Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized

Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Caring for patients with burn injuries Refresh your knowledge of burn types and initial management.

By Alicia L. Culleiton, DNP, RN, CNE, and Lynn M. Simko, PhD, RN, CCRN

Caring for a patient with severe burn injuries offers functions including acting as a protective barrier many challenges for critical care nurses. This article against injury and infection, thermoregulatory con- reviews various types of burns and what you need trol, regulation of fluid loss, synthesis of vitamin D, to know to provide initial resuscitative care for a and sensory contact with the environment. When patient if treatment in a designated burn center the skin is damaged or destroyed by a burn, it may facility or burn ICU isn’t possible. result in or lead to compromised immunity, hypo- Although burn incidence has decreased slightly thermia, increased fluid loss, infection, changes in over the years, burn injuries still occur too frequent- appearance, function, and body image. ly, with an estimated 3,500 fire and burn deaths The skin is divided into three layers: the epider- Ceach year (this figure includes deaths from smoke mis, dermis, and subcutaneous tissue. Burn injuries inhalation and poisoning).1 In addition, about 45,000 are described by the causative agent, depth, and patients who sustain burn injuries require medical severity. In the past, burn injuries were classified as treatment or hospitalization yearly. According to the first, second, third, and occasionally fourth degree. American Burn Association (ABA), hospital admis- In recent years, the ABA has recommended a more sion based on the type of burn include: 44% due to precise definition of first-, second-, and third-degree fire or burn injury, 33% due to scald injury, 9% due burns, categorizing them according to depth of skin to contact burn injuries, 4% due to electrical burns, destruction: epidermal or superficial (first-degree), 3% due to chemical burns, and 7% due to miscel- partial-thickness (second-degree), which may also laneous causes of burns.1 Burn injuries are one of be classified as superficial or deep partial-thickness) the most expensive catastrophic injuries to treat. and full-thickness (third-degree) burns (may also be For instance, a burn injury of 30% of total body classified as a deep full-thickness).4 (See The skin surface area (TBSA) can cost as much as $200,000 in and degrees of burns.) initial hospitalization costs; furthermore, for more extensive burns there are significant additional costs Size matters related to reconstructive surgery and rehabilitation The size of the burn is expressed as the percentage efforts.2 Lastly, mortalities are higher for children of TBSA. A partial-thickness burn of more than younger than age 4 (especially for children from 10% TBSA is serious and needs referral to a burn birth to age 1), and for adults over age 65.3 center (see Should my patient go to a burn center?). You can estimate the TBSA burned on an adult Why is the skin important? by using 9 or multiples of 9, known as the Rule of Burn injuries involve the partial or complete Nines. The Rule of Nines varies between infants and destruction of the integumentary system: the skin. adults because infants’ heads are proportionally larg- The layers of the skin are destroyed and this results er compared to adults (see Rule of Nines: Estimating in local and systemic disturbances. The skin is one burn size in adults). Although the Rule of Nines

ILLUSTRATION BY STEVE OH, M.S./PHOTOTAKE © of the largest organs of the body and has many provides a rapid method for calculating the size of

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the injury, it can overestimate the TBSA burned, such as grease and scald burns. Often, the rule of so follow your facility’s protocol for estimating the palms will be completed first as a quick assess- extent of a burn injury. Most burn centers repeat the ment until the Lund and Browder assessment can estimation of TBSA burned in 72 hours, when burns be completed. The patient’s palm (not including the and their depth are more clearly demarcated and the fingers or wrist area) equals 1% TBSA. burned area can be more easily quantified.5 Other common methods for measuring burn Types of burns size include the Lund and Browder chart and the A burn injury is described based on its cause: “rule of palms.” The Lund and Browder method thermal, chemical, electrical, radiation, smoke or is highly recommended because it corrects for the inhalation, or frostbite. large head-to-body ratio of infants and children.6 • Thermal burns result from contact with hot The rule of palms is used for small scattered burns substances that cause cell injury by coagulation,

