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Introduction

Hydrocarbons are used widely as solvents, degreasers, fuels, and lubricants. Besides inadvertent exposure, poisoning also commonly occurs from inhalation of volatile hydrocarbon gases used as drugs of abuse. Hydrocarbons include organic compounds derived from petroleum distillation as well as many other sources, including plant oils, animal fats, and coal. Subcategories include aliphatic (saturated carbon structure), aromatic (containing one or more benzene rings), halogenated (containing chlorine, bromine, or fluorine atoms), alcohols and glycols, ethers, ketones, carboxylic acids, and many others. This chapter emphasizes toxicity caused by common household hydrocarbons. See specific chemicals elsewhere in Section II and in Table IV-3.

Mechanism of Toxicity

Hydrocarbons can cause direct lung injury after aspiration or systemic intoxication after ingestion, inhalation, or skin absorption (Table II-32). Many hydrocarbons are also irritating to the eyes and skin.

TABLE II-32. HYDROCARBON INGESTION

Common CompoundsRisk for Systemic Toxicity After IngestionRisk for Chemical Aspiration PneumoniaTreatment

No systemic toxicity, high viscosity

Petrolatum jelly, motor oil

LowLowSupportive.

No systemic toxicity, low viscosity

Gasoline, kerosene, petroleum naphtha, mineral seal oil, petroleum ether

LowHighObserve for pneumonia; do not empty stomach.

Unknown or uncertain systemic toxicity

Turpentine, pine oil

UncertainHighObserve for pneumonia; consider removal by nasogastric suction and/or administration of activated charcoal if ingestion is more than 2 mL/kg.

Systemic toxins

Camphor, phenol, halogenated or aromatic compounds

HighHighObserve for pneumonia; consider removal by nasogastric suction and/or administration of activated charcoal.
  1. Pulmonary aspiration. Chemical pneumonitis is caused by direct tissue damage and surfactant disruption. Aspiration risk is greatest for hydrocarbons with low viscosity and low surface tension (eg, petroleum naphtha, gasoline, turpentine).
  2. Ingestion
    1. Aliphatic hydrocarbons and simple petroleum distillates such as lighter fluid, kerosene, furniture polish, and gasoline are poorly absorbed from the GI tract and do not pose a significant risk for systemic toxicity after ingestion if they are not aspirated.
    2. In contrast, many aromatic and halogenated hydrocarbons, alcohols, ethers, ketones, and other substituted or complex hydrocarbons can cause serious systemic toxicity, such as coma, seizures, and cardiac dysrhythmias.
  3. Inhalation of hydrocarbon vapors in an enclosed space can cause intoxication from systemic absorption or displacement of oxygen from the atmosphere; in addition, sensitization of the myocardium to catecholamines can cause cardiac dysrhythmias.
  4. Injection of hydrocarbons into skin, subcutaneous tissue, or muscle can cause a severe local inflammatory reaction and liquefaction necrosis.
  5. Skin and eye contact can cause local irritation. Dermal absorption can be significant for some agents but is insignificant for most of the simple aliphatic compounds.

Toxic Dose

The toxic dose is variable, depending on the agent involved and whether it is aspirated, ingested, injected, or inhaled.

  1. Pulmonary aspiration of as little as a few milliliters can produce chemical pneumonitis.
  2. Ingestion of as little as 10-20 mL of some systemic toxins, such as camphor and carbon tetrachloride, can cause serious or fatal poisoning.
  3. For recommended inhalation exposure limits for common hydrocarbons, see Table IV-3.
  4. Injection of less than 1 mL can cause significant local tissue inflammation.
  5. Dermal absorption is insignificant for most simple aliphatic compounds but may occur with other agents.

