Version May 2024
INTRODUCTION — This topic will discuss the clinical toxicity, evaluation, and diagnosis of acute hydrocarbon exposure. The management of acute hydrocarbon exposure and inhalant abuse in children and adolescents are discussed separately. (See "Inhalant misuse in children and adolescents".)
EPIDEMIOLOGY — Hydrocarbon exposures account for over 28,000 cases reported annually to United States regional poison control centers and are an important cause of poisoning worldwide [1]. About 85 percent of hydrocarbon exposures are unintentional. Children five years of age and younger account for the majority of the nearly 14,000 annual pediatric exposures [1]. Although fatalities are rare, moderate effects requiring supportive care are common, especially after hydrocarbon ingestion. Hydrocarbon ingestion is the most common form of exposure in this age group, occurring in about 75 percent of cases [2]. In young children (≤5 years of age), the ingestion typically occurs as a result of exploratory behavior. Frequently, the hydrocarbon is unsecured or improperly stored in a drinking container (eg, soda or water bottle). Among adolescents and adults, hydrocarbon exposure often arises from recreational inhalant abuse (see "Inhalant misuse in children and adolescents"). Fuel siphoning is an important source of unintentional ingestion in adults [3].
PATHOPHYSIOLOGY — The specific toxicity of a hydrocarbon exposure is determined by the route, type of chemical compound, and amount of exposure (see 'Clinical toxicity' below). Although hydrocarbons are toxic to essentially all body systems, the most important toxicities occur in the lungs, brain, and heart [4-6]:
●Lungs – Pulmonary aspiration and chemical pneumonitis are major features of hydrocarbon ingestion. Based on animal studies, the primary pathologic finding is severe necrotizing pneumonia [7]. Other findings include direct destruction of the airway epithelium, alveolar septae, and pulmonary capillaries, as well as solubilization of the lipid surfactant layer. Secondary changes include atelectasis, interstitial inflammation, and hyaline membrane formation. The inflammatory response from chemical irritation generally causes temperature elevation, usually within hours of exposure. The aspiration hazard of hydrocarbon compounds is determined by three properties [4,5]:
•Viscosity – Viscosity refers to the resistance to flow through an orifice or the tendency of a compound to resist stirring. Lower viscosity facilitates deeper penetration into the tracheobronchial tree. Viscosity is the most important chemical characteristic that determines the aspiration potential for hydrocarbons.
•Surface tension – Surface tension refers to the adherence (or cohesiveness) of molecules along a liquid surface. Low surface tension allows compounds to spread or "creep" over a larger area.
•Volatility – Volatility refers to the ability to vaporize or to exist in a gaseous form. The greater the volatility, the greater the risk of pulmonary absorption and central nervous system (CNS) depression.
The aspiration hazard of hydrocarbons is inversely related to viscosity and surface tension and directly related to volatility [4-6]. Thus, hydrocarbons with decreased viscosity, low surface tension, and high volatility are more likely to be aspirated and cause pulmonary injury. The low viscosity permits greater penetration into the distal airways while the low surface tension facilitates spread over a larger area. Examples of such hydrocarbons include kerosene, gasoline, mineral spirits, mineral seal oil, turpentine, and other petroleum distillates. These compounds have high potential to cause aspiration pneumonitis but rarely cause systemic symptoms except in the setting of massive ingestion [6,8].
Aromatic hydrocarbons (eg, benzene and toluene), halogenated hydrocarbons (eg, trichloroethylene), and pine oil primarily produce toxicity through systemic absorption via the gastrointestinal tract or the lungs [6]. However, vomiting with pulmonary aspiration and chemical pneumonitis can also occur [9-11]. In addition, inhalation of high concentrations of highly volatile hydrocarbons, particularly halogenated hydrocarbons, can cause lung irritation with pulmonary edema [12-14].
●Central nervous system – CNS depression commonly accompanies exposure to many hydrocarbons and is caused by direct neuronal effects of specific agents and/or hypoxia secondary to severe lung injury.