The skin and degrees of burns6,8,9,15

The epidermis is the nonvascular outer layer of • Depths of burns the skin and is as thick as a sheet of paper. The Epidermis epidermis is a protective barrier for the skin, Superficial holding in ﬂ uids and electrolytes and aiding in (1st degree) Partial body temperature regulation. thickness • The dermis lies beneath the epidermis and is 30 to (2nd degree) 45 times thicker than the epidermis. Connective tissues with blood vessels, hair follicles, nerve Full thickness endings, and sweat glands are found in the dermis. (3rd degree) Dermis • Under the epidermis is the subcutaneous tissue, which contains major vascular networks, nerves,

fat, and lymphatics. The subcutaneous tissue Subcutaneous acts as a heat insulator for underlying structures, tissue including the muscles and internal organs. • Superfi cial burns caused by the sun or low-intensity heat fl ashes damage only the epidermis. These part of the dermis, and 2 to 6 weeks for deep partial- fi rst-degree burns cause erythema, skin blanching on thickness burns, which involve more of the dermis. pressure, mild pain and swelling, and no blisters or • Full-thickness burns may extend into the subcutaneous vesicles, although after 24 hours the skin may blister tissue, meaning the skin can’t heal on its own. These and peel. Symptoms include hyperesthesia, mild pain, burns, classifi ed as third- and fourth-degree burns, are and tingling. Healing typically takes 3 to 6 days. caused by prolonged exposure to chemicals, electrical • Partial-thickness burns caused by chemicals, fl ame, current, fl ame, hot liquids, or tar. The skin appears dry, or hot liquids damage the epidermis and part of waxy, white, leathery, or hard. Thrombosed vessels the dermis. These second-degree burns appear as will be visible, and muscles, tendons, and bones may fl uid-fi lled vesicles that be involved. Signs and are red and shiny (and symptoms include lack wet if the vesicles have of pain, possible hema- ruptured). Symptoms turia, possible entrance include edema, hyper- and exit wounds from esthesia, pain caused an electrical burn, and by nerve injury, and shock. Skin grafting sensitivity to cold air. is often required for Healing typically takes healing, and patients 10 to 21 days for super- may lose function of fi cial partial-thickness Deep partial-thickness (second extremities or digits, or A full-thickness (third degree) burns, which involve degree) burns of the hands. need amputation. burn of the foot.

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Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. including flame, hot liquids, hot solid objects, and Should my patient go to a burn steam.7 The longer the skin is in contact with these center?19 hot substances the deeper the wound. Oil-based liquids such as grease and cooking oil have higher Patients who should be referred to a burn center boiling points, and cause deeper burns than scalds include: with water or other liquids.8 Burns from hot solid • All burn patients under age 1. objects such as solid metal, hot plastic, glass, or • All burn patients ages 1 to 2 with burns over 5% or stone are all considered thermal burns. more of TBSA. • Chemical burns destroy tissue and continue • Patients of any age with full-thickness burns of to do damage up to 72 hours unless neutralized. any size. Causes of chemical burns are strong acids, alkalis, • Patients over age 2 with partial-thickness burns and organic compounds.9 Acids are commonly greater than 10% of TBSA. found in household cleaners such as rust removers • Patients with burns of special areas such as the face, hands, feet, genitalia, perineum, or major joints. and bathroom cleaners, and cause protein coagula- • Patients with electrical burns, including lightning tion, which results in less extensive injuries. Alkalis injuries. such as oven cleaners and fertilizers cause deeper • Patients with chemical burns. burns due to liquefaction necrosis of tissue, which • Patients with inhalation injury resulting from a ﬁ re lets the chemical penetrate deeper into tissues.9 or hot liquid burn. Organic compounds that cause chemical burns • Patients with circumferential burns of the limbs include gasoline and chemical disinfectants, which or chest. can cause severe coagulation necrosis and produce • Patients with preexisting medical conditions a layer of thick, nonviable tissue called eschar, that could complicate burn management, prolong 9 which is normally present in full-thickness burns. recovery, or affect mortality. • Electrical burns are classified as low voltage • Patients with burns and concomitant trauma. (under 1,000 volts) or high voltage (1,000 volts or • Children with burns who are suspected to be victims higher).9 Electrical injuries can cause death by of child abuse. producing ventricular fibrillation or paralysis of • Patients whose burns require treatment that exceeds the respiratory muscles; dysrhythmias can occur the capabilities of the referring facility. with low voltage, but are more commonly seen in • Patients with septic burn wounds. high-voltage injuries. The extent of damage from an electrical burn may initially appear minor—the the patient has thermal burns, the signs of inhala- patient may only have small entry and exit wounds. tion burns are facial burns, hoarseness, soot in the Extensive damage can appear within several days nose or mouth, carbon in the sputum, lip edema, to weeks, a phenomenon known as the iceberg and singed eyebrows or nasal hair. Manufacturing effect because the skin surface shows little injury of illegal methamphetamine can cause thermal and hides massive injury beneath.9 Instead of and chemical burns and associated inhalation conducting the electricity, bones, muscle, tendon, burns.9 Regardless of the cause of the inhalation and fat respond to electrical injury by producing injury, the patient needs immediate respiratory heat. Most injuries occur to muscles surrounding interventions such as bronchoscopy, endotracheal the long bones.9 intubation, and measurement of carboxyhemoglo- • Radiation burns result from exposure to bin (COHgb) levels. sunlight, tanning booths, X-rays, or nuclear emis- • Frostbite is temporary or permanent tissue sions or explosions. Ionizing radiation can produce damage resulting from exposure to very cold tissue damage directly by striking a vital molecule temperatures. Any area left uncovered in very cold such as DNA.8 Sunburn is usually a first-degree or temperatures can become frostbitten, but the most superficial burn, but radiation therapy can cause commonly affected areas are the fingers, toes, full-thickness burns. chin, earlobes, cheeks, and nose.10 Blood flow to • Smoke and inhalation burns can occur the skin’s outer layer is reduced and the skin tis- concurrently with thermal or chemical burns. If sue freezes and begins to die. Without treatment, www.nursingcriticalcare.com January l Nursing2013CriticalCare l 17

