Flame burn

Thermal burns result from tissue exposure to an external source of heat and remain prevalent in pediatric burn injuries. They account for approximately 40% of all admissions to burn units in the United States. Injuries from contact or flame are the most common cause of burn in children older than 5 years, with scald burns being more frequent in children younger than 5 years. Up to 90% of burn injuries are minor and can be managed on an outpatient basis with good outcomes. However, in larger burns, mortality is greatly influenced by burn (TBSA burn), patient age, and the presence or absence of concomitant inhalation injury. ^, Another main risk factor for death is sepsis, with rates of sepsis-specific death of 50% to 84% in adult and 55% in pediatric burn patients. ^, In general, the extent of soft tissue damage highly depends on the duration of exposure and presence and type of clothing material, all of which should be investigated during the initial evaluation.

Scald burn

Scald is a frequent mechanism of burn. An analysis of 127,016 patients who were hospitalized in US burn centers showed that approximately 30% were due to scald burns. The majority of scald injuries result from domestic accidents and are potentially preventable (e.g., spilling or splashing hot water). Infants and toddlers have a higher incidence of scald burns compared with older children. ^, In low-income countries, this is mainly due to unsafe and open cooking.

Scald injuries are commonly associated with the preparation or consumption of food. ^, Accidental hot liquid spills account for many of these injuries; a thorough history of the patient at admission should include the type and consistency of the causative liquid. Compared with water and thin liquids, oil and thick soups have a higher heat capacity and are more viscous. This may translate into longer contact time and higher temperatures, causing greater skin and soft tissue damage. In general, water heated to a temperature of 60°C (140°F) will cause a deep burn after 5 seconds of contact; water heated to 68°C (155°F) will cause the same burn after 1 second of contact.

Scald burns are more likely to be associated with child abuse than other types of burn injuries. Classic scald patterns consistent with child abuse include glove-like or stocking-like burns to the hands or feet and/or symmetric burns to the buttocks, legs, or perineum. Concomitant injuries (including bruising, fractures, and retinal hemorrhages) and delays in seeking treatment and/or inconsistencies in the patient history should trigger concern. These scenarios must prompt a full evaluation by social services with a referral to the appropriate state or government agencies regardless of the depth or extent of the burn.

Electrical burn

Electrical injuries accounted for less than 5% of all admission to US burn centers in 2016. The prevalence in low-income countries is up to 20% of all burns. Electrical burns are accompanied by a higher overall morbidity and mortality than flame or scald burns. ^, The majority of injuries involve electrical cords and outlets, with rare cases from lightning. Most homes in the United States use alternating current (AC). Although more efficient than direct current (DC), AC is more dangerous. Tissue damage typically results from heat generated by tissue resistance to current flow. Thus, the determinants of injury are voltage, tissue resistance, and time of contact to the body.

Young males are affected more often than their female counterparts (80%), and electrical injuries often occur at work (>90% in adults). Also, children are generally more susceptible to electrical injuries owing to their propensity to chew on cords or insert objects into outlets. Many of those burns are so-called “balcony injuries” that mainly occur owing to poor safety standards in low-income countries.

Wet or moist skin, including the mucous membranes around the mouth, has low resistance and permits electrical current entry. These injuries often result in considerable soft tissue trauma. Nerves, blood vessels, and muscles exhibit the least resistance as compared with bone, fat, and tendons. Higher-resistance tissues tend to heat and cause damage nearby, especially when no adjacent lower-resistance pathway is available (wrists and ankles).

The lack of overt skin damage may mask more significant underlying soft tissue damage. This leads to a significantly higher rate of major amputations compared with nonelectrical burns. Patients with electrical injuries are more prone to complications, such as neurologic symptoms or compartment syndrome. Cardiac arrhythmias occasionally are seen after burn injury, usually atrial tachycardia or atrial fibrillation. In some cases, the electrical injury may unmask an accessory pathway, resulting in a post-electrical injury reentry tachycardia. Cataracts are an additional complication of some electrical burn injuries; these may be noted prior to discharge on dilated eye examination or within 24 months of the electrical injury.