Volatile hydrocarbons (eg, aromatic and halogenated hydrocarbons) are highly lipid soluble and are systemically absorbed via the lungs through inhalation or the gastrointestinal tract after ingestion. They rapidly diffuse throughout the body and into the CNS, where, based upon animal studies, they appear to cause CNS depression by a complex effect on a variety of neurotransmitter receptors, including the excitatory N-methyl-D-aspartate receptor and inhibitory gamma aminobutyric acid receptor [5,15,16]. The euphoria associated with inhalation of toluene and chlorinated hydrocarbons make them attractive for recreational abuse by older children and adolescents. (See "Inhalant misuse in children and adolescents", section on 'Hydrocarbons'.)
Pine oil cleaners contain polycyclic terpene hydrocarbons, isopropanol, and soaps and are absorbed via the gastrointestinal tract. They cause rapid onset of lethargy that is primarily attributable to the hydrocarbon component although, in children, isopropanol may also play a role [9-11].
CNS depression may also occur secondary to severe pulmonary injury and hypoxia caused by severe chemical pneumonitis.
●Heart – Hydrocarbons, especially halogenated and aromatic hydrocarbons, sensitize the heart to catecholamines, which can lead to malignant arrhythmias (eg, ventricular fibrillation, ventricular tachycardia, and sudden cardiac arrest). Proposed mechanisms for this effect are described separately. (See "Inhalant misuse in children and adolescents", section on 'Cardiovascular effects'.)
Other toxic effects that have been reported after acute hydrocarbon exposure include:
●Mucosal and gastrointestinal irritation (common and associated with vomiting after ingestion) [4-6]
●Hemolysis [17]
●Hepatotoxicity (primarily after occupational exposure to chlorinated hydrocarbons, such as carbon tetrachloride) [5]
●Dermal irritation and, after prolonged contact with the skin or mucosa, partial or full thickness burns [18]
COMMERCIAL PRODUCTS THAT CONTAIN HYDROCARBONS — The types of hydrocarbons and household products that may contain them are provided in the table (table 1). The structural classes of hydrocarbons include [4,5]:
●Aliphatic hydrocarbons – The aliphatic hydrocarbons consist of straight-chain compounds and include butane, propane, kerosene, and mineral seal oil. They are found in furniture polishes, lamp oil, and lighter fluid. Gasoline and naphtha contain mixtures of aliphatic hydrocarbons that also contain other substances such as xylene, toluene, benzene, naphthalene, and, when added to enhance octane, tetraethyl lead. Petroleum distillates are derived from crude oil processing and contain gasoline, naphtha, mineral spirits, kerosene, paraffin wax, and tar.
●Terpene hydrocarbons – The terpenes are cyclic hydrocarbons that include turpentine (often used as a paint thinner) and pine oil (contained in many pine-scented cleaning products).
●Aromatic hydrocarbons – Aromatic hydrocarbons are cyclic compounds containing a benzene ring (eg, benzene, toluene, and xylene). They are used primarily in solvents, glues, nail polishes, paints, and paint removers.
●Halogenated hydrocarbons – Halogenated hydrocarbons are brominated, fluorinated, or chlorinated. Chlorinated hydrocarbons (eg, methylene chloride, chloroform, carbon tetrachloride, trichloroethylene, or tetrachloroethylene) account for the most common toxic encounters with this type of hydrocarbon.
CLINICAL TOXICITY — The type of hydrocarbon and the route and amount of hydrocarbon exposure determine the severity and type of clinical toxicity as described below.
Hydrocarbon ingestion — Hydrocarbon ingestion is the most common type of exposure, with clinical toxicity determined by the chemical substance:
●Petroleum distillates, turpentine, and other aliphatic hydrocarbons – Petroleum distillates (eg, kerosene, gasoline, naphtha, and mineral spirits), turpentine, and mineral seal oil have toxicity after ingestion that largely consists of pulmonary aspiration with chemical pneumonitis. Clinical findings of toxicity include cough, vomiting, and, later in the course, tachypnea and respiratory distress [4-6]. Fever is frequently present at initial evaluation. Lethargy or coma may develop in patients with severe lung injury secondary to hypoxemia and hypercarbia.