frostbite can progress to necrosis, gangrene, hypo- the perineal area are prone to autocontamination thermia, and cardiac arrest. Because frostbite causes by urine and feces.11,12 Lastly, burns over the joints damage to the skin, some patients are treated in the immediately affect the patient’s range of motion, ICU as burn patients, although initial treatment for which may be exacerbated later by hypertrophic frostbite is different than that for burns. scarring (see Troublesome scars). Intensive therapy to prevent permanent disability is crucial. Location matters The location of a burn injury can predispose a The body’s response to burns patient to initial complications or complications Understanding the pathophysiology of a burn during healing.11 Circumferential burns of the injury (sometimes called burn shock) is key to extremities (see Ring of fire) can lead to vascular effective management. Different causes lead to dif- compromise resulting in compartment syndrome, ferent burn injury patterns, which require different and circumferential burns to the thorax can impair management. chest wall expansion, causing pulmonary insuffi- The body’s compensatory mechanisms start with ciency. Burns of the chest, head, and neck are also the inflammatory response, which is initiated by associated with pulmonary complications. Facial cellular injury. The most important activator of burns are associated with corneal abrasions, burns the inflammatory response is the mast cell, which of the ears with auricular chondritis, and burns of releases biochemical mediators, such as histamine and chemotactic factors, and synthesizes other mediators, such as prostaglandins and leukotri- Rule of Nines: enes.13 Histamine, the major vasoactive amine Estimating burn size in adults released by the mast cells, causes increased capillary permeability and exudation resulting in edema, decreased intravascular volume, hypotension, 41⁄2% 1 4 ⁄2% tachypnea, tachycardia, oliguria, and shock.13 The sympathetic nervous system (SNS) is stimulated and the fight-or-flight response activated, causing thirst, gastrointestinal hypomotility (ileus), adrenal stimulation (causing increased catecholamine secretions, 18% 18% increased metabolic rate, and increased aldosterone secretion), hepatic stimulation (causing release of 441⁄2% 1⁄2% glycogen stores), increasing blood glucose levels, 41⁄2% 41⁄2% and vasoconstriction.13

1% Ring of ﬁ re

9% 9%

Source: Anatomical Chart Company. Pathology/Laboratory Medicine; 2008. Circumferential burns of the extremities can lead to compartment syndrome.

