Inhalation Injury Clinical Presentation

The presence of underlying lung disease, including asthma, makes a child more susceptible to airway irritation.

Children and adults are often exposed to smoke together. The extent of disease can be notably different between children and adults, despite similar exposures. Children have higher minute ventilation and smaller body size, which increase toxin exposure. Children also have increased disorientation and delayed escape that may prolong exposure.

A history of patient exposure can help determine the risk for inhalation injury. The duration of exposure, the dose inhaled, and the actual toxins determine toxicity. Unfortunately, these details are often not known, although some information can be garnered from rescuers and other observers present at the scene.

Exposure to fire in a closed space, prolonged duration of entrapment, evidence of carbonaceous sputum, the requirement for cardiopulmonary resuscitation (CPR) at the scene, the presence of respiratory distress, and obtundation all increase the risk for significant pulmonary disease and hypoxic injury.

Fires involving the combustion of cellulose, nylon, wool, silk, asphalt, and polyurethane increase the risk for hydrogen cyanide poisoning.

Damage varies with the chemical activity of the particular inhalants, their size, solubility, and the duration and concentration of exposure. Upper airway injuries tend to be caused by the more irritating, water-soluble, larger particles. Substances of smaller size and lower water solubility cause alveolar and parenchymal injury.

Gasoline self-extinguishes when oxygen concentrations in the surrounding gas fall below 15%. Other substances may continue to undergo thermal decomposition, further decreasing ambient oxygen tension.

Inhalation injuries occur without skin burns or other obvious external injury; hence, a high degree of suspicion must be maintained. A retrospective review of 4,451 children with thermal injuries over 10 years demonstrated that inhalation injury was often not recognized, manifested late, and usually had significant consequences, including parenchymal injury and secondary pneumonia.^[1]

Because of its vast heat capacitance, thermal injury is generally confined to the upper airway. Inhalation of steam is a notable exception, in which lower airway and pulmonary parenchymal thermal injury are common. Theoretically, continued combustion of inhaled particulate matter could possibly produce more distal airway injury.

Thermal injury to the mucosa produces burns and edema of the nose, mouth, pharynx, and larynx, much like the damage from burns. The loose tissues of the upper airway swell readily in response to injury. Fluid resuscitation and loss of colloid oncotic pressure can obstruct the airway.

The full extent of airway compromise may not be evident until 12-24 hours after the initial injury. For patients with extensive surface burns, chest wall restriction may occur because of eschar formation.

Simple carbon soot is not particularly toxic, although it may carry and deposit other toxins directly onto the airway surfaces, thereby increasing exposure.

Children frequently become disoriented and may attempt to hide from flames and smoke, thereby prolonging their exposure to toxic inhalants. In addition, children have greater minute ventilation relative to body size than do adults, further increasing their exposure to toxic inhalants.

Pulmonary injury from smoke inhalation is characterized by both hyperinflation and atelectasis. Debris from cellular necrosis, inflammatory exudate, and shed epithelium combine with carbonaceous material to narrow airways that are already compromised by edema. Reflex bronchoconstriction further exacerbates the obstruction. Both inspiratory and expiratory resistance are increased, and the premature closure of small airways occurs, producing hyperinflation and air trapping. Surfactant production and activity are both impaired, leading to alveolar collapse and segmental atelectasis.

Low-pressure pulmonary edema plays an important role in the development of lung injury from smoke inhalation. Damage to the alveolar capillary membrane increases its permeability, and intravascular leakage into the pulmonary interstitium ensues. Eventually, increased lymphatic flow may be overwhelmed, resulting in alveolar edema. Alveoli fill with thick bloody fluid. Loss of compliance, further atelectasis, and increasing edema can result in severe ventilation-perfusion mismatch and hypoxia.

Pulmonary injury may also occur as a direct result of hypoxia. As with many pediatric illnesses and injuries, hypoxia itself may produce system dysfunction in many organs. The decrease in ambient oxygen tension that occurs during fires in closed spaces depends on the substances that are burned. Even small decrements in oxygen tension have a potentiating effect on inhaled asphyxiant gases, such as CO and hydrogen cyanide, resulting in severe lactic acidosis and a high fatality rate.

CO is a colorless odorless gas produced by the incomplete combustion of carbon-containing compounds, such as wood, coal, and gasoline. It is a major component of the smoke produced in open fires. The combustion of wood, coal, gasoline, and other organic substances increases the risk of CO poisoning. CO is a major component of smoke produced in most open fires and must be considered in any person injured in a fire. Remember that significant CO exposure can occur in the absence of open flames with malfunctioning domestic equipment (eg, poorly ventilated space heaters, cooking gas) and exposure to automobile exhaust fumes either from a suicide attempt or accidentally from poor ventilation.

Significant toxicity occurs with the inhalation of asphyxiants, including CO, nitrogen, and methane. These asphyxiants cause injury by interrupting the delivery of oxygen to the tissues. Asphyxiants either displace oxygen from the air or interfere with tissue oxygen delivery by blocking the action of hemoglobin or cytochrome oxidase (eg, CO, cyanide).

