In 1953, a 49% total body surface area (TBSA) burn in a child was associated with a 50% risk of mortality. Today, following major advancements in burn care, even an estimated 99% TBSA burn is associated with an expected survival of 50%. , Despite such significant improvements in burn care, burns continue to be a major cause of unintentional death and injury in children less than 14 years of age. In the United States, burns remain one of the top 10 causes of unintentional death in children, with more than 3000 deaths reported from 2010 to 2020. , Scald and contact burns continue to make up the majority of pediatric burns, with most burns measuring less than 10% of TBSA. , A prerequisite for the optimal management of pediatric burns continues to be a multidisciplinary approach by a team of healthcare providers, therapists, and social workers.
Pathophysiology
Skin is a complex, multilayer organ with a surface area ranging from 0.2 to 0.3 m 2 in the newborn to 1.5–2.0 m 2 in the adult. An understanding of its basic structure and regenerating ability is critical to burn management. The skin provides protection, participates in thermoregulation and vitamin D production, and is involved in sensation. The epidermis is the avascular and aneural superficial layer made up of keratinocytes (95%), melanocytes, Langerhans cells, and Merkel cells. Desquamation of cells formed in the basal layer takes 2 to 4 weeks, with the entire epidermis being replaced by new cells every 48 days. The dermis has a deep reticular layer and a superficial papillary region that are connected to the epidermis via the basement membrane. Composed primarily of collagen and elastin from fibroblasts, the dermis provides support for the skin.
There are several important factors to consider when assessing any burn injury: temperature of the heated object, duration of contact with the skin, thickness of the skin, and blood supply to the affected area. These four factors play an important role in how severe the injury is, how deep it will extend, and how it is treated. Scald burns constitute between 40% and 50% of pediatric burns, usually occurring in toddlers. Scald burns tend to be superficial epidermal burns. Flame burns, on the other hand, are more common in adolescents and can result in deep injury. Contact burns are also common, primarily among toddlers. At our facility, contact burns are the second most common mechanism of burn injury and are related primarily to stove tops and fireplace glass covers.
In 1953, Jackson described the zones of burn injury that remain important to the understanding and management of burns today ( Fig. 12.1 ). The zone of coagulation occurs at the site of maximal damage and is defined by irreversible tissue loss due to protein coagulation. The zone of stasis surrounds this area and has decreased tissue perfusion but remains salvageable with aggressive resuscitation and wound management. Outside the zone of stasis is the zone of hyperemia, where tissue perfusion is increased and the integument often survives unless faced with infection or severe hemodynamic deterioration.
Three zones of burn injury: coagulation, stasis, and hyperemia.
The systemic response to burn injury is mediated by the release of inflammatory mediators such as thromboxane A 2 , bradykinin, oxidants, and cytokines, which can impair flow to the zone of stasis through thrombosis, vasoconstriction, and capillary blockage. The administration of antioxidants, bradykinin antagonists, and thromboxane A 2 inhibitors may improve blood flow and possibly mitigate injury. In addition, the administration of β-glucan, through its immunomodulatory effects, antioxidant properties, and ability to reduce the inflammatory response, has been shown to improve reepithelialization in a rat model of burn injury. Small studies in human subjects have shown promising results; topical administration of β-glucan improved wound healing in burn wounds, was well tolerated with no significant adverse effects, and was a cost-effective method of wound dressing. ,
The systemic effects of burn injury extend beyond these three zones and can potentially lead to multiorgan dysfunction. Burns larger than 15% TBSA can lead to the initiation of a systemic inflammatory response requiring aggressive fluid resuscitation in an attempt to prevent burn shock and death. The sudden and massive surge in proinflammatory mediators can lead to a number of different organ responses. In large burns, the cardiovascular system usually exhibits an initial hyperdynamic state followed by varying degrees of myocardial depression and hypovolemia. Pulmonary vasoconstriction and edema lead to respiratory failure. Splanchnic vasoconstriction can result in gut dysmotility and malabsorption by causing epithelial apoptosis and decreased epithelial proliferation. This results in atrophy of small bowel mucosa, increased intestinal permeability, bacterial translocation, and sepsis. Splanchnic vasoconstriction and activation of stress-induced hormones and mediators, such as angiotensin, aldosterone, and vasopressin, lead to a decrease in renal perfusion that can lead to oliguria. When unrecognized, this can progress to acute tubular necrosis, renal failure, and ultimately death. , While the initial phase of burn injury is characterized by a proinflammatory state, the next phase is predominantly antiinflammatory. In this phase, there is a systemic decrease in immune function due to impaired production and function of neutrophils, macrophages, and T-lymphocytes, placing the patient at risk for infectious complications.