Because hydrocarbons are irritating to mucosal membranes and have a noxious taste, unintentional hydrocarbon ingestions are usually small-volume exposures (eg, one swallow [5 to 15 mL]). Mineral seal oil, an aliphatic hydrocarbon sometimes contained in furniture polish, is an important exception; it has a sweet taste, and a large ingestion of several ounces is possible if a young child has free access to it [19]. In adults, accidental ingestion during fuel siphoning is typically a small-volume exposure [3].
Intentional aliphatic hydrocarbon ingestions in adolescents and adults frequently consist of larger volumes, although coughing and gagging often limit the total amount of chemical that can be ingested.
●Pine oil – Pine oil is frequently combined with isopropanol and soap in household cleaners [11]. After ingestion, it causes rapid onset of lethargy and coma. Pulmonary aspiration with chemical pneumonitis has also been described but is less common than with petroleum distillates, turpentine, and aliphatic hydrocarbons.
●Aromatic or halogenated hydrocarbons – Ingestion of aromatic hydrocarbons (eg, benzene, xylene, or styrene) or halogenated hydrocarbons (eg, trichloroethylene or trichloroethane) commonly causes dizziness, euphoria, headache, blurry vision, muscular weakness, numbness, and muscular weakness soon after ingestion [5]. Subsequently, the patient may develop slurred speech, ataxia, diplopia, lethargy, and/or coma [4-6]. These agents also sensitize the myocardium to endogenous and administered catecholamines (eg, epinephrine) with the potential for life-threatening ventricular arrhythmias.
●Toxicity from co-ingestants – Many commercial preparations use petroleum distillates as a solvent with ingredients that can cause severe toxicity such as organophosphate pesticides, organotin compounds, and heavy metals (eg, tetraethyl lead in gasoline). Ingestion can produce the typical systemic toxicity associated with these exposures and/or pulmonary aspiration with chemical pneumonitis or lipoid pneumonia [20].
The clinical manifestations and management of organophosphate poisoning are described in detail separately. (See "Organophosphate and carbamate poisoning".)
●High-viscosity hydrocarbons – High-viscosity hydrocarbons (eg, tar, mineral oil, petroleum jelly, or motor oil) typically do not cause significant harm after ingestion unless gross aspiration occurs [5]. Lipoid pneumonia has been described after small-volume aspiration of paraffin oil in fire-breather entertainers [21].
Hydrocarbon inhalation — Hydrocarbon inhalation is most frequently due to intentional recreational abuse (see "Inhalant misuse in children and adolescents", section on 'Hydrocarbons'):
●Asphyxiant hydrocarbon gases – Gases such as methane, ethane, propane, and butane cause asphyxia by replacing alveolar gas and are readily absorbed through the lungs and into the circulatory system. After absorption, they also have the potential to cause central nervous system (CNS) depression, seizures, and ventricular arrhythmias.
●Aromatic or halogenated hydrocarbons – Inhalation of aromatic or halogenated hydrocarbons causes neurotoxicity and sensitization to catecholamine-induced cardiac arrhythmias that is similar to the toxicity seen after ingestion of these agents. The clinical effects of inhalation of these agents are discussed in detail separately.
Dermal exposure — Brief and small-volume dermal hydrocarbon exposure to liquid hydrocarbons is associated with localized redness due to chemical irritation. Hydrocarbons cause cell membrane injury and lipid dissolution, which may result in skin necrosis with prolonged exposure. Most burns are superficial or partial thickness. However prolonged exposure may cause full thickness burns. Once skin damage has occurred, hydrocarbons are readily absorbed and, depending upon the specific chemical compound, can rarely cause systemic toxicity, including severe pulmonary, neurologic, cardiac, hepatic, and/or renal injury. (See 'Pathophysiology' above and "Topical chemical burns: Initial evaluation and management", section on 'Hydrocarbons'.)
Dermal exposure to heated asphalt or tar during paving causes thermal burns. (See "Topical chemical burns: Initial evaluation and management", section on 'Tar and asphalt'.)