Chemical burn

Chemical burns are less common, representing only 3% of admissions to burn centers in the United States. ^, These result from contact with acid, alkali, or organic compounds, with acids being the most frequent agents. In 2017, the National Poison Data System reported more than 2.6 million poison exposures in the United States. Children younger than 3 years were involved in 35.5% of poison exposures, and children younger than 6 years accounted for approximately half of all exposures to poison (48.0%). Household cleaning substances account for one of the top five common exposures in children 5 years or younger. This includes alkali drain cleaners, which are composed of sodium hydroxide; they can cause significant tissue injury from interaction with cutaneous lipids in the skin. Other common exposures in this age group were cosmetic/personal care products, analgesics, foreign bodies/toys and topical preparations.

The severity of injury is determined by not only the type and concentration of the chemical but also the duration of exposure. The appropriate treatment of chemical burns does not involve neutralization of the acid or base since the resultant exothermic reaction would worsen tissue injury. Instead, the initial treatment of chemical burns includes copious irrigation with tepid water for at least 15 minutes. Hydrofluoric (HF) acid burns represent a distinct clinical scenario. Stuke et al. reported that 17% of 35 patients admitted to their burn unit in a 15-year interval were exposed to HF acid. In addition to being a corrosive agent, fluoride causes severe, deep liquefaction necrosis. Copious irrigation will attenuate the initial chemical burn, but neutralization with calcium or magnesium is occasionally necessary to halt further necrosis. Current HF acid treatment recommendations include topical calcium and close monitoring of serum calcium levels (with supplementation as needed). Cardiac arrhythmias resulting from calcium sequestration are common with significant HF acid exposures and are typically treated with parenteral calcium.

Superficial burns

Traditionally, depth has been categorized as either first-, second-, third-, or fourth-degree burn. First-degree (superficial burns) are erythematous and usually very painful but do not form blisters. Traditionally, most sunburns can be classified as superficial burns. Damage is isolated to part of the epidermis only, sparing the dermis and dermal structures. These burns blanch easily on examination and heal within 2 to 3 days after the damaged epidermis desquamates and is replaced by regenerating keratinocytes. The wounds usually heal without scarring, and surgical treatment is not needed. Superficial burns are neither included in calculations of the burn size nor in estimates for the need of fluid demands.

Superficial partial-thickness burns

Superficial partial-thickness burn wounds differ from first-degree burns in that the entire epidermis and superficial dermis is injured. These burns typically form fluid-containing blisters at the dermal-epidermal junction. After debridement, the underlying dermis is erythematous, appears wet, is painful, and blanches with pressure. As the deeper dermis is left undamaged, wounds heal within 2 weeks without the need for skin grafting, typically without hypertrophic scarring (although there may be long-term pigment changes).

Deep partial-thickness burns

Both superficial and deep partial-thickness burns have traditionally been classified as second-degree burns. These two categories merit distinction as deep partial-thickness burns behave clinically similarly to third-degree burns. Deep partial-thickness burns blister, but as tissue damage extends deep into the dermis, the blister base may appear to have a mottled pink and white appearance. The blood vessels of the dermis are partially damaged, giving rise to variance in discoloration of the wound base. These wounds are less painful than superficial burns owing to nerve injury and because the capillaries refill slowly when pressure is applied. Treatment of these wounds customarily requires excision and grafting when not expected to heal within 3 weeks. Decisions on the actual burn depth can usually be made when the dynamic process of burn evolution peaks at 3 days after injury. Some burn surgeons advocate initial monitoring for up to 14 days to allow for demarcation. Serial clinical examinations for partial thickness scald burns for 14 days have been shown to either reduce the excision area or avoid surgery altogether. Rarely, these wounds will heal without surgical intervention but will remain at risk for developing hypertrophic burn scars and/or contractures.

Full-thickness burns

Full-thickness burns are synonymous with third-degree injuries and involve all skin layers. These wounds need definitive surgical treatment in order to heal. On examination, these wounds are white, cherry red, brown, or black in color and do not blanch with pressure. The burned areas are dry, charred, and often leathery compared with unburned skin. Wounds are typically insensate because of the superficial nerve injury. In some cases, full-thickness burns may appear translucent, with clotted vessels shining through them. Early excision and grafting are needed to reduce rates of infection and hypertrophic scarring.