Initial Management
Most pediatric burns are minor, often resulting from scald accidents and affecting <10% TBSA, or from thermal injuries isolated to the hands. Such burns are usually limited to partial-thickness injury of the skin and can be managed on an outpatient basis. Larger burns require inpatient admission and special attention. All large burns (>10% TBSA) should undergo initial Advanced Trauma Life Support evaluation beginning with the primary survey. Issues with airway, breathing, and circulation should be addressed immediately. Signs and symptoms including increased respiratory effort, wheezing, stridor, and tachypnea should raise concern for impending airway loss, and the decision to intubate a patient with a tenuous airway should be made early. Inhalation injury can result in edema that may worsen over the first few hours, so repeated evaluation of the airway is important. If inhalation injury is suspected, arterial blood gas analysis and measurement of carboxyhemoglobin levels should be obtained. Patients need support with 100% supplemental oxygen. Burn injuries can have a negative effect on breathing mechanics, not only through smoke inhalation, but also from blast injury causing blunt chest trauma and from the restrictive effects of a burn eschar that limits full chest expansion. Escharotomy should be performed for the latter.
The source of thermal injury needs to be removed from the patient as quickly as possible, ideally at the scene but certainly during the primary survey, if not done previously. Active cooling may limit the depth of the burn but can result in hypothermia and is discouraged. Chemicals need to be removed from the skin, and the area should be thoroughly irrigated with warm water for 15–30 minutes. Except for a few specific chemicals such as hydrofluoric acid, neutralization of chemicals is not needed and may actually produce additional heat that could lead to a deeper burn. Blankets should be used to keep the patient warm, as the risk of hypothermia increases with increasing burn area.
Two large-bore intravenous (IV) lines should be placed and fluid resuscitation started as soon as possible. When extremity burns limit peripheral IV access, or if there is difficulty obtaining central venous access, intraosseous access should be utilized as a temporary (<24 hours) alternate route for fluid administration. A urinary catheter should be inserted, and heart rate, blood pressure, and urine output should be continuously monitored. No attempt at burn wound debridement or application of dressing should be made at the initial evaluation. All burn patients should be covered with warm, dry sheets when not being actively examined.
A decision should be made after initial evaluation, resuscitation, and wound dressing as to whether the patient needs to be transferred to a burn center. The American Burn Association has published referral criteria regarding which patients should be referred to these centers ( ).
A fundamental component of initial burn care is an accurate measurement of the TBSA of the injured skin. There are several techniques to estimate the TBSA of a burn. The Wallace rule of nines estimates burn area fairly well for adolescents and older patients. Each upper extremity and the head represent 9% of the TBSA. The lower extremities and the anterior and posterior trunks are 18% each. The perineum, genitalia, and neck each measure 1%. Due to differences in body proportions for infants and children, the rule of nines has been modified to determine the burned area more accurately in these patients. In this modification, the head represents 18% of the TBSA and each leg is 13.5%. Other modifications have been proposed to better estimate TBSA burn in obese patients.30 The Lund and Browder chart provides a more accurate determination of the burn area in children, as it compensates for variations in body shape and proportions (Fig. 12.2 ). For a rapid estimation of burn size, the “palm” method can be used. The palm of the patient’s hand, excluding the fingers, is approximately 0.5% of the TBSA; the palmar surface of the patient’s entire hand including fingers is approximately 1% of the TBSA.31 This method is best used for estimating small surface area burns. Smartphone applications have also been developed to help providers estimate the size of the burn. After inputting the patient’s age and weight, the user draws in the areas of full and partial-thickness burns, which are then used to calculate the estimated TBSA. Fluid resuscitation calculations are also automatically performed.32 Superficial burns, formerly referred to as first-degree burns, should never be included in burn size calculations using any of these techniques. Despite the numerous printed, online, and smartphone applications currently available for estimating TBSA, recent studies demonstrate that referring hospitals continue to overestimate TBSA.33–36 In one study, almost 60% of patients were administered more fluid at the referring hospital than would have been expected based on burn size estimates.34 Smaller burns in particular (<20% TBSA) are disproportionally overestimated and thus can result in inappropriate transfers to a burn center from the referring hospital, incurring unnecessary healthcare costs, leading to overuse of limited resources, delaying appropriate care, and causing undue stress on the patient and family.36 It is thought that the overestimation of burn size from referring hospitals may be due to a number of different factors. First, there is an absence of any TBSA guidelines in Pediatric Advanced Life Support courses. Second, adjacent reactive hyperemia may be confused with partial-thickness burns. Finally, there appears to be a relative inexperience with burn care by emergency department house staff personnel secondary to insufficient exposure to burn injuries. Despite overestimates in TBSA, it appears that most pediatric patients are not overresuscitated, and those who are do not suffer statistically significant complications.33 , 34 , 37
The Lund-Browder burn diagram is depicted for estimating the body surface area for burns in children.
