Hydrocarbons are a heterogenous group of organic substances that are primarily composed of carbon and hydrogen molecules. They are quite abundant in modern society. Some of the most commonly ingested hydrocarbons include gasoline, lubricating oil, motor oil, mineral spirits, lighter fluid/naphtha, lamp oil, and kerosene.[1] Other common sources of hydrocarbons include dry cleaning solutions, paint, spot remover, rubber cement, and solvents. In addition, many volatile substances that contain hydrocarbons (eg, glue, propellants) are commonly abused for their euphoric effects.
Hydrocarbons can be classified as being aliphatic, in which the carbon moieties are arranged in a linear or branched chain, or aromatic, in which the carbon moieties are arranged in a ring. Halogenated hydrocarbons are a subgroup of aromatic hydrocarbons, in which one of the hydrogen molecules is substituted by a halogen group. The most important halogenated hydrocarbons include carbon tetrachloride, trichloroethylene, tetrachloroethylene, trichloroethane, chloroform, and methylene chloride.
The hydrocarbons can be derived from either petroleum or wood. Petroleum distillates include kerosene, gasoline, and naphtha, whereas wood-derived hydrocarbons include turpentine and pine oil. The length of the chains as well as the degree of branching determine the phase of the hydrocarbon at room temperature; most are liquid, but some short-chain hydrocarbons (eg, butane) are gas at room temperature, whereas other long-chain hydrocarbons (eg, waxes) are solid at room temperature.
Toxicity from hydrocarbon ingestion can affect many different organs, but the lungs are the most commonly affected. The chemical properties of the individual hydrocarbon determine the specific toxicity, while the dose and route of ingestion affect which organs are exposed to the toxicity. Unlike the aromatic or aliphatic hydrocarbons, the halogenated hydrocarbons tend to cause a wider range of toxicity.
The recreational use of inhaling hydrocarbons and other volatile solvents for the purposes of creating a euphoric state is becoming increasingly common. Several methods are used for this abuse, including "sniffing" (directly inhaling vapors), "huffing" (placing a hydrocarbon-saturated rag over the mouth and nose and then inhaling), or "bagging" (inhaling via a plastic bag filled with hydrocarbon vapors).
The toxicity of hydrocarbons is directly related to their physical properties, specifically the viscosity, volatility, surface tension, and chemical activity of the side chains. The viscosity is a measure of resistance to flow and is measured in Saybolt Seconds Universal (SSU). Substances with a lower viscosity (SSU < 60, eg, turpentine, gasoline, naphtha) are associated with a higher chance of aspiration. The surface tension is a cohesive force created by van der Waals forces between molecules and is a measure of a liquid's ability to "creep." Like the viscosity, the surface tension is also inversely related to aspiration risk; the lower the viscosity, the higher the risk of aspiration. The viscosity is the single most important chemical property associated with the aspiration risk.[2]
Volatility is the tendency for a liquid to change phases and become a gas. Hydrocarbons with a high volatility can vaporize and displace oxygen, which can lead to a transient state of hypoxia. Not surprisingly, the degree of volatility is directly related with the risk of aspiration. The amount of hydrocarbon ingested has not consistently been linked to the degree of aspiration and hence pulmonary toxicity.
Toxicity from hydrocarbon exposure can be thought of as different syndromes, depending on which organ system is predominately involved. Organ systems that can be affected by hydrocarbons include the pulmonary, neurologic, cardiac, gastrointestinal, hepatic, renal, dermatologic, and hematologic systems. The pulmonary system is the most commonly involved system.[3]
Pulmonary
Pulmonary complications, especially aspiration, are the most frequently reported adverse effect of hydrocarbon exposure. While most aliphatic hydrocarbons have little GI absorption, aspiration frequently occurs, either initially or in a semidelayed fashion as the patient coughs or vomits, thereby resulting in pulmonary effects. Once aspirated, the hydrocarbons can create a severe pneumonitis.
