usually occurs on the face, dorsum of the hands and feet, or any area chronically exposed to a coldenvironment. Signs and symptoms include pruritic, reddened skin lesions that with continued exposure, ulcerate or develophemorrhagic lesions that progress to scarring, fibrosis, or atrophy with itching, tenderness, and pain. Symptoms arecontrolled by protection from further exposure, and the use of antiadrenergics or calcium channel blockers.

BURN ASSESSMENT

Burn depth and extent are assessed to determine the severity of burn injury. In many cases final determination is not madefor several days.

Depth of Burn

Burns are described as partial thickness or full thickness. Identification of the depth of injury may be difficult initially becausedepth may actually increase over time as edema forms and circulation to the area of injury is compromised. This processusually peaks at 48 hours; therefore a more accurate determination of depth can be made between 48 and 72 hours. Depthdetermination is not a priority during initial resuscitation.

Extent of Burn

Extent of injury for thermal and chemical injuries is assessed by using formulas such as the rule of nines (Figure 26-2),Berkow formula, or Lund and Browder table (Figures 26-3 and 26-4). The caregiver should remember that the rule of ninesmust be modified for children. As noted in Figure 26-2, B, the head and neck of an infant represent 18% of BSA, whereaslegs represent 14% for each lower extremity. To correct for age 1% is subtracted from the head for each year of age through10 years, and 0.5% is added to each lower extremity. To estimate scatter burns, the size of the patient’s palm (includingfingers) is used to represent 1% of total BSA (TBSA). The palm is visualized over the burned areas. To obtain a moreaccurate estimate of the extent of burns, both burned and unburned areas are calculated. The two estimates should then becompared. If the total is more or less than 100%, the areas should be reestimated. Assessing extent of injury in electricalburns is more difficult because surface damage is minimal when compared with underlying damage. When discussing anelectrical injury, describing the injury anatomically is more important than calculating percentage of BSA burned.

FIGURE 26-2 Rule of nines. A, Adult. B, Child. (A from Ignatavicius DD, Workman LM: Medical-surgicalnursing: critical thinking for collaborative care, ed 5, Philadelphia, 2006, WB Saunders. B from Sole ML,Klein DG, Moseley MJ: Introduction to critical care nursing, ed 4, Philadelphia, 2005, WB Saunders.)

FIGURE 26-3 Lund and Browder formula. (From Cornwell P, Gregory C: Management of clients withburn injury. In Black J, Hawks J, editors: Medical-surgical nursing, ed 7, St. Louis, 2005, Elsevier.)

FIGURE 26-4 Lund and Browder formula. (From Artz CP, Moncrief JA: The treatment of burns, ed 2,Philadelphia, 1979, WB Saunders.)

Severity of Burn

The severity of burn injury is based on assessment of extent and depth of injury, patient age, presence of concomitantinjuries, smoke inhalation, and preexisting diseases. The American Burn Association’s guidelines for classification ofseverity of burn injuries are listed in Table 26-1.

Table 26-1 -- AMERICAN BURN ASSOCIATION’S CLASSIFICATION OF SEVERITY OF INJURY

Classification Characteristics Treatment Facility

Minor SPT

DPT, <15% TBSA adult <40 years of age

Outpatient or inpatient

(for 24 hr)

DPT, <10% TBSA adult >40 years of age

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DPT, <10% TBSA adult >40 years of age

<10% TBSA burn in children <10 years of age

With<2% TBSA full-thickness burn and no cosmetic or functional risk to the face, eyes,ears, hands, feet, or perineum

Moderate DPT, 15% to 25% TBSA adult <40 years of age Community hospital

DPT, 10% to 20% TBSA adult >40 years of age

10% to 20% TBSA burn in children <10 years of age

With<10% TBSA full-thickness burn without cosmetic or functional risk to the face,eyes, ears, hands, feet, or perineum

Major DPT, 25% TBSA adult <40 years of age Burn center

DPT, 20% TBSA adult >40 years of age

20% TBSA burn in children <10 years of age

Burns of face, eyes, ears, hands, feet, and perineum

Burns with concomitant inhalation injury or major trauma

All major electrical injuries

Data from Cornwell P, Gregory C: Management of clients with burn injury. In Black J, Hawks J, editors: Medical-surgicalnursing, ed 7, St. Louis, 2005, Elsevier.

DPT, Deep partial thickness; SPT, shallow partial thickness; TBSA, total body surface area.

Care of patients with burns of different severity is determined by availability of specialized care facilities. Initial stabilization ofthe burn patient should be available in any community hospital with 24-hour emergency capabilities. Patients with minorburns may be treated as outpatients or admitted to the community hospital. Patients with moderate burns may be treated ina community hospital with appropriate staff and facilities to deliver burn care or transferred to a specialized burn care facility.Patients with major burns require care in a specialized burn care facility. Transfer agreements with special-care unitsshould be developed in advance to facilitate timely and uneventful transfer. Box 26-1 summarizes criteria for transfer to aburn center. Any patient with concomitant trauma that poses increased risk for morbidity or mortality should be treated in atrauma center until he or she is stable and then transferred to a burn center as appropriate.

