IV. Burns

SECTION IV. BURNS


Amanda Bettencourt and Melissa Gorman


Caring for a child with a burn injury is challenging; depending on the size and depth of the burn, dramatic alterations in fluid and electrolyte balances, ventilation, and thermoregulation can occur and if not managed properly can result in organ dysfunction and ultimately death. Pediatric burn care has progressed significantly over the past several years, and with proper care and treatment children today can survive burn injuries that involve almost all of their body surface area (BSA). Nursing care of the burned child involves knowledge of the pathophysiology of burn inflammation; management of burn shock; performance of complex wound care; adequate pain and anxiety management; and providing for the psychosocial needs of the child, his or her family, and community. The American Burn Association (ABA) is the interprofessional organization for those who care for patients with burn injuries. In addition to this chapter, nurses who care for burned children on a regular basis are encouraged to familiarize themselves with the ABA and its clinical practice guidelines, which can be found on the organization’s website (www.Ameriburn.org).


A.    Incidence



1.    According to the World Health Organization (2018), an estimated 265,000 deaths are caused worldwide every year by burns. The vast majority of these deaths occur in low- and middle-income countries.



2.    According to the ABA (2016), there are approximately 486,000 burn injuries and 40,000 burn-related hospital admissions in the United States annually.



3.    Unintentional injury is the leading cause of death for children over the age of 1 year in the United States. Unintentional fire/burn is the fifth leading cause of unintentional injury death in children age 1 to 4 and the third leading cause in children 5 to 9 years of age (CDC, 2016a, 2016b).



4.    Children ages 4 and younger are at the greatest risk of suffering burn-related injuries, with an injury rate more than twice that of children aged 5 to 15 years (ABA, 2017).



5.    Scald injuries are most prevalent in children younger than 5, whereas fire/flame injuries are the most common in the remaining age categories (ABA, 2017).


B.    Types of Burn Injury


Burn types can be classified into four main categories: thermal, electrical, chemical, and radiation. Thermal burns can be further divided into subtypes of scald, flame, contact, and hypothermic. See Table 9.26 for descriptions of each type of burn.


C.    Pathophysiology of Burn Injury



1.    Local Inflammation



a.    The local burn wound is the result of direct damage of skin cells and results in coagulation necrosis of tissue that has both breadth and depth, or more common, a percentage of total body surface area (%TBSA) and degree (i.e., first, second, or third degree) of burn injury. The depth or extent of the burn injury depends on the intensity of the heat, the duration of exposure, and the type of tissue involved.



b.    If the absorption of heat energy exceeds the ability of the tissue to dissipate the absorbed heat, cellular injury occurs at various depths in the skin organ. This phenomenon can best be described by Jackson’s functional classification system (Figure 9.10; Lewis, Heimbach, & Gibran, 2012). In this model, the depth of injury is dependent on the relative heat exposure area and the healing process as represented by three distinct zones of injury.



i.    The zone of hyperemia is the most superficial area of viable tissue and will heal itself in a matter of days (i.e., sunburn).



ii.    The zone of stasis is a deeper area inside the zone of hyperemia where vascular damage and inflammation have resulted in some compromise of tissue perfusion but not immediate cell death. This zone is evolving continuously over the first 2 to 3 days postinjury, and may undergo progressive tissue destruction or heal on its own depending on the quality of care the child receives and other physiological factors. Effective resuscitation and immediate postinjury care have been shown to positively affect viability in the zone of stasis (Lewis et al., 2012).



iii.    The third zone is the zone of coagulation, where the heat has damaged the skin most intimately, and cells in the skin have necrosed. Because this zone is characterized by cellular death, coagulation necrosis is the result of injuries in this zone.


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FIGURE 9.10    Zones of tissue injury.







c.    At the injury site, the inflammatory response mediated by histamine and prostaglandin causes increased permeability of the cell membrane separating the intravascular and interstitial compartments, resulting in altered exchange of fluid and plasma in the wound bed. When this occurs, it causes all elements of the intravascular space except RBCs to escape, and edema forms, causing a relative intravascular hypovolemia. This is also how a blister forms on the burn wound. As the child’s %TBSA and depth of injury increase, the severity of this inflammatory response increases. Thus, children with large burns (>15% TBSA) have local edema formation as well as potential for systemic capillary leak formation, and resultant need for fluid resuscitation to maintain homeostasis. Edema that is the result of increased capillary permeability is at its peak 12 to 24 hours postburn injury. Very large and deep burns can take up to 2 to 3 days to regain capillary cell membrane integrity (Warden, 2014).



7962.    Systemic Responses



a.    A large burn injury (>15% TBSA and deep) affects all organ systems and can cause a phenomenon known as burn shock. SIRS is present in burned children to varying degrees after injury. In addition to burn shock, a hypermetabolic and systemic immune response occurs. The events, magnitude, and duration of the systemic manifestations of burn shock are proportional to the extent of burn injury and plateau at approximately 50% to 60% burn surface area. Although the exact etiology of burn shock is not totally understood, characteristic fluid volume shifts and hemodynamic changes that accompany burn shock have been identified. Within several hours of injury, as edema forms, the fluid shift and intravascular volume deficit result in hemoconcentration (Kramer, 2014). The hematocrit increases secondary to loss of circulating plasma volume. Blood viscosity also increases.



b.    With increased catecholamine and glucagon production, there is a mobilization of hepatic glycogen stores, coupled with a relative decrease in insulin production that commonly results in high serum glucose levels in the early postburn period. Within 24 to 48 hours after the burn, there is an increase in metabolism directly related to the severity of the injury. This hypermetabolic state is characterized by increases in oxygen consumption and heat production, with an increase in both core and skin temperatures. Both protein synthesis and breakdown are increased. In patients not meeting nutritional goals, breakdown rates exceed synthesis, resulting in a negative nitrogen balance. As capillary integrity is restored, electrolyte replacement therapy becomes an ongoing process and continues until wound closure is achieved. As the wounds heal, either spontaneously or by skin grafting, the metabolic rate gradually returns to normal levels. The decrease in metabolic requirements is a gradual process. In children with large burns, metabolic requirements remain elevated even after the burn wound is fully mature (Jeschke & Herndon, 2014).