Hydrocarbon pneumonitis results from a direct toxic affect by the hydrocarbon on the lung parenchyma. The type II pneumocytes are most affected, resulting in decreased surfactant production. This decrease in surfactant, results in alveolar collapse, ventilation-perfusion mismatch, and hypoxemia. Hemorrhagic alveolitis can subsequently occur, which peaks 3 days after ingestion.[4] The end result of hydrocarbon aspiration is interstitial inflammation, intra-alveolar hemorrhage and edema, hyperemia, bronchial necrosis, and vascular necrosis. Rare pulmonary complications include the development a pneumothorax, pneumatocele, or bronchopleural fistula.[5]
Nervous system
CNS toxicity can result from several mechanisms, including direct injury to the brain or indirectly as a result of severe hypoxia or simple asphyxiation.
Many of the hydrocarbons that affect the CNS directly can make their way across the blood-brain barrier because certain hydrocarbons are highly lipophilic. In addition, for individuals who are huffing or bagging, the act of rebreathing can result in hypercarbia, which can contribute to decreased level of arousal.
Prolonged abuse of hydrocarbons can result in white matter degeneration (leukoencephalopathy) and atrophy.[6, 7] In addition, prolonged exposure to certain hydrocarbons (eg, n -hexane or methyl-n -butyl ketone [MnBK]) can result in peripheral neuropathy, blurred vision, sensory impairment, muscle atrophy, and parkinsonism.[8]
Cardiovascular
Exposure to hydrocarbons can result in cardiotoxicity.[9]
Most importantly, the myocardium becomes sensitized to the effects of catecholamines, which can predispose the patient to tachydysrhythmias, which can result in syncope or sudden death.
Gastrointestinal
Many of the hydrocarbons create a burning sensation because they are irritating to the GI mucosa. Vomiting has been reported in up to one third of all hydrocarbon exposures.
Hepatic[10]
The chlorinated hydrocarbons, in particular carbon tetrachloride, are hepatotoxic. Usually, the hepatotoxicity results after the hydrocarbon undergoes phase I metabolism, thereby inducing free radical formation. These free radicals subsequently bond with hepatic macromolecules and ultimately cause lipid peroxidation. This metabolite creates a covalent bond with the hepatic macromolecules, thereby initiating lipid peroxidation.
The common histopathologic pattern is centrilobular (zone III) necrosis.
Liver function test results can be abnormal within 24 hours after ingestion, and clinically apparent jaundice can occur within 48-96 hours.
Methylene chloride, a hydrocarbon commonly found in paint remover, is metabolized via the P450 mixed function oxidase system in the liver to carbon monoxide (CO). Unlike other cases of CO exposure, with methylene chloride, CO formation can continue for a prolonged period of time.
Renal
Chronic exposure to toluene, an aromatic hydrocarbon, can result in a distal renal tubular acidosis and present with an anion gap acidosis (see the Anion Gap calculator). A patient may have chronic exposure either via an occupational environment or by repeated recreational inhalation.
Hematologic
Prolonged exposure to certain aromatic hydrocarbons (especially benzene) can lead to an increased risk of aplastic anemia, multiple myeloma, and acute myelogenous leukemia. In addition, hemolysis has been reported following the acute ingestion of various types of hydrocarbons.[11]
In 2015, 32404 cases of hydrocarbon poisoning were reported to US poison control centers. Of those, 13,074 were in patients aged 19 years or younger.[1]
International
In developing nations, kerosene is implicated in approximately one third of pediatric poisonings.
Mortality/Morbidity
In 2015, 16 deaths due to hydrocarbons were reported to US poison control centers.[1] However, several other deaths are classified as being due to "chemicals, cleaning substances, fumes/gases/vaporizers," and "pesticides." Thus, the true number is probably slightly higher. In addition, the poison control data are widely known to be an underestimate of the true incidence because of underreporting.
Age
Proportionately, more fatalities are associated with children younger than 5 years who often accidentally ingest hydrocarbons, and among adolescents, who are more likely to abuse volatile hydrocarbons.