Box 26-1

CRITERIA FOR TRANSFER TO A BURN CENTER

1. Partial-thickness and full-thickness burns greater than 10% total body surface area (TBSA) in patients less than 10

years or over 50 years of age. 2. Partial-thickness and full-thickness burns greater than 20% TBSA in other age groups 3. Burns that involve the face, eyes, ears, hands, feet, genitalia, perineum, or major joints. 4. Full- thickness burns greater than 5% TBSA in any age-group. 5. Electrical burns, including lightning injury. 6. Significant chemical burns. 7. Inhalation injury.

8. Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or

affect mortality.

9. Any patient with a burn injury that has concomitant trauma poses an increased risk of morbidity or mortality, and may

be treated initially in a trauma center until stable before being transferred to a burn center. 10. Children with burn injuries in hospitals without qualified personnel or equipment for the care of children.

11. Burn injury in patients who will require special social, emotional, or long-term rehabilitative intervention, including

cases involving suspected child abuse and neglect.

Data from American College of Surgeons: Advanced trauma life support student manual, Chicago, 2008, The College.

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PATHOPHYSIOLOGY

Burn injury occurs when skin is exposed to more energy than it can absorb. The cause of the burn may vary, but local andsystemic responses are generally similar. To understand the pathophysiology of burns, one must first understand thefunctions of the skin, which consists of two layers: the epidermis and the dermis. The epidermis, the outer layer of thebasement layer of cells, consists of cells that migrate upward to become surface keratin. The dermis, or inner layer,consists of collagen and elastic fibers and contains hair follicles, sweat and sebaceous glands, nerve endings, and bloodvessels. The skin is the largest organ of the body and acts as an infection barrier, vapor barrier, and a heat regulator.

Three zones of tissue damage occur at the burn site. First is the central zone of coagulation, an area of irreversible damage.Concentrically surrounding this area is the zone of stasis, where capillary and small vessel stasis occurs. The ultimate fateof the burn wound depends on resolution or progression of the zone of stasis. Edema formation and prolongedcompromise of blood flow to this area cause a deeper, more extensive wound; therefore depth and severity of burn woundsmay not be known for 2 or more days after the initial injury. The third zone of damage is the zone of hyperemia, an area ofsuperficial damage that heals quickly on its own.

The body responds to the burn injury with varying degrees of tissue damage, cellular impairment, and fluid shifts. A briefdecrease in blood flow to the affected area is followed by a marked increase in arteriolar vasodilation. Damaged tissuesrelease mediators that initiate an inflammatory response. Histamine, serotonin, prostaglandin derivatives, and thecomplement cascade are all activated. Release of proinflammatory mediators combined with vasodilation causesincreased capillary permeability, leading to intravascular fluid loss and wound edema. For burn injuries less than 20%TBSA, these actions are usually limited to the burn site with 90% of the edema present by 4 hours. The edema tends toreside within the dermis, and resorption is complete by 4 days. As the affected TBSA goes beyond 20%, local responsebecomes systemic. With large burns the overwhelming inflammation, coagulation, and fibrinolysis can continue andconstantly be reactivated. The cytokine activity creates a state of exaggerated or reactivated inflammation that includes organinvolvement such as acute respiratory distress syndrome (ARDS), systemic inflammatory response syndrome (SIRS), andmultiple organ dysfunction syndrome (MODS). Large burns cause a hypermetabolic state that has multiple harmfulphysiologic derangements associated with it. Derangements noted are muscle catabolism, hepatic dysfunction, andimmunosuppression. Treatments such as tight glycemic control and beta blockade may be used to attenuate thehypermetabolic state. Basal metabolic rate increases from insensible fluid loss, which, along with fluid shift, produceshypovolemia. Hypoproteinemia resulting from increased capillary permeability aggravates edema in nonburned tissue.Capillary permeability increases for 2 to 3 weeks with the most significant changes occurring in the first 24 to 36 hours.

