Introduction
Most burn injuries in the United States are minor and treated in the outpatient setting in urgent care or emergency departments. The American Burn Association (ABA) Burn Injury Summary Report (2016–2022) documented approximately 30,000 annual hospital admissions for burn injuries in the United States each year. Of that, approximately 25% were pediatric patients. Overall, this represents a steady decline over the last several decades, although the percentage of pediatric patients requiring admission has remained relatively unchanged and disproportionately high. ,
Whereas house fires are the leading overall cause of burn injury and mortality in the United States in all age groups, scald injuries remain the most common type of burn injury in children. According to the ABA Burn Injury Summary Report (2016–2022), the overall mortality in the United States from burn injuries in children was 0.5% as compared with 3.2% overall mortality in all age groups. Children aged 16 years or younger account for 41% of all scald burns in all age groups, and 88% of scald burns in these children were less than 20% of total body surface area (TBSA). Scald burns represented 62% of the reported burn injuries in children with an average mortality of 0.4%. In contrast, flame injuries accounted for only 15.2% of the total burns in children but carried a 3.4% mortality rate , ( Table 48.1 ). Children under the age of 1 are more likely to suffer a chemical burn and disproportionately constitute 2.1% of all chemical burn injuries in all age groups. Approximately 13% of pediatric burns require admission.
Table 48.1
Burns According to Known Etiology of Patients Aged 0–16 Years Old in the United States (2016–2021)
Image provided with permission from the American Burn Association. All rights reserved..
| Etiology | Cases (N = 34,763) | Percentage |
|---|---|---|
| Scald | 21,586 | 62% |
| Contact | 5,760 | 16.5% |
| Flame | 5,288 | 15.2% |
| Flash | 958 | 2.8% |
| Chemical | 595 | 1.8% |
| Electrical | 576 | 1.7% |
Whereas mortality in burned children in the United States has decreased over the years, , global mortality has remained high. The World Health Organization Global Burn Registry, launched in 2018, reports a 10% mortality rate in children aged 18 years or younger. , This represents a global disparity in pediatric burn care that remains to be addressed in low-resource countries.
Children have physiologic and psychosocial differences that make their care more challenging than that of the average adult patient. Their high ratio of body surface area to body mass creates a higher risk for fluid imbalances than one might see in an adult. Thinner skin and less subcutaneous tissue in children put these patients at higher risk for deeper injuries from a burn mechanism than might be seen in an adult with the same type of injury. Children have smaller airways, and early intubation should be considered more aggressively than that in an adult. Sedation and analgesia needs make wound care in this patient population more complex and labor intensive. Child life specialists are essential in any inpatient pediatric burn unit and are ideal in the outpatient center as well. Child psychiatrists and therapists are often needed to help children and their families cope with the stress of severe injury and hospitalization. Child abuse and neglect are also major considerations and may account for up to 25% of the burns seen in the pediatric population.
Significant improvements in fluid resuscitation, early excision and grafting, infection management, and modulation of the hypermetabolic response have all led to the steady decline in the morbidity and mortality in pediatric burn patients. Yet, burn injuries remain one of the leading causes of unintentional death in these patients.
Initial management
Burn patients need to be treated first as trauma patients. The primary survey of advanced burn life support and advanced trauma life support is used to rule out other life-threatening injuries and conditions. The airway is assessed and stabilized first, and inhalation injury must be considered. Next, breathing and ventilation are addressed and maintained. Finally, circulation is assessed and supported with large-bore intravenous (IV) lines being established for fluid resuscitation. If IV access is not able to be achieved, intraosseous line placement may be required, especially in smaller children. If distal extremity pulses are lost or compromised or difficulty in ventilation is observed, immediate surgical intervention with escharotomy or fasciotomy may be required. Cooling the burn is also recommended. The application of cool running water to the burn site for 20 minutes in children within 3 hours of burn injury is associated with reduced skin grafting and faster reepithelialization. However, this is precluded by the presence of life-threatening injuries, or if the burned area is so extensive that hypothermia would result.
The secondary survey then allows a more detailed evaluation of the patient with a more in-depth history and head-to-toe examination to rule out other injuries and to calculate an accurate assessment of the extent of the injury, defined in TBSA. The TBSA will help guide the need for admission to the hospital or if outpatient care can be initiated. If the injury is large enough, fluid resuscitation is then initiated based on the TBSA and is adjusted based on urine output. Urine output is monitored by the use of a urinary catheter. Patients with larger TBSA burns may require nasogastric drainage. Nutritional support via nasogastric or nasojejunal tube may also be recommended early in the management of pediatric patients. In larger burns, special attention to preventing hypothermia is important. Fluid warmers, covering with clean, dry sheets, and higher-than-normal ambient room temperatures can help to avoid this problem.