Inhalant abuse is becoming increasingly common among adolescents. It is estimated that approximately 20% of students in middle school and high school have abused volatile substances.[12]
In cases of suspected hydrocarbon intoxication, it is important to determine the agent ingested, the route of ingestion (eg, oral, dermal, inhalational) the amount of substance ingested, and the time of the ingestion. In addition, the history should include questions about co-ingestants, any vomiting or coughing prior to arrival, and any attempt to treat the patient prior to arrival.
Respiratory distress
The lung is the primary site of most common toxicity following hydrocarbon exposures. Pulmonary toxicity most often occurs following ingestion and subsequent aspiration of hydrocarbon. Respiratory symptoms (eg, coughing, gagging, choking) usually occur within 30 minutes of exposure but often can be delayed several hours.
Many patients develop a transient cough. A prolonged cough and hypoxia, however, is more concerning for aspiration. Lack of coughing does not exclude the possibility of aspiration.
Nervous system
The most common CNS symptoms include headache, lethargy, and decreased mental status. Nonspecific symptoms such as weakness and fatigue may also be reported.
Because many of the solvents are highly lipophilic, solvent abuse causes a transient euphoria.
With prolonged exposure to n -hexane, MnBK, and possibly toluene, an axonopathy can occur. This peripheral neuropathy usually begins in the extremities and then progresses more proximally.
Cardiovascular
The patient may complain of dyspnea or syncope.
In addition, because of sensitization of the myocardium to catecholamines, a relatively young and previously healthy patient can present in full cardiac arrest after being suddenly startled or following strenuous athletic events. A common scenario for the cardiac arrest patient is the teenager who is huffing, or bagging alone in a dark room, who then gets startled when a parent opens the door. This "sudden sniffing death syndrome" results in ventricular fibrillation or ventricular tachycardia, following a large catecholamine exposure to a myocardium that is already sensitized to the effects of the catecholamines. This syndrome is more common following exposure to the halogenated hydrocarbons, but it can occur following exposure to aromatic hydrocarbons as well.
Gastrointestinal
Nausea, vomiting, and sore throat are frequent but are relatively mild.
Local reactions such as a burning sensation in the mouth, pruritus, or a perioral rash are not uncommon and are usually mild.
Prior to instituting the physical examination, the patient should be appropriately decontaminated, if indicated.
The physical examination should focus on the patient's airway, breathing, and circulation (ABCs).
Patients who are experiencing any respiratory compromise should be placed on supplemental oxygen. For those patients who are in severe respiratory distress, or who are too lethargic to be able to adequately protect their airway, advanced airway management may be required.
Respiratory
See the list below:
Coughing
Gagging
Choking
Tachypnea
Hemoptysis
Rales
Rhonchi
Wheezes
Hypoxia
Cyanosis
Cardiovascular
See the list below:
Tachycardia
Dysrhythmias
Hypotension
CNS
See the list below:
Headache
Ataxia
Weakness
Lethargy to coma
Seizures
GI - Nausea/vomiting
Dermal
See the list below:
Erythema
Blistering
Pain
Nasal dermatitis or perioral dermatitis (with chronic abuse)
Skin irritation (with single use) at an intravenous, intramuscular, or subcutaneous injection site
Hydrocarbon exposure can be divided into the following 4 broad categories:
Nonintentional nonoccupational exposure: Accidental ingestions are the most frequent type and commonly involve young children tasting a hydrocarbon. Typically, children do not drink large quantities, as hydrocarbons generally taste bad. Adults and older children occasionally consume a hydrocarbon if liquid is placed in an unlabeled can or bottle resulting in accidental ingestion.
Recreational exposure: Inhaling of hydrocarbons or other volatile solvents for the purpose of producing a transient state of euphoria is becoming more common. This pattern of use is most common in junior high and high-school aged children.
Occupational exposure: This type of exposure is most often industrial, where a worker has either a dermal exposure to the liquid or an inhalational exposure to the vapors.
Intentional: This type of exposure usually involves consuming a large amount of the hydrocarbon as an oral ingestion during a suicide attempt.