Initially blood viscosity increases when hematocrit rises secondary to vascular fluid shifts into the interstitium. Because of amarked increase in peripheral vascular resistance, decreased intravascular fluid volume, and increased blood viscosity,cardiac output falls. Capillary leakage and depressed cardiac output can depress central nervous system function, causingrestlessness, followed by lethargy, and finally coma. Decreased cardiac output, decreased blood volume, and intensesympathetic response cause a decreased perfusion to the skin, viscera, and kidneys. Levels of thromboxane A2, a potentvasoconstrictor, are significantly increased in burned patients and contribute to mesenteric vasoconstriction and decreasedsplanchnic blood flow. Decreased flow can convert a zone of stasis to a zone of coagulation, which increases depth of theburn. Decreased circulating plasma with increased hematocrit can cause hemoglobinuria, which can lead to renal failure.Immediate hemolysis of red cells occurs, with the life span of remaining red cells reduced by approximately 30% of normal.Platelet count and platelet survival time initially drop drastically then continue to decrease for 5 days after injury. This periodis followed by a rebound increase in platelets over the next 2 to 3 weeks.

Cardiovascular changes begin immediately after a burn; their extent varies with burn size and presence of additionalinjuries. Patients with an uncomplicated burn less than 15% TBSA can usually be treated with oral fluid resuscitation. Burnpatients who surpass 20% TBSA have massive shifts of fluid and electrolytes from intravascular to extravascular spaces.This shift begins to resolve in 18 to 36 hours; however, normal extracellular volume is not completely restored until 7 to 10days after the burn injury. If intravascular volume is not replenished, hypovolemic shock occurs. If untreated, the patient candie of cardiovascular collapse. Inadequate treatment may lead to renal failure from acute tubular necrosis.

The vasoconstriction of the mesentery mentioned above predisposes the patient to gastric distension, aspiration, andulceration (Curling’s ulcer). A patient with a burn greater than 20% TBSA should have a gastric tube placed to decompressthe stomach and avoid aspiration. Admission orders will include medication to reduce gastric secretion and early enteralfeedings (within 24 hours of injury) to meet basic energy needs.

The hypermetabolic response after burn trauma far exceeds the response seen in other forms of trauma. The patient’smetabolic rate can increase as much as two to three times the normal rate. Release of catabolic hormones, includingcatecholamines, cortisol, and glucagon, initiates a persistent hypermetabolic response. This response causes acceleratedbreakdown of skeletal muscle, decreased protein synthesis, increased peripheral lipolysis, and increased utilization ofglucose, which rapidly depletes glycogen stores. It manifests clinically as severe muscle wasting, decreased musclestrength, and increased liver fat with hepatomegaly and functional impairment. The hypermetabolic response iscommensurate with the size of the burn. The adverse effects of the response are managed through nutritional andpharmacologic intervention to improve net nitrogen balance, preserve lean body mass, decrease cardiac work, anddecrease hepatic fatty infiltration.

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Burn injuries can affect every organ system in the body, causing cerebral perfusion abnormalities, impaired coronary bloodsupply, renal insufficiency, and acid-base imbalance. Realization of these broad effects can enhance management of theburn patient.

Pulmonary Response to Smoke Inhalation

Inhalation injury or smoke inhalation is a syndrome comprising three distinct problems: carbon monoxide intoxication, upperairway obstruction, and chemical injury to the lower airways and lung parenchyma. The majority of deaths from fires are dueto smoke inhalation rather than the burn injury or its sequelae. A burn injury with associated inhalation injury increases themortality rate. Pulmonary complications associated with inhalation injury directly contribute to death in up to 77% of patientswith combined cutaneous and inhalation injury.

Carbon monoxide intoxication is the most common killer of victims of fire. Of the patients admitted to burn centers,approximately 10% to 20% have inhalation injuries. This incidence increases with the size of the burn. Most people whodie in a fire have been overcome by carbon monoxide before they sustain a burn injury. In the body, carbon monoxide has a240-times greater affinity for hemoglobin than oxygen, which causes inadequate oxygen delivery to the tissues. Carbonmonoxide combines with myoglobin in muscle cells, causing muscle weakness. Tissue hypoxia and the resultantconfusion and muscle weakness may be the major reasons for most fire fatalities. Carbon monoxide poisoning ischaracterized by pink to cherry-red skin, tachypnea, tachycardia, headache, dizziness, and nausea. An arterial blood gassample is drawn to measure the carboxyhemoglobin level. Levels below 15% are rarely associated with symptoms ofcarbon monoxide poisoning and can be normal for a heavy smoker. Levels of 15% to 40% are associated with varyingdisturbances such as headache and confusion. Levels greater than 40% are associated with coma. Reliance on pulseoximetry or an oxygen saturation of arterial blood (SaO ) that is calculated from the partial pressure of oxygen (PO ) ratherthan measured on a CO oximeter may result in failure to diagnose carbon monoxide poisoning. Most pulse oximeterscannot reliably differentiate between oxygenated hemoglobin and hemoglobin with carbon monoxide and will give a falsehigh measurement. All patients with suspected carbon monoxide poisoning should be placed on 100% oxygen.