It is useful to categorize burns not only by the extent of injury but also by mechanism, which may give some indication as to the depth of injury. The size of the injury is useful in deciding fluid resuscitation, as well as the need for potential hospitalization. Categorization of burns into minor, moderate, and major based on TBSA has been helpful in creating a plan for the care of these children. Minor burns (<5% TBSA) are the most commonly seen injuries and can usually be treated as outpatient. The risk of complications and the need for operative intervention are low in these patients. The use of dressings that do not need to be changed daily has allowed the treatment of most patients with minor burns as outpatients. , Moderate burns (5%–10% TBSA) can be managed either inpatient or outpatient, depending on depth and location of the injuries and other factors such as age, comorbidities, and social factors. Most children, especially younger children, with burns of this size are best managed with admission to a pediatric burn center. Major burns (>10% TBSA) virtually all require hospitalization in a pediatric burn center. Scoring systems such as the Pediatric Risk of Mortality score and Abbreviated Burn Severity Index can be used to determine burn mortality in severely burned children. Table 48.2 highlights the current recommendations for potential burn center referral.
Table 48.2
Burn Center Referral Criteria
Bettencourt AP, Romanowski KS, Joe V, et al. Updating the burn center referral criteria: results from the 2018 eDelphi consensus study. J Burn Care Res. 2020;41(5):1052-1062.
| 1 | Full-thickness burns >5% TBSA |
| 2 | Partial-thickness burns >10% TBSA |
| 3 | Any deep partial- or full-thickness burns involving the face, hands, genitalia, feet, perineum, or over any joints |
| 4 | Patients with burns and other comorbidities |
| 5 | All patients with suspected inhalation injury |
| 6 | Pediatric (<16 years) partial- and full-thickness burns <10% TBSA may benefit from burn center referral because of pain, dressing change needs, rehabilitation, patient/caregiver needs, or nonaccidental trauma |
| 7 | Older adults (>55 years) may benefit from multidisciplinary team resources available at burn center |
| 8 | All chemical injuries |
| 9 | All high-voltage electrical injuries (>1000 V) |
| 10 | Lightning injury |
| 11 | Grades II–IV frostbite |
| 12 | Stevens-Johnson syndrome or toxic epidermal necrolysis with epidermal slough |
TBSA, Total body surface area.
Calculation of the extent of the burn in TBSA can be achieved in several ways. Quick assessments can be made by the “palmar method,” whereby the palmar surface of the patient’s hand and fingers approximates 1% of the patient’s body surface area. This is most accurate in young children (1–4 years old) and becomes likely to underestimate TBSA in older children, whose hand surface area is approximately 1.5% TBSA or more. The “rule of nines” must be modified in children to account for larger surface area of the head and smaller surface area of the legs. The most accurate way to assess TBSA can be calculated by using standard charts such as the Lund and Browder, which takes into account each body part involved and the age of the patient ( Fig. 48.1 ). Electronic medical systems exist that will allow computer-based algorithms to assist in these calculations.
Methods of estimating burn size.
The depth of the injury is also an important factor in determining wound management and the need for surgical versus nonsurgical intervention. Standard burn-depth categories remain the same as the adult population and are described in Table 48.3 . Clinical judgment is often used to assess burn depth, but the most experienced burn surgeons can make an inaccurate depth assessment up to one-third of the time. Other modalities exist to determine burn depth. Historically, laser Doppler technology has been held as the gold standard in depth injury but more recently, indocyanine green laser imaging, infrared imaging, and other light-based devices have been developed. These devices have not yet been widely accepted because of cost, additional labor, and time but may be useful in guiding patient care in the future.
Table 48.3
Burn Depth Categories
| Depth | Clinical Characteristics | Prognosis |
|---|---|---|
| Superficial (1°) | Dry, erythematous, painful, no blistering | Heals spontaneously within 1 week without scarring |
| Superficial partial thickness (2°) | Weeping blisters, exposed dermis bright pink/red with brisk capillary refill, very painful | Heals spontaneously within 1–2 weeks, usually without scarring; pigmentation may be irregular |
| Deep partial thickness (2°) | Some blisters, drier, exposed dermis paler/whiter, mottled | Heals spontaneously, but usually after 3 weeks, with high risk of hypertrophic scarring; autografting usually required |
| Full thickness (3°) | White, brown, black, gray, or yellow, with dry, leathery, insensate eschar; sometimes may have cherry-red color caused by carbon monoxide poisoning | Healing by secondary intention and wound contraction with high risk of hypertrophic scarring and functional problems; autografting required |
| Subdermal (4°) | Similar to full-thickness burns; thrombosed veins may be visible through eschar | Healing by secondary intention and wound contraction with high risk of hypertrophic scarring and functional problems; autografting required |
Resuscitation
Fluid resuscitation is challenging in the pediatric burns for a variety of reasons. When compared with adults, children have higher insensible fluid losses because of their greater ratio of body surface area to mass. They also have a smaller intravascular volume per unit of surface area burned. This creates a greater risk for both hemodilution and fluid overload. In these younger patients with immature kidneys that are less capable of concentrating urine, there is an increased risk of dehydration. Younger children also have smaller hepatic glycogen stores, therefore their resuscitation fluids must contain some dextrose, necessitating stricter blood glucose monitoring. Fluid resuscitation requires close monitoring to ensure maximal tissue and organ perfusion while avoiding the complications of inadequate or excessive resuscitation. Young children especially are more prone to develop a systemic inflammatory response to relatively small TBSA burns, so we use the ABA Consensus Formula to resuscitate any child with partial-thickness and/or full-thickness burns of 15% TBSA or greater.