A key component to the initial management of the severely burned patient includes escharotomy when indicated (Fig. 12.3 ). Full-thickness circumferential burns anywhere on the body can produce a constricting eschar that, together with the associated edema, can impede venous outflow and impair arterial flow. If pulses are absent, a bedside escharotomy should be performed with a scalpel or electrocautery along the lateral and medial aspects of the affected extremity. Incisions can be carried onto the hypothenar and thenar eminences and dorsolateral aspects of the digits if the hands or fingers are involved (Fig. 12.4 ). The escharotomy should be carried down to subcutaneous fat. After the escharotomy has been completed, the compartment should feel much softer, and perfusion should immediately improve. A continued absence of perfusion in an affected extremity may require a fasciotomy. Vascular compromise is only one indication: escharotomies should also be performed on the chest or abdomen for circumferential torso injuries, particularly in the setting of increased peak airway pressures (respiratory expansion limited by eschar constriction) or suspected abdominal compartment syndrome.
Escharotomies. The incisions are made on the medial and lateral aspects of the extremity. Hand escharotomies are performed on the medial and lateral digits and on the dorsum of the hand.
From Eichelberger MR, ed. Pediatric Trauma: Prevention, Acute Care, Rehabilitation . Mosby; 1993.
A 13-year-old girl was involved in a motor vehicle collision where the vehicle caught fire, and she suffered approximately 30% TBSA flame burns to the face, torso, and extremities. The extremity burns were circumferential with concern for impending limb compromise, and she underwent escharotomies of the right forearm (A) and hand (B) during the initial resuscitation. Incisions should be carried onto the hypothenar and thenar eminences and dorsolateral aspects of the digits if the hands or fingers are involved (C).
Fluid Resuscitation
The practice of fluid resuscitation for burn victims dates back several centuries.38 Prior to 1940, fluid resuscitation did not involve standardized formulas. Not until after the 1942 Cocoanut Grove nightclub fire experience did the relationship between the amount of fluid resuscitation required and the size of the burn become a central component of all burn formulas.39
Once adequate intravenous or intraosseous access is obtained, fluid resuscitation is initiated. The Parkland formula is the most widely used formula in adults but is not as applicable in young children because children have a greater TBSA relative to their weight than adults. As a result, weight-based formulas can underresuscitate children with minor burns and can grossly overresuscitate children with extensive burns.40 , 41 TBSA-based formulas, such as the Shriners-Galveston formula, are therefore better at estimating fluid requirements in children weighing less than 20 kg.42 For major burns, there are currently two main formulas that are being utilized in large pediatric burn centers: the Cincinnati and Galveston formulas (Table 12.1 ). The Cincinnati formula is a modification of the Parkland formula with added maintenance fluid calculation based on body surface area (BSA), while the Galveston formula uses a similar BSA-based maintenance fluid calculation plus the burn surface area.38 The Galveston formula tends to underpredict 24-hour fluid needs but allows for more physiologic variability.43 Due to their limited glycogen stores, dextrose-containing solutions are used as the primary solution for children younger than 2 years of age. An isotonic solution such as lactated Ringer’s (LR) solution with 5% dextrose is therefore given during the first 24 hours in these patients.
Table 12.1
Pediatric Burn Resuscitation Formulas
| Formula | Crystalloid | Colloid | Glucose | Instructions for Administration |
|---|---|---|---|---|
| Cincinnati (younger children) | 4 mL/kg/% TBSA burn + 1500 mL/m 2 total BSA of LR | 12.5 g of 25% albumin per liter of crystalloid in the last 8 h of first 24 h | 5% dextrose as needed |
Half over the first 8
h, half over the next 16
h. Composition of fluid changes every 8
h
First 8 h, 50 meq/L of sodium bicarbonate was added. Second 8 h was LR alone. Third 8 h, albumin is added |
| Cincinnati (older children) | 4 mL/kg/% TBSA burn + 1500 mL/m 2 total BSA of LR | None | 5% dextrose as needed | Half over the first 8 h, half over the next 16 h |
| Galveston | 5000 mL/m 2 BSA burn + 2000 mL/m 2 total BSA of LR | 12.5 g of 25% albumin per liter of crystalloid | 5% dextrose as needed | Half over the first 8 h, half over the next 16 h |
BSA, Body surface area; LR, lactated Ringer’s; TBSA, total body surface area.