3.    Associated Complications



a.    General. Although the exact mechanisms of the immunologic and inflammatory response are not known, characteristic pathophysiologic activities are being recognized as a result of the burn injury. Alteration in the skin’s protective function provides opportunity for invasion of microorganisms and primes the defensive mechanisms of the inflammatory and immune systems. It is hypothesized that a massive systemic inflammatory response is caused by the local trauma of a burn. It appears that a burn is a mediator-induced injury; although the local effects occur immediately, the systemic response to the mediators produced within a burn progresses and peaks 5 to 7 days after the injury. It is unclear whether the immunosuppression after a burn injury is the result of biochemical substances (i.e., oxidants, histamine, prostaglandins, arachidonic acid metabolites) liberated from the burn itself, or is produced in response to the burn. In addition, the immunosuppressive effects of anesthetic agents, surgical procedures, multiple transfusions, and the use of systemic antibiotics emphasize postburn immunologic abnormalities during the clinical course of burn therapy (Murphy, Sherwood, & Toliver-Kinsky, 2012).



b.    Hypothermia. Children are more prone to the development of hypothermia related to their increased body surface-area-to-mass ratio, resulting in greater evaporative water loss and conductive heat loss. Hypothermia remains a major problem until the wounds have been skin grafted or healed. Hypothermia alone, without any injuries, can cause apnea, progressive metabolic acidosis, and ventricular arrhythmias. Every effort should be made to minimize heat loss in children with burn injuries, including providing care in a heated and humidified hospital room (Lee, Norbury, & Herndon, 2012).



c.    Compartment syndrome. Circumferential deep partial-thickness and full-thickness burns of the extremities may impair circulation as a result of rapid edema formation. Thus, it is imperative to maintain continuous elevation of the burned extremities and evaluate skin color, sensation, and capillary refill at frequent intervals during the first 24 to 48 hours after injury. The use of an ultrasonic flow device is indicated if pulses are not palpable or color and sensation assessments are complicated by the burn injury (Advanced Burn Life Support [ABLS] Advisory Committee, 2015). Another assessment strategy is to apply a pulse oximetry probe distal to the circumferential injury and monitor the waveform to assess flow. Because compartment syndrome is associated with loss of life and limb, escharotomies should be performed by an experienced clinician provider at the earliest sign of circulatory compromise (i.e., [early] paresthesia, pain with passive 797stretch, or [later] decreased pulse or complaints of deep aching muscle pain).



i.    Escharotomy/fasciotomy. An escharotomy is performed when the edema from a circumferential deep burn wound is compromising circulation to the deeper tissues. The skin loses elasticity with deep burn injury, and thus cannot expand to accommodate this increased edema, causing circulatory compromise.



ii.    Escharotomies are performed most often at the bedside with a scalpel or electrocautery device, and involve mechanical release of the eschar layer of the skin only on the longitudinal plane. If compartment syndrome becomes severe and escharotomy does not relieve the pressure, a fasciotomy may be required. This procedure is typically performed in the operating room and involves mechanical release of the underlying fascia to alleviate pressure from edema in the muscular compartment. Without prompt intervention, nerve damage and muscle necrosis can result.



d.    Abdominal compartment syndrome. If the resuscitation volumes are excessive, or the child has suffered from massive (>80%) burns, abdominal compartment syndrome may develop (Lee, Norbury, & Herndon, 2012). In children with abdominal compartment syndrome, mortality risk increases significantly, as multiorgan system failure often results. Careful monitoring and surgical laparotomy intervention or percutaneous peritoneal drainage when abdominal compartment syndrome is suspected/confirmed is key to improving survival and reducing morbidity in children with massive burns.



e.    Electrical injuries. The complications associated with electrical injuries are related to the type and duration of electrical current that the child has come in contact with. The injuries of most concern for the critical care nurse are high-voltage injuries. According to Ohm’s law, electrical current flows through areas that have the least resistance (highest conductivity) to the electrical current flow. When electricity comes in contact with the skin, the skin is injured at the contact points as well as deeper within the skin and underlying tissues where the current has flowed. If electrical current has flowed through the torso, cardiac rhythm disturbances can occur. In addition to cardiac rhythm disturbances, cutaneous injury can occur. Typically, the contact points (or “entrance and exit wounds”) appear dry, circumscribed, and depressed.



i.    Electrical injuries are often referred to as “iceberg” injuries, as the true extent of tissue injury is often not visible on the surface of the skin itself. A common complication of high-voltage electrical injury is subfascial edema and tissue necrosis between the contact points. Thus, it is imperative that the nurse measure pulse quality, color, motor function, and sensation in the electrically injured limb closely during the first 24 hours after injury. When a change in color, motor function, sensation, or pulse quality is detected, a provider should be notified and escharotomies or fasciotomies may be performed to relieve the pressure and restore perfusion (ABLS Advisory Committee, 2015). If these symptoms are not recognized and intervened upon, loss of limb can occur.



ii.    Any child who has an electrical injury should have a 12-lead ECG performed to check for arrhythmia. If a loss of consciousness occurred at the scene or any abnormality is detected in the ECG, continuous cardiac monitoring is indicated.



iii.    If the electrical injury is extensive and muscle necrosis has occurred, a common and serious side effect is myoglobinuria due to the hemochromogens present in the bloodstream. If the urine of a child with an electrical injury becomes pigmented, an increase in intravenous fluid rate and addition of bicarbonate or mannitol to the treatment plan is often indicated, as acute tubular necrosis and renal failure can result (ABLS Advisory Committee, 2015).



iv.    Other, less common complications associated with electrical injuries include the following:



1)  Pathologic fractures of long bones due to muscle tetany



2)  Spinal cord injuries due to falling/trauma or spinal fracture



3)  Neurologic complications such as headaches, seizures, diminished memory, difficulty concentrating, and emotional fluctuations that may persist for months to years after injury



f.    Chemical injuries. The complications associated with chemical injury vary based upon the nature of the chemical. Typical caustic chemicals that can cause injury are acids, alkalis, and petroleum-based products. The most important intervention in the child with a chemical injury is to remove clothing and to brush off all powders, 798followed by decontamination with tap water. Once the agent has been identified, treatment may be directed at neutralizing the agent, but irrigation should occur continuously from the time of exposure through the evaluation stage in the hospital. Typically, alkalis cause deeper skin damage than acidic compounds due to their high affinity for elements found in the tissue.



i.    If the chemical has made contact with the eyes, contact lenses should be removed and immediately flushed with copious amounts of water. Irrigation with normal saline or a buffered solution is preferred, but tap water is appropriate if nothing else is readily available (ABLS Advisory Committee, 2015). A prompt consultation to an ophthalmology provider and corneal exam are very important due to the risk of permanent vision loss.



ii.    The specific treatment modality for each chemical the child has been exposed to can be obtained by contacting a poison control facility, the hazardous materials division of the fire department, or the chemical manufacturer. Prompt treatment with the appropriate antidote is key to minimizing morbidity and mortality in chemically injured children.


