Hydrocarbon Inhalation Injury

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Background

Inhalation injury due to hydrocarbons can occur as a result of either accidental or intentional exposure. Inhalant abuse, the deliberate inhalation of hydrocarbons as a form of recreational drug use, has become a significant health issue affecting children. Epidemiologic data state that, among adolescents, inhalants are the second most widely used class of illicit drugs; more than 2 million children aged 12-17 years report using inhalants at least once in their lifetime. Death from intentional inhalation of hydrocarbon fumes is not uncommon and is usually due to sudden cardiac events or CNS depression. The recognition and treatment of inhalant abuse remain challenges for pediatricians and emergency physicians.

Deliberate inhalation of volatile hydrocarbons for their mood-altering effects is popular among adolescents. Their low cost, ready availability, and ease of use contribute to this problem. Volatile hydrocarbons are contained in glues, solvents, lighter fluid, gasoline, and paints. Most inhalants are composed of several compounds, and almost all pressurized aerosol products can be abused because the propellants are volatile hydrocarbons. Inhalation is most commonly achieved by sniffing, huffing, or bagging.[1, 2]

In young children, ingestion typically occurs as an exploratory behavior. The hydrocarbon is frequently unsecured or improperly stored in a drinking container. Since 2001, The US Consumer Product Safety Commission has required child-resistant packing of products that have low viscosity and contain greater than 10% hydrocarbon by weight.[3]

The majority of intoxication reports of hydrocarbons are due to inhalation or ingestion, but a few case reports have described intravenous ingestion of gasoline for suicide.[4]

Pathophysiology

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.[5] The second theory suggests that potentiation of the GABA receptors occurs; a cross-tolerance between 1,1,1-trichloroethane, toluene, ethanol, barbiturates, and benzodiazepines is noted.[6]

Recreational abuse of hydrocarbons by inhalation is accomplished in 3 ways: sniffing, huffing, and bagging. Sniffing, the least potent delivery method, is the inhalation of the volatile substance through the nostrils (ie, sniffing glue). Huffing is the placing of a rag soaked with an inhalant such as gasoline or lighter fluid over the nose and mouth. Bagging involves repeated deep inhalations from a plastic or paper bag filled with a particular hydrocarbon such as spray paint or another propellant.

Chronic 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.

Two primary organ systems are affected by inhalation hydrocarbon toxicity: the CNS and the cardiopulmonary system. Volatile hydrocarbons are highly lipid soluble and readily cross the blood-brain barrier. Rapid absorption occurs across the large surface area of the pulmonary vascular bed, and peak blood levels are noted approximately 15-30 minutes after inhalation. Confusion, disorientation, disinhibition, and euphoria are exhibited early. Speech becomes slurred, and motor function becomes impaired, with gait becoming staggered. Hallucinations are frequently described, followed by CNS depression, drowsiness, and sleep. Coma can occur with prolonged or repeated exposures; however, this is unusual because the intentional exposure ceases as the user becomes drowsy.

Sudden sniffing death syndrome was first described by Bass in 1970.[7] Death occurs after the user is startled during or soon after inhalation. Hydrocarbons can sensitize the myocardium to endogenous and exogenous catecholamines, which can precipitate ventricular dysrhythmias and sudden death.[8, 9] In addition, some limited data have shown toxic effects of hydrocarbons directly on the myocardium, and excess catecholamine concentrations may cause an increase in oxygen demand, coronary artery spasm, platelet aggregation, and thrombus formation.[10] Numerous case reports also detail acute myocardial infarction as a complication following hydrocarbon inhalation.[11, 12, 13]

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.

Other reported complications include renal tubular acidosis with subsequent hypokalemia and hyperchloremia; frostbite with facial injury and burns to the trachea, mainstem bronchi, esophagus, and oral cavity due to intentional inhalation of fluorinated hydrocarbon; bone marrow damage, aplastic anemia, and leukemia due to benzene exposure; and toxic hepatitis due to toluene exposure.[14, 15, 13, 16, 17] In contrast to pulmonary injury from aspiration of liquid hydrocarbons, direct pulmonary injury from acute inhalation exposure has not been described.