Pulse oximetry should be performed on all patients to evaluate oxygenation.
Complete blood count
Chronic benzene exposure may produce either acute myelogenous leukemia or aplastic anemia.
In the acute ingestion, leukocytosis can occur.
Anemia can occur as a result of intravascular hemolysis.
A CBC should be ordered if there is concern for any of the above findings. However, it is not necessary to routinely obtain a CBC in all hydrocarbon exposures.
Chemistries
A routine basic metabolic panel should be performed to determine the BUN, creatinine, glucose, electrolytes, and anion gap (see the Anion Gap calculator).
Any patient appearing intoxicated should have the serum glucose level checked expeditiously.
The anion gap will most likely be normal, but in acute toluene intoxication, an elevated anion gap can be present. The presence of an anion gap, especially if associated with a profound acidosis in a patient appearing intoxicated, however, should prompt an evaluation for other etiologies (eg, methanol, ethylene glycol, salicylates).
Acute renal failure following massive hydrocarbon ingestion can occur but is rare.
Testing of the hepatic transaminase levels should be performed, as these can be elevated following hydrocarbon ingestion (particularly the halogenated hydrocarbons).
A serum creatine kinase (CK) level should be obtained, as acute rhabdomyolysis has been reported in association with isolated hydrocarbon intoxication.
Specific diagnostic testing for hydrocarbon poisonings is available, but it is unlikely to be clinically helpful, as these tests are not routinely available.
All symptomatic patients should have a chest x-ray performed.
Patients who are asymptomatic (eg, no coughing or signs/symptoms of respiratory distress) should not have a chest radiograph obtained immediately. Rather, asymptomatic patients should have chest radiography performed at the end of a 6-hour observation period.
See the image below.
View Image
Anteroposterior view of the chest of 14-month-old boy 30 hours after ingesting lamp oil. Note the central right lower lobe infiltrate obscuring the ri....
An electrocardiogram should be obtained to assess for arrhythmias, especially in those individuals with suspected hydrocarbon abuse (ie, individuals who were huffing or bagging).
Prehospital care should focus on decontamination, followed by immediate transport to a medical facility capable of managing such a patient. GI decontamination has no role in prehospital care. Decontamination should focus on removing any remaining hydrocarbon that might be on the clothes or skin, in the correct clinical setting.
Patients should be kept calm to prevent arrhythmia as a result of myocardial sensitization.
All patients should have their airway, breathing, and circulation managed per routine advanced life support protocols.
Symptomatic patients should receive intravenous access and cardiac monitoring.
The hydrocarbon agent should be transported with the patient to the hospital, if this can be done in a safe manner. Bringing the substance to the hospital can permit identification.
Management for hydrocarbon intoxication is largely supportive.
Asymptomatic patients should be observed with continual pulse-oximetry for a period of at least 6 hours. If the patient remains asymptomatic (eg, no coughing, vomiting, tachypnea, or other evidence of respiratory difficulties), then a chest radiograph may be obtained to evaluate for aspiration.
Other etiologies of altered mental status should be investigated as deemed clinically appropriate by the treating clinician.
Patients who show signs of impending respiratory failure despite supplemental oxygen may require rapid sequence intubation for definitive airway management. Intubation and positive pressure ventilation may be required for evidence of on-going respiratory distress.
If arrhythmias occur, electrolytes, including magnesium and potassium, should be replaced.
If ventricular fibrillation occurs, and is thought to reflect myocardial sensitization, treatment with catecholamines, including epinephrine, should be avoided. In this setting, lidocaine or beta-blockers can be used.
Decontamination of the GI tract remains controversial. Activated charcoal does not absorb hydrocarbons well, and gastric lavage should not be routinely performed. The use of ipecac-induced emesis is contraindicated.