D.    Initial Assessment and Management



1.    Assessment and Management at the Scene



a.    The most important first-aid treatment is minimizing the burn wound depth and extent, which is accomplished by eliminating the source of the injury and stopping the burning process (ABLS Advisory Committee, 2015).



b.    After the burning agent is eliminated, cover the burns with clean, dry linen. Measures to conserve body heat are essential for all burn survivors, particularly for the infant and young child. Wet compresses may be applied to small wounds but not to large injuries and need only be applied during the first few minutes after injury (Sheridan, 2012). Water increases body heat loss through evaporation and can lead to hypothermia. This is a principal concern in small children, where wet dressings may accentuate the shock state, causing a further decrease in tissue perfusion, cardiac output, and perfusion to vital organs (Lee, Norbury, & Herndon, 2012). Ice or ice water should never be used directly on the skin because of the potential for cold injury or for conversion of a lesser burn to a deeper injury (due to vasoconstriction; ABLS Advisory Committee, 2015).



c.    Rapid primary and secondary assessment



i.    At the accident scene, the primary and secondary assessments are performed as later described but in a more rapid manner. The priority quickly becomes to expediently transport the patient to a hospital.



ii.    Burn patients are considered multiple trauma victims and must be assessed for other traumatic injuries in addition to the burn, especially if the burn is the result of a motor vehicle crash or an explosion of some kind. Any coexisting trauma must be evaluated and treated during the primary and secondary surveys.



iii.    Begin fluid resuscitation if the burn appears to be bigger than 15% of the TBSA and deep according to the ABLS prehospital resuscitation rates (Table 9.27). Lactated Ringer’s or NS are appropriate choices for resuscitation fluid in the field (ABLS Advisory Committee, 2015).


Example of Calculating Fluid Resuscitation







Parkland Burn Resuscitation Formula



First 24 Hours Postburn



4 mL Ringer’s lactate × weight in kg × %burn surface area



Give half of the calculated amount in the first 8 hours postburn and the remaining amount over the next 16 hours; plus daily maintenance volume with dextrose as needed.



Example: 10-kg child with 50% burn surface area:



4 mL × 10 kg × 50% burn surface area = 2,000 mL Ringer’s lactate* over 24 hours



First 8 hours = 1,000 mL RL = 125 mL/hr



Second 8 hours = 500 mL RL = 62.5 mL/hr



Third 8 hours = 500 mL RL = 62.5 mL/hr



* The fluid is recommended to be lactated Ringer’s, but could be normal saline.







2.    Assessment and Management in the Emergency Department



a.    Primary assessment. The primary assessment follows the “ABCDE” methodology, beginning with airway and breathing, followed by circulation, disability, and expose/examine.


799TABLE 9.27    Burn Resuscitation Fluid Calculation Recommendations




















Practice Setting


Age of Patient


Recommended Formula


Prehospital (start if burn looks >15%TBSA and deep)


Infant


Child


Adolescent/Adult


125 mL/hr of LR or NS


250 mL/hr of LR or NS


500 mL/hr of LR or NS


Emergency department (ABLS consensus formulas)


Adults


Children


Electrical injury (any age)


2 mL LR × %TBSA × weight (kg)


3 mL LR × %TBSA × weight (kg)


4 mL LR × %TBSA × weight (kg)


Take this total and divide by ½. Give the first ½ in the first 8 hours, rest over next 16 hours.


Remember to monitor urine output hourly and titrate up/down as needed to meet UOP target of 0.5–1 mL/kg/hr or 2 mL/kg/hr if electrical injury is present.


Inpatient unit/burn center


Adults


Children


Electrical injury (any age)


Parkland formula


Brooke formula


Nurse-driven resuscitation


All formulas are estimates, careful measurement of clinical endpoints of resuscitation is the key intervention to titrate fluid requirements appropriately.


LR, lactated Ringer’s; NS, normal saline, TBSA, total body surface area; UOP, urine output.



b.    Assess the airway and breathing. Airway management for the burn patient should be managed as for any trauma victim, including performing basic life-support measures if indicated, providing 100% FiO2 via face mask, assessing respirations for adequacy of rate and depth, and assessing for bilateral breath sounds.



i.    Special considerations. The upper airway is susceptible to edema and obstruction as a result of exposure to heat and smoke. Because of relatively small airways in children, upper airway obstruction may occur early and rapidly. Circumferential full-thickness burns to the neck or chest may restrict ventilation.



ii.    Upper airway obstruction or lower airway compromise should be identified and treated accordingly and may require endotracheal intubation and mechanical ventilation.



c.    Assess circulation.



i.    Determine the exact extent and depth of the burn. Children with deep burns covering 20% or more of their TBSA require circulatory volume support (Sheridan, 2012). See Table 9.27 for appropriate resuscitation formula choices during emergency department stabilization.



ii.    Establish intravenous (IV) access for fluid resuscitation if indicated. Place two peripheral large-bore IV catheters, appropriate for the size of the child. The peripheral percutaneous route is the method of choice for immediate initial access; if the only accessible veins have overlying burned skin, do not hesitate to use them (ABLS Advisory Committee, 2015). Cannulation of small veins may be difficult in any infant or child but even more so in a child with severe vasoconstriction. Maintaining venous access is a major priority. Adhesive tape is ineffective in securing IV catheters to burned tissue and may compromise blood flow in edematous extremities if applied circumferentially. An intraosseous needle is the vascular access of choice in the child who will need fluids or pain management and peripheral IV access cannot be obtained in a timely fashion (Lee, Norbury, & Herndon, 2012). In the event the child needs continual resuscitation and/or pain management, central venous catheterization is indicated.