Cyanide poisoning may also occur during a fire and can rapidly result in death. Hydrogen cyanide is highly toxic and can beformed in high-temperature combustion from materials such as polyurethane, acrylonitrile, wool, cotton, and nylon. Cyanidebinds to a variety of iron-containing enzymes, one of which plays a critical role in electron transport during oxidativephosphorylation. Even minute amounts of bound cyanide can inhibit aerobic metabolism and rapidly result in death.

The patient with cyanide poisoning will rapidly develop coma, apnea, cardiac dysfunction, and severe lactic acidosis.Diagnosis can be difficult when combined with carbon monoxide poisoning, and the patient can have sublethal levels ofcarbon monoxide and cyanide and still die due to the combination. The two are synergistic because carbon monoxideprimarily affects oxygen delivery and cyanide affects oxygen utilization.

Thermal injury to the upper airway is usually associated with facial burns. Upper airway obstruction is the result of intrinsicor extrinsic edema that may lead to airway occlusion at or above the vocal cords Edema progresses rapidly, totally occludingthe airway in minutes to hours (Figure 26-5). This injury is primarily a thermal injury, resulting in tissue damage in theposterior pharynx. Figure 26-6, B, shows radiographic evidence of epiglottitis secondary to thermal/chemical injury. Upperairway edema will usually manifest within 24 hours of the injury. Management for airway edema is early intubation ortracheostomy if intubation is not possible. If the patient exhibits dyspnea, stridor, or cyanosis, suspect impending airwayobstruction and be prepared to assist with intubation that may be difficult.

FIGURE 26-5 Facial edema. A, Four to 5 hours after burn. B, Thirty hours after burn, showing distortionof facial features and necessity of intubation before the full extent of burn edema development. C, Facialcontour 3 months after burn. (Courtesy Anne E. Missavage, MD, UC Davis Regional Burn Center,Sacramento, Calif.)

FIGURE 26-6 A, Photograph of 22-month-old child showing burn primarily to the anterior chest wall. B,Lateral airway radiograph of the same child demonstrating effects of thermal or chemical epiglottitis.(From Barkin RM: Pediatric emergency medicine: concepts and clinical practice, ed 2, St. Louis, 1997,Mosby.)

Actual thermal injury below the vocal cords is rare because the posterior pharynx is such an efficient heat exchange system.True thermal injury below the vocal cords is usually the result of superheated steam in which water vapor carries heat intothe lungs. Injuries that occur in an oxygen-enriched atmosphere or one in which the person was inhaling explosive gases(e.g., during inhalation anesthesia) also cause true thermal injury below the vocal cords. True thermal injury to the lungs isalmost always fatal.

Chemical injury to the lower airway is a common problem with inhalation of smoke. Many lower-molecular-weightconstituents of smoke are toxic to the mucosa and alveoli because of their pH or the ability to form free radicals. Chemicalinjury, from acids and aldehydes in the smoke, may damage the lung parenchyma. These chemicals, attached to carbonparticles in the smoke, are heavier than air, so they are readily inhaled and find their way down the bronchi into alveoli. Thischemical injury causes hemorrhagic tracheobronchitis, increased edema formation, decreased surfactant levels, and

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decreased pulmonary macrophage function. Although the compounds produce acute neutrophilic airway inflammation, thesymptoms, cough, bronchorrhea, dyspnea, and wheezing, may not appear for 12 to 26 hours. Many centers perform earlybronchoscopy to determine if there is injury to the lower airways. The bronchoscopy will reveal erythema, edema,carbonaceous debris, and ulceration of the airways. This condition may lead to rapid development of ARDS over 24 to 48hours. Severe inhalation injury may increase the patient’s fluid needs in the first 24 hours by as much as 50% of calculatedvalues.

PATIENT MANAGEMENT

The burn patient may have other injuries in addition to the burn; therefore the patient should be initially evaluated using theABCDE survey for trauma. The cervical spine is protected while assessing for an adequate airway. Assessment ofspecific burn injuries should be done after the primary assessment is completed. A history is obtained as time and patientcondition permit. How did the injury occur? What caused the injury—flame, scald, etc? Was smoke involved? Did injury occurin a confined space? What was the patient doing before the injury? Did the patient have a stroke or myocardial infarctionbefore the injury? Does the patient have any medical problems or allergies? General assessment and interventions for theburn patient are described in this section.

Airway

A primary trauma survey should be performed with appropriate management. Look for evidence of respiratory distress andsmoke inhalation injury. A high index of suspicion for smoke inhalation is essential for these patients. Burns that occur insmall spaces are often associated with smoke inhalation. Administration of high-flow oxygen should be started in anattempt to reverse tissue hypoxia resulting from a low fraction of inspired oxygen (FiO ) at the fire and to begin displacingcarbon monoxide and cyanide from their protein-binding sites. If the patient has a history of chronic obstructive pulmonarydisease and is a suspected carbon dioxide retainer, immediate intubation is recommended to prevent progressive carbondioxide retention.

