Pediatric Burns By Bradley J. Phillips

and is typically injured from direct heat to the mucosa. This injury responds with formation of edema within 45 to 60 minutes. Patients with inhalation injury may initially present with a patent airway but can rapidly deteriorate within 12 to 24 hours of injury as edema peaks from aggressive fluid resuscitation. Some warning signs of exposure to high heat include singed nasal hairs and facial burns.¹ Common signs of a compromised airway include progressive hoarseness, stridor or inspiratory grunting, and increased respiratory rate and work of breathing. Providers should continue to monitor the patient’s airway throughout the emergent phase, with a low threshold for intubation in burn patients. Upon any sign of a deteriorating airway, an endotracheal tube should be placed, as delay in securing the airway can lead to a difficult and potentially dangerous emergent intubation. Edema can be minimized by elevating the head of the bed 20° to 30° and typically resolves in 2 to 3 days¹²; thus, tracheostomy is typically not required.¹

Particular care must be taken to properly secure the endotracheal tube once placement is confirmed. Failure to secure the tube may be disastrous due to the difficulty of reintubation in the setting of massive edema. The tube may be secured carefully with umbilical tape, but the surrounding skin must be monitored regularly for signs of pressure necrosis.¹

Breathing—Lower Airway Injury

Lower airway inhalation injuries (defined as injury below the glottis, including the lung parenchyma) greatly increase the severity of the burn. Lower airway injuries are the result of smoke inhalation, usually within an enclosed space, such as a house fire. The inhalation of smoke results in exposure of the terminal bronchioalveolar tree to chemical irritants. With the notable exception of steam injuries, lower airway injuries are not a result of direct thermal injury, since the upper airway dissipates the energy prior to exposure to the lower airway.⁸ Pediatric patients become disoriented easily and may hide rather than making an attempt to escape from an enclosed space.¹³ Young children in particular are at high risk of inhalation injury due to relative immobility and lack of situational awareness.⁷

The diagnosis of lower airway injury in pediatric patients is typically clinical. Visualization of subglottic structures via bronchoscopy requires an internal diameter of at least 8.0 mm and can be technically demanding in small children. Any patient who presents with a history of being involved in an enclosed space fire, loss of consciousness, or change in mental status should be presumed to have some degree of inhalation injury and closely monitored. These injuries may occur in the absence of cutaneous damage and may present with dyspnea, rales and rhonchi, and carbonaceous sputum.⁸

These signs and symptoms typically develop within 24 to 48 hours of the initial insult.¹

The treatment of lower airway injuries is mainly supportive.¹⁴ Bronchodilators may be useful in treating bronchospasm caused by aerosolized irritants. Mechanical ventilation with positive end expiratory pressure may be necessary in the event of a declining respiratory status. Permissive hypercapnia is allowed in patients with inhalation injury as long as the pH remains above 7.20.¹² Meticulous pulmonary toilet plays an important role, particularly in younger children, where the small diameter of pediatric endotracheal tubes can result in an increased risk of obstruction by secretions as well as wound exudates and topical wound care agents.¹

Systemic poisoning caused by inhaled toxins, frequently carbon monoxide and cyanide, is also very common. Carbon monoxide poisoning is the leading cause of death at the scene of a fire.⁸ This toxin binds over 200 times more efficiently to hemoglobin than oxygen does, thereby impairing oxygen uptake and delivery to tissues.¹³ Patients can present with headaches, dizziness, nausea, and seizures. A high clinical suspicion is required based on the history and mechanism of injury. Pulse oxymetry will be unreliable in carbon monoxide poisoning, as hemoglobin will be detected in its bound form. Treatment with high-flow oxygen via a non-rebreather mask is initiated while blood carboxyhemoglobin levels are measured to confirm the diagnosis. Treatment is continued until carboxyhemaglobin is less than 10% total hemoglobin.⁸

Cyanide poisoning is associated with incomplete combustion of nitrogenous materials such as silks and polyesters.¹⁵ The severity of poisoning is directly related to the extent of smoke exposure and results in metabolic acidosis. Patients with cyanide poisoning present with nonspecific symptoms such as nausea, tachypnea, and changes in mentation. Unfortunately, treatment is limited and the patient is notably unresponsive to supplemental oxygen.³ There is no available widespread testing method, and patients are typically diagnosed postmortem.⁸

Circulation

Predictable hemodynamic changes occur following severe burn injury. The patient exhibits an elevated cardiac output and decreased total peripheral resistance, making assessment of intravascular volume difficult.¹² Intravenous access is very important in patient management. In large burns, 2 large-bore peripheral IVs are required.¹ Obtaining access may be difficult secondary to distribution of the burn, edema, and reluctance to penetrate burned skin. Though not ideal, access may be obtained through areas of burn injury, followed by venous cut-downs and intraosseous access.