Pulmonary complications, especially aspiration, are the most frequent adverse effects of hydrocarbon exposure. Typically, this involves the unintentional childhood ingestion of small amounts of aliphatic hydrocarbon mixtures commonly stored in the household. Aliphatic hydrocarbons have a limited GI absorption; toxicity usually results from aspiration of the low-viscosity compounds or inhalation (intentional or inadvertent) of compounds with high volatility. Although ingestion of aromatic or halogenated hydrocarbons may also result in aspiration, GI absorption is greater. Hence, CNS and other systemic toxicity secondary to GI absorption often predominate after aromatic and halogenated hydrocarbon ingestion.
Aspiration is not dependent on volume ingested. Experimentally in rats, as little as 0.2 mL instilled intratracheally has caused pneumonitis. Pulmonary toxicity does not result from GI absorption but occurs from direct aspiration of the hydrocarbon into the pulmonary tree. This occurs at the time of ingestion when the hydrocarbon migrates from the hypopharynx into the airway. There is no evidence that hydrocarbons reflux from the stomach into the airway. Spontaneous vomiting, however, does increase the risk of aspiration.6 Pulmonary toxicity manifested as acute bilateral pneumonitis has also been reported from the inhalation of an aerosolized aliphatic hydrocarbon such as gasoline or kerosene.
Hydrocarbon aspiration causes chemical pneumonitis by direct toxic injury to the pulmonary parenchyma and altered surfactant function. Destruction of alveolar and capillary membranes results in increased vascular permeability and edema. Early distal airway closure and alveolar collapse produces clinical bronchospasm and ventilation/perfusion mismatch. The CNS manifestations seen after ingestion of a poorly GI-absorbed aliphatic hydrocarbon are thought to be from hypoxia secondary to the hydrocarbon induced pneumonitis and/or direct CNS toxicity following the pulmonary absorption of a volatile hydrocarbon. Studies performed in animals in which hydrocarbons were instilled into the stomach after ligation of the esophagus demonstrate negligible absorption of aliphatic compounds from the GI tract with no evidence of subsequent pneumonitis.7 Pneumatoceles, pneumothoraces, and/or pneumomediastinum are occasionally associated with hydrocarbon aspiration. Other complications include bacterial superinfection, acute respiratory distress syndrome, and death. Long-term pulmonary dysfunction may occur.
In one study of 950 children who ingested products containing hydrocarbons and who were brought to the hospital, 19 percent had clinical or radiographic evidence of pulmonary aspiration.8 In another study of 184 pediatric hydrocarbon ingestions called to a poison center, 35 percent had initial symptoms, but only 3 percent had progressive pulmonary symptoms.9 The clinical manifestations of pulmonary aspiration are usually apparent almost immediately on ingestion. The early effects result from irritation of the oral mucosa and tracheobronchial tree. Symptoms include coughing, choking, gasping, dyspnea, and burning of the mouth. Patients with these symptoms should be assumed to have aspirated until proven otherwise. Physical examination may reveal grunting respirations, retractions, tachypnea, tachycardia, and cyanosis. An odor of the hydrocarbon may be noted on the patient's breath. An elevated temperature of 39°C (102.2°F) or greater is common and may occur upon initial presentation or be delayed for 6 to 8 h.
Auscultation may be normal, or reveal wheezing, and decreased, or absent breath sounds. Arterial blood gas analysis may demonstrate a widened alveolar-arterial oxygen gradient or frank hypoxemia. The development of a necrotizing pneumonitis and hemorrhagic pulmonary edema usually occurs within hours in severe aspiration.
Most fatalities from these complications occur within 24 to 48 h. With less severe damage, symptoms usually subside within two to five days, except with pneumatoceles and lipoid pneumonias whose symptoms may persist for weeks to months.
Although most patients with clinically significant aspiration have abnormal chest x-rays, the time course of radiographic changes varies and correlation with physical examination may be poor. Changes may be seen as early as 30 min after aspiration, but the initial radiograph in the symptomatic patient may be deceptively clear. Radiographic changes usually appear by 2 to 6 h and are almost always present by 18 to 24 h if they are to occur. The infiltrates range in appearance from streaking to flocculent to homogeneous, and are usually located in the dependent lobes. Multilobar involvement is more common than single-lobe involvement and right-sided involvement is more common than left-sided involvement. Radiographic changes limited to bilateral perihilar regions with clear lung bases are also common.
High-viscosity compounds such as lubricants, mineral oil, or tar, are not aspirated readily and tend to be less toxic when ingested. Occasionally, however, aspiration occurs that results in the development of lipoid pneumonia. Deaths from hydrocarbon lipoid pneumonia have been reported.
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