Parenteral injection — Parenteral injection of hydrocarbons is a rare form of unintentional injury occurring in painters using airless paint guns or intentional exposure seen in suicidal patients or malingering prisoners [22-24]. Soft tissue or intravenous (IV) injection causes swelling, redness, and blistering of the skin with necrosis of the underlying tissues. Within one to two days, thrombophlebitis (after IV injection) [22], soft tissue phlegmon, sterile abscess [23,25], compartment syndrome [26], and/or rhabdomyolysis [27] can develop.
IV injection of gasoline has been associated with the acute onset of severe hemorrhagic pneumonitis and pulmonary edema secondary to capillary breakdown [22]. Patients may rapidly progress to severe hypoxemia, respiratory failure, and multisystem organ failure.
STABILIZATION — Prior to evaluation, patients should undergo rapid assessment of airway, breathing, circulation, and disability and appropriate resuscitation, as needed. (See "Acute hydrocarbon exposure: Management", section on 'Stabilization'.)
EVALUATION
History — Essential history after acute hydrocarbon exposure includes:
●Which hydrocarbon? – Identification of the hydrocarbon compound provides key information regarding the expected toxic effects (see 'Pathophysiology' above and 'Clinical toxicity' above). Household products and the typical hydrocarbons they contain are provided in the table (table 1). Hydrocarbons are often listed as "petroleum distillates" on product labels. In adults with acute occupational hydrocarbon exposures in the United States, detailed chemical information may be available from the Safety Data Sheet (SDS) or, in other countries, its equivalent. Regional poison centers are available to provide detailed ingredients by product brand name and to provide other assistance with identification of the toxic agent (in the United States, call 1-800-222-1222). Contact information for poison centers around the world is provided separately. (See 'Additional resources' below.)
In some instances, the hydrocarbon has been inappropriately stored in an unlabeled plastic or glass container located in a basement or garage, and the composition unknown. The clinician may sometimes identify the compound or class of hydrocarbon based upon its use. For example, hydrocarbons used for painting include turpentine, xylene, mineral spirits, and other petroleum distillates while gasoline, citronella oil, naphtha, and kerosene are common hydrocarbon fuels kept at home.
●What kind of exposure? – The clinician should identify the amount and primary route of exposure: ingestion, inhalation, dermal, or injection (rare), which informs the likely type and severity of toxicity. (See 'Clinical toxicity' above.)
Patients with inhalational exposures should be questioned regarding recreational inhalant abuse to guide evaluation for chronic toxicity related to specific chemical compounds (table 2). (See "Inhalant misuse in children and adolescents".)
Intentional and industrial exposures are often high-volume exposures of highly concentrated agents that are more likely to result in life-threatening toxicity.
●What symptoms are present? – Most exposures consist of exploratory ingestions of small amounts of aliphatic or terpene hydrocarbons (eg, kerosene, mineral spirits, gasoline, or turpentine) by young children at home or small-volume accidental ingestions in adults [1,5]. Many of these patients have a history of choking, gagging, or vomiting shortly after ingestion but are initially asymptomatic during emergency evaluation. Patients with respiratory distress and/or hypoxemia soon after ingestion often progress rapidly to respiratory failure. (See 'Hydrocarbon ingestion' above.)
Early onset of headache, dizziness, nausea, euphoria, and lethargy is characteristic of exposure to aromatic and halogenated hydrocarbons or pine oil, or asphyxial exposure to aliphatic or terpene hydrocarbons [5]. (See 'Clinical toxicity' above.)
Physical examination — Physical examination findings of hydrocarbon exposure include:
●Odors – Characteristic odors can occasionally help identify the presence of hydrocarbon exposure when history of exposure is lacking or the ingestant is unknown [28]:
•Petroleum distillate odor (kerosene, mineral spirits, naphtha, turpentine, or gasoline)
•Pine scent (pine oil cleaners)
•Sweet solvent odor (halogenated hydrocarbons)
●Vital signs – Patients may have or develop tachypnea, tachycardia, and decreased oxygen saturation by pulse oximetry. Fever commonly occurs soon after aliphatic hydrocarbon ingestion and may range from 38 to 40ºC (100.4 to 104°F) [28-30]. Thus, a high fever does not indicate the presence of infection at initial presentation. Persistence of fever beyond 48 hours suggests bacterial superinfection [29].