The half-life of carboxyhemoglobin on room air is approximately 240 minutes. When the patient is placed on 100% FiO , thehalf-life is reduced to approximately 75 to 80 minutes. Hyperbaric oxygen at 2.0 atm decreases the half-life ofcarboxyhemoglobin to approximately 20 minutes and appears to hasten the resolution of symptoms. The use of hyperbaricoxygen in the treatment of carbon monoxide poisoning is controversial. Centers that advocate hyperbaric oxygen use it forpatients with a carboxyhemoglobin level greater than 40%, loss of consciousness, or in pregnant women with acarboxyhemoglobin level greater than 20% or evidence of fetal distress.

Hyperbaric chambers are limited in availability and most are small and hold only the patient. Larger multiplace chambersallow an attendant to dive with the patient, but even then, complex medical interventions are difficult to perform in this setting.Therefore an unstable patient who may require intensive therapy should not be placed in a chamber. A complication ofhyperbaric therapy is barotrauma to the ear due to the inability of the patient to equalize the pressure within the ear as theatmospheric pressure increases. Myringotomy with tube placement has been used as a preventative measure because thepressure difference that leads to barotrauma cannot occur with a hole in the tympanic membrane.

If the patient has suspected cyanide poisoning, antidotal treatment includes induction of methemoglobinemia, use of sulfurdonors, and binding of cyanide. Outside the United States the combination of sodium thiosulfate and hydroxocobalamin hasbeen successful in the treatment of severe poisoning. In the United States the Taylor cyanide antidote package is used andincludes amyl nitrate and sodium nitrite to induce methemoglobinemia and sodium thiosulfate to act as a sulfur donor. Thekit will treat two adult patients. If the patient also has carbon monoxide poisoning, the treatment with amyl nitrite or sodiumnitrite is contraindicated until normal carbon monoxide levels can be confirmed. Pending test results for carboxyhemoglobin,sodium thiosulfate may be given intravenously.

The oropharynx and vocal cords should be inspected for redness, blisters, and carbonaceous particles. The patient isobserved for increasing restlessness, dyspnea, difficulty swallowing, increasing hoarseness, and rapid, shallowrespirations. The patient may have increasing difficulty managing secretions with a significant risk for impending airwayobstruction. Early intubation is recommended before complete obstruction occurs. Tracheostomies should be avoidedinitially because edema of the neck makes this procedure difficult.

Breathing

Circumferential full-thickness burns of the chest can impair breathing by limiting chest wall excursion and preventingadequate gas exchange. The chest should be visually inspected for tight, leathery eschar that circles the chest. Evidence ofbreathing compromise includes inadequate chest expansion, restlessness, confusion, decreased oxygenation, decreasedtidal volume, and rapid, shallow respirations.

Escharotomy is indicated for circumferential burns that compromise breathing. Surgical incisions are made in burnedtissue on the chest to release eschar and expose underlying subcutaneous tissue. Improvement in chest wall expansionshould occur immediately after incisions are made. General anesthesia is not required because the incisions are made ina full-thickness burn. Intravenous (IV) narcotic analgesia is usually adequate to relieve any pain associated withescharotomy.

The patient with a burn injury is also at risk for carbon monoxide poisoning. Altered breathing patterns such as decreasedrespirations or apnea may be evident, as may the characteristic cherry-red skin, or the skin can appear slightly cyanotic.

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Confusion, irritability, or coma may be present. Carboxyhemoglobin level and chest radiograph are obtained to assess forcarbon monoxide poisoning and the presence of pulmonary damage or associated injuries. High-flow oxygen with anonrebreather mask or bag-mask device is administered as appropriate. If the patient does not respond after 1 to 11⁄2hours of regular oxygen therapy, hyperbaric oxygen therapy may be used.

ARDS occurs in patients with carbon monoxide poisoning but is usually not a problem until approximately 18 hours afterinjury. Clinical findings associated with ARDS include decreased oxygenation, increased secretions, rapid respirations,confusion, and increasing patchy infiltrates on the radiograph. Treatment includes intubation and ventilation with positiveend-expiratory pressure (PEEP). Bronchodilators may be indicated; however, corticosteroids are not. Giving corticosteroidsto patients with burns and smoke inhalation can increase morbidity and mortality. Refer to Chapter 30 for additionalinformation on ARDS.

The burn patient should be assessed for other injuries that can affect breathing, such as pneumothorax, hemothorax,tension pneumothorax, and flail chest. These problems can occur with a burn injury from a motor vehicle crash or explosion.Additional injuries may be present when a patient has jumped to escape the fire. Preexisting health problems that may affectrespiratory functions (e.g., chronic obstructive pulmonary disease, asthma) should be noted.