iii.    Evaluate skin color, sensation, and capillary refill. Circumferential deep second- to third-degree burns of the extremities may impair circulation as a result of edema formation. Regardless of circumferential injury, maintain continuous elevation of the burned extremities.



iv.    Monitor arterial pulses hourly for 24 to 48 hours on all extremities with deep burns, 800circumferential burns, or electrical burns. Use an ultrasonic flow device or pulse oximetry probe with a pleth waveform if pulses are not palpable. Escharotomies should be performed at the earliest sign of circulatory compromise (i.e., decreased pulse, complaints of deep aching muscle pain) in consultation with an experienced provider.



v.    Insert a urinary catheter to monitor the effectiveness of fluid resuscitation.



d.    Assess disability/neurologic status. Use the alert, voice, pain, unresponsive (AVPU) method to assess neurologic status (ABLS Advisory Committee, 2015). Typically, the burn survivor is initially alert and oriented. If a decreased level of consciousness is present, consider an associated injury, substance abuse, hypoxia, or preexisting medical condition.



e.    Expose and examine



i.    Remove all clothing so the extent and severity of injury can be examined. In the case of chemical burns, the clothing could be contaminated and cause further injury and should be immediately removed entirely. Keep any clothing removed from the child in a safe place until it is determined whether it will be needed for law enforcement evidence review.



ii.    Remove all jewelry as soon as possible, as jewelry will create a tourniquet effect as systemic and burn wound edema form, restricting blood flow and causing tissue loss (ABLS Advisory Committee, 2015).



f.    Secondary assessment



i.    Obtain a history of the burn injury. Initial management and definitive care are guided by the mechanism, duration, severity, and time of the injury. As much information as possible should be obtained regarding the incident:



  What was the cause of the burn?



  Did the injury occur in a closed space?



  What was the timing of the injury?



  Were harmful chemicals involved?



  Were others involved?



  Is there suspicion for nonaccidental trauma?



ii.    Obtain medical history. Underlying medical conditions frequently complicate burn management and prolong recovery. Determine the presence of preexisting disease or associated illness; medications, alcohol, or drugs; allergies or sensitivities; recent exposure to communicable diseases (i.e., varicella, tuberculosis); status of tetanus immunization (burn wounds are tetanus-prone wounds and immunizations should be consistent with the recommendations of the American College of Surgeons); and status of other immunizations (ABLS Advisory Committee, 2015). The tetanus status, however, must be documented so as not to be overlooked. As an aid to gaining necessary information, the mnemonic “AMPLET” can be used:


A = Allergy


M = Medications


P = Previous illness


L = Last meal/fluids


E = Events related to the injury


T = Tetanus



iii.    Complete physical examination. This includes a complete head-to-toe examination and physical assessment to evaluate more fully any and all injuries or abnormalities, including the burn injury. The severity of a burn injury and its morbidity and mortality are determined by the type of burn; size, depth, and anatomic location of the wound; the patient’s age; and any preexisting illness or associated trauma.



iv.    Determine burn size.



1)  The extent of a burn is calculated as a %TBSA burned. Various methods are available to determine the %TBSA. The exact %TBSA is necessary to calculate definitive resuscitation formulas and ensure adequate volume, but not too much volume, is given to the patient. Superficial first-degree burns with erythema (redness) alone should not be included in %TBSA calculations.



2)  In the rule of the palm, the entire palmar aspect of the patient’s hand (including the fingers) represents approximately 1% of the TBSA. Therefore, using the child’s hand as a visual guide, the extent of a small burn or one with an irregular outline or distribution can easily be estimated by determining how much of that child’s palms would cover the injured 801area, and multiplying that by 1% to calculate the percentage of TBSA burned.



3)  The rule of nines measures the percentage of burn surface area by dividing the body into multiples of nine. In the infant or child, the rule is adjusted because the child’s head has a larger proportional percentage of the TBSA and thus is not the most accurate estimation of burn extent in children (ABLS Advisory Committee, 2015).



4)  The Berkow formula, or Lund and Browder chart allows for a more accurate assessment in children, as it takes into account differences in BSA related to age and divides the body into smaller areas (e.g., foot, lower leg, thigh).



5)  Another method uses a standard height and weight nomogram to calculate the BSA burned in square meters (m2).



6)  Regardless of the calculation method used, accurate communication of the %TBSA calculated upon admission used for resuscitation volume calculations must occur. In most cases, a burn diagram should be completed by a nurse or provider and filed in the child’s medical record.



v.    Type of burn. Identify the type of burn: Although appropriate initial interventions often occur before arrival at the emergency department, never assume this step has been completed (i.e., chemical burns).



vi.    Obtain baseline diagnostic studies. Baseline laboratory studies are essential to evaluate the patient’s subsequent progress. Evaluate ABGs and carboxyhemoglobin (if a closed space injury has occurred), hematocrit and hemoglobin, electrolytes, albumin, urinalysis, BUN, chest radiographic examination, and 12-lead ECG with electrical injury, ectopy, or history of underlying cardiovascular disease.



vii.    Initial wound care. Wound care is not considered a component of emergency care except in chemical burns, in which immediate removal of the agent is essential. Substantial wound care, such as excessive manual debridement or application of topical antimicrobials (in the field or primary hospital), is not necessary if the patient will be transferred to a burn care facility in a relatively timely fashion (ABLS Advisory Committee, 2015).



viii.    NPO status. Patients must have nothing by mouth (NPO) until they have been seen and evaluated in a hospital and, if necessary, transported to a burn center. A nasogastric tube should be inserted in all patients with a burn size of over 15% BSA, as they are susceptible to gastric dilatation due to a paralytic ileus, and in all patients who are intubated (ABLS Advisory Committee, 2015).



3.    Admission and Transfer Criteria



a.    Children who have suffered deep burns on greater than 15% of their TBSA should be admitted to a pediatric intensive or intermediate level-of-care environment to allow for close monitoring of hydration status and organ perfusion. Criteria established by the ABA exist to guide clinicians in decisions related to transfer of a child to a verified burn center. These criteria are listed in Table 9.28.



b.    Additional criteria to consider for a potential admission to a burn critical care environment include the following:



i.    Suspected inhalation injury



ii.    Concomitant trauma



iii.    Circumferential deep burn wounds



iv.    Electrical injuries



v.    Children who require continuous pain medication infusions



vi.    Fluid over-resuscitation in the field/emergency department



vii.    Delayed resuscitation



c.    Regardless of the care location, priorities of care in the inpatient setting include maintaining intravascular volume to allow for end-organ perfusion, maximizing pain relief, monitoring ventilation, and minimizing wound complications such as compartment syndrome and infection.