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 mid face, wide nasal bridge, abnormal palmar creases, and blunt fingertips. The syndrome of toluene embryopathy closely resembles the phenotypic features found in fetal alcohol syndrome.[18, 19]

With long-term hydrocarbon inhalation, CNS damage occurs, including loss of cognitive functions, gait disturbances, and loss of coordination. Radiographic tests have demonstrated loss of brain mass and white-matter degeneration. Additionally, certain chemicals have been shown to have associations with specific CNS injuries, including peripheral neuropathy, deafness, and optic neuropathy. Other, less common complications of long-term hydrocarbon inhalation include restrictive pulmonary disease, pulmonary hypertension, and reduced diffusion capacity.[20, 21, 22]

Pulmonary toxicity can occur as a result of hydrocarbon aspiration. This injury differs from hydrocarbon inhalation injury. The most common clinical scenario of hydrocarbon aspiration is a young child unintentionally ingesting a hydrocarbon-containing compound such as lamp oil or a cleaning solvent (see the image below).[23]



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....

Hydrocarbons cause direct injury to the respiratory epithelium, producing inflammation and bronchospasm. Direct contact with alveolar membranes can lead to hemorrhage, hyperemia, edema, surfactant inactivation, leukocyte infiltration, and vascular thrombosis. The result is poor oxygen exchange, atelectasis, and pneumonitis.[24] For more information, see Toxicity, Hydrocarbons.

Epidemiology

Frequency

United States

National surveys of adolescents in the United States have revealed that, after marijuana, inhalants are the most commonly used class of illicit drugs for 8th and 10th graders; inhalants are the third most widely used illicit drugs for 12th graders.[25] The low cost, ease of use, and ready availability of organic solvents perpetuate their abuse. Epidemiologic data suggest a decrease in the prevalence of inhalant abuse, but overall abuse rates remain high.

Inhalant abuse by adolescents in the United States is common. In 2000, more than 2 million adolescents aged 12-17 years reported using inhalants at least once in their lifetime.[26] Since 1975, the National Institute on Drug Abuse annual survey of high-school seniors has documented a lifetime incidence of inhalant abuse of 15-20%, with the highest prevalence of use being in 8th graders.[27, 28]

Although the trend of lifetime use decreases between the 8th and 12th grades, these data may underestimate the true lifetime use of older adolescents because many students have dropped out of school by the 12th grade and, thus, are no longer included in the survey.

The typical person who abuses inhalants is a young male of lower socioeconomic class. Overall, males are twice as likely to abuse inhalants as females; however, between the 8th and 12th grades, the difference is less pronounced. Immigrants from Latin America and American Indians have a higher prevalence of use, and blacks have a low prevalence of inhalant abuse. Although inhalant abuse is typically thought of as being most common among adolescents, abuse among adults is also well described, and abuse in children as young as age 4-6 years has been reported.[29, 30, 27]

A study reported that inhalant use prevalence rates generally declined from 1991 to 2011, however, the proportion of females and Hispanics among lifetime users increased.[31]

According to the National Institute on Drug Abuse, research shows that inhalant users initiate use of cigarettes, alcohol, and almost all other drugs at younger ages than those who did not use inhalants. In addition, early inhalant users are more likely to develop substance abuse disorders, including abuse of prescription drugs, compared with other substance abusers with no history of inhalants use.[32]

International

The United Kingdom is the only major country in the Western world that tracks inhalant abuse fatalities; an incidence of 2 deaths per week has been documented. In Canada, the patterns of inhalant use are similar to those associated with other illicit substances for experimenters, intermittent users, and long-term abusers. Long-term use tends to be endemic in both the inner-city areas and remote communities, and data show an association between chronic use, lower socioeconomic class, and family dysfunction.

Mortality/Morbidity

Although hydrocarbon inhalation was previously thought to be a benign fad, permanent and significant pulmonary and neurologic sequelae clearly may persist even after abuse has discontinued. Recreational solvent inhalation may account for as much as 2% of all deaths among adolescent males. In the United Kingdom, 15% of deaths caused by inhalants occur as a result of suffocation, 15% are a result of accidental trauma, and 15% are a result of aspiration, whereas the remaining 55% are a result of sudden sniffing death syndrome.[33, 34] The fact that 22% of victims of sudden sniffing death syndrome had no history of inhalant abuse is of significant concern, demonstrating that death can result from any episode of inhalant abuse.