Although mention has been made of the different burn resuscitation formulas, there are no standard agreed-upon guidelines that are used at all burn centers across the country, as there have been no adequate controlled studies comparing the different formulas. The American Burn Association clinical practice guidelines simply recommend administering a maintenance fluid rate to burned children in addition to their calculated fluid requirements caused by injury, without clearly favoring one resuscitation formula over another.44 In general, each center adopts its own formula likely based on historical resuscitation protocols at each institution.45 Some centers adopt a resuscitation formula based on 15% or greater TBSA, while others use 20% or greater TBSA as a trigger for formula-based resuscitation. It is important to note that these formulas are only estimates of the volume of fluid that will be required for resuscitation; they should be used to initiate IV fluid therapy, but the rate must be reevaluated and adjusted hourly as both over- and underresuscitation are problematic. To this end, most centers adopt slightly different algorithms for patients who fail to respond to initial resuscitation fluids (difficult-to-resuscitate algorithms).
At our institution, we have adopted a formula using a preinjury cutoff weight of 20 kg. We utilize a 20% TBSA burn as our indicator for needing formula-based fluid resuscitation. All burn patients admitted to our pediatric intensive care unit with a burn greater than 20% TBSA are resuscitated using the following formula:
We divide the total fluid volume by 2 and administer half of the fluid over the first 8 hours from the time of the burn injury and the remaining half over the next 16 hours. In the presence of known or suspected inhalation injury, our resuscitation formula will be based on 6 mL/kg instead of 3 mL/kg. For children >20 kg, we use LR as our resuscitation fluid of choice, and for those <20 kg, we use D 5 LR. We monitor urine output (UOP) as a surrogate for volume status. For patients >20 kg, our goal UOP is >0.5 mL/kg/h. For patients <20 kg, we use >1 mL/kg/h. For UOP of >1 mL/kg/h or <0.5 mL/kg/h in patients weighing <20 kg, we titrate the total IV fluid (IVF) rate up or down 20%, accordingly. For a patient >20 kg, we use <1 mL/kg/h or >1.5 mL/kg/h as cutoffs for titration.
At the time of admission, we calculate the maximum fluid to be given over the first 24 hours based on our formula and annotate it on the nursing bedside flowsheet. The flowsheet is updated at least hourly. If the patient exceeds this total fluid volume within the first 24 hours (>6 mL/kg/h without inhalation injury or >9 mL/kg/h with cutaneous burns and inhalation injury), we reclassify these patients as difficult-to-resuscitate. We then institute our difficult-to-resuscitate algorithm (Table 12.2 ).
Table 12.2
Difficult-to-Resuscitate Algorithm.
Courtesy Jenna Miller, MD and Jennifer Flint, MD, Children’s Mercy Hospital, Kansas City, MO.
|
|
With hypotension or other evidence of poor end organ perfusion. Consider epinephrine (Epi) or norepinephrine (NE) based on the following:
|
|
| → Start NE at 0.02 μg/kg/min. If CVP or UOP remains low, consider fluid bolus (10 mL/kg) or increasing IVF by 20% | |
| OR | |
| → Start Epi at 0.02 μg/kg/min | |
| ↓︎ | |
| Assess BP in addition to SVO 2 , CVP, and UOP | → If improved, continue current management |
| ↓︎ | |
|
If continued hypotension or other evidence of poor end organ perfusion:
Titrate the Epi or NE by 0.02 μg/kg/min up to 0.1 μg/kg/min to obtain hemodynamic parameters above. Notify pediatric intensive care unit provider if patient requires 0.1 μg/kg/min |
|
| ↓︎ | |
| Assess BP in addition to SVO 2 , CVP, and UOP | → If improved, continue current management |
| ↓︎ | |
| If continued hypotension or other evidence of poor end organ perfusion: Start vasopressin 2 milliunits/kg/min. DO NOT TITRATE | |
| ↓︎ | |
| Assess BP in addition to SVO 2 , CVP, and UOP | → If improved, continue current management |
| ↓︎ | |
If continued hypotension or other evidence of poor end organ perfusion consider the following:
|
|
BP, Blood pressure; CN, cyanide; CVP, central venous pressure; IVF, intravenous fluid; LR, lactated Ringer’s; UOP, urine output.
