Epidemiology

Adolescents 12 to 17 years old comprise the most likely age group to abuse volatile substances; U.S. eighth grade students have a 15% lifetime prevalence of this abuse. Volatile substance use should be suspected in this population. The habitual abuser of volatile substances may have paint stains or other telltale findings on the clothing or skin (see “Presenting Signs and Symptoms”).

Many hydrocarbons have a characteristic odor similar to that of gasoline or lighter fluid. Solvents containing aldehyde or ketone groups smell sweet or fruity. Essential oils are characteristically pungent or aromatic. In acutely intoxicated patients, these odors are rarely missed.

Pathophysiology

A hydrocarbon is an organic compound composed mainly of carbon and hydrogen atoms. In modern society, these compounds are virtually everywhere. Hydrocarbons are so common in our society that exposures—even illnesses related to exposures—are not usually documented. Hydrocarbons derive most commonly from distillation and processing of petroleum, but many derive from plants (pine oil, essential oils), animal fats, and natural gas. An example is gasoline, which is a mixture of alkanes, alkenes, naphthenes, and aromatic hydrocarbons. Commercial gasoline contains hundreds—up to 1500—individual chemical species.

The term solvent is often used to refer to an organic solvent—typically a hydrocarbon mixture—that is used to dissolve other substances. Occupational literature often uses the terms solvent and hydrocarbon interchangeably. Organic solvents are common in industry, and workers may suffer dermal or inhalational exposures. Children may suffer unintentional hydrocarbon exposures, often ingestions, with a risk of pulmonary hydrocarbon aspiration. More concerning is a trend toward greater intentional abuse of volatile hydrocarbon inhalants by adolescents and young adults. This form of substance abuse, often termed volatile substance abuse (VSA), is a growing problem worldwide.

One can predict many of the physical properties of hydrocarbons by knowing the molecular shape and size (number of carbon atoms in the molecule’s chain). The nonpolar, covalent bonds between carbon-carbon and carbon-hydrogen atoms produce dispersion forces, which result in the attraction between hydrocarbon molecules. These same forces repel polar molecules (e.g., water) and make hydrocarbons generally hydrophobic. Once dissolved in aqueous solution, nonpolar hydrocarbons can transit rapidly through lipid membranes, including cell membranes and the blood-brain barrier. Small, light, aliphatic hydrocarbons with up to 4 carbons are gases at room temperature; those with 5 to 19 carbon molecules are liquids; and longer molecules form solids or paraffins. Branching in the molecule destabilizes intermolecular forces, so less energy is required to separate molecules. This makes it easier for a molecule to leave the liquid phase and enter the vapor phase (to volatilize). Therefore, for a given molecular size, more branching means a lower boiling point, and the compound is typically more volatile. Gaseous or volatilized hydrocarbons are likely to cause toxicity by inhalation.

Lipid-soluble solvents (aromatic, aliphatic, or halogenated hydrocarbons) are more likely than water-soluble hydrocarbons (alcohols, ketones, or esters) to cause acute central nervous system (CNS) effects. Clinicians are familiar with these effects from experience with inhaled anesthetic agents, which cause CNS sedation similar to that resulting from other hydrocarbons. The Meyer-Overton hypothesis suggests that inhaled anesthetics dissolve into some critical lipid compartment of the CNS and cause generalized inhibition of neuronal transmission. This mechanism is probably oversimplified, but it helps to explain partly the nonspecific inhibition of neuronal transmission that hydrocarbons produce in the CNS. Specific membrane interactions may also contribute to this process,¹ and several receptor-mediated interactions are known to occur.

Specific physical properties of ingested hydrocarbons help to predict the risk of pulmonary aspiration (Table 152.1). In particular, viscosity, surface tension, and volatility determine aspiration potential and the contribution to pulmonary toxicity.² Viscosity is a measure of a fluid’s resistance to flow, commonly described in units of Saybolt universal seconds (SUS). This property is not the same as the fluid’s density; in fact, these two properties correlate poorly.

Low-viscosity substances (less than 60 SUS), such as turpentine, gasoline, or naphtha, have higher tendency for aspiration in animal models. A lower viscosity value predicts a higher risk. The U.S. Consumer Products Safety Commission now requires child-resistant packaging for products that contain 10% or more hydrocarbons and have a measured viscosity less than 100 SUS.

