Hydrocarbons are a heterogeneous 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 abused hydrocarbons include gasoline, lubricating oil, motor oil, mineral spirits, lamp oil, and kerosene. Other common sources of hydrocarbons include dry cleaning solutions, paint, spot remover, rubber cement, solvents, model glue, and lacquers, while aerosol sources include spray paints, butane fuel, lighter fluid, cooking sprays, cosmetics, hairspray, toiletries, and deodorants.[1]
Chemicals found in abused inhalants include the following:
Propane
Butane
n-Hexane
Trichloroethylene
Freon
Benzene
Toluene[2]
Xylene
Acetone
Methyl isobutyl ketone
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, and 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 hydrocarbons and other volatile solvents by inhalation, 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), and "bagging" (inhaling via a plastic bag filled with hydrocarbon vapors).
Chronic inhalation abusers generally inhale 3-4 times daily for 10-15 minutes each time, although prolonged sessions of inhaling 6-7 hours a day as a group activity have been described. Tolerance and physical dependence can occur, although withdrawal symptoms are only infrequently reported.
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 viscosity is the single most important chemical property associated with the aspiration risk.[3]
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 to the risk of aspiration. The amount of hydrocarbon ingested has not consistently been linked to the degree of aspiration and hence pulmonary toxicity.
The exact mechanism of action for the volatile substances on the whole is unknown. Two theories have been postulated for the mechanism of action of inhalants. One hypothesis is that the volatile solvents produce a generalized slowing of axonal ion-channel transport by altering the membranes, similar to anesthetic gasses.[4] The second theory suggests that potentiation of the gamma-aminobutyric acid (GABA) receptors occurs (GABA being a major inhibitory neurotransmitter in the brain); a cross-tolerance between 1,1,1-trichloroethane, toluene, ethanol, barbiturates, and benzodiazepines is noted.[5]
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.[6]
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.
A 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.[7] 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 of pneumothorax, pneumatocele, or bronchopleural fistula.[8]
Nervous system
Central 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 can directly 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 a decreased level of arousal.
As solvent abuse becomes chronic, damage to the CNS becomes irreversible, with changes occurring in the cerebellar and cerebral white matter, including demyelination and gliosis.[9] 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.[10]
Cardiovascular
Exposure to hydrocarbons can result in cardiotoxicity.[11] 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.
In addition, ventricular fibrillation, myocardial infarction, and multifocal premature ventricular contractions have been observed.
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[12]
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 with 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.[13]
Fetal
Many solvents, particularly toluene, are lipophilic and readily cross the placenta, resulting in characteristic fetal anomalies that include microcephaly, narrow bifrontal diameter, short palpebral fissures, hypoplastic midface, wide nasal bridge, abnormal palmar creases, and blunt fingertips. The syndrome of toluene embryopathy closely resembles the phenotypic features found in fetal alcohol syndrome.[14, 15]
A literature review by Kounlavong et al reported that fetal growth restriction and preterm delivery (< 37 weeks) were among the most frequent fetal outcomes linked to inhalant use by pregnant persons. Withdrawal symptoms, including jitteriness, trouble feeding, and dystonia, were found in affected neonates, with subsequent demonstration of developmental delays (such as cognitive and speech impairments) and postnatal growth restriction (including microcephaly).[16]
Hydrocarbon exposure can be divided into the four broad categories summarized below.
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 exposure
This type of exposure usually involves consuming a large amount of the hydrocarbon as an oral ingestion during a suicide attempt.
According to the 2022 Annual Report of the National Poison Data System (NPDS) from America’s Poison Centers, hydrocarbons ranked 12th in nonpharmaceutical substance exposures, with 27,701 hydrocarbon exposures for the year. This included 18,066 exposures in adults over age 20 years. Nineteen fatalities in which hydrocarbon exposure was involved were reported, including three in adolescents aged 13-19 years.[17] (However, poison control data are widely known to be an underestimate of the true incidence because of underreporting.)
Inhalant abuse is common among adolescents. It is estimated that approximately 20% of students in middle school and high school have abused volatile substances.[18]
Pulmonary, renal, gastrointestinal (GI), cardiac, and even neurologic dysfunction usually resolves with abstinence. Prolonged abuse increases the risk that residual organ dysfunction, particularly neurologic sequelae, will persist.