As with any trauma patient, large-bore peripheral IV access is preferred for any child with a major burn injury. Unburned sites are ideal but not always available. Care must be taken to secure lines well when placed through burned skin. Placing central venous and arterial lines in the emergency department should be avoided to minimize infection risk. Unless absolutely necessary, it is better to place these lines in the more controlled setting of the burn unit. If peripheral vascular access is not immediately possible in the emergent setting, intraosseous lines may be placed. Fluid volumes in excess of 100 mL/h can be administered directly into the bone marrow. A 16- to 18-gauge bone marrow aspiration needle, spinal needle, or commercially available intraosseous needle can be used to cannulate the bone marrow compartment. Although previously advocated only for children younger than 3 years, intraosseous fluid administration can be safely performed in all pediatric age groups. , The proximal anterior tibia, medial malleolus, anterior iliac crest, and distal femur are preferred sites for intraosseous infusion. The needle should be introduced into the bone, avoiding the epiphysis, either perpendicular to the bone or at a 60-degree angle, with the bevel facing the greater length of bone ( Fig. 48.2 ). The needle has been properly inserted when bone marrow can be freely aspirated. Fluid should be allowed to infuse by gravity drip. The use of pumps should be discouraged in case the needle becomes dislodged from the marrow compartment.
Intraosseous line placement in the (A) proximal tibia and (B) distal femur.
(From Fleisher G, Ludwig S, eds. Textbook of Pediatric Emergency Medicine. 2nd ed. Williams & Wilkins; 1988:268.)
Many formulas are available for calculation of pediatric burn resuscitation volumes and the type of fluids used. Class I or II data do not exist supporting one particular formula or type of crystalloid. What has been well-established is that delays in resuscitation are related to increased mortality, sepsis, and renal failure, so instituting resuscitation immediately and efficiently is key. A commonly used resuscitation formula in pediatric patients calls for the administration of 5000 mL/m 2 TBSA burned plus 2000 mL/m 2 TBSA for maintenance fluid given over the first 24 hours after burn. At our center, we use the ABA Consensus Formula ( Table 48.4 ). Traditionally, the 24-hour totals obtained by formula calculations are front loaded so that half of the volume is given over the first 8 hours after injury. In practice, fluids must be titrated hourly based on the clinical response, mainly by following urine output. Any formula is just a starting point that provides an initial rate. Our practice is to calculate the initial rate per the formula, start resuscitation at that rate regardless of the time elapsed since injury, and titrate closely to clinical response. As in adults, bolusing fluids is avoided unless warranted by hypotension. Calculations are based on an accurate assessment of TBSA of partial- and full-thickness burns only (superficial burns are not included) and must use an accurate dry weight. Isotonic crystalloid solution is used for resuscitation; most centers use lactated Ringer’s solution, as it is isotonic with plasma and avoids causing hyperchloremic metabolic acidosis. After the first 24 hours postinjury and for the rest of the time the burn wounds are open, the 24-hour fluid requirement to replace burn wound losses is 3750 mL/m 2 TBSA burned (or remaining open area) plus basal maintenance fluids. The fluid requirement decreases as a patient achieves more wound coverage and healing. Hyponatremia is a frequently observed complication in pediatric patients after the first 48 hours postburn. Frequent monitoring of serum electrolytes is necessary to guide appropriate electrolyte and fluid management.
Table 48.4
Pediatric (13 Years and Under) Fluid Resuscitation Guidelines for Initial 24 Hours Postburn Injury
| EXTENT OF BURN | |
| <10% TBSA | 1× maintenance rate |
| 10%–14% TBSA | 1.5× maintenance rate |
| ≥15% TBSA | American Burn Association Consensus Formula |
| 3 mL LR per kg body weight per % TBSA burned (2° and 3° only) | |
|
|
|
|
|
|
| For children <30 kg, add 1× maintenance rate | |
D 5 LR, Dextrose 5% in lactated Ringer’s solution; LR, Lactated Ringer’s solution; TBSA, total body surface area.
Assessment of resuscitation
The most common way to monitor response to fluid resuscitation remains urine output, despite attempts to find more accurate modalities using modern technology. In reality, the entire clinical picture must be taken into account when assessing fluid status, including heart rate and blood pressure, capillary refill/extremity perfusion and mental status, base deficit, and serum lactate levels. All of these parameters can be useful but are also subject to various pitfalls, especially in children. Renal compensatory mechanisms for hypovolemia (e.g., tubular concentration) are not well-developed in young children, contributing to hypovolemia with sustained urine production despite reduced intravascular volume. The routine clinical signs of hypovolemia in adult burn patients, such as low blood pressure and decreased urine output, are late manifestations of shock in the pediatric patient, and tachycardia is ubiquitous. Because of their cardiopulmonary physiologic reserve, pediatric patients do not show overt signs of hypovolemia until a decrease of at least 25% of the total blood volume occurs; at this point, hemodynamic decompensation occurs abruptly.
