Hydrocarbon Toxicity

Etiology

Hydrocarbons come in four structural classes.

1. Aromatic - contain a benzene ring (most toxic) and are used in solvents and glues but also in paint and paint remover.  
2. Aliphatic - petroleum distillates found in polishes, lamp oils, and lighter fluid.
3. Halogenated - fluorinated, chlorinated, or brominated, and are used for refrigeration (freon) and as insecticides and herbicides. 
4. Terpene - found in turpentine and pine oil. Some of these hydrocarbons may be found in various mixed forms and used as an aerosol spray propellant.

Hydrocarbon's ability to cause disease is dependent on three factors.

Route of Exposure

Direct skin contact can happen, causing local skin irritation and, rarely, systemic disease. However, prolonged exposure can lead to tissue breakdown and superficial, partial thickness chemical burns. Severe, full-thickness chemical burns can lead to absorption and acute toxic systemic manifestations. Ingestion and inhalation/aspiration of hydrocarbons can also occur, which may signify disease and lead to systemic toxicity and morbidity and mortality.

The Chemical Properties

The hydrocarbon's chemical properties, including its volatility, viscosity and surface tension, affect the disease-causing potential of the hydrocarbon. Volatility refers to the rate at which the hydrocarbon can vaporize or exist as a gas. Chemicals with high volatility have an increased risk for pulmonary absorption and can lead to central nervous system (CNS) depression. Viscosity refers to the ability to resist flow. Low viscosity allows for deeper penetration into the lungs. The ability of the molecules to adhere along a liquid surface is surface tension. Low surface tension can allow compounds to spread easily over large areas.

Amount of Exposure

Hydrocarbon exposure, either in a single or cumulative dose, can determine the systemic CNS effects on the patient.

Epidemiology

Hydrocarbon exposure in the symptomatic patient will typically occur three ways. First, the unintentional ingestion of household products by children. Second, dermal or inhalational occupational exposure. Lastly, the intentional recreational inhalation of hydrocarbons by adolescents and adults. In a 2016 report, the American Association of Poison Control Centers reports hydrocarbon exposure as a top 25 most frequently involved exposure, showing 29,796 exposures with 24 deaths. The techniques used in intentional inhalation were sniffing, huffing, and bagging. Sniffing refers to inhaling directly from the container or an alternate container into which the substance was added. Huffing refers to soaking a towel or cloth with the substance and placing it over the mouth and nose to inhale it. Bagging is when the abuser places the substance in a plastic or paper bag and inhales, maximizing the concentration. Exposure can not only affect the respiratory system and CNS but also the cardiovascular system, gastrointestinal tract, and kidneys. Exposures resulting in seizure and death are usually caused by respiratory failure, arrhythmias (sudden sniffing death), or severe CNS effects.[5]

Pathophysiology

Exposure to hydrocarbons may be systemic, affecting many organ systems.[6][7][8][9]

Pulmonary effects

Inhalation or aspiration may lead to an asthma-like reactive airway syndrome as well as a chemical pneumonitis. Hydrocarbon has low surface tension and a low viscosity, therefore it penetrates deep into the lungs. This leads to a severe necrotizing pneumonia. The chemicals may also destroy surfactant, airway epithelium, alveolar septae, and pulmonary capillaries, leading to inflammation, atelectasis, and fever. Symptoms typically present as a cough and/or shortness of breath.

CNS Effects

CNS effects can be both short and long-term. In an acute setting, generalized depression may be seen with slurred speech, disorientation, headache, dizziness, ataxia, syncope, nausea, hallucination, agitation, violent behavior, and seizure activity. The exact mechanism by which hydrocarbons affect the CNS is not exactly known; however, some studies show that the hydrocarbons may affect NMDA, serotonin, nicotinic, glutamate receptors, voltage-gated ion channels, and the dopamine and GABA pathways in the brain. Some effects also may be due to the metabolism of the hydrocarbon into a neurotoxin. Prolonged exposures, such as seen in workplace exposures, also can result in neuropathy, reduction in brain size, and encephalopathy.Cardiovascular Effects

Arrhythmias may be induced following exposure. The hydrocarbons, mostly in halogenated form, may increase myocardial sensitivity to epinephrine, leading to a nonperfusing rhythm. They also may have a negative inotropic effect and dromotropic and chronotropic effects on the myocardium. The exact mechanism is unknown but appears to be due to altered function of calcium, potassium, and sodium channels in the myocardium. Chronic abusers may demonstrate murmurs associated with pulmonary hypertension such as a load S2.[10]Gastrointestinal Effects

Ingestion may cause GI tract irritation and breakdown of the epithelium, leading to nausea, vomiting, abdominal pain, and hematemesis. Some solvents may lead to hepatic toxicity. Vomiting hydrocarbons may lead to aspiration and pneumonitis.Renal Effects

Hydrocarbons (mostly due to toluene) may cause a metabolic acidosis, leading to renal tubular acidosis, urinary calculi, glomerulonephritis, hyperchloremia, and hypokalemia. Abuse may lead to both proximal and distal tubular injury.Dermatologic Effects

Skin exposure may cause mild irritation, or with prolonged exposure, chemical burns ranging from superficial to full thickness burns. Full thickness burns may lead to systemic symptoms. Skin irritation found periorally is known as “glue sniffer's rash.” Skin lesions may present as bullae or blistering. Other skin manifestations include jaundice and/or mucous membrane irritation.