Immersion scald burns that have full-thickness depth can sometimes be confused with partial-thickness burns owing to their red color. Fourth-degree burns are full-thickness injuries involving the underlying subcutaneous fat, muscle, and tendons. These injuries are more commonly associated with limb loss and/or need for extensive reconstruction in addition to grafting.

Zones of injury

Burn wounds continue to evolve for days after the initial injury; the subsequent inflammatory process may last for several months. ^, The wound is divided into three zones of injury: zone of coagulation, zone of stasis, and zone of hyperemia. The zone of coagulation is easily identified, as it comprises the necrotic tissues closest to the injury site. The zone of hyperemia consists of normal, uninjured skin with a physiologic increase of blood flow in response to local tissue injury. The zone of stasis is located between the zones of coagulation and hyperemia, representing an area of ongoing injury. Poor perfusion of this zone can result in the progression of initially viable tissue, which furthers necrosis and deepens wounds. Tobalem et al. used a rat burn model to demonstrate that early erythropoietin administration prevented burn progression, mainly by improving vascular perfusion. Although this is not currently used for the treatment of pediatric burns, current research is targeting new methods to salvage these zones of intermediate injury.

Estimating the extent of the burn

An accurate assessment of both the extent and depth of the burn is necessary to guide initial care. The percent of TBSA burned is an independent risk factor that correlates with length of hospital stay and mortality in pediatric burns. However, the extent of burn injuries may be overestimated up to 75% by the initial care provider. This results in over-resuscitation with potentially devastating complications and poor use of limited resources (e.g., inappropriate transfer to burn centers). Future methods to accurately calculate TBSA burn include using computerized imaging, two- and three-dimensional graphics, and body contour reproductions.

Current methods of calculating combined second- and third-degree burn size in adults include burn diagrams, the “rule of nines,” and a general estimate that the palm and fingers of one hand account for 1% of the normal BSA. Palaski and Tennison developed the rule of nines, which is a rough estimation of adult BSA divided into multiples of 9%. This calculation rarely underestimates TBSA but often overestimates it, especially in children. BSA is distributed differently in children and infants owing to proportionally larger heads and smaller extremities. This supports the need for age-specific surface area charts, such as the Lund-Browder diagram, to better estimate the extent of burns in children ( Fig. 116.2 ).

Shriners Hospitals for Children diagram used for estimation of burn depth and extent in pediatric burned patients.

Additionally, the rule of nines, which is currently the most commonly used method, may not be accurate in overweight patients. Williams and Wohlgemuth suggest the “rule of sevens,” which includes a higher trunk proportion. There is also growing interest in the application of the software BurnCase 3D (RISC Software) in burn centers, which considers the body mass index (BMI).

Colloid resuscitation

The timing and the use of colloids in burn resuscitation are controversial. Historically, colloids have been used in varying amounts throughout the common formulas for burn resuscitation. ^, Since plasma proteins maintain oncotic pressure and the need to administer large volumes of crystalloid fluids (to prevent burn shock), colloids could theoretically mitigate the effect of decreased plasma protein concentrations. This theory led to the assumption that in pediatric patients with extensive burn injury, colloid replacement is sometimes necessary due to rapid serum protein depletion resulting in crystalloid resuscitation failure. Lawrence et al. described the addition of colloid to resuscitation of severely burned patients, which eventually reduced the hourly fluid requirements, restored normal resuscitation ratios, and ameliorated fluid creep. However, prior evidence has shown that colloid resuscitation provides no long-term benefits, does not affect mortality, and is more expensive compared with crystalloid solutions.

Complications of resuscitation

Inadequate resuscitation may result in poor perfusion to both vital organs and the evolving zone of stasis. This leads to the necrosis of previously viable tissue and to the progression of superficial burns to deeper injuries, requiring grafting. The complications of fluid overload in burn patients are associated with pneumonia, bloodstream infections, acute respiratory distress syndrome (ARDS), pulmonary edema, acute respiratory failure, multiple-organ failure, extremity compartment syndrome, abdominal compartment syndrome, and death. The volume infused should be continuously titrated to avoid both over-resuscitation and under-resuscitation with little to no role for fluid bolus therapy during initial burn management. Hemodynamic parameters should be monitored continuously, especially during the first days following burn. Parameters such as cardiac output, cardiac index, or extravascular lung water index obtained via transpulmonary thermodilution or urine output can assist in adjusting fluid demands. ^,

Risks for the development of compartment syndrome in the extremities, torso, or abdomen have been linked to the presence of deep, full-thickness circumferential burns as well as the volume of fluid infused during resuscitation. Severe burn injury results in a systemic inflammatory response leading to microcirculatory leak, vasodilation, and decreased cardiac output and contractility. Compartment syndrome may develop with tissue edema, reperfusion injury following resuscitation, and external compression from circumferential burns; it is most common within the first 24 to 48 hours. Excessive fluid resuscitation increases the incidence of compartment syndrome and leads to additional complications, such as pulmonary edema and heart failure.