Any patient receiving Consensus Formula resuscitation requires an indwelling urinary catheter. These patients are assessed hourly for adequate urine output. For children under 30 kg body weight, the goal is 1 mL/kg/h. Similar to adults, in children over 30 kg, the goal is to maintain a urine output of 30 to 50 mL/h. In cases of smoke inhalation injury and with younger children, calculated fluid volumes as high as 6 mL/kg/% TBSA over the initial 24-hour period is required for effective resuscitation. Patients who require more than 6 mL/kg/% TBSA may be considered to have failed standard resuscitation techniques; in these cases, the use of colloid, inotropic, or pressor support and more invasive monitoring may be needed. The use of colloid remains controversial in burn resuscitation. Some studies have demonstrated that the use of colloid can reduce total fluid volumes given in resuscitation but makes no difference in longer-term outcomes. , Children are particularly prone to the development of edema from both vasogenic and hydrostatic sources. Vasogenic edema occurs in the early postburn period when vascular integrity is impaired. The maintenance of intravascular osmotic pressures reduces the likelihood of edema development. In difficult resuscitation, colloids such as albumin can be used. Albumin can be expected to remain in the intravascular space if administered more than 8 hours after burn. At our center, we use a resuscitation protocol that allows for the introduction of 5% albumin when patients are not responding well to crystalloid alone, if at least 8 hours have passed since the time of injury.
Overresuscitation must be avoided because it can lead to congestive heart failure, pulmonary edema, abdominal and extremity compartment syndromes, and cerebral edema. In children, cardiac output depends mainly on the heart rate because of the low compliance of the heart, which limits the increase in stroke volume. In addition, the heart is more susceptible to volume overload. Cardiac output can be measured using transpulmonary thermodilution devices, which are less invasive than a pulmonary artery catheter and only require an arterial catheter and a central venous line. Transthoracic or transesophageal echocardiograms should be used early to assess cardiac function in patients who are not responding to conventional therapy.
Evaluation and management of the airway
Early airway evaluation and management in children is essential. Children have a funnel-shaped larynx and are more prone to obstruction than adults because of the smaller aperture of their airway with the narrowest portion located at the level of the cricoid cartilage. With a smaller-diameter airway, a few millimeters of edema induced by an inflammatory or inhalational mechanism can cause exponential airway resistance when compared with adults ( Fig. 48.3 ). Pediatric patients also have shorter mandibles, disproportionately larger tongues, and prominent adenoids that can complicate intubation and contribute to airway resistance. Children may appear stable initially, but airway edema can progress rapidly over the first 24 hours. Both the failure to recognize impending airway compromise and the misjudgment of intubating unnecessarily can cause significant morbidity or even mortality. However, the risks of delayed intubation and a difficult airway are potentially more catastrophic than the risks of aspiration or other collateral damage from overzealous intubation, so it is better to err on the aggressive side of airway management if the clinical picture is uncertain.
Age-dependent effects of reduction in airway caliber on airway resistance and air flow to demonstrate the effect of airway edema, secondary to inhalation injury, on the respiratory mechanics in children compared with adults. One millimeter of circumferential edema will reduce the diameter of the airway by 2 mm, resulting in a 16-fold increase in airway resistance for the pediatric airway versus a threefold increase for the adult airway. It is possible the resistance can increase by 32-fold when a child is crying in the resuscitation room.
(From Wheeler OS, Spaeth JP, Mehta R, et al. Assessment and management of the pediatric airway. In: Wheeler OS, Wong HR, Shanley TP, eds. Resuscitation and Stabilization of the Critically Ill Child . Springer; 2008:224. With permission.)
Early intubation in burned children should be considered if there is concern for inhalation injury (see Inhalation Injury section), if a long transfer is anticipated (>3 hours), when deep anterior neck/facial burns are present, if a history of asthma or concomitant upper airway infection is present, or in larger (>20% TBSA) burns as these patients typically develop airway edema secondary to large-volume resuscitative fluid administration.
The ideal endotracheal tube (ETT) in a pediatric burn patient is the largest cuffed tube that the airway will allow. Cuffed tubes have been associated with reduced rates of air leak and reintubation without increased risk of subglottic tracheal injury when compared with uncuffed tubes in children. A larger-diameter tube will offer less airway resistance and facilitate efficient removal of airway debris if inhalation injury is present. A readily available estimate of airway diameter and ETT size in children is the width of the patient’s small fingernail, an age-based formula [(age/4) + 3.5 mm], the use of Broselow tape, or more recently by ultrasound.
The ETT must be secured and can be a difficult task in children with facial burns. Adhesives do not adhere well to open exudative burn wounds, and commonly used fixation methods may limit wound care. A simple method using cloth tape around the head, both above and below the ears, can be used to secure the ETT until more definitive fixation can be established. Multiple novel ETT fixation methods are available for children with facial burns. A 25-gauge ivy loop wire fixation between the maxillary lateral incisor and canine and a technique using two orthodontic brackets on the maxillary central incisors with a stabilizing stainless steel ligature wire have been described. , These methods allow access for wound care and surgical treatment of facial burns with good fixation of the ETT and avoid trauma to deciduous and erupting teeth in children.
Inhalation injury
Inhalation of flames, superheated air, smoke, and toxic fumes can cause direct airway and pulmonary damage and systemic toxicities commonly referred to as inhalation injury. The overall incidence of inhalation injury in children is approximately 5% to 7% and increases to 20% to 30% in severe burns (>20% TBSA). , , , , Inhalation injury remains a harbinger of mortality in children with burns. Overall mortality in children (0.5%–1.5% without vs. 16.4% with inhalation injury), risk of pneumonia, and length of stay are significantly increased when a cutaneous burn is compounded by inhalation injury. , , , , Furthermore, inhalation injury was found to significantly decrease the lethal percentage TBSA (LA10 and LA50) in children ( Table 48.5 ).