Resuscitation Endpoints
The key to successful resuscitation is based on constant reassessment of the physiologic status of the patient. Over- and/or underresuscitation are equally fraught with complications. Historically, UOP has been the primary parameter used for assessing fluid status in burn patients. Goal UOP should be 1 mL/kg/h for children less than or equal to 20 kg and 0.5 mL/kg/h for children greater than 20 kg. Although UOP has long been used as a surrogate of perfusion in critical care, it is important to note that it is several steps removed from the indirect measurement of cardiac output and has a weak relevance to actual tissue oxygenation.46 With this in mind, using UOP as a sole or major indicator of adequate tissue perfusion can lead to misinterpretation of fluid status. A global assessment including mental status, vital signs, invasive hemodynamic monitoring when indicated, and trends in laboratory values such as lactate and base deficit should be used to monitor resuscitation more accurately in patients with large burns. The concept of permissive oliguria has even been proposed as an appropriate management strategy in burn patients and is one that we occasionally use at our own institution.47 This strategy aims to limit overly aggressive fluid resuscitation by tolerating an hourly UOP at the lowest end of the acceptable range of 0.5–1 mL/kg/h, and even brief periods of anuria.
Inadequate resuscitation and/or overresuscitation can result in hypoperfusion to the zone of stasis, with subsequent deepening of the burn, as well as hypoperfusion of major organs. Capillary permeability is increased during the first 6–12 hours, and fluid moves from the intravascular space to the interstitial tissues, with worsening edema. Overly aggressive fluid administration can result in significant tissue edema, tissue hypoxia, and elevated compartment pressures, possibly necessitating surgical decompression of the affected body cavity or extremity.48
The use of colloids such as albumin, fresh frozen plasma, or synthetic starches/dextrans, remains a controversial topic in the burn literature. Large-volume crystalloid resuscitation can decrease plasma protein concentration and therefore osmotic pressure, resulting in fluid shifts from the intravascular to extravascular spaces, leading to worsening edema. In theory, the use of colloids such as plasma, albumin, and dextran should mitigate the effect of losing plasma into the extravascular space, and the addition of colloid solutions might reduce crystalloid requirements and more rapidly establish a balanced fluid intake to output ratio.49 , 50 However, the capillary integrity seen in the first 8–24 hours after burn injury is not enough to prevent efflux of colloids into the extravascular space, therefore not affecting the oncotic pressure of the intravascular space enough to maintain adequate intravascular volume.51 This effect is limited to approximately the first 12 hours. There may be some benefit to the use of colloids in the second half of the resuscitation algorithm. At our institution, for difficult-to-resuscitate patients, we change half of our resuscitation fluids to albumin only after the first 8 hours.
Although there are no high-quality randomized controlled studies comparing the use of colloids versus crystalloids in burn victims, a 2018 Cochrane Database Review found that colloid resuscitation has no effect on mortality in critically ill adults requiring resuscitation.52 Another meta-analysis also failed to show a mortality benefit unless two of the studies with a high risk of bias were excluded.41 All of these studies fall short of clear evidence, but that is likely due to the heterogeneity of the population and of the studies. Other solutions, such as hypertonic saline, have been used to provide a high osmotic pressure, which might keep more volume in the intravascular space. Hypertonic saline may also have antiinflammatory effects. Hypertonic saline should be used with caution as it causes hypernatremia and has not been shown to improve outcomes for hypotensive trauma patients.53
Unlike adults, children do not show hemodynamic changes reflecting hypovolemia until they are significantly volume depleted. Tachycardia may be a sign of compensation for a low-volume state or a stress response to injury. Signs of inadequate perfusion include lethargy and decreased capillary refill with cool, clammy extremities. Laboratory tests should be performed along with serial clinical exams to follow the response to resuscitation. Resolving acidosis, for example, may serve as an objective marker of improvement. Hyponatremia is a frequent complication in pediatric burn patients after aggressive fluid resuscitation, and correction is required to avoid severe electrolyte imbalance.
Inhalation Injury
Concomitant or isolated inhalation injury can lead to increased mortality and significant morbidity in all burn victims. For infants and children with large burns, the incidence of associated inhalation injury has been reported to be between 20% and 30%.54 One large multicenter review of pediatric burn patients diagnosed with inhalation injury demonstrated an overall mortality of 16%, with the majority of deaths resulting from sepsis and pulmonary dysfunction. Mortality increased to 50% if the patients required more than 1 week of mechanical ventilation.55 Diagnosing inhalation injury begins with a detailed history of the events related to the burn and a careful primary and secondary exam. Patients found in enclosed buildings or spaces are at high risk of inhalation injury. Physical exam findings such as facial burns, singed hairs in the nares, eyebrows, or head, and/or carbonaceous sputum are all nonspecific signs of smoke inhalation.