Circulation

The patient with a burn injury is at significant risk for hypovolemia from actual fluid loss and fluid movement from increasedcapillary permeability and vasodilation. Assess the patient for increased respirations, increased pulse, decreased bloodpressure, decreased urine output, diminished capillary refill, restlessness, confusion, nausea, and vomiting. Additionalindications of volume compromise include central venous pressure less than 3 cm H O, hematocrit greater than 50 mg/dL,presence of an ileus, and urine output less than 0.5 mL/kg/hr.

One or two large-bore IV catheters should be started. A single IV catheter is adequate for a burn less than 40% TBSA. Twoperipheral access sites are established if the burn is greater than 40% TBSA or the patient will be transferred. Leg veins areavoided because of increased risk for thrombophlebitis. The IV catheter can be inserted into burned tissue if no otheraccess is available, but this should be considered a last resort. Fluid volume requirements are calculated using anaccepted formula such as the Parkland or Baxter formula (Table 26-2). These formulas are guidelines for fluid replacementtype and volume and should be adjusted to the patient’s response to the fluid. Ideally, fluid resuscitation is adequate if pulseand blood pressure are within normal limits for age and urine output is 0.5 mL/kg/hr for adults and 1 to 1.5 mL/kg/hr forinfants.

Table 26-2 -- FLUID REPLACEMENT FORMULAS

Formula Electrolyte Solution Colloid Water Rate Example:70 kg/45%TBSA(per 24 hr)

Evans 1 mL/kg/% TBSA of NS 1mL/kg/%

2000mL

½ in first 8 hr; ½ in next 16 hr

3150 mLNS

3150 mLcolloid

2000 mLwater

8300 mLtotal

Brooke 1.5 mL/kg/% TBSA of LR 0.5mL/kg/%

2000mL

½ in first 8 hr; ½ in next 16 hr

4725 mLLR

1575 mLcolloid

2000 mLwater8300 mLtotal

ModifiedBrooke

2-3 mL/kg/% TBSA of LR None None ½ in first 8 hr; ½ in next 16 hr 6300-9450mL LR

Parkland(Baxter)

4 mL/kg/% TBSA of LR None None ½ in first 8 hr; ½ in next 16 hr 12,600 mLLR

Hypertonicformula(Warden)

4 mL/kg/% TBSA of LR plus 50 mEqNaHCO (180 mEq of Na) per liter forfirst 8 hr

None None Switch to LR when pHnormalizes or at 8 hr Adjust ratebased on urine output

Unknown

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(Warden) first 8 hr based on urine output

Modified from Greenhalgh D: Burn resuscitation, J Burn Care Res 28:4, 2007.

LR, Lactated Ringer’s solution; NS, normal saline; TBSA, total body surface area.

No formula exists for calculating fluid resuscitation in electrical injuries. An infusion of lactated Ringer’s solution isadministered at 1 to 2 L/hr in the average adult until he or she shows signs of adequate resuscitation. Urine output shouldbe maintained at two to three times the normal volume to facilitate excretion of myoglobin. After urine output is established,an osmotic diuretic such as mannitol may be given to increase urine flow and aid in excretion of myoglobin. Significantacidosis can occur, so repeated administration of sodium bicarbonate may be required to prevent dysrhythmias. Once fluidtherapy corrects acidosis, repeated administration may not be necessary.

Disability and Exposure

If not yet done, all clothing and jewelry should be removed and a head-to-toe assessment done to check for any concomitanttrauma and to estimate burn depth and size. Refer to the earlier section on burn assessment for estimate of burn depth andsize. Because the burn patient has lost ability to control body temperature, it is important to increase the temperature in theroom and to monitor the patient. Body temperature below 35° C should be avoided.

Diagnostic Procedures

Diagnostic procedures that may assist during the resuscitation of the burn patient are the following:

Laboratory 1. Complete blood count with differential 2. Serum electrolytes 3. Carboxyhemoglobin 4. Type and crossmatch/screen blood 5. Urinalysis, pregnancy test in females of childbearing age 6. Arterial blood gas

Radiography 1. Chest 2. Other x-ray examinations as indicated for associated trauma

Other special studies as indicated for associated trauma 1. Focused assessment sonography for trauma (FAST) 2. Computed tomography (CT) scan as indicated by assessment findings 3. Possible peritoneal lavage 4. 12-lead electrocardiogram (ECG) if electrical or lightning injury

Protection Against Infection

The patient with a burn injury has lost the greatest protection against invasion by various pathogens and must be protectedwith scrupulous aseptic technique. Gloves, masks, caps, and gowns must be worn. Sterile technique is necessary for allprocedures. Wounds are kept covered with clean sheets while other care is provided. If the patient is transferred, sterilesheets are used to cover the patient. If treatment is followed by discharge, the nurse should debride the burn, apply a topicalantibiotic, and cover the wound with a fluffy dressing. Systemic antibiotics are rarely indicated even in severe burns untilinfection is confirmed by culture. Exceptions to this guideline may include young children, older adult patients, diabeticpatients, or those with immune system compromise.

