The pathophysiology and severity of inhalation injury varies with the aerosolized toxins particular to the circumstances of individual injuries. Years ago, the products of combustion in a structural fire were less toxic, due to extensive use of plastics in household items today. But all of the injuries are some combination of (1) upper airway obstruction secondary to progressive edema; (2) reactive bronchospasm from aerosolized irritants; (3) small airway occlusion initially from edema and subsequently from sloughed endobronchial debris and loss of the ciliary clearance mechanism; (4) diffuse microatelectasis from loss of surfactant and alveolar edema; and (5) interstitial and alveolar edema secondary to loss of capillary integrity. The physiologic consequences of these changes are upper and lower airway obstruction with increased airway resistance, decreased compliance, an increase dead space and intrapulmonary shunting.
The diagnosis of inhalation injury remains difficult because the components of the smoke to which any individual patient has been exposed are generally unknown. As current treatment is exclusively supportive, diagnosis provides only prognostic information. Bronchoscopy frequently reveals carbonaceous endobronchial debris and mucosal pallor, erythema or ulceration (Figure). But findings at the time of initial evaluation frequently only loosely correlate with the subsequent clinical course and long term sequelae.
The earliest consequence of inhalation injury is upper airway edema which is commonly seen during the first 6 to 24 hours after injury. It is common in patients with large surface area injuries who develop more significant loss of capillary integrity, resulting in soft tissue edema. Children with very severe injuries will slough casts of endobronchial debris that can cause small and large airway obstruction and may occasionally occlude the endotracheal tube. Steam inhalation will cause direct injury to the distal tracheobronchial tree, but most distal airway injuries are caused by aerosolized toxins (from burning plastics) rather than direct heat, as the upper airway is an effective heat sink.
Early obstruction of the upper airway is managed with intubation. In equivocal cases, bronchoscopy is performed and patients with significant upper airway edema are intubated using the bronchoscope as a stylet. Children can generally be extubated (if mechanics and mental status and gas exchange are satisfactory) when facial edema has largely resolved and there is an audible airleak around the endotracheal tube at a moderate pressure (20-30 cm H2O).
The later physiologic consequences of small airway obstruction and intrapulmonary shunting become more prominent after several days. Children with more serious injuries will develop progressive respiratory failure. Endobronchial debris and the loss of the ciliary clearance mechanism result in a high rate of pneumonia, which occurs in 20% to 50% of patients who suffer inhalation injury.
Management of patients with inhalation injury often requires aggressive pulmonary toilet, aided by frequent chest physiotherapy and toilet bronchoscopy. Positive pressure ventilation facilitates management of patients with large intrapulmonary shunts or mechanics poor enough to result in an excessive work of breathing. Although moderate inflating pressures will help to expand recruitable segments, peak inspiratory pressures in excess of 35-40 cm H2O should be avoided because they are associated with both overt barotrauma as well as more subtle overpressure injuries (“volutrauma”) to the pulmonary microvasculature and alveoli which can themselves exacerbate respiratory failure. High inflating pressures are also ineffective in recruiting additional lung, because the compliance decrements are not homogeneous and high pressures simply overdistend more compliant segments. Setting optimal levels of positive end-expiratory pressure may be effective in alveolar recruitment. When ventilating children with poor compliance we use pressure control ventilation and tolerate moderate hypercapnia and respiratory acidosis to facilitate control of inflating pressures . Neither steroids nor prophylactic antibiotics are routinely recommended. We rarely use early tracheostomy, and only then in those very exceptional circumstances when it is required for pulmonary toilet in those children who are sloughing large amounts of endobronchial debris.
Hyperbaric oxygen therapy may be indicated in selected children with documented or suspected clinically significant exposure to carbon monoxide (CO) to hasten clearance of carboxyhemoglobin (COHb), thus limiting ischemia secondary to a physiologic anemia, and to hasten clearance of CO bound to cytochrome enzymes, presumably limiting cellular injury. There is an extensive favorable uncontrolled literature, but major controversy persists over who should be treated. Many believe that stable patients with clear neurologic dysfunction and elevated COHb should be treated if it can be safely done, considering risks associated with transport and compromised monitoring during treatment. Children with more subtle exposures present more difficult decisions, acknowledging that obtundation after extrication from structural fires can be multifactorial in origin, secondary to anoxia, cyanide, CO, hypotension, and drugs.
Outcome for most children is very good if secondary lung injury from high inflating pressures, high concentrations of oxygen, or the adverse pulmonary sequelae of wound sepsis are avoided. Most will have clinically normal lung function, although there are subtle restrictive and obstructive changes reported with later pulmonary function studies.
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