Table 48.5
Lethal Percentage Total Body Surface Area With and Without Inhalation Injury in Pediatric Patients 0–18 Years of Age
Thombs BD, Singh VA, Milner SM. Children under 4 years are at greater risk of mortality following acute burn injury: evidence from a national sample of 12,902 pediatric admissions. Shock. 2006;26(4):348-352; and Barrow RE, Spies M, Barrow LN, Herndon DN. Influence of demographics and inhalation injury on burn mortality in children. Burns. 2004;30(1):72-77.
| With Inhalation Injury | Without Inhalation Injury | |
|---|---|---|
| LA10 | 45% TBSA | 67.6% TBSA |
| LA50 | 77.3% TBSA | 99.7% TBSA |
LA10 and LA50 refer to the % TBSA required for 10% and 50% mortality in children, respectively.
TBSA, Total body surface area.
As expected, children who suffer flame burns are much more prone to inhalation injury than their scald burn counterparts (17.4% vs. 0.2% incidence, respectively). Therefore any patient with a flame-related injury, particularly those sustained in a closed environment, should be evaluated for inhalation injury. If inhalation injury is suspected, arterial blood gas and carboxyhemoglobin levels should be obtained, and the patient should be placed on 100% oxygen. Signs of potential inhalation injury include facial burns, singed nasal hairs, carbonaceous sputum, altered mental status, dyspnea, drooling, stridor, hoarseness, wheezing, or an elevated carboxyhemoglobin level of greater than 10%. A spectrum of neurologic symptoms exists as carboxyhemoglobin levels increase ( Table 48.6 ). In retrospective reviews of patients with inhalation injury, predictors of intubation included edema of true or false vocal cords, soot in nares or oropharynx, facial burns, and large body burns. , If any evidence of respiratory compromise is evident, expedient intubation may be lifesaving.
Table 48.6
Carbon Monoxide Poisoning Symptoms According to Carboxyhemoglobin Level
| Carboxyhemoglobin (%) | Symptoms |
|---|---|
| 0–10 | Normal |
| 10–20 | Headache, confusion |
| 20–40 | Disorientation, fatigue, nausea, visual changes |
| 40–60 | Hallucination, combativeness, convulsion, coma, shock state |
| 60–70 | Coma, convulsions, weak respiration and pulse |
| 70–80 | Decreasing respiration and stopping |
| 80–90 | Death in less than 1 hour |
| 90–100 | Death within a few minutes |
Direct inhalation injuries are typically separated into two anatomic regions, as the glottis reflexively protects the lower airway when subjected to a thermal stimulus. Direct thermal injury within the upper airway results in sequelae similar to cutaneous burns such as erythema, blistering, and ulcerations of the oropharynx. This manifests as hoarseness, stridor, and dyspnea and can lead to rapidly progressing airway edema. Swelling develops quickly over a few hours, is worsened by fluid resuscitation, and peaks 24-hours postinjury. Lower-airway injury typically results from chemical irritation from inhaled smoke. The noxious chemicals cause bronchoconstriction of the lower airways and a resultant inflammatory response leading to exudative secretions filling the tracheobronchial tree and damage to the ciliary lining of bronchial epithelium. Lung parenchyma injury typically manifests 24 hours or more after initial injury. Inflammation results in obstruction and collapsing of alveoli, edema, and ventilation/perfusion mismatches.
Tissue hypoxia caused by inhaled asphyxiants is a potentially highly lethal component of inhalation injury. Younger children are less able to quickly escape the scene of an enclosed fire and have higher minute ventilation, resulting in greater exposure to carbon monoxide (CO) and hydrogen cyanide, the most clinically important toxins present in smoke. CO has an affinity for hemoglobin 200 times that of oxygen. Hemoglobin preferentially binds CO and forms carboxyhemoglobin, resulting in hypoxia as tissue delivery of oxygen is impaired. Plasma pulse oximetry is unreliable as infrared wavelength changes are the same for carboxyhemoglobin and oxyhemoglobin. Carboxyhemoglobin levels can be measured via serum CO oximetry. The patient should be placed on 100% oxygen until carboxyhemoglobin levels normalize, as the half-life of carboxyhemoglobin is 60 minutes with 100% FiO 2 compared with 5 hours at room air. If the patient’s condition permits, hyperbaric oxygen therapy is an adjunctive therapy, as oxygen at 2.5 atmospheres reduces the half-life of carboxyhemoglobin to 20 minutes. Hydrogen cyanide is released with burning of synthetic material and disrupts the mitochondrial generation of adenosine triphosphate at the cellular level. No rapid diagnostic test is available for cyanide poisoning; however, an anion gap metabolic acidosis, serum lactate greater than 8, and high methemoglobin concentration are all highly suggestive of the diagnosis. Hydroxocobalamin (70 mg/kg IV over 15 minutes) remains the first-line treatment of cyanide poisoning for its rapid onset, safety, and efficacy. ,
Children under the age of 4 years with concomitant inhalation injury and severe cutaneous burns are at higher risk of death than their adult counterparts. Contrary to conventional belief, increased mortality in children with inhalation injury was not found as a result of a systemic proinflammatory cytokine surge in burned children. The increased mortality may be a result of children’s higher fluid requirements leading to underresuscitation, smaller anatomic airways that are more at risk for obstruction, and immature immune systems unable to combat infection and sepsis.
