Ally son A. Kreshak
Hydrocarbons are among the 25 most frequent exposures reported to the American Association of Poison Control Centers.
Approximately 3.5% to 10% of young people have tried volatile substance inhalation.
Products containing hydrocarbons are found in many household and workplace settings; these include fuels, lighter fluids, paint removers, pesticides, polishers, degreasers, and lubricants.
Volatile substances containing hydrocarbons such as glue, propellants, and gasoline are occasionally used for recreational abuse.
Pulmonary toxicity manifests as chemical pneumonitis which results from direct parenchymal injury and altered surfactant function. This results either from aspiration of a low-viscosity compound or from inhalation of a high-volatility compound.
Cardiac toxicity manifests as dysrhythmias that are mediated by endogenous catecholamines.
Central nervous system (CNS) toxicity can be caused directly by systemically absorbed hydrocarbon, or indirectly from hypoxia due to pulmonary toxicity.
Peripheral neuropathy secondary to demyelination and retrograde axonal degeneration results from P450 metabolism of six-carbon hydrocarbons to the toxic metabolite 2,5-hexanedione.
Chlorinated hydrocarbons can cause lipid peroxidation and hepatic injury.
With methylene chloride exposure, carbon monoxide formation may continue after cessation of exposure; this is caused by gradual release of methylene chloride from the tissues prior to its metabolism to carbon monoxide.
Toxicity depends on the route of exposure (ingestion, inhalation, or dermal), physical characteristics of the agent (volatility, viscosity, and surface tension), chemical characteristics (aliphatic, aromatic, or hydrogenated), and the presence of toxic additives (eg, lead or pesticides).
Table 113-1 lists the most common clinical manifestations of hydrocarbon toxicity; pulmonary and cardiac effects are most common.
Aspiration of highly volatile aliphatic substances such as gasoline, kerosene, methane, or butane may result in chemical pneumonitis, pneumodeiastinum, pneumothorax, and pneumatocele.
Patients may present with coughing, dyspnea, choking, and gasping. Physical examination may reveal tachypnea, wheezing, grunting, and decreased breath sounds. Chest radiographic findings lag behind the clinical picture by 4 to 6 hours.
Cardiac toxicity from aromatic and halogenated hydrocarbons is due to sensitization of the myocardium to catecholamines that may cause serious or fatal dysrhythmias.
CNS toxicity occurs most commonly with the volatile petroleum distillates such as toluene and trichloroethane. Symptoms range from giddiness, slurred speech, ataxia, and hallucinations to seizures, lethargy, obtundation, and coma. Chronic exposure can cause cerebellar ataxia and mood lability.
Halogenated hydrocarbons such as carbon tetrachloride and chloroform cause direct hepatocellular injury. Liver enzymes may be elevated within 24 hours, and right upper quadrant abdominal pain and jaundice develop within 48 to 96 hours. Chronic exposure causes cirrhosis and hepatoma.
Hematologic toxicity from gasoline, kerosene, and trichloroethane can lead to hemolysis. Chronic benzene abuse can cause aplastic anemia and hematologic malignancies.
Dermal toxicity includes rashes (erythema, papules, vesicles, or scarlatiniform rash), eczematous dermatitis, and burns.
Carbon monoxide poisoning from methylene chloride metabolism may result in a metabolic acidosis.
TABLE 113-1 Clinical Manifestations of Hydrocarbon Exposure
DIAGNOSIS AND DIFFERENTIAL
Diagnosis is made by history and the accompanying physical examination findings.
Helpful laboratory tests include arterial blood gas, liver function panel, BUN, creatinine, hematocrit, and carboxyhemoglobin level (in methylene chloride exposure).
A chest radiograph should be ordered to evaluate for aspiration pneumonitis immediately in symptomatic patients and after a 6-hour observation in asymptomatic patient.
A kidney, ureter, and bladder radiograph (KUB) may show the presence of chlorinated hydrocarbons (eg, carbon tetrachloride) in the gastrointestinal (GI) tract as polyhalogenated substances are radiopaque.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Decontamination of the patient should follow standard HAZMAT measures, and should preferably occur in the out-of-hospital setting.
Administer supplemental oxygen and place all symptomatic patients on a cardiac monitor.
Consider endotracheal intubation for patients with significant respiratory distress. Positive end-expiratory pressure may be added to improve oxygenation, but pneumothorax or pneumatocele are potential complications.
In severe pulmonary aspiration with refractory hypoxemia, successful treatment with extracorporeal membrane oxygenation or high-frequency jet ventilation has been reported.
Treat hypotension with IV crystalloid infusion. Catecholamines may precipitate life-threatening dysrhythmias and should be avoided, except in cases of cardiac arrest.
Treat tachydysrhythmias with a beta-adrenergic antagonist (eg, propranolol 1 milligram, which can be repeated if well tolerated).
Seizures are managed using standard regimens.
Hydrocarbons referred to with the CHAMP acronym (camphor, halogenated hydrocarbons, aromatic hydrocarbons, metals, pesticides) have potential inherent systemic toxicity or solubilize into toxic agents. GI decontamination using gastric emptying should be considered when exposure to these hydrocarbons has occurred, but is generally contraindicated in other hydrocarbon ingestions.
The majority of hydrocarbon ingestions, which consist of aliphatic mixtures, are poorly absorbed from the GI tract and carry a risk of aspiration during GI decontamination measures.
Activated charcoal and cathartics are of no benefit for any hydrocarbon ingestion.
Hyperbaric oxygen therapy may be indicated for patients who develop significant carbon monoxide toxicity after exposure to methylene chloride.
Because most fatalities occur in the first 24 to 48 hours, admit all patients who are symptomatic at the time of evaluation.
Asymptomatic patients with a normal chest radiograph who remain symptom-free after 6 hours of observation can be discharged. All discharged patients should receive close follow-up for delayed toxicity.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 193, “Hydrocarbons and Volatile Substances,” by Paul M. Wax and Stella C. Wong.