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Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Burns affect every body system: Troublesome scars • Respiratory system effects include direct airway injury; inhalation injury; carbon monoxide poisoning; smoke inhalation (damage to epithe- lial cells in the lower respiratory tract secondary to inhaling oxides, the products of combustion); alveolar damage; pulmonary edema; and decreased oxygen diffusion.8 • Cardiovascular system effects include fluid volume deficit, decreased mean arterial pressure, decreased cardiac output, hypovolemic shock (secondary to extensive fluid shifts), and decreased myocardial contractility (impaired cardiac function improves 24 to 30 hours postinjury).9 Electrical burns can Hypertrophic scarring of a deep partial-thickness burn cause ECG changes, myocardial infarction, ven- can cause pruritus, warmth, and other patient discomfort, tricular fibrillation, and cardiac arrest.9 and the raised scar can limit function if joints are affected. • Renal system effects are indirect. Decreased cardiac output leads to decreased renal perfusion and oligu- Assessment and initial management ria that can culminate in acute kidney injury (AKI). The emergency management of a patient with a In addition, after a burn injury, damaged red blood burn injury begins with the initial assessment and cells release hemoglobin and potassium, and skele- treatment of life-threatening injuries. Stabilize the tal muscle cells release myoglobin. Both hemoglobin patient’s cervical spine if this hasn’t already been and myoglobin are filtered by the glomerulus and done. The true mechanism of injury may not be degraded, releasing heme pigment. Heme pigment, clear (for example, the patient may have been especially in the setting of fluid volume deficit, can burned and propelled in an explosion). cause AKI.14 Marked release of hemoglobin or myo- Follow these specific aspects of the ABCDE globin usually causes red or brown urine. (Airway, Breathing, Circulation, Disability, and • Gastrointestinal system effects include ileus sec- Exposure/Environmental control) assessment:5,9,15 ondary to SNS activation. Stress ulcer formation • Airway. The airway is the primary concern, is triggered by the stress response and the his- especially if a patient has an inhalation injury. tamine released in the inflammatory response. Assess for stridor (an ominous sign that suggests Intra-abdominal hypertension and abdominal the patient’s upper airway is at least 85% nar- compartment syndrome can damage the gut, rowed), facial burns, soot in the nares or mouth, kidneys, and liver.5,9 singed facial hair or nasal hair, edema of the lips • Neuroendocrine system effects include increased and oral cavity, coughing, hoarse voice, and cir- metabolic rate to compensate for the initial low cumferential neck burns.5,9 core body temperature due to loss of skin. The • Breathing. Determine adequacy of ventilation by increased metabolic rate increases caloric needs and assessing the patient’s respiratory rate and depth leads to catabolism and a negative nitrogen balance and observing for dyspnea and adventitious breath that slows tissue building and healing.9 Increased sounds. Obtain a pulse oximetry reading (remem- cortisol levels may cause insulin resistance and bering that it may be inaccurate in the presence hyperglycemia.13 of carbon monoxide), and a co-oximetry reading if • Immune system effects include immunosuppression indicated and available.5,9,15 secondary to the immediate, prolonged, and severe • Circulation. Assess for the presence, rate, and immunologic and inflammatory response to a major rhythm of pulses; evaluate capillary refill time, burn injury.13 skin color, and temperature; and observe for obvi- • Musculoskeletal system effects include contractures ous arterial bleeding.5 and complications secondary to immobility and the • Disability. Use the AVPU (Alert, Verbal, Pain healing process. stimuli, Unresponsive) Scale (see A look at the www.nursingcriticalcare.com January l Nursing2013CriticalCare l 19