Surface tension indirectly measures dispersion forces between molecules in a fluid, but it also characterizes the interaction with the surface that the fluid contacts. This property can be quantified on a modified Wilhelmy balance, which measures adherence of the fluid along a surface (“the inability to creep”). In theory, the lower the surface tension is, the higher is the aspiration risk.² A lower surface tension value predicts a higher risk.

Volatility is the tendency for a liquid to enter the gas phase. Hydrocarbons that are highly volatile have a high vapor pressure and so tend to vaporize, enter the lungs, displace oxygen, and cause hypoxia. A higher volatility value predicts a higher risk.

Mechanisms of Toxicity

Although organ-specific pathophysiology is often unique to individual agents, much of the toxicity of hydrocarbons results from their ability to dissolve fats or, similarly, to diffuse across hydrophobic barriers intended to protect anatomic structures (e.g., lipid bilayers, myelin). Hydrocarbon solvents cause irritation of skin and mucous membranes. Recurrent or prolonged contact results in “defatting” of skin, dissolving lipid components, and disrupting the normal architecture of the stratum corneum.³

Most hydrocarbons are flammable or combustible. Under appropriate conditions, most hydrocarbons can explode. The widespread availability of hydrocarbons and their use as organic solvents account for the frequent finding of stored quantities of these solvents in clandestine illicit drug laboratories and other places. Storage and use of these flammable agents appreciably contribute to the health hazards of these facilities.

Presenting Signs and Symptoms

The route of exposure considerably influences the organs affected. The principal organ systems affected by hydrocarbons are the skin (from dermal contact), the GI system (when ingested), the CNS, and the lungs. Some classes of hydrocarbons are cardiotoxic. Certain agents may cause organ-specific toxicity to cranial or peripheral nerves, the liver, or the kidneys. Typical presenting symptoms can be found in Table 152.2.

Table 152.2 Symptoms Associated with Hydrocarbon Exposure

The intentional inhalation in VSA can be challenging to diagnose because affected patients frequently withhold relevant history. Several common inhalational techniques have been identified. Sniffing involves inhaling vapor from an open container. Huffing involves placing a volatile hydrocarbon in a rag or cloth, then covering the nose and mouth with the cloth or rag and inhaling the agent through it. Bagging implies placing the substance inside a plastic (or other) bag and then putting the bag over the face to inhale hydrocarbon vapor.

Respiratory findings are uncommon after inhalation, but the patient may manifest tachypnea or cyanosis or may suffer sudden cardiac arrest. Classically, cardiac arrest occurs after a sudden fright or physical exertion (e.g., running to avoid an authority), with a sudden catecholamine surge and a sensitized heart. This phenomenon is termed the sudden sniffing death syndrome.

Cutaneous findings may be the chief complaints, with dermal exposure to solvents from work or hobbies. Drying, cracking, pitting, or eczematous lesions occur in up to 9% of workers who are repeatedly exposed. Allergic reactions are uncommon but may be seen with exposure to certain essential oils or to pine oil. Nonspecific skin irritation is the most common finding, and it may progress to blistering or contact dermatitis with recurrent, prolonged, or protracted VSA. With continued or recurring exposure, the skin changes may even progress to partial- or even full-thickness chemical burns.⁴ When the dermatitis involves the skin surrounding the nose and mouth, it has been dubbed “huffer’s rash” (Fig. 152.1). Abusers of volatile solvents may have telltale paint, shoeshine, or solvent stains on clothes or skin. Nonfreezing cold injury (frostbite) may occur on or about the face because of intentional release of liquid hydrocarbon propellant, which cools as it suddenly exits its container (Fig. 152.2).

Fig. 152.1 A and B, “Huffer’s rash” resulting from repeated “sniffing” of liquid propane.

Both contact dermatitis and nonfreezing cold injury likely contribute to the skin findings in this characteristic distribution.

(Courtesy of E. O’Connell, MD.)

Fig. 152.2 Nonfreezing cold injury resulting from intentional release and attempted inhalation of halocarbon propellant.