Clinical Presentation

  1. Pulmonary aspiration usually causes immediate onset of coughing or choking. This can progress within minutes or hours to a chemical pneumonitis characterized by respiratory distress, including tachypnea, retractions, grunting, wheezing, rales, hypoxia, and hypercarbia. Death may ensue from respiratory failure, secondary bacterial infection, and other respiratory complications.
  2. Ingestion often causes abrupt nausea and vomiting, occasionally with hemorrhagic gastroenteritis. Some compounds may be absorbed and produce systemic toxicity.
  3. Systemic toxicity caused by hydrocarbon ingestion, inhalation, intravenous injection, or dermal absorption is highly variable, depending on the compound, but often includes confusion, ataxia, lethargy, and headache. With significant exposure, syncope, coma, and respiratory arrest may occur. Cardiac dysrhythmias can occur as a result of myocardial sensitization, especially with halogenated and aromatic compounds. Atrial fibrillation, ventricular fibrillation, and sudden cardiac death are reported. Many agents also can cause hepatic and renal injury.
  4. Injection of hydrocarbons can cause local tissue inflammation, pain, and necrosis. Severe scarring and loss of function have occurred after injection into a finger with a paint gun or another high-pressure spray device containing a hydrocarbon solvent. Often, the puncture wound and local swelling appear minor, but tracking of hydrocarbon solvent down fascial planes into the palm and forearm can cause widespread inflammation and injury.
  5. Skin or eye contact can cause local irritation, burns, or corneal injury. Chronic skin exposure often causes a defatting dermatitis (resulting from removal of oils from the skin). Some agents are absorbed through the skin and can produce systemic effects.

Diagnosis

  1. Aspiration pneumonitis. Diagnosis is based on a history of exposure and the presence of respiratory symptoms such as coughing, tachypnea, and wheezing. Chest radiograph, oximetry, and arterial blood gases may assist in the diagnosis, although radiographic findings can be delayed for more than 24 hours.
  2. Systemic intoxication. Diagnosis is based on a history of ingestion or inhalation, accompanied by the appropriate systemic clinical manifestations.
  3. Specific levels are not generally available or useful in the diagnosis or management.
  4. Other useful studies. For suspected aspiration pneumonitis, obtain pulse oximetry or arterial blood gas and a chest radiograph. For suspected systemic toxicity, obtain electrolytes, glucose, BUN, creatinine, and liver aminotransferases. Obtain an ECG and continuous cardiac monitoring.

Treatment

  1. Emergency and supportive measures
    1. General. Provide basic supportive care for all symptomatic patients.
      1. Maintain an open airway, administer supplemental oxygen, and assist ventilation if necessary.
      2. Monitor pulse oximetry, co-oximetry (especially for methemoglobin formers), arterial blood gases, chest radiographs, and ECG.
      3. Use epinephrine and other beta-adrenergic medications with caution, as these agents can induce dysrhythmias.
      4. Admit symptomatic patients to a setting with continuous cardiac monitoring.
    2. Pulmonary aspiration. Patients who remain completely asymptomatic after 4 hours of observation can be discharged.
      1. Administer supplemental oxygen and treat bronchospasm and hypoxia if they occur.
      2. Do not use steroids or prophylactic antibiotics. A randomized, controlled trial of antibiotics for aspiration pneumonitis in children demonstrated no benefit.
    3. Ingestion. In the vast majority of accidental childhood ingestions, less than 5-10 mL is actually swallowed and systemic toxicity is rare. Treatment is primarily supportive.
    4. Injection. Injections into the fingertip or hand, especially those involving a high-pressure paint gun, often require urgent surgical intervention. Consult a plastic or hand surgeon immediately.
  2. Specific drugs and antidotes
    1. There is no specific antidote for aspiration pneumonitis; antibiotics and corticosteroids are of no proven value.
    2. Specific drugs or antidotes are available for systemic toxicity of some hydrocarbons (eg, acetylcysteine for carbon tetrachloride and methylene blue for methemoglobin formers) or their solutes (eg, chelation therapy for leaded gasoline and antidotes for pesticides).
  3. Decontamination
    1. Inhalation. Move the patient to fresh air and administer oxygen.
    2. Skin and eyes. Remove contaminated clothing and wash exposed skin with water and soap. Irrigate exposed eyes with copious water or saline and perform fluorescein examination to rule out corneal injury.
    3. Ingestion. For agents with no known systemic toxicity, avoid gut decontamination because it increases the risk for aspiration. For systemic toxins, consider removal of the liquid via nasogastric tube and administration of activated charcoal. Take precautions to prevent pulmonary aspiration in obtunded patients.
    4. Injection. See Item A.4 above.
  4. Enhanced elimination. There is no known role for any of these procedures.