Clinical suspicion of compartment syndrome is supported by findings of delayed capillary refill, cyanosis, paresthesia, and diminished pulses. It is imperative to make the diagnosis before the loss of pulses, as this indicates long-standing compartment syndrome with a higher likelihood of muscle necrosis and nerve damage. Compartment pressures can be measured using the Intra-Compartmental Pressure Monitor (Stryker Orthopaedics) or an 18-gauge needle inserted under the eschar into the subcutaneous or subfascial layer and connected to an arterial pressure transducer. A pressure greater than 30 mm Hg is considered diagnostic, mandating decompression through escharotomy and/or fasciotomy. Escharotomies are performed at the bedside under sedation with electrocautery, which is used to incise the full length of eschar down to subcutaneous fat along defined lines of incision ( Fig. 116.3 ).

Recommended lines of incision for escharotomies of the extremities and torso.

Bulging of surrounding tissues leads to adequate decompression. Fasciotomies are generally performed in the operating room under general anesthesia. All extremity compartments must be opened with evaluation of muscle for signs of necrosis. Escharotomies and fasciotomies should be performed only by experienced practitioners owing to increased morbidity from incorrectly executed procedures. ^,

Abdominal hypertension with subsequent compartment syndrome significantly decreases perfusion to vital organs, including the small and large bowel, liver, and kidneys, contributing to the development of multisystem organ failure. ^, Patients will often present clinically with abdominal distention and decreased urine output. Additionally, decreased pulmonary compliance secondary to elevated abdominal pressures can compound respiratory challenges. The incidence of intraabdominal hypertension in patients with extensive burns is approximately 70%, with up to 20% of those identified requiring decompressive laparotomy. Preventive measures to avoid abdominal compartment syndrome include appropriate titration of resuscitation fluid as well as early recognition of abdominal hypertension through serial bladder pressure evaluations. ^, Timely decompressive laparotomy should be performed at the onset of increased compartment pressures to avoid significantly increased morbidity and mortality related to fluid loss with an open abdomen. In children, percutaneous drainage using peritoneal dialysis catheters may be an effective alternative to laparotomy provided that the increased intraabdominal pressure is related to fluid accumulation and not organ edema. In a pilot study, Latenser et al. compared percutaneous drainage with surgical decompressive laparotomy in adult and pediatric patients with greater than 40% TBSA burns. They concluded that percutaneous drainage is safe and effective as a decompression modality for decreasing intraabdominal hypertension and preventing acute compartment syndrome in patients with less than 80% TBSA burns.

The development of pulmonary complications, including pulmonary edema and ARDS, has been attributed to excessive fluid resuscitation. ^, In the absence of inhalation injury, the systemic inflammation seen after severe burn injury results in third spacing of fluids (fluid moving from the intravascular to the interstitial space) and in accumulation of interstitial edema in the lungs. The treatment of this immune response remains challenging.

Topical therapy

Minor superficial burns of small size can usually be treated topically with moisturizing creams such as Eucerin or aloe vera. Superficial partial-thickness burns to the face are treated in a similar fashion. Nonadherent gauze or petroleum gauze can be placed over triple antibiotic ointment to provide a comfortable protective environment that promotes epithelialization.