For minor or moderate burns, tetanus immunization is given if the patient has not been immunized within the past 10 years.In major burns or grossly contaminated burns, tetanus immunization is given if previous immunization has occurred within 5years. If the patient has never been immunized or no clear history of immunization exists, tetanus hyperimmune globulin(HyperTET) and tetanus immunization is given.

Pain Management

Burn wounds are exquisitely painful and deserve special consideration. The pain of primary tissue damage and nervedamage may be worsened by primary and secondary hyperalgesia. Intravenous opioid administration should be the primetreatment for burn pain. During initial resuscitation, analgesics or anesthetics should be titrated to effect. After 24 hours,decreased plasma protein levels increase bioavailability of free drugs, especially those that are protein bound. Giving painmedication as needed may increase the patient’s awareness of pain and other symptoms. Administering opioids on aschedule, based on drug half-life or by continuous infusion, can facilitate the patient’s ability to cope with the pain. The

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opioid of choice has been IV morphine at 25 to 50 mcg/kg/hr, titrating to avoid respiratory depression. Fentanyl may also beused for some patients. For the burn victim, pain can be made worse by fear of pain or disfigurement, anxiety related to lossof control, and distress over losing family members or material possessions at the time of injury. Anxiety decreases paintolerance. Reducing anxiety minimizes interplay between acute pain and sympathetic arousal. For the burn patient,anxiolytics may help decrease anxiety and improve pain tolerance. They are especially helpful during painful procedures.The most commonly used anxiolytics are benzodiazepine drugs. Diazepam has a long half-life and high lipid solubility. Afterrepeated use in the burn patient, prolonged mental impairment may occur when the drug is stopped. Therefore short-termadministration of lorazepam and midazolam are preferred.

Patients with burn-induced or traumatic nerve injury may develop neuropathic pain. Pain is usually described as tingling,burning, shooting, or numbing. When a postburn patient comes to the ED with this type of pain, it is because the pain did notrespond to opiate analgesics. Drugs that decrease neuronal excitability by mechanisms other than opiate receptors areuseful for this type of pain. Tricyclic antidepressants in low doses are often successful in relieving neuropathic pain. Sodiumchannel–blocking drugs such as IV lidocaine, carbamazepine, phenytoin, and mexiletine have also produced successfulanalgesia.

Wound Care

Wound care should be delayed until the patient’s condition is stabilized; however, initial management must include removalof jewelry and constrictive clothing. Wounds must be kept covered with clean sheets until more definitive care can beprovided. All patients with full-thickness burns are assessed for circulatory problems. Capillary refill and the presence ofparesthesia are evaluated with distal pulses checked by Doppler ultrasonography. Because burn tissue does not stretch,swelling beneath burned tissue compromises circulation because of lack of elasticity. If the patient has signs ofcompromise, escharotomy is indicated. Figure 26-7 illustrates placement of these surgical incisions. Significant bleedingthat occurs with escharotomy can be controlled with an electrocautery unit or small hemostats (Figure 26-8). After theprocedure is completed, a topical antibacterial agent is applied to the open wound, a light pressure dressing is applied, andthe extremity is slightly elevated.

FIGURE 26-7 Placement of escharotomies.

FIGURE 26-8 Control of bleeding from escharotomy.

Thermal burns may be secondary to flame, flash, scalds, or hot objects. Figure 26-9 shows an example of a thermal burn.Thermal burns are cleaned with mild soap and water. The use of skin disinfectant, such as povidone-iodine (Betadine), hasbeen shown to inhibit the healing process and is discouraged. Ruptured blisters should be removed, but intact blisters maybe left alone and should never be aspirated with a needle because this increases the chance of infection. The wound iscovered immediately with a topical antibacterial agent such as silver sulfadiazine (Silvadene) or bacitracin. Burns of the faceshould be left open and covered by a topical antibiotic ointment such as bacitracin, which is reapplied every 6 hours aftergently washing the skin.

FIGURE 26-9 Flame burns to back.

Chemical burns should be immediately irrigated with tap water or normal saline for at least 5 to 10 minutes to remove thechemical. Clothing and jewelry are removed, and unburned areas adjacent to the burned areas are rinsed. These areas canbe injured but may not hurt, blister, or turn red immediately. If the chemical is dry, it can be brushed from the patient beforeirrigating. After the wound is thoroughly irrigated, it is treated like a thermal burn. Chemical burns of the eye are anophthalmologic emergency. The eye must be irrigated thoroughly with copious amounts of water or saline. (Refer to Chapter 45 for additional discussion of chemical eye injuries.)