Hydrocarbons cause CNS depression. Transient excitation may initially occur after inhalation or ingestion, but early sedation is more common. Initial findings include behavioral changes, impaired sense of smell, impaired concentration, and mildly unsteady movements or gait. As with alcohol or other sedatives, mild exposures produce euphoria, likely contributing to abuse potential. Further acute exposure leads to slurred speech and progressive incoordination. Physical signs are nystagmus, tremor, spasticity with hyperreflexia, abnormal plantar reflexes, hearing loss, impaired vision, and a broad-based, staggering gait. Pain inhibition explains why hydrocarbons were chosen as general anesthetic agents. Stupor, lethargy, or obtundation is seen in overdose. Coma and seizures occur in up to 3% of cases.¹⁴

Chronic CNS dysfunction occurs in recurrent abusers of volatile substances, and reports include optic neuropathy, sensorineural hearing loss, equilibrium disorders, ataxia, and cognitive deficits. Occupational solvent exposures are also associated with persistent CNS abnormalities, although the exposures and the clinical findings are typically less impressive than those in habitual VSA. Most published reports involve exposure to toluene, a very common workplace and household hydrocarbon solvent. Neurologic deficits are tremor, ataxia, impaired fine-motor skills, and mild cognitive defects. Long-term occupational exposures are associated with a clinical syndrome consisting of fatigue, poor short-term memory, attention difficulties, visuospatial abnormalities, personality changes, and mood disorder. Clinically, this presentation has been dubbed “the painter’s syndrome.”

Abdominal pain and vomiting are common, and diarrhea is likely after ingestion, particularly of insoluble hydrocarbons (mineral oil, paraffins). Vomiting increases the risk of pulmonary aspiration.

A typical case in the emergency department (ED) involves a young child who is suspected to have unintentionally ingested a hydrocarbon mixture. Infrequently, a parent may have witnessed the ingestion; more typically, the situation was discovered shortly thereafter. The caregiver often identifies the specific agent. A parent may report that the child was coughing, gagging, or vomiting, or that he or she noticed an odor of the suspected hydrocarbon. If the ingestion was unwitnessed, it may be difficult to quantify the amount ingested, but a “worst case scenario” can often be ascertained. A history of coughing, choking, or vomiting should heighten the ED’s suspicion of pulmonary aspiration. Respiratory findings include coughing, choking, gagging, grunting, tachypnea, retractions, fever, cyanosis or poor coloration, and abnormal sounds on chest auscultation. Mental status depression is common in patients with larger ingestions but may not occur for 30 to 60 minutes after ingestion. In a prospective, multicenter study of 760 pediatric kerosene ingestions, no association was found between the age of the patient and the amount ingested. The risks of pulmonary toxicity and of CNS depression were significantly higher in children who ingested more than 30 mL of kerosene (according to history). The incidence of pulmonary aspiration was higher in children who vomited after ingestion.¹⁵

Differential Diagnosis and Medical Decision Making

The differential diagnosis in hydrocarbon exposure is usually limited because the history often elucidates the exposure. Some possible differential diagnoses include adult respiratory distress syndrome, toxic alcohol exposure, barbiturate or benzodiazepine toxicity, and toluene exposure.

The diagnostic evaluation of a patient with hydrocarbon exposure depends heavily on the known patterns of toxicity associated with specific hydrocarbon agents and the route of exposure. It is more crucial to obtain and verify the history, with particular attention to identifying the specific type and composition of the agent or agents involved. The route of exposure should direct the clinician to the anticipated target organ or organs, which guide testing.

Renal function, serum electrolyte levels, and acid-base status should be evaluated in all patients with a history of chronic or recurrent toluene exposure. Liver transaminases and bilirubin should be assayed in patients with significant exposure to halocarbons or to benzene. Electrocardiographic monitoring and a formal 12-lead electrocardiogram are indicated when a patients has significant exposure to heart-sensitizing hydrocarbon agents. Head computed tomography and magnetic resonance imaging are valuable to assess the extent of brain involvement in chronic exposures. Pulse oximetry or arterial blood gas testing helps assess the severity of pulmonary injury. Carboxyhemoglobin or methemoglobin measurements are indicated for exposures involving specific agents (see “Other Effects”).

Early chest radiography may be indicated for severely symptomatic patients, to gauge the extent of pulmonary injury and guide the inpatient placement decision. Radiographic evidence of pneumonitis may develop as early as 15 minutes or as late as 24 hours after hydrocarbon aspiration. Ninety percent of patients who have radiographic abnormalities do so within 4 hours.¹⁶ After the initial episode of coughing, gagging, or choking, most patients with persistent respiratory signs and symptoms have pneumonitis and radiographic changes. Typical findings in hydrocarbon pneumonitis are audible abnormalities on chest auscultation, fever, leukocytosis, and abnormalities on chest radiograph (Fig. 152.3). These findings do not differ clinically from those of community-acquired pneumonia. Only the history differentiates the two entities. The elevated temperature initially noted in hydrocarbon aspiration often spikes at 8 to 12 hours, then declines over several days, unless bacterial superinfection intervenes. For an asymptomatic patient with hydrocarbon ingestion, however, early radiography does not help predict aspiration pneumonitis, and it is not cost-effective.