In the United States, inhalant abuse was responsible for 12.2% of the deaths reported to poison control centers in the group aged 13-19 years. Given that many inhalant-related deaths are never reported to poison control centers, this statistic grossly underestimates the true mortality due to inhalant abuse.[27]

Ongoing inhalant use has been associated with significant psychosocial pathology, including failure in school and delinquency; a high correlation between poor academic performance and inhalant abuse is noted. In patients with neurologic symptoms who abused toluene as an inhalant, nearly one third showed deficits in orientation, attention, learning, arithmetic calculation, abstraction, construction, and recall.[35, 29]

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.[36] Psychiatric disorders, spasticity, cognitive changes, and secondary Parkinson disease have been reported. Attention deficit and decreased memory retrieval may also occur.[37]

Race

Previous data suggested the highest inhalant abuse to be among Latin American immigrants. In adolescents aged 12-17 years, inhalant users were more likely to be American Indian or Alaskan Native (13.2%), followed by multiracial (11.2%) and white (9.5%).[38, 27] Lowest reported rates were among blacks (5.3%) and Asians (6.5%).

Sex

According to data from Wu et al in 2004, the lifetime prevalence rates of inhalant abuse were not significantly different for males and females aged 12-17 years.[27]

Age

Peak age of inhalant abuse is 14-15 years, with onset of abuse occurring from ages 6-8 years. Use typically declines by the late teenage years; however, some users continue to abuse inhalants into adulthood.

History

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.

Populations at higher risk should be questioned more carefully; high-risk populations include children and adolescents from families of low socioeconomic status, in whom unemployment and poverty rates are high, as well as those lacking adult supervision.

Common symptoms between episodes of abuse include poor social functioning, underachievement at work or school, apathy, chest pain, and thirst.

Carefully investigate the possibility of illicit solvent inhalation in all patients presenting with the following unexplained symptoms or factors:

When inhalant abuse is identified, make efforts to specifically identify the toxins involved because abusers often ingest various solvent-inhalants and frequently misidentify the substances involved. Hydrocarbons are not often part of a routine toxicology screen; therefore, if such an exposure is clinically suspected, the laboratory must be alerted and specific identifying tests must be obtained.

Physical

Patients who have acute decompensation from solvent-inhalant abuse are frequently found near the offending agent; however, many patients who present to medical care have no obvious physical findings to suggest hydrocarbon exposure or inhalant abuse. Some patients may present with subtle signs of abuse, such as paint staining around the mouth or nose. A characteristic odor may be detectable on presentation because a significant proportion of the absorbed chemical exits the body via the lungs. Also, the product may have been spilled onto clothing during use.

Evidence of chronic inhalant abuse may be subtler. Patients presenting with unexplained peripheral neuropathy and weakness, diffuse GI symptoms, or neuropsychiatric symptoms should raise suspicion of chronic solvent-inhalant abuse. Electrolyte abnormalities, including hypokalemia, hypophosphatemia, and acidosis, should further raise suspicion. However, the nature of these symptoms is not diagnostic of solvent-inhalant abuse; therefore, a very broad differential diagnosis is required.

Signs and symptoms

A single, loud S2 may be evident as a result of pulmonary hypertension. Ventricular arrhythmias or bradycardia may be observed. Discolored urine may be evident from rhabdomyolysis.

Adolescents who present with unexplained obtundation or seizures should be examined carefully for evidence of recent solvent-inhalant exposure. Physical findings of recent solvent-inhalant abuse include flecks of paint around the nose and mouth and staining of the fingers, nails, and clothing.

A solvent aroma may be present on the breath. Rhinitis, nasal mucosal erosions, epistaxis, hoarse voice, and conjunctivitis may result from local exposure.

The acute neurologic effects of inhaled solvents generally wear off within minutes to a few hours, but the effects of more chronic use may persist.

Muscle weakness, diffuse GI symptoms, and neuropsychiatric symptoms are 3 major symptom patterns of chronic abuse.

Causes

The common idea that solvent inhalation is innocuous undoubtedly contributes to solvent-inhalant abuse. The wide availability of organic solvents in commonly used household products makes them readily accessible.

Commonly abused products include the following:

Chemicals found in abused inhalants include the following:

Laboratory Studies

When solvent-inhalant abuse is suspected, specific solvent identification should be requested from the laboratory because solvent inhalants are infrequently included in routine toxicologic screening tests.[39]

Complete toxicology screening should be performed because patients who abuse one drug may be simultaneously abusing others.