In an enclosed space, damage can occur via two mechanisms: heated air and inhaled gases. With heated air, most of the damage occurs in the upper airway as the reflexive glottis closes and the heated air cools significantly, causing minimal to no direct damage to the lower airways but potentially causing significant damage to the upper airway. The subsequent development of erythema or ulceration of the oropharynx can then lead to worsening obstruction over the first several hours after the injury. Additionally, aggressive fluid resuscitation results in worsening tissue edema in the upper airway with hoarseness, stridor, or dyspnea.56
Injury below the vocal cords occurs because of inhaled smoke. For enclosed fires, the greatest risk of immediate mortality and morbidity is carbon monoxide (CO) and hydrogen cyanide (HCN) toxicity. Smoke from burning wood generates high concentrations of CO and aldehydes, while the burning of synthetic material produces HCN. Both CO and HCN produce concentration-dependent hypoxia at the cellular level, but the mechanisms are distinct.
The affinity of CO for hemoglobin is more than 200 times that of oxygen, displacing oxygen from hemoglobin. It also shifts the oxyhemoglobin dissociation curve to the left, further increasing its affinity and significantly impairing the ability of hemoglobin to unload oxygen in the tissues. This decreases perfusion of oxygenated blood to organs and cells. Prolonged exposure causes high concentrations of CO in the blood and profound hypoxia, brain damage, and if unchecked, brain death.57 If CO toxicity or exposure is suspected, carboxyhemoglobin (COHb) levels can be obtained and are readily available in most hospitals. Approximately 5% of inhalation injuries in children involve inhaling CO.56 It is important to keep in mind that a normal or near normal serum carboxyhemoglobin level does not exclude CO toxicity, particularly in patients who have been on high-flow oxygen for extended periods of time prior to arriving at the hospital. Symptoms of CO toxicity with COHb levels of 15%–40% include headaches, flu-like symptoms, blurred vision, nausea, vomiting, and circulatory collapse. At levels above 40%, loss of consciousness, seizures, Cheyne-Stokes respirations, and death can occur.58
HCN, a gaseous form of cyanide, also leads to tissue hypoxia by disrupting mitochondrial generation of adenosine triphosphate through the binding of ferric ions in cytochrome c oxidase, which subsequently blocks aerobic cellular metabolism.59 While small amounts can safely be metabolized in the liver, larger amounts inhaled through the lungs overwhelm hepatic metabolism, leading to toxic levels.60 Neurologic deficits, persistent and unexplained acidosis, and serum lactate levels >8 mmol/L are major manifestations of cyanide toxicity. Persistent hypotension, metabolic acidosis, increased lactate, and cardiac arrhythmias, as well as decreased serum or mixed venous oxygen after adequate resuscitation are signs that can be seen with HCN toxicity.56 Cyanide levels can be measured directly in the blood or indirectly with serum lactate, anion gap, and methemoglobin concentrations.
Damaged epithelium in the lung due to activation of immune systems by inhaled smoke releases vasoactive substances (thromboxanes A 2 , C3a, and C5a) that lead to hypoxia, increased airway resistance, decreased pulmonary compliance, increased alveolar epithelial permeability, and increased pulmonary vascular resistance.61 Secondary injury is due to impaired ciliary clearance of airway debris. Neutrophil infiltration occurs, macrophages are destroyed, and bacteria accumulate, leading to pneumonia.
Any signs of impending respiratory difficulty should be carefully monitored, as respiratory collapse can occur quickly, and endotracheal intubation may become difficult in the face of significant tissue edema in the oropharynx. Chest films in the acute setting are nondiagnostic of inhalation injury. Although CT scans and xenon lung scans with xenon-133 isotope may be diagnostic, the most widely used and reliable method of diagnosing extent, severity, and progression of inhalation injury continues to be fiberoptic bronchoscopy62 (Fig. 12.5 ).
Representative images of bronchoscopic findings following inhalational injury in three separate patients. The degree of injury can range from mild (A) to severe (B) edema and congestion with carbon soot deposition (C) and formation of pseudomembranes.
From Bai C, Huang H, Yao X, Zhu S, Li B, Hang J, Zhang W, Zarogoulidis P, Gschwendtner A, Zarogoulidis K, Li Q, Simoff M. Application of flexible bronchoscopy in inhalation lung injury. Diagn Pathol . 2013;8:174.