However, the benefits of gastric decontamination may outweigh the real risks of inducing aspiration in patients who have ingested hydrocarbons with significant systemic toxicity. These are outlined in the following mnemonic, CHAMP:
Camphor (toxicity is seizures)
Halogenated hydrocarbons (toxicity is arrhythmias and hepatotoxicity)
Aromatic hydrocarbons (toxicity is CNS toxicity, myelosuppression, and malignancy)
Metals (heavy metals)
Pesticides (cholinergic symptoms, seizures)
Antibiotics are frequently given to patients who develop a pneumonitis following hydrocarbon aspiration. However, there is no evidence to support prophylactic administration of antibiotics.[13] In animal models, the empiric administration of antibiotics altered the lung flora compared with controls and did not yield any benefit.
Clinically, superinfection can definitely occur. Because the pneumonitis itself can create abnormal lung sounds, fever, and leukocytosis, determining whether those effects represent a superimposed infection or the pneumonitis itself is often difficult. Any abnormal finding on a chest radiograph within a few hours of the exposure, however, is unlikely to be pneumonia, and much more likely to be a pneumonitis.
Steroids have not been proven to be beneficial.
Several commercial surfactant preparations are available for use with other conditions, such as hyaline membrane disease (HMD). Animal data on its use demonstrate conflicting results, and currently no human data exist to support its routine use.
Clinical Context:
Class II antiarrhythmic, nonselective, beta-adrenergic, receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.
Effective for treating aggression resulting from head injury. Also used for reducing restlessness and disinhibition. Treatment for persistent agitation and aggression in organic brain syndromes.
Clinical Context:
Short-acting IV cardioselective beta-adrenergic blocker with no membrane depressant activity. Half-life of 8 min allows for titration to effect and quick discontinuation prn.
After a 6-hour observation period during which a patient has a normal chest radiograph and never developed any symptoms (including coughing, vomiting, respiratory difficulty) of hydrocarbon exposure, the patient can be safely discharged home with close follow-up (reevaluation in 24 h).
Patients who develop any symptoms of hydrocarbon exposure during the 6-hour observation should be admitted to a unit capable of continuous pulse oximetry.
Patients should be closely observed for any evidence of respiratory deterioration.
Patients with radiographic evidence of pneumonitis should receive repeat chest radiographs every 24 hours (or sooner, if clinically indicated) to ensure that the pneumonitis is not progressing.
Michael D Levine, MD, Assistant Professor, Department of Emergency Medicine, Section of Medical Toxicology, Keck School of Medicine of the University of Southern California
Disclosure: Nothing to disclose.
Coauthor(s)
Chip Gresham, MD, FACEM, Emergency Medicine Physician, Medical Toxicologist, and Intensive Care Consultant, Department of Emergency Medicine, Clinical Director of Medication Safety, Middlemore Hospital; Consultant Toxicologist, National Poisons Centre; Director, Auckland Regional Toxicology Service; Senior Lecturer, Auckland University Medical School, New Zealand
Disclosure: Nothing to disclose.
Specialty Editors
John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals
Disclosure: Nothing to disclose.
John G Benitez, MD, MPH, Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center
Disclosure: Nothing to disclose.
Chief Editor
Michael A Miller, MD, Clinical Professor of Emergency Medicine, Medical Toxicologist, Department of Emergency Medicine, Texas A&M Health Sciences Center; CHRISTUS Spohn Emergency Medicine Residency Program
Disclosure: Nothing to disclose.
Additional Contributors
David A Peak, MD, Associate Residency Director of Harvard Affiliated Emergency Medicine Residency; Attending Physician, Massachusetts General Hospital; Assistant Professor, Harvard Medical School
Disclosure: Partner received salary from Pfizer for employment.
Acknowledgements
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Timothy P Barron, DO, and Jeremiah J Johnson, MD, to the development and writing of this article.
Anteroposterior view of the chest of 14-month-old boy 30 hours after ingesting lamp oil. Note the central right lower lobe infiltrate obscuring the right heart border.
Anteroposterior view of the chest of 14-month-old boy 30 hours after ingesting lamp oil. Note the central right lower lobe infiltrate obscuring the right heart border.
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