Defining diagnostic criteria for inhalation injury is made difficult by the extreme heterogeneity of clinical presentation. Diagnosis is confirmed with a suggestive history and physical as mentioned earlier and with visualization of the airway with fiberoptic bronchoscopy. CT findings of ground glass opacities, atelectasis and consolidation near large airways, and a 133Xe ventilation perfusion scan can serve as adjuncts to diagnosis. , Grading scales of inhalation injury based on bronchoscopy are available and may be helpful in predicting severity of injury, development of acute lung injury, and mortality ( Table 48.7 ). ,
Table 48.7
Abbreviated Injury Score Grading Scale for Inhalation Injury on Bronchoscopy
Endorf FW, Gamelli RL. Inhalation injury, pulmonary perturbations, and fluid resuscitation. J Burn Care Res. 2007;28(1):80-83.
| Grade | Class | Description |
|---|---|---|
| 0 | No injury | Absence of carbonaceous deposits, erythema, edema, bronchorrhea, or obstruction |
| 1 | Mild injury | Minor or patchy area of erythema, carbonaceous deposits, bronchorrhea, or bronchial obstruction |
| 2 | Moderate injury | Moderate degree of erythema, carbonaceous deposits, bronchorrhea, or bronchial obstruction |
| 3 | Severe injury | Severe inflammation with friability, copious carbonaceous deposits, bronchorrhea, or obstruction |
| 4 | Massive injury | Evidence of mucosal sloughing, necrosis, or endoluminal obstruction |
Grades greater than 2 have increased mortality.
Treatment modalities for inhalation injury are mostly supportive and include airway management, secretion clearance, and pharmacologic management. Endotracheal intubation is essential for upper airway obstruction but has risks and should not be performed prophylactically in all cases of inhalation injury. , Mechanical ventilation increases the incidence of pneumonia; if required for more than 1 week, mortality rate increases to 25% through 50%. , If the patient requires intubation, the largest appropriately sized, cuffed ETT allows adequate suctioning and better sealing of the airway should positive end-expiratory pressure be required. Infants and toddlers have a much higher oxygen consumption and CO 2 production than adults, thus they require a high respiratory rate. The optimal ventilator mode for pediatric burn patients with inhalation injury remains unclear. Studies have shown that high tidal volumes (15 ± 3 mL/kg TV) result in decreased incidence of acute respiratory distress syndrome and reduced ventilator days in children with inhalation injury but are also associated with increased pneumothoraces and higher ventilation pressures. High-frequency percussive ventilation is also effective in pediatric inhalation injury and may help facilitate evacuation of airway debris. Airway pressure release ventilation and high-frequency oscillatory ventilation benefits remain unproven and are reserved as rescue modes. Aggressive pulmonary toilet with chest physiotherapy, suctioning and lavage, therapeutic bronchoscopy, and early ambulation are vital. Extracorporeal membranous oxygenation may also be considered for severe refractory pulmonary failure. Finally, pharmacologic management has been shown to decrease duration of mechanical ventilation after inhalation injury and is summarized in Table 48.8 . , Steroids have not been shown to improve long-term pulmonary function and are not routinely recommended in inhalation injury.
Table 48.8
Pediatric Inhalation Treatment Protocol
Mlcak RP, Suman OE, Herndon DN. Respiratory management of inhalation injury. Burns. 2007;33(1):2-13.
| Titrate humidified oxygen | SaO 2 > 90% |
| Cough, deep breathing exercises | q2h |
| Turn patient side to side | q2h |
| Chest physiotherapy | q4h |
| Aerosolized bronchodilators (0.5% albuterol with 3 mL 20% NAC) | q4h |
| Aerosolized heparin 5000 U with 3 mL NS | q4h |
| Nasotracheal suctioning | As needed |
| Early ambulation | Postoperative day 5 or earlier |
| Sputum cultures for intubated patients | Every Monday, Wednesday, and Friday |
| Pulmonary function studies | Before discharge and outpatient visits |
| Patient/family education on inhalation injury | Continued |
Protocol is continued for 7 days. Alternate aerosolized albuterol/NAC and aerosolized heparin/NS so that the patient receives a treatment every 2 hours.
NAC, N -aceylcysteine; NS, normal saline; q2h, every 2 hours; q4h, every 4 hours; SaO 2 , arterial oxygen saturation.
Hypermetabolism
Children have 1.5 to 2 times higher total and basal metabolic rates than adults. Profound hypermetabolism is a classic feature of children with large (>40% TBSA) burns and increases with increasing burn size. However, even children with less severe burns (4% TBSA) have been found to exhibit a dysregulated metabolism. There is no other pathologic state that produces as dramatic an effect on the metabolic rate as severe burn injury.