History and Physical

Hydrocarbon exposure can present in many different ways. A detailed history of the incident is needed to determine the nature of the exposure. In unresponsive patients, it is necessary to question caregivers, emergency medical services, and bystanders in order to get a complete picture of the exposure. If possible, try to obtain the container or bottle that was used to determine the exact chemicals to which the patient has been exposed. A thorough history with a detailed past medical and psychological history is pertinent. A review of the patient records also may contribute to whether there is a history of abuse. The initial physical exam should focus on inhalation/aspiration. The patient may be coughing and have difficulty breathing and shortness of breath. Evaluation of vital signs may show tachycardia, tachypnea, hypoxia, and fever. A physical exam will need to be thorough and include a respiratory, cardiovascular, neurological, and dermatological exam. Wheezes may be present on the respiratory exam. The patient with CNS effects may present with euphoria, agitation, hallucinations, or confusion, which may then progress to CNS depression or seizures. This initial evaluation will help to determine the best next step. Signs of huffing, sniffing, or bagging may be present, for example, as perioral pain residue or dermatitis.

Evaluation

Diagnosis is typically deducted clinically based on history and physical.

Treatment / Management

Initial treatment should be based on presentation and should focus on possible respiratory or cardiac failure. Providers must be prepared to protect the airway when needed, using noninvasive or invasive techniques. Beta-agonists may be used for wheezing but may not be beneficial. If severe pulmonary toxicity is found, move toward intubation as patients may decompensate quickly. High positive end-expiratory pressure is generally indicated to maintain alveoli. Antibiotics may be warranted if a concomitant infection is suspected. Those presenting with cardiovascular symptoms will need aggressive, intravenous fluid hydration in cases of hypotension. Ventricular dysrhythmias should be treated with beta-blockers to prevent catecholamine surges. Catecholamines like epinephrine should be avoided given the increased sensitivity of the conducting system associated with hydrocarbons. 

Patients presenting with skin exposure will need to have their clothes removed and be decontaminated with soap and warm water. Contact precautions should be used for the safety of staff and providers. Patients are presenting agitated, or seizing should be given benzodiazepines. The patients may need to be restrained for their own protection of the safety of the staff or providers. GI symptoms generally do not need treatment or decontamination. Local poison control should be consulted before starting GI decontamination. The pneumonic CHAMP is helpful in determining serious/life-threatening ingestions.

• C - Camphor
• H - Halogenated hydrocarbons
• A - Aromatic hydrocarbons
• M - Metals
• P - Pesticides

Halogenated hydrocarbons may cause dysrhythmias and hepatotoxicity, where aromatic hydrocarbons may cause bone marrow suppression and cancer.  

Initial orders should include a chest radiograph to aid in determining the extent of lung injury. Laboratory studies are generally not helpful when assessing acute exposure, but may determine the effect on other organ systems. Useful laboratory tests may include complete blood count, oxygen saturation, serum electrolytes, liver function tests, creatinine, glucose, and urinalysis. An electrocardiograph also may be useful. Prolonged QT, ST-segment elevation, bradycardia, SVT, AV blocks, atrial fibrillation, premature ventricular contractions, and ventricular fibrillation are all possible ECG findings with exposure to hydrocarbons. The patient should be placed on a cardiac monitor for possible arrhythmias and pulse oximetry for hypoxia. Replace electrolytes as needed as hypokalemia is common in hydrocarbon exposure. The mainstay treatment for hydrocarbon toxicity is supportive care, and the majority of symptoms resolve within a short observational time. If after an observation period of 4 to 6 hours there are no signs of pulmonary or systemic toxicity, including a clear chest radiograph, the patient may be discharged home with outpatient follow up and strict return precautions. If after observation, systemic or pulmonary symptoms persist, admission and prolonged observation may be necessary. N-acetylcysteine may be considered in cases of liver toxicity associated with specific toxins such as carbon tetrachloride. Other considerations include treating toxicity of additives that may coexist with hydrocarbons.

Differential Diagnosis

History and physical determine hydrocarbon toxicity. However, if the diagnosis is unclear, consider other signs presenting in the altered patient, including sleep disorders, major depression/anxiety, substance abuse, neurodegenerative disease, neoplasms, metabolic causes, trauma, and toxic encephalopathy.