1353CHAPTER 116 Burn and Inhalation Injury research is being performed to examine the utility and efficacy of noninvasive computational algorithms89,94 and invasive trans pulmonary thermodilution moni[.]
CHAPTER 116 Burn and Inhalation Injury 1353 TABLE Common Pediatric Formulas for Burn Fluid Resuscitation 116.1 Formula Crystalloid Colloid Glucose Instructions Galveston 5000 mL/m2 BSA burn 2000 mL/m2 total BSA of LR 12.5 g 25% albumin/L crystalloid 5% dextrose, as needed Half over the first h, half over the next 16 h Cincinnati (children , y) mL/kg/% TBSA burns 1500 mL/m2 total BSA of LR 12.5 g 25% albumin/L crystalloid in the last h of the first 24 h 5% dextrose, as needed Half over the first h, half over the next 16 h Composition of fluid changes every h First h, add 50 mEq/L sodium bicarbonate Second h, LR alone Third h, add albumin Cincinnati (children y) mL/kg/% TBSA burn 1500 mL/m2 total BSA of LR None 5% dextrose, as needed Half over the first h, half over the next 16 h BSA, Body surface area; LR, lactated Ringer solution; TBSA, total body surface area research is being performed to examine the utility and efficacy of noninvasive computational algorithms89,94 and invasive transpulmonary thermodilution monitoring devices (Pulse index Continuous Cardiac Output [PiCCO] device).95 Wurzer et al compared cardiac outcome measurements with PiCCO and echocardiography, showing that echocardiography often underestimates the hyperdynamic state.96 Additionally, chest radiographs often are performed daily or when central lines are placed, which can be used to assess for potential pulmonary edema following over-resuscitation 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.82–84,92 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.91 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.97 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.98 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.58 The complications of fluid overload in burn patients are associated with pneumonia, bloodstream infections, acute respiratory distress syndrome (ARDS), pulmonary edema, acute respiratory failure, multipleorgan failure, extremity compartment syndrome, abdominal compartment syndrome, and death.99–103 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.104 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.95,105 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.106 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.102 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.106 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) 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.107,108 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.83,109 Patients will often 1354 S E C T I O N X I I Pediatric Critical Care: Environmental Injury and Trauma The development of pulmonary complications, including pulmonary edema and ARDS, has been attributed to excessive fluid resuscitation.114,115 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 Treatment of Burn Wounds • Fig 116.3 Recommended lines of incision for escharotomies of the extremities and torso present clinically with abdominal distention and decreased urine output.83 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.110 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.111,112 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.113 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.113 Burn wounds evolve over time on the basis of several factors, including mechanism of injury and fluid resuscitation, sometimes requiring 10 to 14 days for complete demarcation.116 It is not uncommon for previously diagnosed superficial partial burn wounds to demarcate as full-thickness burns and vice versa If the burn wound is improperly managed and is allowed to desiccate or become infected, it can convert to a deeper wound requiring definitive surgical management Initial cleansing and debridement of the wound are absolutely essential for accurate diagnosis of size and depth Mild soap and water or chlorhexidine mixed in saline washes is recommended for cleaning, with adequate pain control to allow complete debridement of necrotic tissue Most burn experts recommend debridement of all blisters (unless smaller than 0.5 cm or in a difficult-to-manage area) to reduce the risk of bacterial colonization or infection The blisters should be removed immediately when cleaning the wounds under sterile conditions Most burn wounds become colonized in the first few hours with gram-positive bacteria such as Staphylococcus aureus and Staphylococcus epidermidis and are predominantly colonized with gut flora such as Pseudomonas aeruginosa, Enterobacter cloacae, and Escherichia coli by days.117 Healthcare workers involved with the cleansing and debridement of burn wounds must be vigilant in handwashing and in maintenance of a clean environment around the wound for prevention of cross-contamination in these immunocompromised patients Culture swabs of all wound beds should be obtained on arrival and on a scheduled basis to monitor for changes in colonization (ideally, when changing the dressings) Bacterial colonization of burn wounds does not require systemic antibiotics However, it should be managed with early debridement, appropriate topical and/or biological dressings, and scheduled dressing changes.116 Topical therapy is not intended to sterilize the burn wound but, instead, to control colonization Gauze and sterile dressings are used