Management of pediatric burn patients with suspected inhalation injury starts with the establishment of an adequate and stable airway and assessment of the risk of CO and HCN toxicity. Young children are often unable to escape from the scene of an enclosed fire, and their exposure to inhaled toxins can be significant. After the airway is secured, an inhalation treatment protocol is utilized in the intensive care unit (ICU) that focuses on the clearance of secretions and control of bronchospasm. Humidified 100% high-flow oxygen should be administered to displace CO from hemoglobin. The half-life of COHb is 60 minutes when 100% FiO 2 is administered, compared with 5 hours on room air.56 Although there have been many study design flaws, to date there is no conclusive evidence that supports the routine use of hyperbaric oxygenation for CO poisoning.63 For treatment of HCN toxicity, some studies have shown efficacy with hydrocobalamin, a cobalt compound that binds to cyanide and transforms cyanide to cyanocobalamin, which is then excreted in the urine. However, current evidence does not support the empiric administration of the drug.64 Sodium thiosulfate, a chemical that binds to cyanide to donate a sulfur group to form the less toxic compound thiocyanate, can also be used. Nitrites are avoided in pediatric patients as they can lead to methemoglobinemia.
Early and aggressive pulmonary therapy consisting of chest physiotherapy, frequent suctioning, and early mobilization should be started on all patients with a confirmed diagnosis of inhalation injury. Bronchodilators and racemic epinephrine are used to treat bronchospasm. Clearance of secretions can be assisted with inhalation treatments composed of heparin and acetylcysteine. Human autopsy and animal models have shown nebulized heparin (5000–10,000 units per 3 mL of NS every 5 hours) can reduce tracheobronchial cast formation, improve minute ventilation, and decrease peak inspiratory pressures after smoke inhalation.65–67 The addition of 20% acetylcysteine (3 mL every 4 hours) also improves the clearance of tracheobronchial secretions and minimizes bronchospasm. Pediatric and adult studies have shown this combination of medications decreases reintubation rates and mortality.68–70 Our protocol uses 5000 units of nebulized heparin every 4 hours alternating with 3 mL of 20% N -acetylcysteine every 4 hours for 7 days or until extubated, whichever comes first.
Assessment of Burn Depth
The accurate measurement of burn depth and TBSA of the burn victim is central to their management. Historically, a structural-anatomical classification into four categories has been utilized to characterize the depth of a burn.71 These categories are epidermal, superficial partial thickness, deep partial thickness, and full thickness. First, second, third, and fourth degree are no longer a part of the professional lexicon among burn care providers, or in the literature. Epidermal burns, although exquisitely painful, require no special medical attention. Superficial partial-thickness burns extend into the papillary dermis and are generally characterized by blisters and blanching tissue with pressure (Fig. 12.6 ). They are also painful when the underlying viable tissue is exposed. In otherwise healthy patients, these wounds will reepithelialize within 7–10 days with no untoward long-term functional or cosmetic deficits. On the other hand, deep partial-thickness burns extend into the reticular dermis and involve variable amounts of damage to skin appendages such as hair follicles. In these wounds, blanching is delayed, and the surface of the wound may be white and mottled (Fig. 12.7 ). Also, these wounds are usually less painful.
Two examples of a superficial partial-thickness burn are shown. (A) This child suffered a scald burn to the back. The characteristic blisters with this degree of burn injury are seen. (B) After removal of the blister, the wounds are painful and blanch when pressure is applied. (C) This child suffered also suffered a scald burn to the abdomen and groin. This photo was taken after several days in a silver-impregnated dressing.
A deep partial-thickness burn of the back is seen. Note the mottled and white appearance of the burned areas.
Full-thickness burns involve the entire dermis and extend into the subcutaneous tissue. These appear charred, leathery, and firm (Fig. 12.8 ). Patients typically are insensate in the burned regions and may not feel pressure. Blanching does not occur when pressure is applied. Full-thickness injuries should be excised and grafted early.72
This child sustained a 42% TBSA flame burn to his torso, anterior neck, and upper extremities. The white, leathery areas are full thickness burns, while the periphery of the burn is a deep partial-thickness injury.