AVPU scale) to determine the patient’s level of alcohol), Pertinent history, Last oral intake, and consciousness and carefully evaluate any abnor- Events leading up to the injury.16 Determine the malities. Assess for hypoxia, decreased cerebral extent and depth of the burn, and ask the follow- perfusion related to hypovolemia, and cerebral ing questions: injury resulting from head trauma. Assess the • What is the patient’s chief complaint (for patient’s pupillary response to light and sensory example, dyspnea or pain)? and motor function.3,9 • Did the burn occur in an enclosed space? • Exposure/environmental control. Gently remove • Were explosives or chemicals involved? the patient’s nonadherent clothing and jewelry to • What was the source of the burning agent (for prevent continued tissue damage. If the patient’s example, liquid, metal, or chemicals)? face is burned, remove glasses or contact lenses. • What is the status of the patient’s tetanus immu- Cover the patient with a dry sterile sheet to prevent nization?6 further contamination of the burn wounds and to provide warmth.3,5,6,15 Stages of burn management Obtain vital signs and establish I.V. access The care of the burn patient is organized into three with two large-bore catheters if the patient has overlapping stages: emergent (resuscitative), acute burns over 15% or more of TBSA. Elevate burned (wound healing), and rehabilitative (restorative).5 extremities above heart level to decrease edema. The assessment and management of specific prob- Administer I.V. analgesia as prescribed and assess lems aren’t limited to these stages and take place its effectiveness often, using a valid and reliable throughout the care of patients with burn injuries. pain intensity rating scale. For example, rehabilitation begins on the first day After the initial focused assessment is completed after the burn injury, with the formal rehabilitative and the patient is stabilized, obtain a history of the phase beginning when the burn wound is almost events while performing a comprehensive physical healed.15 assessment. Your main priorities are to determine the potential for an inhalation injury, presence of About ﬂ uid resuscitation concomitant injuries or trauma, and any preexist- Fluid resuscitation efforts are started as soon as ing conditions that may influence the physical possible for patients with burns of more than assessment or patient outcomes. A simple way 15% of TBSA; otherwise, the patient may experi- to initially accomplish this is to use the SAMPLE ence hypovolemic shock.9 Insert an indwelling mnemonic: Signs and symptoms, Allergies, cur- urinary catheter to monitor fluid balance. Fluid rent Medications (including illegal substances or resuscitation is usually accomplished with an isotonic crystalloid such as lactated Ringer’s solution; A look at the AVPU scale the lactate helps to buffer the metabolic acidosis commonly seen with hypoperfusion and burn This scale, a shortened form of the Glasgow Coma shock.9 Several fluid resuscitation formulas are Scale, can be used to determine a patient’s level of available, and a formula usually is prescribed by consciousness. the burn trauma surgeon. Alert: patient is alert, awake, responds to voice, and is oriented to time, place, and person. You can obtain All formulas are based on the percentage of subjective information from the patient. TBSA burned, the patient’s weight in kilograms Verbal: The patient opens his or her eyes to verbal (kg), and the patient’s age. Half of the fluid volume stimuli, but isn’t fully oriented to time, place, or is administered in the first 8 hours post-burn, and person. the remainder is given over the next 16 hours. Painful: The patient responds to painful or noxious The ABA recommends titrating the fluids to main- stimuli, such as a hand squeeze or sternal rub, but tain a urine output of 30 to 50 mL/hour in adults doesn’t respond to verbal stimuli. and 1 mL/kg/hour in children weighing less than Unresponsive: The patient is nonverbal and doesn’t 30 kg.9 In the case of a patient who has sustained respond to painful stimuli. a high-voltage electrical burn, the target range for Source: http://www.ahrq.gov/research/esi/esi2.htm. urine output is 75 to 100 mL/hour to prevent renal

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Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. tubular obstruction from heme interventions for common types pigment.9 Avoid administering of burns: diuretics, which may aggravate • Thermal. Assess the patient for dehydration.9 The patient’s men- inhalation injuries. For adults tal status, vital signs, hourly urine with burns of more than 15% output, and urine specific gravity, TBSA, begin fluid replacement are valuable indicators of the as prescribed and insert an patient’s response to fluid resus- indwelling urinary catheter. citation. • Chemical. Assess the patient’s Because of the massive ABCs before starting decontami- volumes of I.V. fluids adminis- nation procedures. Endotracheal tered to burn patients (rates of intubation and mechanical 1,000 mL/hour are common), ventilation may be needed for diligently assess the patient’s Only 25% of initial patients with significant inhala- hemodynamic status to avoid ﬂ uid resuscitation tion injuries or circumferential inducing fluid overload. Signs actually stays in the full-thickness burns to the neck and symptoms of “fluid creep,” intravascular space. or chest. Remove dry chemi- or fluid resuscitation in excess of cals from the patient’s skin, that predicted by the Parkland then use saline or tap water to formula, include abdominal flush chemicals from the burn. compartment syndrome, extremity compartment Contact the poison control center for more infor- syndrome, and acute respiratory distress syn- mation on handling chemicals, and protect yourself drome (ARDS).17,18 from potential exposure.5,15 Fluid resuscitation after the first 24 hours is • Electrical. Check pulses distal to the burn. Monitor accomplished by using isotonic crystalloids as the patient for myoglobinemia (myoglobin released well as colloids. Dextrose solutions and electrolyte from injured muscle tissue and hemoglobin from replacement (especially potassium replacement) damaged red blood cells). Be prepared to administer is initiated. Lactated Ringer’s solution is isotonic I.V. mannitol, an osmotic diuretic, to maintain urine and doesn’t increase intravascular oncotic pres- output, and I.V. sodium bicarbonate to alkalinize sure. Because of increased capillary permeability the urine.5,15 in patients with burns, only 25% of the lactated • Inhalation. Obtain an arterial blood gas analysis, Ringer’s solution infused in the initial fluid resusci- COHgb level, and chest X-ray. Be prepared if fiber- tation will actually stay in the intravascular space. optic bronchoscopy or endotracheal intubation are This is one reason for the large fluid volumes needed needed. in fluid replacement.9 Once the increased capillary permeability has A good start decreased (8 to 12 hours after the burn injury), By understanding the types of burns and how to colloids such as albumin may be given to help assess and manage them, you can help patients restore intravascular volume. Colloids increase the until they can be transferred for specialized burn oncotic pressure in the vascular space, pulling inter- care. In future articles, we’ll describe manag- stitial fluid into the intravascular space. This helps ing burn patients in the ICU, skin grafting, and decrease the edema associated with burn injuries. inhospital rehabilitation. ❖