●Respiratory – Pulmonary manifestations secondary to aspiration generally occur within 30 minutes, although their onset may be delayed for 12 to 24 hours [28-30]. Immediate signs of aspiration include coughing, choking, gagging, and vomiting.
Respiratory examination findings vary with the degree of pulmonary injury and may include tachypnea, dyspnea, cyanosis, wheezing, diminished resonance on percussion, suppressed or tubular breath sounds, rales, nasal flaring, and/or grunting respirations [5,28,30].
Displacement of alveolar gas by vaporized hydrocarbon may aggravate hypoxemia caused by inflammation and edema. However, normal initial lung examination does not exclude hydrocarbon aspiration [5,28,30].
As pulmonary toxicity progresses over the first 24 to 48 hours, clinical findings may include persistent hypoxemia caused by asphyxia, necrotizing chemical pneumonitis, lipoid pneumonia, and hemorrhagic pulmonary edema, which can quickly progress to shock and respiratory arrest [31,32]. Pneumothorax, subcutaneous emphysema of the chest wall, and pleural effusion, including empyema, may also occur. Secondary bacterial or viral infection may exacerbate the chemical pneumonitis. Pneumatoceles rarely develop in areas of extensive consolidation one to two weeks after ingestion [33,34].
●Central nervous system – Hydrocarbon ingestion or inhalation of aromatic or halogenated hydrocarbons may rapidly cause direct central nervous system (CNS) effects, including somnolence, headache, ataxia, dizziness, blurred vision, weakness, fatigue, lethargy, stupor, seizures, and coma, depending on the amount ingested [5,6,30].
In addition, hypoxia caused by hydrocarbon aspiration may cause secondary CNS toxicity, including drowsiness, tremors, or seizures [35]. (See "Acute toxic-metabolic encephalopathy in children".)
●Cardiovascular – Cardiac arrhythmias and myocardial dysfunction may occur after hydrocarbon ingestion or inhalation. Solvent hydrocarbons (eg, halogenated hydrocarbons), in particular, are known to produce fatal ventricular arrhythmias because they sensitize the myocardium to endogenous and exogenous catecholamines ("sudden sniffing death"). (See "Inhalant misuse in children and adolescents", section on 'Cardiovascular effects'.)
●Gastrointestinal – Ingestion of hydrocarbons causes contact irritation of the pharynx, esophagus, stomach, and small intestine, with edema and mucosal ulceration. Orogastric and intestinal irritation may be associated with nausea, vomiting, and hematemesis [4,5,30]. These effects usually are mild and rarely require treatment.
Halogenated hydrocarbons may cause hepatic and/or renal tubular necrosis one to two days after ingestion. (See "Inhalant misuse in children and adolescents", section on 'Other effects'.)
●Skin – Patients with prolonged skin exposure to hydrocarbons or heated tar should be assessed for the presence of chemical or thermal burns. (See "Assessment and classification of burn injury" and "Topical chemical burns: Initial evaluation and management".)
Ancillary studies
Symptomatic — During stabilization, all symptomatic patients and, regardless of symptoms, those who have ingested aromatic or halogenated hydrocarbons should undergo the following studies:
●Electrocardiogram to evaluate for prolonged QT intervals and continuous monitoring for early detection of ventricular arrhythmias
●Chest radiograph to identify chemical pneumonitis (see 'Diagnosis' below)
●Arterial blood gas or venous blood gas with pulse oximetry
●Complete blood count
●Serum glucose
●Serum electrolytes
●Urinalysis
Because of the risk for liver and kidney injury, patients exposed to halogenated hydrocarbons, regardless of symptoms, should also undergo measurement of:
●Aspartate aminotransferase (AST)
●Alanine aminotransferase (ALT)
●Blood urea nitrogen
●Serum creatinine
The initial blood gas and pulse oximetry findings after hydrocarbon aspiration often reveal a mild respiratory alkalosis with hypoxemia. If hypoxemia is not corrected, the patient will later develop a metabolic acidosis.