for coverage to minimize evaporative water losses and further entrance of infectious agents.118 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.116,119 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.120,121 Sulfamylon cream is also easy to apply but can be painful when used on CHAPTER 116 Burn and Inhalation Injury 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.120 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.122,123 Newer agents—such as hydrocolloid, hydrogel, and polyurethane film dressings—provide effective humidity and control of exudate but are lacking in antimicrobial coverage.124 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.116 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.125 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.119 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.119 Although no consensus exists on the timing of burn wound excision, most experienced burn surgeons advocate early wound excision—within the first to days after thermal injury—to attenuate the inflammatory response of burn and reduce the risk of sepsis.126–128 A staged approach is often performed for more extensive injuries whereby the wound is excised and controlled on day 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.119 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.129 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.130,131 It is generally incapable of engraftment and best used for temporary coverage, providing effective protection.116 The allograft has revolutionized burn care by providing medium-term coverage for patients requiring excision without available autografts An allograft is typically rejected within to 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 1355 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 or 6:1.116 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.132 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 to weeks to grow, and usually result in hypertrophic scarring and unstable epithelium.133 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 collagenbased scaffold.134,135 This leads to fewer complications related to placement and healing postoperatively as well as less hypertrophic scarring and improved aesthetic results.136 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.119 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.137 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.138 Following the discovery of adipose-derived stem cells (ASCs) in adipose tissue,139 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 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.140 Inhalation Injury It was initially reported in 1985 that presence of inhalation injury is a main contributor to mortality following burn.141,142 Although sepsis is currently the most common cause of death following severe burn,20,143 about two-thirds of children who die have inhalation injury.3,144 In age-specific studies of mortality, the presence of concomitant inhalation injury increased mortality across all ages, but its effect on mortality was largest in the pediatric burn patient population.145 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 1356 S E C T I O N X I I Pediatric Critical Care: Environmental Injury and Trauma evaporative cooling capacity in addition to other natural defense mechanisms.27,146 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.71,147 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.148 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.149 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.150 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.148,151 Loss of ciliary action in the respiratory mucosa can lead to increased pulmonary infections, ultimately resulting in irreparable damage to the respiratory tree.71 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.148 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.152 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.148 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.153 It is well known that high concentrations of nitric oxide (NO) contribute to developing ARDS in the ovine model of burn and smoke inhalation.154 During the first 48 hours after inhalation injury, there are significant increases in pulmonary fluid flux and edema that are linked to oxidative stress.155 Additionally, increased collagen deposits are associated with an increase in oxidative stress and arginase activity, which can lead to lung dysfunction.156 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.11,157 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.71 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 Pao2/Fio2] # 300 mm Hg), moderate (100 mm Hg , Pao2/Fio2 # 200 mm Hg), and severe (Pao2/Fio2 # 100 mm Hg) It also includes four ancillary variables for severe ARDS: radiographic severity, respiratory system compliance (#40 mL/cm H2O), positive end-expiratory pressure (PEEP; 10 cm H2O), and corrected expired volume per minute (10 L/min).158 Albeit controversial, this ratio has been proposed as an indicator of poor outcome in burn patients.159,160 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.161 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 days after the injury.162 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.153 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.163,164 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 10year 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.142 