Determination of burn wound depth can sometimes be difficult. Initial evaluation even by an experienced surgeon as to whether an indeterminate dermal burn will heal in 3 weeks is only about 50%–70% accurate.73–75 Scald injuries are particularly difficult to assess for depth and extent of injury. A number of techniques or tools have been described to improve accuracy. These techniques utilize the physiology of the skin and the alterations that occur with burn injury. Detection of dead cells or denatured collagen using ultrasound (US), biopsy, or vital dyes have been trialed.76–79 Appropriate US equipment is expensive; biopsies are invasive, painful, and lead to scarring; and interpretation of both modalities requires an experienced pathologist or radiologist. Other technologies such as analyzing altered blood flow using fluorescein, laser Doppler imaging (LDI), and thermography have shown some promise.80–83 LDI in particular has been shown to increase the accuracy of burn depth assessment when compared with evaluation by experienced burn surgeons. LDI measures the extent of the superficial microvascular blood flow, which can then correlate with the depth of the burn. Studies utilizing LDI in pediatric patients suggest high positive value and negative predictive values, providing a more accurate estimation and an earlier determination of burn depth than clinical judgment alone.84–86
Wound Care
Burn surgeons prefer to divide burn wounds into one of two categories: superficial wounds that will heal without surgery and deep wounds that will require surgical intervention. For deep partial-thickness burns, the management strategy may not be entirely clear. Many partial-thickness burns can be managed nonoperatively for 10–14 days with topical therapies and dressings. Using this strategy, the goal of burn care is to optimize reepithelialization by providing a warm and moist environment, removal of exudate and potentially contaminated or necrotic material (eschar), and control of bacterial proliferation. Deep partial-thickness burns should be excised and grafted if the surgeon does not believe that the wounds will heal by 3 weeks. It has been shown that if a partial-thickness burn wound heals within 2 weeks, scarring is unlikely to occur, but after 3 weeks, the risk of hypertrophic scar formation is extremely high.87 , 88 However, distinguishing between superficial and deep partial-thickness burns is not always clear and can be challenging even for experienced burn surgeons. This implies a great deal of clinical expertise because one would have to make that decision between post-burn day 10 and 14 at the latest. When possible, the burn surgeon should strive to excise and graft all known deep partial-thickness burns and all deep burns within the first 24–48 hours.
Antimicrobial Agents
The initial treatment of partial-thickness burns is debridement and coverage with a topical agent or dressing that has antibacterial properties and allows for separation of the burn eschar when present.89–91 Various topical antimicrobial agents have been used (Table 12.3 ). These agents decrease bacterial content, but they do not eradicate or prevent colonization.
Table 12.3
Burn Wound Dressings
| Dressings | Advantages | Disadvantages |
|---|---|---|
| Antimicrobial Salves | ||
| Silver sulfadiazine (Silvadene) | Painless; broad spectrum; rare sensitivity | Leukopenia; some gram-negative resistance; mild inhibition of epithelialization |
| Mafenide acetate (Sulfamylon) a | Broad spectrum; penetrates eschar; effective against Pseudomonas | Painful; metabolic acidosis; mild inhibition of epithelialization |
| Bacitracin/neomycin/polymixin B | Ease of application, painless, useful on face | Limited antimicrobial property |
| Nystatin | Effective in inhibiting fungal growth; use in combination with Silvadene, bacitracin | Cannot use in combination with mafenide acetate |
| Mupirocin (Bactroban) | Effective against Staphylococcus , including MRSA | Cost; poor eschar penetration |
| Antimicrobial Soaks | ||
| 0.5% silver nitrate | Painless; broad spectrum; rare sensitivity | No eschar penetration; discolors contacted areas; electrolyte imbalance; methemoglobinemia |
| Povidone-iodine (Betadine) | Broad-spectrum antimicrobial | Painful; potential systemic absorption; hypersensitivity |
| 5% mafenide acetate | Broad-spectrum antimicrobial | Painful; no fungal coverage; metabolic acidosis |
| 0.025% sodium hypochlorite (Dakin’s solution) | Effective against most organisms | Mildly inhibits epithelialization |
| 0.25% acetic acid | Effective against most organisms | Mildly inhibits epithelialization |
| Silver Impregnated | ||
| Aquacel, Acticoat, Mepitel Ag, Mepilex Ag | Broad-spectrum antimicrobial; no dressing changes | Cost |
| Synthetic Dressings | ||
| Suprathel | Provides wound barrier; minimizes pain; useful for outpatient burns, hands (gloves) | Requires extensive wound debridement for adequate adherence |
| OpSite, Tegaderm | Provides moisture barrier; minimizes pain; useful for outpatient burns; inexpensive | Exudate accumulation risks invasive wound infection; no antimicrobial property |
| Transcyte | Provides wound barrier; accelerates wound healing | Exudate accumulation risks invasive wound infection; no antimicrobial property |
| Integra, Alloderm | Complete wound closure, including dermal substitute | No antimicrobial property; expensive; requires training, experience |
| Biologic Dressings | ||
| Allograft (cadaver skin), xenograft (pig skin or tilapia skin) | Temporary biologic dressings | Requires access to skin bank; cost |
| Amniotic membrane | Minimizes dressing changes | Not widely used |
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