E.    Ongoing Assessment and Management



1.    Depth of Injury Assessment



a.    It may take up to several days for the burn wound to fully “declare itself” with respect to the depth of injury. Depth of injury is best assessed by visual inspection of the burn wound and palpation of several areas of the burn wound to determine the extent of capillary and tissue injury. As a general rule, a burn wound that is moist and has blisters is a second-degree (partial-thickness) burn wound. If the skin appears dry and tough, it is most likely a third-degree (full-thickness) burn wound. Skin that appears red and does not have blisters is first degree (superficial) and is not included in %TBSA calculations (ABLS Advisory Committee, 2015).


802TABLE 9.28    American Burn Association Burn Center Referral Criteria






Burn injuries that should be referred to a burn center include the following:


1.    Partial-thickness burns greater than 10% TBSA


2.    Burns that involve the face, hands, feet, genitalia, perineum, or major joints


3.    Third-degree burns in any age group


4.    Electrical burns, including lightning injury


5.    Chemical burns


6.    Inhalation injury


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


8.    Any patient with burns and concomitant trauma (such as fractures) in which the burn injury poses the greatest risk of morbidity or mortality; in such cases, if the trauma poses the greater immediate risk, the patient may be initially stabilized in a trauma center before being transferred to a burn unit; physician judgment will be necessary in such situations and should be in concert with the regional medical control plan and triage protocols


9.    Burned children in hospitals without qualified personnel or equipment for the care of children


10.  Burn injury in patients who will require special social, emotional, or rehabilitative intervention


TBSA, total body surface area.


Source: Excerpted from Committee on Trauma American College of Surgeons. (2014). Resources for optimal care of the injured patient (p. 101). Chicago, IL: American College of Surgeons.



b.    Most burn wounds are a mixture of all three depths of injury, so the nurse must be able to assess depth and healing of the mixed burn wound at the bedside. To assess the depth of a wound that has a mixture of blisters and dry, tough tissue, palpate the tissue with a gloved finger or sterile cotton swab and assess capillary refill, or “blanching” of the wound. A wound with brisk capillary refill when pressed upon is more superficial than one with slower capillary refill when pressed upon. Thus, the part of the wound with slower capillary refill is deeper than the part with the brisk refill. If there is an absence of capillary refill, blood supply to that area is permanently compromised, and that wound is full thickness and will eventually most likely need surgical intervention (see Figure 9.11).



2.    Assessment of Systemic Responses to Burn Injury



a.    Burn Shock. An extensive burn affects all organ systems and is manifested by a biphasic pattern of early hypofunction (i.e., decreased cardiac output, increased capillary permeability) followed by hyperfunction (i.e., hypermetabolism). The events, magnitude, and duration of the systemic manifestations of burn shock are proportional to the extent of burn injury and plateau at approximately 50% to 60% burn surface area. Although the exact etiology of burn shock is not totally understood, there are several characteristic fluid volume shifts and hemodynamic changes that accompany burn shock that have been identified.



b.    Cardiovascular response



i.    The initial response to a large burn injury is characterized by a decrease in cardiac output and increased peripheral vascular resistance. An uncharacterized factor present in the circulation following massive burns has been implicated for this characteristic myocardial depression. The increased peripheral vascular resistance develops as an initial physiologic response to hypovolemia, decreased cardiac output, and the release of vasoactive mediators from the stress response following injury (Kramer, 2014).



ii.    Cardiac output returns to normal 24 to 36 hours after the burn (Kramer, 2014). Peripheral vascular resistance returns to normal as cardiac output improves. As cardiac output improves, it exceeds normal values as the characteristic hyperdynamic state develops. Tachycardia develops as a physiologic response to hypovolemia, decreased cardiac output, and elevated catecholamine levels.








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FIGURE 9.11    Schematic cross-sectional representation of the skin.







iii.    Microvasculature changes in the cell membranes result in the disruption of normal capillary barriers separating the intravascular and interstitial compartments, resulting in free exchange of fluid and plasma. This increased permeability permits essentially all elements of the vascular space, except RBCs and platelets, to escape, creating a relative hypovolemia. The fluid requirement necessary to restore and maintain tissue perfusion is directly related to the burn size. Capillary leak and edema following small burns are localized to the burn wound. Injury greater than 20% burn surface area produces not only a localized burn wound edema but also a systemic capillary permeability and general body edema (Sheridan, 2012). The rate of progression of tissue edema is dependent on the adequacy and volume of fluid resuscitation. The maximal amount of edema occurs 8 to 12 hours after injury in small burns but can last up to 24 hours after injury in large burns. Capillary integrity is restored approximately 18 to 24 hours postburn. Large burns may take up to 30 hours to regain capillary integrity.



c.    Pulmonary response



i.    In large burns without an inhalation injury, early alterations in pulmonary function occur indirectly through the release of inflammatory mediators (i.e., thromboxane) and intravascular hypoproteinemia resulting in a transient hydrostatic pulmonary edema with a mild derangement in oxygenation.



ii.    A decrease in lung compliance may be related to chest-wall edema, circumferential burns to the chest wall, smoke-inhalation injury, preexisting lung disease, or fluid volume overload (Traber, Herndon, Enkhbaatar, Maybauer, & Maybauer, 2012).



d.    Hematologic response



i.    Within several hours of injury, as edema forms, the fluid shift and intravascular volume deficit result in hemoconcentration. The hematocrit increases secondary to loss of circulating plasma volume. Blood viscosity also increases (Kramer, 2014).



ii.    The characteristic anemia associated with burn injuries has multiple causes. Only about 10% of the RBC mass is lost to hemolysis during the burning process or by the extravasation of RBCs into the wound (Posluszny, Gamelli, & Shankar, 2012). Heat-injured RBCs have a shortened half-life and increased clearance. The ongoing postburn RBC hemolysis has been attributed to the release of inflammatory mediators (i.e., oxygen radicals, lipid peroxides). Although the exact nature is not known, there is an impaired production of new RBCs by the bone marrow with a shortened RBC lifespan (Posluszny et al., 2012). In addition, there is an ongoing effective blood loss related to daily wound care and multiple surgical procedures.