Patients who abuse solvent-inhalants are frequently abusers of other drugs and alcohol.
Hypocalcemia is frequently encountered during fluid and electrolyte repletion and may be severe enough to precipitate tetany or seizures.
Many abusers perform poorly in school, are chronically unemployed as adults, and commit criminal acts; therefore, efforts at early recognition and provision of long-term care with frequent monitoring are justified.
With acute intoxication, deaths due to asphyxiation from a plastic bag over the head or from aspiration of stomach contents are not unusual. Also, trauma-related injury and motor vehicle accidents have been reported, resulting from disinhibition and disorientation following inhalation.
Although mild ingestions are usually devoid of complications, the morbidity and mortality associated with such poisoning are primarily related to pulmonary aspiration. Subsequent complications—most importantly, secondary bacterial infections—can worsen the clinical condition.
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 a cardiac arrest patient is a 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.
A high index of suspicion is required because exposure to most volatile substances is not detectible by physical examination and because people who intentionally abuse inhalants initially deny hydrocarbon inhalation. Presentation of a patient with a characteristic odor of gasoline or kerosene likely suggests exposure; however, patients who present with altered mental status or intoxication should be scrutinized for the possibility of inhalation abuse in addition to abuse of other common drugs.
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 are too lethargic to be able to adequately protect their airway, advanced airway management may be required.
Respiratory findings include:
Coughing
Gagging
Choking
Tachypnea
Hemoptysis
Rales
Rhonchi
Wheezes
Hypoxia
Cyanosis
Cardiovascular findings may include tachycardia, dysrhythmias and hypotension. Nausea/vomiting may be present.
CNS findings include:
Headache
Ataxia
Weakness
Lethargy to coma
Seizures
Dermal findings include:
Erythema
Blistering
Pain
Nasal dermatitis or perioral dermatitis (with chronic abuse)
Skin irritation (with single use) at an intravenous, intramuscular, or subcutaneous injection site
The workup depends on the exposure. Pulse oximetry should be performed on all patients to evaluate oxygenation.
Complete blood count
Acute ingestion of benzene commonly results in leukocytosis. Anemia can occur as a consequence of intravascular hemolysis. Chronic benzene exposure may produce either acute myelogenous leukemia or aplastic anemia.
A complete blood cell count (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 blood urea nitrogen (BUN), creatinine, glucose, and electrolyte levels and permit calculation of the anion gap (see the Anion Gap calculator).
Obtain serum electrolyte levels to diagnose hypokalemia, hypophosphatemia, hypercalcemia, and acidosis from distal renal tubular acidosis caused by chronic hydrocarbon abuse.
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, should prompt an evaluation for other etiologies (eg, methanol, ethylene glycol, salicylates).
Acute kidney injury following massive hydrocarbon ingestion can occur but is rare.
Other
Testing of 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.
Pregnancy testing should be performed in all solvent-abusing females of reproductive age because of the risk of toluene embryopathy.
Specific diagnostic testing for hydrocarbon poisoning exists but is unlikely to be clinically helpful, as these tests are not routinely available.
All symptomatic patients should have a chest radiograph 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....
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 dysrhythmia 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.
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.
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 ongoing respiratory distress.
If dysrhythmias 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 dysrhythmias and hepatotoxicity)
Aromatic hydrocarbons (toxicity is CNS toxicity, myelosuppression, and malignancy)
Metals (heavy metals)
Pesticides (cholinergic symptoms, seizures)
After a 6-hour observation period during which a patient has a normal chest radiograph and has not 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 a pneumonitis should receive repeat chest radiographs every 24 hours (or sooner, if clinically indicated) to ensure that the pneumonitis is not progressing.
All hydrocarbon ingestions should be discussed with the regional poison control center (800-222-1222) or a medical toxicologist.
For severe disease, pediatric intensive care and or pulmonology should be consulted for intensive care unit (ICU) management and for consideration of surfactant and extracorporeal membrane oxygenation (ECMO) use. If the treating facility does not have access to these subspecialties and medical resources, transfer to such as site should be considered.