Leukocytosis occurs early in the clinical course of hydrocarbon aspiration unrelated to pneumonitis and may last as long as one week [36]. Hemolysis, hemoglobinuria, and consumptive coagulopathy may occur rarely after large ingestions [5,37].
Ancillary studies for patients with co-ingestion of organophosphate or leaded gasoline are provided separately. (See "Organophosphate and carbamate poisoning" and "Childhood lead poisoning: Clinical manifestations and diagnosis" and "Lead exposure, toxicity, and poisoning in adults".)
Asymptomatic — Asymptomatic patients who ingest hydrocarbons should receive a chest radiograph four to six hours after exposure to assess for chemical pneumonitis (algorithm 1). (See 'Diagnosis' below.)
DIAGNOSIS — Acute hydrocarbon exposure is a clinical diagnosis made based upon history and physical findings.
Chemical pneumonitis caused by hydrocarbon aspiration is determined by chest radiograph. In patients who ultimately manifest pulmonary aspiration after hydrocarbon ingestion, the radiographic findings of hydrocarbon aspiration are evident in most individuals within six hours of exposure [38]. In patients who are initially asymptomatic on evaluation, radiographic findings frequently precede the development of physical findings.
Initial radiographic findings of pulmonary aspiration/chemical pneumonitis consist of multiple, small, patchy densities with ill-defined margins (image 1). The lesions become larger and coalesce as the injury progresses [4,32]. In some cases, the radiographic findings may be minimal at a few hours and then rapidly progress to extensive infiltrates. Emphysema or pneumothorax may develop.
Radiographic abnormalities typically peak by 48 hours after aspiration [32]. The resolution of radiographic changes is gradual and lags behind clinical improvement. Pneumatoceles may develop within one to two weeks after aspiration despite clinical improvement.
Although exposure to some hydrocarbons may be confirmed by detection of urinary metabolites (eg, trichloroethanol after chlorinated hydrocarbon exposure or hippuric acid after toluene exposure) or directly measured in the blood (eg, toluene), these laboratory studies are not rapidly available and do not change management priorities.
DIFFERENTIAL DIAGNOSIS — The clinician should consider the following alternative diagnoses when hydrocarbon exposure is not certain or is associated with findings suggestive of other poisonings:
●Bronchopneumonia – Patients with bronchopneumonia typically have fever and tachypnea and may appear similar to patients with hydrocarbon aspiration. However, patients with pneumonia do not display a characteristic petroleum distillate odor and do not have findings of chemical pneumonitis on chest radiograph. (See 'Evaluation' above and 'Asymptomatic' above.)
●Salicylate overdose – Patients who have ingested salicylates may have fever and tachypnea with altered mental status but typically do not have abnormal chest radiographs soon after ingestion. Some clinicians may think the fruity odor of ketoacidosis is similar to that caused by halogenated hydrocarbon ingestion.
●Other toxins – Any toxin that produces metabolic acidosis (eg, iron, metformin, isoniazid, toxic alcohol) or cellular hypoxia (eg, carbon monoxide, cyanide) may cause tachypnea. Blood gas measurement will often differentiate these toxins from hydrocarbon exposure with its typical respiratory alkalosis, and in more serious cases, arterial blood hypoxemia.
●Diabetic ketoacidosis – Diabetic ketoacidosis commonly causes tachypnea, fruity breath odor, and metabolic acidosis. The presence of hyperglycemia, glycosuria, and ketonuria distinguishes this condition from hydrocarbon ingestion.
Hydrocarbons are sometimes used as solvents for other dangerous toxins (eg, organophosphates, organotin compounds, and heavy metals). Thus, the clinician should seek to identify the exact compound that was ingested when managing a patient with hydrocarbon poisoning to ensure timely recognition and treatment of all possible toxic agents.
ADDITIONAL RESOURCES
Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)
Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General measures for acute poisoning treatment" and "Society guideline links: Treatment of acute poisoning caused by specific agents other than drugs of abuse".)