Hydrogen cyanide is an asphyxiant that is released during the incomplete combustion of products such as plastics and acrylics.

Cyanide has a characteristic almondlike odor. Hydrogen cyanide is absorbed rapidly, producing an almost immediate effect if exposure is by inhalation. In contrast, cyanide salts (eg, potassium, sodium cyanide, and, particularly, silver and copper cyanide), which are typically ingested, must be converted to hydrogen cyanide and are absorbed more slowly.

At higher levels of exposure, obtundation, seizures, and apnea occur. Low levels of cyanide increase cardiac output. At higher levels, a wide variety of bradyarrhythmia and tachyarrhythmia occur.

Symptoms at clinical presentation range from mild to severe smoke inhalation with coexistent burns and toxic gas exposure. In most cases, the presentation of a person injured in a fire is obvious and usually witnesses and evidence of burns or smoke inhalation are present.

Respiratory injury

Patients with respiratory injury present with many symptoms, ranging from minor eye irritation, cough, and uncomfortable breathing to acute respiratory failure. The full extent of respiratory tract injury may not be evident at initial presentation, although symptoms are usually present within 12-24 hours. Patients presenting with dyspnea, hemoptysis, cough, tachypnea, rales, rhonchi, wheezing, facial burns, carbonaceous sputum, pulmonary infiltration on radiography, and hypoxemia with or without acidosis should be closely observed because these findings increase the risk of progressive disease.

Burns on the face, soot marks, and singed eyebrows or facial hair are indicative of smoke inhalation. Inhalation injury can also occur without evidence of burns. Recognizing that upper airway swelling may take several hours to develop is imperative; thus, facial burns, hoarseness, stridor, upper airway injury with mucosal lesions identified upon oral examination or bronchoscopy, and carbonaceous sputum are indications to promptly secure artificial airway access.

Symptoms of lower respiratory tract injury include tachypnea, dyspnea, cough, decreased breath sounds, wheezing, rales, rhonchi, and retractions. Cyanosis is an unreliable indicator of hypoxia because of the bright-red color imparted to the skin when carboxyhemoglobin levels are elevated.

Neurologic injury

This may take longer to appear than evidence of respiratory injury. Neurologic injury may be the result of hypoxia at the time of injury or may result from hypoxia secondary to pulmonary dysfunction. Fear, severe pain, and obtundation from inadequate perfusion may cloud the neurologic examination in the burned child. Serial examinations assessing the sensorium are extremely helpful in guiding the initial resuscitation and stabilization.

Patients exposed to asphyxiants, including CO and cyanide, present with hypoxic injury and subsequent CNS depression, lethargy, and obtundation. Hypoxia is caused by an asphyxiant and is usually evident upon presentation. Irritability, severe temporal headache, and generalized muscle weakness are also common findings.

The presence of coma following exposure to fire is nearly always indicative of CO poisoning and should be promptly treated with 100% oxygen. Suspect cyanide toxicity in the child whose sensorium remains clouded and who does not respond to oxygen therapy.

Red retinal veins resulting from elevated venous oxyhemoglobin saturation may be noted on funduscopic examination.

Cardiovascular injury

Complex cardiovascular changes associated with surface burns may coexist with inhalation injury. Heart rate, capillary refill, warmth of unburned extremities, and blood pressure should be promptly evaluated at presentation and at frequent regular intervals during the initial stabilization.

Findings of acute ischemia on ECG in patients with young, otherwise healthy hearts are nearly always indicative of CO poisoning.

Other injury

Pay careful attention to narrowed pulse pressure because this may indicate inadequate volume resuscitation. Hypotension is invariably a late finding of volume loss.

The respiratory, cardiovascular, and neurologic organ systems are commonly injured because of their direct exposure and exquisite sensitivity to hypoxia respectively. However, renal tubular acidosis, hepatitis, and bone marrow insufficiency are not uncommon, particularly when hypoxic injury is either severe or prolonged.

Organ system dysfunction is also common as a result of the complex hemodynamic and inflammatory reactions associated with significant burns. In the obtunded patient, assume coexistent spine injury. CO poisoning may produce cutaneous erythema, blisters, and edema that can easily be mistaken for thermal burns.

Most often, inhalation injury results from direct damage to exposed epithelial surfaces and often causes conjunctivitis, corneal edema, rhinitis, pharyngitis, laryngitis, tracheitis, bronchitis, bronchiolitis, and alveolitis. Systemic absorption of toxins also occurs. Ascertaining if respiratory insufficiency is due to direct pulmonary injury or is the result of the extensive metabolic, hemodynamic, and subsequent infectious complications of surface burns is difficult.

Inhalants are classified as irritant, asphyxiant, or systemic toxins. Irritants cause extensive cell injury within the respiratory tract. Asphyxiants interrupt the delivery of oxygen to the tissues. Systemic toxins are absorbed through the respiratory tract and go on to damage other organ systems. Toxic gases are liberated during the combustion of various substances, as listed below.

Table. Inhalants^{[2, 3]} (Open Table in a new window)