Perform serologic investigation of renal and hepatic dysfunction, as well as blood and urine testing for rhabdomyolysis.

Obtain serum electrolyte levels to diagnose hypokalemia, hypophosphatemia, hypercalcemia, and acidosis from distal renal tubular acidosis caused by chronic hydrocarbon abuse.

If indicated from the history and physical examination, laboratory tests should be performed for sexually transmitted disease and, possibly, pregnancy (due to disinhibition and poor judgment). Pregnancy testing should be performed in all solvent-abusing females of reproductive age because of the risk of toluene embryopathy.

Other Tests

The following are also indicated:

Medical Care

The care of patients with inhalation abuse is mainly supportive. Because many potential complications involving the pulmonary, cardiovascular, and neurologic systems may be present, careful assessment and stabilization of the ABCs should be paramount in the initial management. In addition to acute medical treatment, patients suspected of chronic solvent-inhalant use should be carefully evaluated by a team trained in the treatment of childhood substance abuse.

Acute inhalant abuse

Medical care of patients following acute decompensation from hydrocarbon inhalation is primarily supportive. Those with significant neurologic impairment who are unable to protect their airway should undergo endotracheal intubation and mechanical ventilation to prevent aspiration and respiratory deterioration. Hypoxic injury to other organ systems, particularly the heart, should be sought and treated.

Because of the sensitization of the myocardium to catecholamines, inotropic agents and bronchodilators should be avoided. Some authors suggest the use of amiodarone to treat ventricular arrhythmias if used early in treatment. Epinephrine administration during resuscitation may be harmful and can lead to recurrence of ventricular fibrillation.

Electrolyte abnormalities should be corrected.

Chronic inhalant abuse

Management of chronic solvent-inhalant abuse should be directed at preventing further abuse.

Therapy for commonly involved organs, including the central and peripheral nervous systems, kidneys, liver, lungs, heart, and bone marrow, is primarily supportive.

In patients with significant electrolyte abnormalities, typically due to distal renal tubular acidosis, parenteral fluid and electrolyte repletion may be necessary. Correction of potassium and phosphorus deficiency may result in rapid improvement in muscle strength. Hypocalcemia is frequently encountered during fluid and electrolyte repletion.

Apneic aversion and covert sensitization have been used as a treatment of hydrocarbon inhalation addiction.[40]

Consultations

Patients who are suspected of solvent-inhalant abuse should be carefully evaluated by experts who are trained in the treatment of childhood substance abuse. Consultation with specialists, including cardiologists and neurologists, may also be warranted, depending on the individual needs of the patient. Any patient who has unstable hemodynamics or cardiac arrhythmias or who has significantly altered mental status should be admitted to and observed in the pediatric intensive care unit.

Diet

Patients should remain on a diet of nothing by mouth (NPO) until muscle weakness clearly will not necessitate institution of mechanical ventilation. Also, because of the risk of hypocalcemic seizures, patients should remain NPO during initial fluid and electrolyte repletion.

Medication Summary

For acute inhalant abuse, some authors suggest the use of amiodarone to treat ventricular arrhythmias if used early in treatment. Electrolyte abnormalities should be corrected.

For patients with chronic solvent-inhalant abuse with significant electrolyte abnormalities, typically due to distal renal tubular acidosis, parenteral fluid and electrolyte repletion may be necessary. Correction of potassium and phosphorus deficiency may result in rapid improvement in muscle strength. Hypocalcemia is frequently encountered during fluid and electrolyte repletion.

Potassium phosphate/sodium acid phosphate (Neutra-Phos-K, K-Phos)

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 millimols of phosphorus, not milliequivalents of potassium, to avoid confusion as to the phosphorus content.

Calcium gluconate

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.

Class Summary

These agents are used to correct hypokalemia and hypophosphatemia in inhalation cases. Electrolytes are used to correct disturbances in fluid and electrolyte homoeostasis or acid-base balance and to reestablish osmotic equilibrium of specific ions.

Phenobarbital (Luminal, Solfoton)

Clinical Context:  Most helpful if withdrawal symptoms are evident. Can be continued for sedation for 5-10 d. Therapeutic level is 15-40 mg/L.

Diazepam (Valium)

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.

Phenytoin (Dilantin)

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.

Lorazepam (Ativan)

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.

Class Summary

These agents are used for withdrawal symptoms or seizure activity in inhalation cases.