SUMMARY AND RECOMMENDATIONS
●The type of hydrocarbon and the route and amount of hydrocarbon exposure determines the severity and type of clinical toxicity. Ingestion of petroleum distillates, turpentine, and other aliphatic hydrocarbons is most common (See 'Clinical toxicity' above and 'Epidemiology' above.)
●Household products and the typical hydrocarbons they contain are provided in the table (table 1). Hydrocarbons are often listed as "petroleum distillates" on product labels. In adults with acute occupational hydrocarbon exposures in the United States, detailed chemical information may be available from the Safety Data Sheet (SDS) or, in other countries, its equivalent. (See 'History' above.)
●If the hydrocarbon has been inappropriately stored in an unlabeled plastic or glass container located in a basement or garage, and the composition unknown, the clinician may sometimes identify the compound or class of hydrocarbon based upon its use.
●Hydrocarbons are sometimes used as solvents for other dangerous toxins (eg, organophosphates). Thus, the clinician should seek to identify the exact compound that was ingested when managing a patient with hydrocarbon poisoning to ensure timely recognition and treatment of all possible toxic agents. (See 'Commercial products that contain hydrocarbons' above and 'Clinical toxicity' above and 'History' above.)
●Patients with inhalational exposures should be questioned regarding recreational inhalant abuse to guide evaluation for chronic toxicity related to specific chemical compounds (table 2).
●Chemical pneumonitis is the most concerning toxicity for exploratory ingestions of small amounts of aliphatic or terpene hydrocarbons (eg, kerosene, mineral spirits, gasoline, or turpentine) by young children at home or small-volume accidental ingestions in adults. These patients often present with a history of choking, gagging, or vomiting shortly after ingestion but are initially asymptomatic during emergency evaluation. Patients with respiratory distress and/or hypoxemia soon after ingestion often progress rapidly to respiratory failure. (See 'Physical examination' above and 'Hydrocarbon ingestion' above.)
●Early onset of headache, dizziness, nausea, euphoria, and lethargy is characteristic of exposure to aromatic and halogenated hydrocarbons or pine oil, or asphyxial exposure to aliphatic or terpene hydrocarbons. (See 'Physical examination' above and 'Hydrocarbon ingestion' above.)
●Cardiac arrhythmias and myocardial dysfunction may occur after hydrocarbon ingestion or inhalation. Solvent hydrocarbons (eg, halogenated hydrocarbons), in particular, are known to produce fatal ventricular arrhythmias because they sensitize the myocardium to endogenous and exogenous catecholamines ("sudden sniffing death"). (See 'Physical examination' above and "Inhalant misuse in children and adolescents", section on 'Cardiovascular effects'.)
●During stabilization, symptomatic patients and those who have ingested aromatic or halogenated hydrocarbons should undergo the following studies:
•Electrocardiogram
•Chest radiograph
•Arterial blood gas or venous blood gas with pulse oximetry
•Complete blood count
•Serum glucose
•Serum electrolytes
•Urinalysis
Because of the risk for liver and kidney injury, patients exposed to halogenated hydrocarbons, regardless of symptoms, should also undergo measurement of:
•Aspartate aminotransferase (AST)
•Alanine aminotransferase (ALT)
•Blood urea nitrogen
•Serum creatinine
●Asymptomatic patients who ingest hydrocarbons should receive a chest radiograph at four to six hours after exposure to assess for chemical pneumonitis (algorithm 1).
●Acute hydrocarbon exposure is a clinical diagnosis made based upon history and physical findings. Chemical pneumonitis caused by hydrocarbon aspiration (image 1) is determined by chest radiograph. Although exposure to some hydrocarbons may be confirmed by detection of urinary metabolites or directly measured in the blood, these laboratory studies are not rapidly available and do not change management priorities. (See 'Diagnosis' above.)
●Regional poison centers are available to provide detailed ingredients by product brand name and to provide other assistance with identification of the toxic agent (in the United States, call 1-800-222-1222). Contact information for poison centers around the world is provided separately. (See 'Additional resources' above.)
●The management of acute hydrocarbon exposure is discussed separately. (See "Acute hydrocarbon exposure: Management".)
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