After cleansing and debridement of deeper burns, topical agents—including silver sulfadiazine (Silvadene), mafenide acetate (Sulfamylon), and 0.5% aqueous silver nitrate—are options for local care. ^, Silvadene has been in use for many years and has demonstrated effective control of burn wound colonization against a continually widening spectrum of bacteria. Drawbacks include minimal eschar penetration as well as complications related to leukopenia and red blood cell hemolysis. ^, Sulfamylon cream is also easy to apply but can be painful when used on superficial partial-thickness burns. Eschar penetration is greatest using this agent, making it the topical of choice in burns when eschar will not be excised immediately. Its antimicrobial activity includes control of P. aeruginosa , which is a common colonizing bacterium in pediatric burn patients. Sulfamylon is a carbonic anhydrase inhibitor; complications related to metabolic acidosis may occur. Although these two agents are used most often in care of pediatric burns, silver nitrate 0.5% solution has generally fallen out of favor as first-line therapy due to electrolyte abnormalities and poor tissue penetration.

Newer bioactive dressings have begun to replace topical antimicrobials, as they minimize the need for twice-daily dressing changes. Silvadene in particular has been shown to delay wound healing due to a direct toxic effect on keratinocytes in addition to traumatic injury caused by frequent reapplication. ^, Newer agents—such as hydrocolloid, hydrogel, and polyurethane film dressings—provide effective humidity and control of exudate but are lacking in antimicrobial coverage. Silver-impregnated dressings such as Acticoat, Aquacel, and Mepilex provide combined antimicrobial coverage, adequate humidity for the wound, and decreased trauma to healing wounds with less frequent dressing changes.

Surgery (excision and grafting)

Early excision and grafting—within 72 hours of admission—is one of the main approaches to minimizing infections and slowing down the inflammatory and hypermetabolic response. When unable to cover all wounds with autografts, temporary placement of xenograft or allograft can be performed. Further skin grafting procedures should be performed as necessary until all wounds are covered with autograft.

Placement of skin substitutes and replacements requires adequate wound bed excision and preparation. Use of these materials on eschar or an improperly prepared wound bed will lead to graft loss, increased risk of infection, and prolongation of definitive therapy. Although no consensus exists on the timing of burn wound excision, most experienced burn surgeons advocate early wound excision—within the first 1 to 5 days after thermal injury—to attenuate the inflammatory response of burn and reduce the risk of sepsis. A staged approach is often performed for more extensive injuries whereby the wound is excised and controlled on day 1 with subsequent donor site harvest and grafting. The benefits of this approach include shorter operations, tighter temperature control, and ability to perform sheet grafting through improved hemostasis. Additional research is being performed to evaluate adjuncts, including laser Doppler imaging to assess for cutaneous blood flow within burn wounds to best assess appropriate time and wound bed for grafting.

The provision of a xenograft is a less expensive alternative to an allograft (human cadaver skin) for coverage of burn wounds. Although many animal skins have been used for temporary coverage over the years, only pig skin is widely used today. ^, It is generally incapable of engraftment and best used for temporary coverage, providing effective protection. The allograft has revolutionized burn care by providing medium-term coverage for patients requiring excision without available autografts. An allograft is typically rejected within 2 to 3 weeks after placement, although burn patients demonstrate differences in immunocompetence, resulting in varying degrees of rejection. An autograft provides definitive coverage of deep partial- and full-thickness burns. Donor site selection depends on available areas and extent of burn to be covered. If limited, xenografts and allografts provide effective temporizing coverage. An autograft can be applied as a sheet graft or can be meshed in ratios from 1:1 up to 4 or 6:1. The use of large-mesh graft ratios (greater than 2:1) has become less frequent owing to improved local wound management techniques and availability of synthetic skin substitutes.

Cultured epidermal autografts (CEAs) are derived from the patient’s own cells and were first successfully used in the 1980s. For this procedure, only a small punch-biopsy of the skin is needed. When developed and first used, it was hoped that CEAs would provide a solution to the clinical problem of massive wounds. However, these thin grafts are fragile, difficult to work with, take 2 to 3 weeks to grow, and usually result in hypertrophic scarring and unstable epithelium. For these reasons, CEAs are usually reserved for burns greater than 85% TBSA, when there is a dearth of donor sites and when other methods are not feasible. Another approach is to use a cultured skin substitute consisting of autologous keratinocytes and fibroblasts grown on a collagen-based scaffold. ^, This leads to fewer complications related to placement and healing postoperatively as well as less hypertrophic scarring and improved aesthetic results.