Fig. 152.3 Aspiration pneumonitis in a child who ingested a hydrocarbon mixture.

Note the early consolidation in the right upper lobe. Although 75% of cases demonstrate right-sided findings, upper lobe involvement is not common.

Results of bioassays and serum hydrocarbon levels are rarely available to the emergency physician and have little to no value in management of hydrocarbon exposure. These measurements are available through reference laboratories for occupational monitoring or to document exposure in forensic cases.

Treatment

Decontamination

An algorithm for the treatment of hydrocarbon exposure is shown in Figure 152.4. The first priority in managing toxicity is to protect rescuers. Personal protection is paramount at each level of health care delivery. Second, the exposure should be removed from the patient, and the patient should be removed from the exposure. Contaminated clothing and external contamination must be removed before the patient enters any patient care or trafficked area. For most hydrocarbons, soap and water are all that are required for decontamination. Most hydrocarbons are flammable and pose a fire risk to the hospital and staff. Personal protective equipment should be worn by anyone who will touch the patient or any articles brought with the patient. Once the patient is externally decontaminated, standard precautions generally suffice in the ED.

Fig. 152.4 Treatment algorithm for hydrocarbon (HC) exposure.

ABG, arterial blood gases; Chem, chemistry; CT, computed tomography; CXR, chest radiograph; ECG, electrocardiogram; ICU, intensive care unit; IV, intravenous; LFTs, liver function tests; MRI, magnetic resonance imaging; PEEP, positive end-expiratory pressure.

Gastric emptying may be useful when the hydrocarbon is extremely toxic (e.g., carbon tetrachloride), when a large volume of hydrocarbon is ingested (more than 30 mL), or when severe toxicity is predicted (Box 152.1). If gastric lavage is performed, a small-bore (not large-bore) nasogastric tube should be used, to reduce the risk of vomiting and aspiration. Activated charcoal has little ability to reduce GI absorption of hydrocarbons and may cause gastric distention and vomiting. Any role for activated charcoal in isolated hydrocarbon ingestion is limited, at best.

Box 152.1 Mnemonic for Potent Hydrocarbon Toxicants: “CHAMP”

The clinician should consider decontamination/gastric emptying when these agents are ingested:

Camphor

Halogenated hydrocarbons

Aromatic

Metal-containing hydrocarbons

Pesticides

Most hydrocarbons cannot be removed by dialysis, but toxic agents that are water-soluble, small, highly polar molecules can be removed by dialysis. Examples are small alcohols and polyols (e.g., methanol, ethylene glycol). Small ketones (e.g., acetone) are also dialyzable. Chloral hydrate can be successfully removed by hemodialysis. Peritoneal dialysis has been employed to reduce the toxicity of both dichloroethane and trichloroethylene. Unfortunately, many hydrocarbon molecules are too large to be dialyzed. Most are lipophilic, so they dissolve into fat stores (with greater volume of distribution), thus reducing their availability in the central compartment.

Extracorporeal membrane oxygenation can successfully temporize the course of severe pulmonary toxicity. This technique is considered invasive, is not widely available, and requires special expertise. Use of extracorporeal membrane oxygenation is generally reserved for severe cases of hydrocarbon toxicity for which other available modalities have failed to achieve adequate oxygenation.

Follow-Up, Next Steps of Care, and Patient Education

Patients who demonstrate clinical evidence of toxicity, and those who are suicidal or intend self-harm, should be hospitalized.

Patients who have been observed for 6 hours after an ingestion and who demonstrate no abnormal pulmonary findings, have adequate oxygenation, are not tachypneic, and have normal chest radiography findings have a good prognosis with a very low risk of subsequent deterioration.¹⁹ These patients can be safely discharged. Care may be individualized for asymptomatic patients with radiographic abnormalities, as well as for patients who have initial respiratory symptoms but who quickly become asymptomatic during medical evaluation. Reliable patients may be considered for discharge with next-day follow-up.

Special care should be given to patients who ingest, or who otherwise have significant toxicity from, agents known to cause cardiac sensitization, including gasoline. The findings of mental status depression, seizures, or arrhythmias attributed to a known cardiac sensitizer (or to an unknown hydrocarbon ingestion) warrant at least 6 hours of continuous cardiac monitoring.