Psychiatric consultation should be performed if deemed clinically relevant.
Antibiotics are frequently given to patients who develop a pneumonitis following hydrocarbon aspiration. However, there is no evidence to support prophylactic administration of antibiotics.[19] 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, with some case reports of secondary abscess formation. 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.
Although steroids are routinely given for a pneumonitis, there have been no definitive studies demonstrating their benefit.
ECMO use has been reported for severe cases of hydrocarbon pneumonitis.[20]
Moreover, a case report of surfactant use for a hydrocarbon pneumonitis found that ECMO support need was immediately reduced from a cardiac index of 2.5 L/min/m2 to 2.0 L/min/m2, with the fraction of inspired oxygen (FiO2) requirement decreased by 10% within 2 hours.[21]
Prevention of nonintentional poisonings includes clearly labeling containers that contain hydrocarbons. Prevention of toxicities as a result of recreational drug use includes educating teens about the risks associated with such behavior.
Clinical Context:
Class III antiarrhythmic. Has antiarrhythmic effects that overlap all four Vaughn-Williams antiarrhythmic classes. May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Only agent proven to reduce incidence and risk of cardiac sudden death, with or without obstruction to LV outflow. Very efficacious in converting atrial fibrillation and flutter to sinus rhythm and in suppressing recurrence of these arrhythmias.
Has low risk of proarrhythmia effects, and any proarrhythmic reactions are generally delayed. Used in patients with structural heart disease. Most clinicians are comfortable with inpatient or outpatient loading with 400 mg PO tid for 1 wk, because of low proarrhythmic effect, followed by weekly reductions, with goal of lowest dose with desired therapeutic benefit (usual maintenance dose for AF 200 mg/d). During loading, patients must be monitored for bradyarrhythmias. Before administration, control the ventricular rate and CHF (if present) with digoxin or calcium channel blockers.
PO efficacy may take weeks. With exception of disorders of prolonged repolarization (eg, LQTS), may be DOC for life-threatening ventricular arrhythmias refractory to beta blockade and initial therapy with other agents.
Clinical Context:
Preferable to potassium chloride because it allows for correction of both hypokalemia and hypophosphatemia. Contains 4.4 mEq of potassium per 3 mmol of phosphate. Elemental phosphorus equals 31.25 mg/mmol. Should be ordered in millimoles of phosphorus, not milliequivalents of potassium, to avoid confusion as to the phosphorus content.
Electrolytes are used to correct disturbances in fluid and electrolyte homoeostasis or acid-base balance and to reestablish osmotic equilibrium of specific ions.
Clinical Context:
Used for sedation if withdrawal symptoms present. Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Individualize dosage and increase cautiously to avoid adverse effects.
Clinical Context:
Sedative hypnotic with short onset of effects and relatively long half-life. By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation. Important to monitor patient's blood pressure after administering dose. Adjust as necessary.
Clinical Context:
May act in motor cortex, where may inhibit spread of seizure activity. Activity of brainstem centers responsible for tonic phase of grand mal seizures may also be inhibited. Dose should be individualized. Administer larger dose before retiring if dose cannot be divided equally. Therapeutic level is 10-20 mg/L.
Clinical Context:
Class II antidysrhythmic, 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.
Clinical Context:
Patients with hypocalcemia may need replacement, particularly in the presence of carpopedal spasm or hypocalcemic seizures. One gram of calcium gluconate equals 90 mg of elemental calcium.
Derrick Lung, MD, MPH, FACEP, FACMT, Physician, Department of Emergency Medicine, San Mateo Medical Center
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
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.
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.
Divya Salhan, MD, Resident Physician, Department of Internal Medicine, Interfaith Medical Center
Disclosure: Nothing to disclose.
M Frances J Schmidt, MD, Chief of Pulmonary Medicine, Pulmonary Fellowship Program, Teaching Attending Physician, Department of Medicine, Interfaith Medical Center
Disclosure: Nothing to disclose.
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.
Rakesh Vadde, MBBS, Attending Physician in Pulmonary and Critical Care Medicine, Southern Ohio Medical Center; Clinical Assistant Professor of Medicine, Ohio University Heritage College of Osteopathic Medicine
Disclosure: Nothing to disclose.
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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