Dermal constructs have been developed in order to provide heat dissipation, strength, and flexibility. Of these, freeze-dried allogenic dermis is the most promising. Alloderm is an acellular human matrix that does not contain epithelial elements. After placing it over the fully excised wound, this material is intended to be combined with a split-thickness skin graft at the time of the closure. The dermal matrix incorporates with the patient’s tissue.

A newer approach is the use of stem cells. Among biological mediators, the use of stem cells (particularly adult cells) can accelerate wound healing and decrease inflammation. Following the discovery of adipose-derived stem cells (ASCs) in adipose tissue, there has been a surge in clinical trials using ASCs to treat different wound-healing models, including burns. Autologous ASCs are especially favorable for burn wound injury; a layer of subcutaneous fat (which is discarded during excision) contains ASCs. Since burn may affect the resident ASCs in the fat tissue, a study performed in an established rat scald burn model has shown that both the stromal vascular fraction and the ASCs isolated 3 days following burn injury have similar levels of differentiation potential, proliferation rate, cytokine production, and expression of stemness-related cell surface markers, indicating that the discarded tissue can be used as a source to obtain the autologous stem cells.

Pathophysiology of inhalation injury

Inhalation injury involves exposure of the upper airway to heated dry air or to steam. The lower airway, consisting of the tracheobronchial tree and lung parenchyma, is rarely injured by the heated dry air because of reflexive vocal cord closure and evaporative cooling capacity in addition to other natural defense mechanisms. ^, Direct thermal injury of the upper airway, however, manifests with significant inflammation. Also, many of the pathophysiologic changes after inhalation injury are related to severe edema. The edema results from increased transvascular fluid flux. Prolonged extrusion of proteinaceous exudate and associated tissue edema may result in the formation of airway casts and upper airway obstruction, similar to mucous plugging. ^,

With only few exceptions (such as inhalation of steam), the injury is usually due to chemicals and particles in the smoke. While large inhaled particles are filtered by the upper airway, both small particles (<5–10 µm) and noxious gases can reach the lower airway and cause injury. Toxins such as ammonia, sulfur oxides, pyrolysates, and chlorine gas form strong alkalis and acids upon contact with the moist, mucosal walls of the upper and lower airways. Fat-soluble agents, such as aromatics, activate alveolar macrophages and may initiate direct cellular damage resulting in hyperemia, which can be visible by bronchoscopy shortly after injury. While water-soluble irritants cause instantaneous pain, fat-soluble agents tend to be less noxious and reach the distal airways more easily, bypassing natural defense mechanisms. If these inhalants induce an inflammatory response in the pulmonary parenchyma, surfactant synthesis may be disrupted, with further worsening of lung compliance. ^, Loss of ciliary action in the respiratory mucosa can lead to increased pulmonary infections, ultimately resulting in irreparable damage to the respiratory tree.

Carbon monoxide (CO) and cyanide are key components of inhalation injury in the acute burn patient, each posing diagnostic challenges. CO is an odorless, colorless gas generated by incomplete combustion of carbon-containing materials. In CO poisoning, tissue oxygenation is impaired, resulting in a range of symptoms: headache, nausea, irritability in mild intoxication, tachypnea, hypoxia, altered mental status, coma, and, ultimately, death. These clinical signs stem from an increased affinity of CO to bind hemoglobin, resulting in carboxyhemoglobin (COHb) formation as well as a left shift of the oxygen-hemoglobin dissociation curve, interfering with normal unloading of oxygen to tissues. Relative tissue hypoxia ensues, with subsequent metabolic acidosis. Hydrogen cyanide, a colorless gas with an odor described as being similar to bitter almonds, is produced by combustion of carbon and nitrogen-containing substances (i.e., wool, cotton). Cyanide inhibits oxidative phosphorylation via reversible inhibition of cytochrome c oxidase. Similar to CO poisoning, cyanide poisoning produces relative tissue anoxia and metabolic acidosis.

It is well known that high concentrations of nitric oxide (NO) contribute to developing ARDS in the ovine model of burn and smoke inhalation. During the first 48 hours after inhalation injury, there are significant increases in pulmonary fluid flux and edema that are linked to oxidative stress. Additionally, increased collagen deposits are associated with an increase in oxidative stress and arginase activity, which can lead to lung dysfunction.