iii.    Initially there is a depression in serum clotting factors with a concomitant rise in fibrinogen degradation products, followed 804by a postresuscitation rise in increased levels of coagulation components. Platelet alterations include an increase in adhesiveness and shortened survival time (Posluszny et al., 2012).



e.    GI response. Decreased GI tract activity caused by decreased tissue perfusion is the by-product of hypovolemia and the neuroendocrine responses to injury. These responses cause an increased risk for the development of a burn-stress-related ulceration (Curling’s ulcer), and the incidence of ulceration has been greatly reduced by the routine use of antacid or histamine (H2) antagonist therapy. With adequate fluid resuscitation, GI tract activity returns to normal within 24 to 48 hours (Chung & Wolf, 2012).



f.    Renal response. With decreased intravascular volume there is a decrease in renal plasma flow and glomerular filtration rate (GFR), resulting in low urine output (Chung, & Wolf, 2012). If fluid resuscitation is inadequate or if resuscitation is delayed, oliguria ensues leading to acute renal failure. As the capillary integrity is restored, interstitial fluids are pulled back into the intravascular compartment, and diuresis occurs.



g.    Metabolic response



i.    With increased catecholamine and glucagon production, there is a mobilization of hepatic glycogen stores, coupled with a relative decrease in insulin production that commonly results in high serum glucose levels in the early postburn period.



ii.    Within 24 to 48 hours after the burn, there is an increase in metabolism directly related to the severity of the injury. This hypermetabolic state is characterized by increases in oxygen consumption and heat production, with an increase in both core and skin temperatures. Severe injury accelerates nitrogen flow. Both protein synthesis and breakdown are increased. In patients not meeting nutritional goals, breakdown rates exceed synthesis, resulting in a negative nitrogen balance. As capillary integrity is restored, electrolyte replacement therapy becomes an ongoing process and continues until wound closure is achieved. As the wounds heal, either spontaneously or by skin grafting, the metabolic rate gradually returns to normal levels. The decrease in metabolic requirements is a gradual process. In children with large burns, metabolic requirements remain higher for up to 2 years even after the burn wound is fully mature (Lee, Norbury, & Herndon, 2012).



h.    Immune response



i.    Although the exact mechanisms of the immunologic and inflammatory response are not known, characteristic pathophysiologic activities are being recognized as a result of the burn injury. Alteration in the skin’s protective function provides opportunity for invasion of microorganisms and primes the defensive mechanisms of the inflammatory and immune systems. It is hypothesized that a massive systemic inflammatory response is caused by the local trauma of a burn. It appears that a burn is a mediator-induced injury; although the local effects occur immediately, the systemic response to the mediators produced within a burn progresses and peaks 5 to 7 days after the injury.



ii.    It is unclear whether the immunosuppression after a burn injury is the result of biochemical substances (i.e., oxidants, histamine, prostaglandins, arachidonic acid metabolites) liberated from the burn itself, or are produced in response to the burn (Posluszny et al., 2012). In addition, the immunosuppressive effects of anesthetic agents, surgical procedures, multiple transfusions, and the use of systemic antibiotics emphasize postburn immunologic abnormalities during the clinical course of burn therapy. Burn patients are at an increased risk for nosocomial infection and sepsis due to this immune response (Posluszny et al., 2012).



i.    Thermoregulation. Children are more prone to the development of hypothermia secondary to their increased BSA-to-mass ratio, and, as a result, children have greater evaporative water loss and greater heat loss from evaporation and convection. Hypothermia remains a major problem until the wounds have been skin grafted or healed. Hypothermia alone, without any injuries, can cause apnea, progressive metabolic acidosis, and ventricular arrhythmias (Lee, Norbury, & Herndon, 2012).


F.    Inhalation Injury Assessment and Management



1.    Respiratory Injury. An inhalation injury may be the most important determinant of mortality in burn patients, having a greater effect than either TBSA burn or age. Inhalation injury exists in approximately 30% of hospitalized burn patients 805(Traber et al., 2012). Respiratory failure, during the first few hours to days after a burn injury, can be caused by asphyxia, upper airway obstruction, or chemical injury to the airway. The resulting injury can occur alone or in combination with a cutaneous injury.



2.    Classification of injury. Diagnosis of inhalation injury is typically a subjective decision based on smoke exposure in a closed space. Bronchoscopy during the first 24 hours postinjury can be performed to diagnose inhalation injury formally using a grading scale of 0 to 4 (Dries & Endorf, 2013), but oftentimes the diagnosis of inhalation injury is made based on clinical presentation.



a.    Acute asphyxia related to hypoxia and carbon monoxide excess. The process of combustion involves consumption of oxygen; therefore, air inspired by fire victims has considerably lower than normal oxygen concentration, particularly when the fire occurs in a closed space. In a fire, as oxygen is consumed during combustion, carbon monoxide is released because it is a basic by-product of incomplete combustion (Traber et al., 2012).



i.    Carbon monoxide causes toxicity by three mechanisms: the formation of carboxyhemoglobin, shifting the oxygen–hemoglobin dissociation curve to the left, and binding to other heme-containing proteins, namely, cytochrome enzymes and myoglobin. Carbon monoxide is a colorless, tasteless, odorless, nonirritating gas with an affinity for hemoglobin 200 times greater than that of oxygen. As carbon monoxide is transported across the alveolar membrane, it preferentially binds with hemoglobin, in place of oxygen, to form carboxyhemoglobin. Carbon monoxide impedes the dissociation of oxygen from hemoglobin, shifting the oxygen–hemoglobin dissociation curve to the left, thereby impairing oxygen unloading at the tissue level. The result is a major impairment in oxygen delivery. Ninety-seven percent of oxygen is carried to the tissues on hemoglobin. Carboxyhemoglobin also interacts with the myoglobin of cardiac muscle and the cytochrome system, further interfering with oxygen utilization (Traber et al., 2012).