After a large burn, there is an upregulation of catabolic agents such as catecholamines (10–15 times normal), inflammatory mediators and cytokines (100–200 times normal), cortisol, and glucagon, which induce a hyperdynamic cardiovascular response; elevated oxygen consumption as a result of skeletal muscle mitochondrial dysfunction; increased energy expenditure, which ranges from 120% to 180% above predicted levels; proteolysis, lipolysis, and glycogenolysis; loss of lean body and bone mass; and delayed wound healing and immune suppression. Skeletal muscle is broken down to supply vital organs, fuel the immune system, and allow wound healing, leading to a fourfold increase in amino acid requirement. , , Interleukin (IL)-1β and IL-6 increase RANK ligand, which promotes bone resorption by stimulating osteoclastogenesis, elevated glucocorticoids, vitamin D deficiency, and immobilization result in reduced bone mass. , Cardiac dysfunction is typically limited to massive burns of greater than 80% TBSA in children. If hypermetabolism cannot be attenuated, sepsis and/or multiorgan failure can result.
A major determinant of morbidity after severe burn is the extent and duration of the hypermetabolic response. The hypermetabolic state begins on postburn day 5 and persists for up to 2 years in children with significant improvement in the second year after surgery. Therefore treatment of burned children should continue after full healing of the integument as lean body mass and bone mineral content are still lower than normal at 2 years. A higher lifetime incidence of osteoporosis and fracture is also observed in patients with a history of burn in childhood. Advancements in early burn care for children, including early burn-wound excision and closure, adequate resuscitation, early enteral nutrition, new generation antibiotics, and the use of pharmacologic agents, have resulted in attenuation of the hypermetabolic response and thus decreased mortality and morbidity in this population. ,
Pharmacologic agents have been used to attenuate the effects of hypermetabolism in children with large burn injury (>30% TBSA). In attempts to mitigate lean body mass loss, several agents have been used: anabolic hormones such as recombinant growth hormone, insulin, insulin-like growth factor, and insulin-like growth factor binding protein 3; and anabolic steroids such as testosterone. , Propranolol, an adrenergic antagonist, has been used to decrease cardiac work and resting energy expenditure by inhibiting catecholamine binding to B-adrenoceptors. Oxandrolone, a nonaromatizing testosterone analog, has been shown to increase height, bone mineral content, lean body mass, and muscle strength and decrease pediatric intensive care unit length of stay in children postburn injury without significant side effects such as virilization or hepatotoxicity. , The combination of propranolol and oxandrolone along with exercise rehabilitative therapy has shown the most dramatic effect on diminishing hypermetabolic sequelae in children. , Finally, vitamin D supplementation and bisphosphonates have shown to reduce bone loss after pediatric burn injury , , ( Table 48.9 ).
Table 48.9
Common Pharmacologic Agents Used to Treat Hypermetabolism in Children With Associated Dose and Treatment Regimen
| Drug | Dose | Start | Duration |
|---|---|---|---|
| Propranolol | 0.33 mg/kg q4h | On admission | 1 year, titrated to achieve 15%–20% decrease from admission heart rate |
| Oxandrolone | 0.1–0.2 mg/kg bid (not to exceed 5 mg daily) | 48 hours after first surgical intervention | 2 years |
| Pamidronate | 1.5 mg/kg | Within first 10 days of injury | Within first 10 days of injury and again 1 week later |
| Vitamin D | 400 U/day | Upon discharge | 7 years |
bid, Twice daily; q4h, every 4 hours.
Thermoregulation
Thermoregulation is an innate ability of the body to maintain core body temperature independent of environmental temperature. Normal physiologic responses to temperature change include alterations in metabolism, shivering, sweating, and autonomic regulation of subcutaneous blood vessels to alter peripheral heat loss. Thermoregulation is dysfunctional in severely burned patients because of the loss of intact skin and dysregulation of peripheral and central thermoregulatory processes. Hypothalamic dysregulation induced by various inflammatory cytokines and pain causes a baseline elevation in core body temperature to 38°C to 39°C after burn injury.
Children, especially those under 2 years of age, have thinner skin, higher body surface-to-weight ratios, high transdermal permeability, and less insulating subcutaneous fat/muscle tissue; and possess limited shivering capacity to help maintain body temperature. With a large burn injury resulting in loss of skin integrity, children lose heat and water rapidly and are more likely to develop metabolic consequences from hypothermia. In younger children, temperature regulation is partially based on chemical/nonshivering thermogenesis, which may further increase metabolic rate, oxygen consumption, and lactate production.
Hypothermia is described as a core body temperature below 35°C and produces numerous consequences. In burn injury, low body temperatures are likely indicative of overwhelming sepsis or exhausted physiologic capabilities. Hypothermia can further exacerbate hypermetabolism and protein catabolism as the patient attempts to return to the elevated basal range. Other sequelae of hypothermia may include ventricular arrhythmias, impaired peripheral oxygenation, coagulopathy, and central nervous system and respiratory depression.
All efforts to avoid excess heat loss should be employed, including maintaining ambient room temperatures at 30°C to 32°C, which can reduce energy demands and evaporative water loss. Maintaining core temperatures of 37.5°C have been recommended. Preventative treatment strategies for hypothermia in children include draping nonburned body parts with plastic or forced warm-air devices, use of warming lights/blankets, using warm prepping solutions and IV fluids, expeditious dressing changes, and staged surgical procedures to limit patient exposure time and use of heat-loss prevention transport protocols.