Interventions for speciﬁ c types of burns REFERENCES For all patients, monitor vital signs, level of con- 1. American Burn Association. http://ameriburn.org/resources_ sciousness, respiratory status, oxygen saturation, factsheet.php. and cardiac rate and rhythm. Identify and treat 2. TOMA Foundation for Burned Children. http://www.fondtoma found.org/english/index.htm. other associated injuries, such as head injury, pneu- 3. Silvestri LA. Comprehensive Review for the NCLEX-RN Examina- mothorax, or fractures. Now let’s look at specific tion. 5th ed. St. Louis, MO: Elsevier Saunders; 2011. www.nursingcriticalcare.com January l Nursing2013CriticalCare l 21

4. Kagan RJ, Peck MD, Ahrenholz DH, et al. Surgical Management 14. Eustace JA, Kinsella S. Clinical features and diagnosis of heme of the Burn Wound and Use of Skin Substitutes. American Burn pigment-induced acute kidney injury (acute renal failure). 2012. Association; 2009. http://ameriburn.org/WhitePaperFinal.pdf. UpToDate. http://www.uptodate.com. 5. Smeltzer SC, Bare BG, Hinkle JL, Cheever, KH. Brunner & 15. Knighton JA. Nursing management: burns. In: Lewis SL, Suddarth’s Textbook of Medical-Surgical Nursing. 12th ed. Philadel- Heitkemper MM, Dirksen SR, O’Brien PG, Bucher L eds. Medical- phia, PA: Lippincott Williams & Wilkins; 2010. Surgical Nursing: Assessment and Management of Clinical Problems. 6. Stout LR. Burns and common integumentary disorders. In: 7th ed., Vol 1. St. Louis, MO: Mosby Elsevier; 2007:483-507. Morton PG, Fontaine DK, eds. Critical Care Nursing: A Holistic 16. EMT’s Patient Assessment: SAMPLE. http://voices.yahoo.com/ Approach. 9th ed. Philadelphia, PA: Lippincott Williams & Wilkins; emts-patient-assessment-sample-1314601.html. 2009:1349-1375. 17. Zaletel CL. Factors affecting fl uid resuscitation in the burn 7. Rice PL, Orgill DP. Classifi cation of burns. 2012. UpToDate. patient: the collaborative role of the APN. Adv Emerg Nurs J. 2009; http://www.uptodate.com. 31(4):309-320. 8. Coffee T. Care of patients with burns. In: Ignatavicius DD, 18. James E, Hayes M, McCabe P, Williams G, Takata M, Workman ML. Medical-Surgical Nursing: Patient-Centered Collabora- Vizcaychipi MP. Fluid creep in burn resuscitation: the tide has tive Care. 7th ed. St. Louis, MO: Saunders Elsevier; 2013:511-540. not yet turned. Critical Care. 2012:16(suppl 1):P464. http://ccforum. 9. Ahrns-Klas KS. Burns. In: Sole ML, Klein DG, Moseley MJ. In- com/content/16/S1/P464. troduction to Critical Care Nursing. 5th ed. St. Louis, MO: Saunders 19. Stander M, Wallis LA. The emergency management and Elsevier; 2009:683-728. treatment of severe burns. Emerg Med Int. 2011;2011:161375. 10. Frostbite treatment. http://www.essortment.com/frostbite- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3195355. treatment-59888.html. At Duquesne University’s School of Nursing in Pittsburgh, Pa., Alicia L. 11. Moss LS. Treatment of the burn patient in primary care. Adv Culleiton is an assistant clinical professor and Lynn M. Simko is an associate Wound Care. 2010;23(11):517-524. clinical professor. 12. Perrin KO. Understanding the Essentials of Critical Care Nursing. Upper Saddle River, NJ: Pearson Prentice Hall; 2009. The authors have disclosed that they have no fi nancial relationships related to this article. 13. Huether SE, McCance KL. Understanding Pathophysiology. 5th ed. St. Louis, MO: Mosby, Inc.; 2011. DOI-10.1097/01.CCN.0000423824.70370.fa

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