ii.    Tachypnea and cyanosis may be absent because the partial pressure of oxygen in arterial blood (PaO2) as perceived by the peripheral chemoreceptors (the carotid body and aortic arch) is normal. The peripheral chemoreceptors controlling respiratory drive respond to changes in the PaO2, and not to changes in the arterial oxygen saturation (SaO2), even in the presence of high carboxyhemoglobin levels. Standard pulse oximeters are unable to distinguish between hemoglobin molecules saturated with oxygen (oxyhemoglobin) and those saturated with carboxyhemoglobin, producing a false elevation in oxygen saturation in victims with significant carbon monoxide toxicity. Carbon monoxide toxicity is evaluated by measuring the arterial carboxyhemoglobin level. Elevated levels of carboxyhemoglobin serve as indirect evidence for exposure to combustion products. Multiple signs and symptoms have been associated with carboxyhemoglobin levels (Table 9.29). A low carboxyhemoglobin level does not indicate minimal exposure. Administration of 90% to 100% O2 displaces some, if not all, the carboxyhemoglobin before arrival to the emergency department or before an ABG analysis can be performed (ABLS Advisory Committee, 2015). Carbon monoxide has a constant half-life and is reduced by 50% in 4 hours at room air, and in less than 1 hour if an oxygen concentration of 100% is used. Thus 100% FiO2 for 6 hours is the treatment of choice for CO inhalation, as hyperbaric oxygen therapy is not typically feasible or available in the first hours following injury (Sheridan, 2012).



b.    Airway injury related to edema or obstruction. Heat injury, from inhaling hot air, is limited to the upper airways (above the glottis) and may cause sufficient edema to produce mechanical obstruction (Sheridan, 2012). Direct thermal injury to the lower tracheobronchial tree and alveoli is rare because of the protective reflex closure of the glottis and the heat-dissipating capacity of the upper airway. Mucosal damage may result from both the heat and the chemical components of smoke. Mechanical obstruction of the airway is not limited to those with inhalation injury. The edema that accompanies scalds or even grease burns to the face and neck can be associated with enough edema to cause external airway compromise (Sheridan, 2002).



c.    Airway injury related to smoke inhalation. Airway injury due to smoke is essentially a chemical injury caused by inhalation of the by-products of combustion and is related to the composition (i.e., benzene from plastics) and duration of the inhaled smoke. When the toxic material is inhaled, it adheres to the mucous membranes, producing a chemical burn to the tracheobronchial mucosa or as far down as the particles descend into the lung. Diagnosing the severity of the injury may be based more on the clinical course of the disease process than on initial physical findings. In general, admission chest radiographic examinations underestimate the severity of lung damage because the injury is usually initially confined to the airways (ABLS Advisory Committee, 2015).


806TABLE 9.29    Carboxyhemoglobin Level and Associated Signs and Symptoms






















Carboxyhemaglobin Level (%)


Symptoms


0–5


Normal value


<15


Often found in smokers


15–20


Headache, mild dyspnea, confusion


20–40


Disorientation, fatigue, nausea, syncope


>50


Coma, seizures, respiratory failure, death



3.    Clinical Assessment



a.    The onset of symptoms is unpredictable, and a patient with possible inhalation injury must be observed closely. Many patients demonstrate minimal symptoms early after injury, and only when airway edema develops over the next 24 to 48 hours after injury do symptoms become evident (Traber et al., 2012).



b.    Because of their relatively small airways, upper airway obstruction in the pediatric patient may occur early and rapid. Thus, if edema is expected and any suspicion of inhalation injury is present, the child should have a secure airway placed until they overcome this period of increased airway loss risk (Sheridan, 2002). Securing the ETT is a particular problem in the presence of burn injury. Facial edema—coupled with wounds, secretions, and topical creams—increases the difficulty of securing and maintaining proper tube placement. Tape and commercially available securement devices may not be effective in securing ETTs in the presence of facial burns. Twill tracheostomy ties may be utilized to secure ETTs.



4.    Ventilation Strategies



a.    Ventilator strategies must support oxygenation and ventilation and reflect the experience of the clinical team managing the patient. Limitation of pressure, acceptance of permissive hypercapnia, and strategies to manage secretions, such as aggressive pulmonary toileting and suctioning, are important. Many patients with smoke inhalation will develop pneumonia in association with mechanical ventilation.



b.    The nursing care of the child with inhalation injury includes elevation of the head of the bed, frequent position changes and oral care to prevent ventilator-associated events (VAEs). There is no consensus about the most appropriate mode of ventilation, as high-frequency oscillation (HFOV) and airway pressure release ventilation (APRV) have not been shown to improve outcomes in these patients (Dries & Endorf, 2013). Thus, ventilation for the child with inhalation injury includes methods similar to those with ARDS.


G.    Fluid Resuscitation Assessment and Management



1.    Fluid Resuscitation. Ongoing fluid resuscitation is indicated if the child’s TBSA burned exceeds 15% second or third degree. If the burn wound is smaller, maintenance IV fluid and encouragement of oral intake is indicated, along with close monitoring of intake and output by the nurse. The goal of resuscitation is to preserve end-organ perfusion in the setting of burn shock, so indicators of good end-organ perfusion should be followed closely during the entire resuscitation phase. It is possible to administer too much or too little fluid to 807resuscitate the burned child, and care must be taken in this phase of inpatient admission to ensure that just the amount of fluid the child needs is administered, and not more or less than is necessary to perfuse the child’s vital organs. Fluid resuscitation begins at the scene of the injury if possible, and progresses through distinct stages of acute burn care as follows.



2.    Precision Resuscitation. At the scene of the injury or in the ED upon initial arrival, fluid resuscitation with lactated Ringer’s solution is administered using the ABLS prehospital fluid rate based solely on the child’s age (see Table 9.27). Once the primary and secondary survey has been completed in the emergency department and precise %TBSA burned has been calculated using one of the methods described earlier, a more prescriptive resuscitation formula is used to guide resuscitation (see Table 9.27). Fluid resuscitation formulas, such as the Parkland, Brooke, Consensus, ABLS, and so forth, are all estimations of the total fluids the child will require over the first days of resuscitation. Each child is different, thus close monitoring by the nurse of end-organ perfusion adequacy, such as urine output, vital signs, and mental status, are essential to achieve optimal resuscitation outcomes (Warden, 2014).