Diagnosis of inhalation injury

There is no consensus on the diagnostic criteria of inhalation injury. One reason for this is that many of the typical signs and changes occur 48 hours postinjury. ^, The diagnosis of inhalation injury begins with a focused history and physical examination; clinicians should be cognizant that inhalation injury may occur without evidence of cutaneous burns. Closed-space burns involving steam, combustibles, hot gases, or explosions are associated with a higher risk of airway injury. Inhalation injury is also likely when the burn history includes incapacitation requiring extraction from a burning structure by emergency personnel. The physical examination should include inspection for soot in the oropharynx, carbonaceous sputum, singed nasal or facial hairs, and burns involving the face or neck. These signs taken individually have a high false positive in the diagnosis of inhalation injury but should raise clinical suspicion. Impending respiratory failure may manifest as wheezing, stridor, tachypnea, or hoarseness, along with depressed mental status, agitation, or anxiety. Many pediatric patients with inhalation injury will develop progressive respiratory failure, tachypnea, hypoxia, and cyanosis after resuscitation, even when appearing normal upon initial presentation.

In addition to the nonspecific clinical signs and symptoms of inhalation injury, noninvasive monitoring of pulse oximetry in burn patients can be misleading. For this reason, laboratory and invasive studies are pertinent to diagnosis. Initial laboratory studies should include arterial blood gas (ABG) analysis and measurement of COHb. The Berlin definition of ARDS includes three categories: mild (200 mm Hg < partial pressure of arterial oxygen/fraction of inspired oxygen Pa o ₂ /F io ₂ ] ≤ 300 mm Hg), moderate (100 mm Hg < Pa o ₂ /F io ₂ ≤ 200 mm Hg), and severe (Pa o ₂ /F io ₂ ≤ 100 mm Hg). It also includes four ancillary variables for severe ARDS: radiographic severity, respiratory system compliance (≤40 mL/cm H ₂ O), positive end-expiratory pressure (PEEP; ≥10 cm H ₂ O), and corrected expired volume per minute (≥10 L/min). Albeit controversial, this ratio has been proposed as an indicator of poor outcome in burn patients. ^, For suspected CO poisoning, COHb values should be drawn and correlated with time from injury. At sea level, when breathing room air, the half-life of CO is 240 to 320 minutes, decreasing to 30 to 40 minutes when breathing 100% oxygen. The half-life of CO falls to 20 minutes when exposed to hyperbaric oxygen conditions. However, the evidence for the use of hyperbaric oxygen for treatment of CO poisoning is somewhat lacking. Given the potential risks of hyperbaric oxygen (including barotrauma and inability to access critically ill patients), treatment of CO poisoning with hyperbaric oxygen is not recommended in every case. Cerebral edema and herniation syndromes are feared complications of CO poisoning; these typically present 3 days after the injury. Careful monitoring of mental status and respiratory adequacy is necessary, and sedative or narcotic agents should be used with great caution, as respiratory acidosis can exacerbate cerebral edema and lead to brainstem herniation. If cyanide poisoning is suspected, blood cyanide levels should be also drawn with prompt administration of antidotes.

Chest radiographs and computed tomography scans are insensitive for the diagnosis of inhalation injury in the first days following burn owing to a relatively normal lung and airway appearance early in the clinical course. ^, Repeated evaluations over time and after resuscitation may demonstrate subsequent development of pulmonary edema or ARDS. Fiberoptic bronchoscopy remains the gold standard for the diagnosis of inhalation injury. Direct visualization of the supraglottic and infraglottic airway allows quantification of hyperemia, exudate, mucosal sloughing, edema, and presence of carbonaceous material. In a study spanning a 10-year period, 71% of pediatric patients with inhalation injury were diagnosed using bronchoscopy versus 25% by history/clinical examination alone and 4% by COHb levels, demonstrating that—even at specialized burn centers—there remains variability in means for diagnosing inhalation injury. However, there is still controversy regarding whether bronchoscopy can provide information on the severity of the inhalation injury. The Abbreviated Injury Score, which is based on bronchoscopic findings, is positively correlated with increased mortality. It includes the evaluation of the presence of carbonaceous deposits, erythema, edema, obstruction, and inflammation, respectively.

Management of inhalation injury

Inhalation injuries can quickly progress to obstruction, hypoxia, and death; thus, timely endotracheal intubation is required ( Box 116.2 ).

• BOX 116.2

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