Amiodarone (Cordarone)

Clinical Context:  Class III antiarrhythmic. Has antiarrhythmic effects that overlap all 4 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.

Class Summary

These agents may be required to treat tachycardias.

Further Outpatient Care

Once abstinence has been established, focus care on returning the patient to the community in a manner in which recidivism is minimized.

Recurrence is likely unless access to solvent-inhalants is eliminated, social and familial dysfunction is remedied, and other psychiatric conditions, including depression and other substance abuse, are addressed and treated.

Further Inpatient Care

Ongoing psychiatric and social intervention is necessary to prevent recidivism. Access to solvent-inhalants should be eliminated as much as possible. Disorganized family settings with inadequate supervision increase the likelihood of return to abuse, and supervised foster care placement may be necessary.

Discontinuation of long-standing solvent-inhalant abuse may result in withdrawal symptoms, including tremor, agitation, tachycardia, hallucinations, and seizures, within hours to days of stopping use. Long-acting sedatives, such as phenobarbital or diazepam, are useful. These drugs should be discontinued over 5-10 days.

Patients who continue to experience seizures after the initial period of withdrawal should be treated with medications with low potential for abuse, such as phenytoin.

Deterrence/Prevention

The nearly ubiquitous availability of organic solvents makes them poor candidates for governmental regulation to reduce abuse.

Preteens are at risk of inhalant abuse; therefore, evidence-based in-school primary prevention education must begin early to ensure that its messages have been delivered before—not in the midst of—youth inhalant abuse. Office-based brief interventions that include a 5- to 10-minute session outlining the risks associated with substance use have been found to be effective in reducing alcohol, marijuana, and tobacco use. However, similar strategies have not been shown to be effective for inhalant abuse, in which perceptions of harm are more strongly correlated with social networks than with future intent to use inhalants. Availability and use of inhalants by peers correlate with inhalant abuse, with many youths reporting abuse at friends’ homes and on school property.[41]

In addition, inhalant abuse is correlated with poverty, hunger, illness, low education levels, unemployment, boredom, and feelings of hopelessness. Thus, it is clear that prevention must also address the influence of social factors, including the social determinants of health. Intersectoral action that includes partnerships among community agencies, the private sector, and government is required to disseminate information and education on inhalant abuse and to develop policies that address inhalant abuse prevention.[41]

Complications

Cardiac arrhythmias, including ventricular tachycardia, ventricular fibrillation, myocardial infarction, multifocal premature ventricular contractions and supraventricular tachycardia, have been observed.

Hypocalcemia is frequently encountered during fluid and electrolyte repletion and may be severe enough to precipitate tetany or seizures.

Prognosis

Pulmonary, renal, 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.

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.

Patient Education

Health professionals should use their knowledge, experience, and community connections to achieve the following[41] :

Community education should be provided regarding the dangers of solvent-inhalant abuse. Education is considered to be the most effective preventive strategy, especially when it is initiated before the usual age of experimentation. School-based curricula that focus on deterring illicit drug use should include inhalants as potential drugs of abuse, and particular focus should be on areas where inhalant abuse is endemic. Pediatricians need to promote education about the health hazards posed by substance abuse to both patients and their families.[12]

For excellent patient education resources, see eMedicineHealth's patient education article Substance Abuse.

Author

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.

Coauthor(s)

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.

Specialty Editors

Mary L Windle, PharmD, Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Charles Callahan, DO, Professor, Chief, Department of Pediatrics and Pediatric Pulmonology, Tripler Army Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Denise Serebrisky, MD, Associate Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director, Division of Pulmonary Medicine, Lewis M Fraad Department of Pediatrics, Jacobi Medical Center/North Central Bronx Hospital; Director, Jacobi Asthma and Allergy Center for Children, Jacobi Medical Center

Disclosure: Nothing to disclose.

Acknowledgements

Heidi Connolly, MD Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center

Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Jason M Kane, MD, FAAP Assistant Professor of Pediatrics, Northwestern University Feinberg School of Medicine; Attending Physician, Department of Pediatrics, Section of Pediatric Critical Care and Cardiac Intensive Care, Children's Memorial Hospital

Jason M Kane, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Emily B Nazarian, MD Assistant Professor of Pediatrics, Fellowship Director, Pediatric Critical Care, Golisano Children's Hospital at Strong

Emily B Nazarian, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

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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.