3.    Monitoring



a.    Once resuscitation has begun, a urinary catheter should be inserted and used to measure urine output quantity and quality at least hourly. The goal urine output during resuscitation is generally 0.5 to 1.0 mL/kg/hr for children and 2 mL/kg/hr in infants (Lee, Norbury, & Herndon, 2012). Urine output targets may be even higher (1.5–2.0 mL/kg/hr or greater) if electrical injury has occurred (ABLS Advisory Committee, 2015).



b.    If the urine output is above this goal, the continuous IV fluid rate should be decreased by 33%, and if it is below the goal the IV fluid rate should be increased by 33% hourly until the child achieves urine output in the goal range (ABLS Advisory Committee, 2015). If the child’s urine output is in the goal range and no other signs of decreased end-organ perfusion exist, no adjustments to the IV fluid rates should be necessary, even if the formula initially used to estimate initial resuscitation fluids calls for more to be given.



c.    Remember, all resuscitation formulas (i.e., Parkland, Brooke) are estimations; the most accurate guides for resuscitation are end-organ perfusion clinical assessment findings such as urine output, vital signs, and mental status (Sheridan, 2012). The nurse caring for a burned child undergoing resuscitation should be in close communication with the provider directing resuscitation regarding the child’s response to fluid therapy.



d.    As a general rule, crystalloid boluses are not recommended during the resuscitation phase. Many burn centers include colloid resuscitation as a part of their overall resuscitation plan once certain volumes of crystalloid have been given as colloids have been shown to restore intravascular volume well in the burned child after 24 hours postburn injury have passed (Warden, 2014).



e.    Many pediatric burn centers use a nurse-driven resuscitation protocol to guide practice. These types of protocols require hourly titrations based on clinical endpoints of resuscitation such as MAP, CVP, and UOP hourly until targets are met. The use of a nurse-driven resuscitation protocol in adults has been shown to improve accuracy and precision in the total volume of resuscitation fluid given as compared with Parkland formula estimations (Fahlstrom, Boyle, & Makic, 2013). See Figure 9.12 for an example of a nurse-driven resuscitation protocol for pediatric patients.


H.    Wound Assessment and Management


Wound assessment and care can be one of the most challenging aspects of caring for the burn patient. It takes time and experience to become proficient at wound assessment, interpretation, and dressing application, particularly in the pediatric burn patient. The potential for wound infection is one of the major considerations in patients who sustain a thermal injury. Wound care, daily wound assessment, and documentation are a vital part of the nursing care of a patient following burn injury. Particular attention should be focused on methods and techniques to prevent infection, facilitate wound healing, promote patient comfort, maintain optimal function, and minimize deformities. Any signs of infection, such as odor, drainage, and redness (cellulitis), must be noted and reported, so as to advocate appropriately for the patient. Wound care begins in the emergent phase and continues through the acute and rehabilitative phases.



8081.    Initial Debridement and Cleaning: Emergent Phase



a.    Wound care should only be initiated after all potentially life-threatening injuries have been addressed as outlined previously.



b.    All clothing and jewelry should be removed from the injured area prior to cleansing wounds, and any decontamination necessary from chemical exposure should occur first.



c.    Wound-cleansing methods are somewhat variable, but the underlying principles are the same.



d.    Wound cleansing involves using water and a mild soap in a bath basin, or various topical agents, to cleanse the wounds. In some burn care areas, hydrotherapy is utilized; however, immersion hydrotherapy is no longer indicated due to increased risk of bacterial translocation (Tredget et al., 1992; Weber, 2014). Hydrotherapy today typically involves the use of a shower or sprayer to cleanse the wounds. Caution must be taken to prevent hypothermia during wound cleansing. This may include only cleansing one part of the body at a time and keeping parts not being cleaned covered with dressings or a dry sheet or blanket, maintaining a warm room temperature, and using warm water for cleansing. It is best to cleanse areas with known or suspected infection or areas close to the perineum last.



e.    Wound debridement involves the removal of necrotic tissue, debris, and foreign material. This can be accomplished by mechanical debridement, chemical debridement, or surgical debridement.



i.    Mechanical debridement can be accomplished by several different methods. This may involve cleaning the wound with coarse mesh gauze, the application and removal of gauze dressings, irrigation, or the use of scissors and forceps to gently lift and trim loose necrotic tissue. It is recommended that all blisters greater than 2 cm be debrided, as this tissue must be removed to minimize infection risk.



ii.    Chemical or enzymatic debridement is accomplished by the use of commercially available topical preparations that cause selective lysis of necrotic tissue. Chemical or enzymatic debriding agents are typically used on partial-thickness wounds to minimize the need for or extent of surgical intervention necessary to close the wound. Enzymatic debridement agents should be applied only within the area of eschar or necrotic tissue and should be discontinued once the eschar has been removed and granulation tissue is present.



iii.    Surgical debridement involves removal of eschar using surgical instruments. This is accomplished via tangential or fascial excision. Tangential excision involves removal of thin layers of eschar until viable tissue is reached. Fascial excision removes all layers of the skin and subcutaneous tissue. Fascial excisions are infrequently required, but may be indicated in burns that involve subcutaneous fat or large full-thickness burns (Sheridan, 2012).



2.    Dressing Application



a.    In the emergent phase, if the patient is being transferred to a burn center, dry sterile dressings should be applied.



b.    Once on the burn unit, wounds should be fully assessed by the nurse with each dressing change and compared to the previous assessment. Assessment findings should be clearly documented and communicated to the patient care team, and any concerning findings escalated to the burn surgeon for evaluation.



c.    Infection prevention is the top priority throughout the dressing-change process. Hand hygiene must be performed prior to the dressing-change procedure and appropriate personal protective equipment must be worn throughout. Sterile supplies should always be used for any dressing procedure, including wound cleansing, debridement, or dressing application. The use of sterile gloves should always be considered during dressing changes to prevent the transfer of organisms to the wound site. Sterile gloves should always be worn for a dressing change that involves sharp debridement or during the first 24 hours after surgery (Iwamoto, 2009).



d.    The choice of dressing is dependent on the area of the body and the size, depth, and type of burn. Dressings are selected and applied to accomplish several goals. The goals of dressing therapy include the following:


Feb 19, 2020 | Posted by in NURSING | Comments Off on IV. Burns
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