However, there is still controversy regarding whether bronchoscopy can provide CHAPTER 116 Burn and Inhalation Injury information on the severity of the inhalation injury The Abbreviated Injury Score, which is based on bronchoscopic findings, is positively correlated with increased mortality.165 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) Oxygen therapy at a Fio2 of 1.0 should be initiated immediately to treat increased COHb levels and provide maximal oxygen delivery to peripheral tissues.148 Duration of oxygen therapy depends on patient condition and can be quantified by documenting return of COHb levels to below 10% and normalization of acidosis.166 Continuous pulse oximetry may be reliably used after normalization of COHb levels Inhalation injuries rapidly evolve over the first few days following injury Acute pulmonary insufficiency may manifest in the first 24 hours, with edema peaking between 48 and 96 hours, and injury culminating in bronchopneumonia to 10 days postburn.167–169 The treatment of inhalation injuries is mainly supportive, consisting of ventilator support, airway clearance, and therapeutic adjuncts In order to early detect pulmonary infection, surveillance cultures should be obtained Ventilator Support Pulmonary function should already be supported at the scene of the injury, if needed When mechanical ventilation is required, measures should be taken to minimize ventilator-associated lung injury (VALI) Following endotracheal intubation, the acute burn patient with inhalation injury may benefit from alternative modes of ventilation as compared with conventional strategies The choice of mode is dictated by patient condition, clinician and staff familiarity, and treatments required (i.e., repeat bronchoscopy, • BOX 116.2 Indications for Early Endotracheal Intubation • • • • • • Extensive burns over face and neck Overt signs and symptoms of airway obstruction by edema Inability to protect airway from aspiration Significance toxicity from carbon monoxide or cyanide Respiratory failure Hemodynamic instability DIFFUSIVE WAVEFORM • Fig 116.4 Volumetric 1357 inhalation agents).170 When used appropriately, standard ventilator strategies may provide adequate support In severe inhalation injury, the use of high-frequency oscillatory ventilation may be beneficial; single centers have shown early and sustained improvement in oxygenation with its use.171 However, use of highfrequency oscillatory ventilation may limit delivery of important inhaled medications and timely serial bronchoscopy, which are important adjuncts in the treatment of inhalation injury Volumetric diffusive respiratory (VDR) mode provides ventilation and oxygenation with a decreased mean airway pressure, reducing the risk of barotrauma (Fig 116.4) VDR mode involves high-frequency ventilation with progressive accumulation of subtidal breaths and passive exhalation once a set airway pressure is met, allowing for gas exchange through more alveoli.172,173 In small prospective studies of pediatric burn patients, Rodeberg et al demonstrated that use of VDR mode significantly increased Pao2, increased Pao2/Fio2 ratio, and decreased mean airway pressure, all without affecting hemodynamic function.172,174 Long term, this mode has been shown to significantly decrease pneumonia and mortality compared with individuals treated with conventional modes of ventilation, but data remain limited in pediatric burn patients.173,175–177 Airway pressure release ventilation (APRV) is a reverse inspiratory/expiratory method of ventilation with two levels of PEEP support (Fig 116.5) High PEEP is continuous during a prolonged inspiratory time, providing for adequate oxygenation and recruitment of closed alveoli, while low PEEP is maintained during expiration, facilitating recruitment of alveoli Theoretically, patients ventilated with APRV benefit from reduced barotrauma, improved oxygenation and ventilation due to better ventilation/perfusion (V/Q) matching, and decreased sedation and paralysis requirements due to increased patient comfort.178 Unlike the VDR mode, there is no percussive component involved.179 Data remain limited regarding use of both these alternative ventilatory strategies in the pediatric burn setting and are extrapolated from adult literature Airway Clearance and Extubation Criteria Appropriately trained respiratory therapists are invaluable in the management of burn patients and are a mainstay in specialized burn care units Together with ventilatory management, other adjunctive therapies (including aggressive pulmonary toilet and chest physiotherapy) are essential components of treatment of inhalation injuries Chest percussion and vibrational treatment with additional focus on early ambulation are effective strategies for secretion mobilization and removal.11 Tracheobronchial suctioning and serial therapeutic bronchoscopies are often necessary PERCUSSIVE WAVEFORM diffusive respiratory ventilation pressure-time tracings Percussive and diffusive waveforms from a pediatric burn patient volumetric diffusive respiratory ventilator ... 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... when used on CHAPTER 116 Burn and Inhalation Injury superficial partial-thickness burns Eschar penetration is greatest using this agent, making it the topical of choice in burns when eschar will... epithelial elements.119 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.137 The dermal matrix