Nutritional support
Nutrition support is especially vital in the pediatric burn patient, as they have limited energy reserves and are in a period of growth and development. Adequate early nutrition blunts the hypermetabolic response of burn injury, preventing depletion of muscle mass and fat stores and decreasing mortality in children. Protein and energy are important for new collagen synthesis and to help maintain visceral protein stores for optimal immune function. Nutritional support should be started as soon as possible, preferably within 24 hours of injury.
Early enteral feeding is best to preserve gut mucosal integrity and improve gut motility. A high-calorie, high-protein formula (1.5–3.0 g/kg/day) with adequate supplementation of vitamin C and zinc is typically used in children. , , Nasogastric tubes or nasojejunal feeds should be used if oral intake is inadequate or in burns greater than 30% TBSA. Several formulas are available to estimate caloric requirements in pediatric burn patients ( Table 48.10 ). Calorie counts should be recorded by a dietician and daily weights obtained. Total parenteral nutrition may be used if enteral feeds are not feasible or suboptimal. In major burn patients who require frequent trips to the operating room, it is safe to continue nasojejunal (postpyloric) feeding throughout the perioperative and intraoperative periods.
Table 48.10
Common Formulas Used to Estimate Caloric Requirements in Burnt Children
| Galveston | Modified Curreri | Mayes | WHO | Schofield | |
|---|---|---|---|---|---|
| Infant (<1 y) | 2100 kcal/m 2 BSA + 1000 kcal/m 2 TBSA |
BMR + 15 kcal/% TBSA
BMR + 25 kcal/% TBSA |
108 + (68 × weight in kg) + (3.9 × % TBSA) |
|
|
|
Toddler (1–3y)
Child (3–10y) |
1800 kcal/m 2 BSA + 1300 kcal/m 2 TBSA |
|
|||
| BMR + 40 kcal/% TBSA | 818 + (37.4 × weight in kg) + (9.3 × %TBSA) |
|
|||
| Adolescent (10–18y) | 1500 kcal/m 2 BSA + 1500 kcal/m 2 TBSA |
|
M: (19.25 × weight in kg) + (1.372 × height in cm) + 515.5
F: (8.365 × weight in kg) + (4.65 × height in cm) + 200 |
BMR, Basal metabolic rate; BSA, body surface area; F, female; M, male; TBSA, total body surface area, WHO, World Health Organization.
Growth delay
Growth delay is a known manifestation of hypermetabolism in severely burned adolescents as lean body and bone mass are reduced. , Without the availability of necessary building blocks in critical adolescent years, growth is interrupted. Hypermetabolism after the burn injury was thought to recede with closure of the burn wound. However, pediatric patients with large burns (>40% TBSA) exert muscle protein catabolism for at least 1 year, linear growth delay for at least 2 years, and a decrease in maximal exercise capacity during the first year after injury, which slowly resolves by postburn year 3. , , Deficits in height are most substantial in massively burned (>50% TBSA) children and can range between 1.6 cm and 5.8 cm when compared with normal height-for-age growth curves.
The growth delay in children is not only attributed to the hypermetabolic state but many compounding factors: reduced vitamin D levels that have been shown to last for up to 7 years postburn injury because of avoidance of sunlight to reduce hypertrophic scarring; immobility because of complications of burn injury; anorexia because of poor emotional adjustment; recurrent infections; and repeated admissions for reconstructive surgeries. The combination of oxandrolone, propranolol, and a rehabilitative exercise regime has shown to ameliorate growth delay secondary to burn injury in children. ,
Management of burn wound
Wound management in pediatric patients can be more complex because of the need for prolonged hospitalization for dressing changes, the need for anesthesia or more complex analgesia to perform dressing changes, and more limited donor areas because of the small size of the patient. Despite these differences, many of the same principles apply to children. Of course, early debridement or excision of eschar and grafting, when necessary, have become the modern standard of care and have revolutionized the outcomes in burn patients worldwide. No longer is it acceptable to allow burns to spontaneously separate and granulate followed by delayed skin-grafting procedures. This led to much longer hospitalizations with higher incidences of infection and sepsis and, ultimately, higher mortality rates. It is generally accepted that if a burn injury is likely to take longer than 2 to 3 weeks to heal spontaneously, then the risk of infection, inflammation, and hypertrophic scarring are significantly increased, leading to higher morbidity in these patients. ,
Initial wound management depends on the depth and TBSA of the injury ( Fig. 48.4 ). Initially, topical antimicrobials are applied to the burn wound to minimize the risk of burn wound infection ( Table 48.11 ). Superficial partial-thickness burns will often receive topical antimicrobial ointments or creams. Silver sulfadiazine cream remains the most commonly used topical agent, but its tendency to leave a pseudoeschar behind makes wound management more painful in pediatric patients and has therefore become less commonly used. If the burn is deeper partia thickness or indeterminate in depth, then collagenase ointment in conjunction with an antimicrobial can be used to begin early enzymatic debridement and help to assess the true depth of the burn wound. This allows for earlier determination of the true depth of the injury, thereby allowing for earlier clinical decision-making.