Electrical injuries are different from thermal and chemical burns. These wounds may have little superficial tissue loss;however, massive muscle injury may be present beneath normal-looking skin or minor to severe exit wounds (Figures 26-10 and 26-11). Wounds should be cleaned gently with a 0.25% povidone-iodine solution using sterile water or 0.9% sodiumchloride; they rarely need immediate debridement. Topical agents such as mafenide acetate (Sulfamylon) solution thatdeeply penetrate tissue are used to cover the wound. Light dressings may be applied to cover these often grotesquewounds; however, dressings must not interfere with assessment for circulatory compromise and possible compartment

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syndrome. High-voltage injuries are associated with severe muscle contractions, so radiographs of the cervical spine maybe indicated.

FIGURE 26-10 Exit wound from direct current. (From Air & Transport Nurses Association: Air & surfacepatient transport: principles and practice, ed 4, St. Louis, 2019, Mosby.)

FIGURE 26-11 Exit wound from alternating current. (From Air & Transport Nurses Association: Air &surface patient transport: principles and practice, ed 4, St. Louis, 2019, Mosby.)

Electrical injuries of the extremities cause significant damage that leads to tissue swelling. Consequently, these patientsare at risk for compartment syndrome. Symptoms associated with this condition include pain, pallor, paresthesia,pulselessness, paralysis, and pressure in the affected area. Fasciotomies are used to relieve compartment syndrome.

Tar or asphalt burns may be deep or superficial depending on the temperature of the tar, which may range from 150° F tomore than 600° F, as well as the length of time the skin was in contact with it. Figure 26-12 shows a tar burn before tarremoval. Immediate treatment of a tar burn is to cool the tar, but do not try to peel it off the patient’s skin. Using mineral oil,petroleum jelly, or a solvent such as Medi-Sol loosens the tar. In areas where the burn is not circumferential, oil or ointmentis applied and the burn is covered with a light dressing. Dressings are removed in 4 to 12 hours, oil or ointment reapplied,and a new dressing applied. For areas with circumferential tar, oil or ointment can be applied with light dressings andchanged every 20 to 30 minutes until tar is removed. After the tar is removed, the burn is treated as a thermal injury.

FIGURE 26-12 Tar burns of chest before removal of tar.

Temperature Regulation

The patient with a burn injury has lost a major control mechanism for temperature regulation. This heat loss is worsened byadministration of room temperature IV fluids, irrigation of burned tissue, and environmental coolness often encountered inthe ED. The patient’s temperature should be documented as soon as possible after arrival in the ED and rechecked within 1hour. Keeping the patient covered, using warmed IV fluids, and increasing room temperature minimizes heat loss.

SUMMARY

Burn injury can be devastating to the patient and family; for the caregiver, it can also be visually disturbing. Regardless ofhow severe the burn may be, a primary survey should be performed for potentially life-threatening injuries. Resuscitation ofthe burn patient includes evaluation of the burn, replacement of fluid losses, wound care, protection against contamination,maintenance of body temperature, and pain control. A multidisciplinary approach to burn care can reduce mortality andmorbidity. Appropriate application of burn center transfer criteria ensures the best outcome for the patient with a major burninjury.

REFERENCES

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2.. American Burn Association: Fact sheet. Retrieved August 20, 2007, fromhttp://www.ameriburn.org/resources_factsheet.php .

3.. American College of Surgeons: Advanced trauma life support student manual, Chicago, 2008, The College.

4.. Auerbach P.: Wilderness medicine. ed 4. St. Louis, Mosby, 2001.

5.. Cornwell P., Gregory C.: Management of clients with burn injury. In: Black J., Hawks J., ed. Medical-surgical nursing, ed7. St. Louis: Elsevier; 2005.

6.. Desai S, Su M: Cyanide intoxication. Retrieved August 20, 2007, from http://www.uptodate.com .

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10.. Hershberger R., Hunt J., Arnoldo B., et al: Abdominal compartment syndrome in the severely burned patient. J BurnCare Res 2007; 28:1.

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12.. Mandel J, Hales: Smoke inhalation. Retrieved August 20, 2007, from http://www.uptodate.com .

13.. Marek K., Piotr W., Stanislaw S., et al: Fibreoptic bronchoscopy in routine clinical practice in confirming the diagnosisand treatment of inhalation burns. Burns 2007; 33(5):554.

14.. Palmieri T.: Inhalation injury: research progress and needs. J Burn Care Res 2007; 28:4.

15.. Rice P: Emergency care of moderate and severe thermal burns in adults. Retrieved December 14, 2007, fromhttp://www.uptodate.com .

16.. Sona C.: Burns. In: Urdan L., Stacy K., Lough M., ed. Thelan’s critical care nursing, ed 5. St. Louis: Mosby; 2006.