Inhalant abuse in children and adolescents

Authors
Erin E Endom, MD
Holly Perry, MD Section Editor
Michele Burns Ewald, MD Deputy Editor
James F Wiley, II, MD, MPH

Last literature review version 17.3: September 2009 | This topic last updated: October 13, 2009 (More)

INTRODUCTION — Inhalants are substances that are abused for their intoxicating properties. They have
significant acute and chronic toxicity. They have a wide variety of chemical structures with the majority
being either hydrocarbons (aliphatic, aromatic, or halogenated), nitrites, or nitrous oxide [1] . They are
similar in that they are all volatile substances, highly lipid soluble, and readily absorbed across the
pulmonary bed.

Inhalant abuse is a common problem in adolescents due to several factors: Inhalants are readily accessible:
an average home has between 30 and 50 products with abuse potential. They are inexpensive and legal to
buy and possess. The perceived risk of use is low [2] .

Frequently, inhalants are the first drugs of abuse used by children and adolescents because of these factors
[1,3] . In addition to being a common problem, inhalant abuse is a serious problem as it is associated with
permanent brain injury, cardiac dysfunction, liver toxicity, acute renal failure, and death.

The epidemiology, clinical manifestations, toxic effects, and management of inhalant use will be reviewed
here. Substances that are snorted (eg, cocaine) or smoked (eg, tobacco, marijuana, cocaine, and opiates)
are discussed separately. (See "Cocaine: Acute intoxication" and see "Marijuana use in children and
adolescents" and see "Opioid intoxication in children and adolescents").

EPIDEMIOLOGY — In the United States, inhalant abuse is common with more than 13 percent of middle
school and high school students reporting having used inhalants in their lifetime [4] . An estimated 800,000
US children experiment with inhalants annually [5] . Unlike nearly all other classes of drugs, their use is
most common among younger adolescents with use peaking between 7th and 9th grade [2] . The incidence
of inhalant abuse in children 12 to 18 years old has fluctuated over the past 25 years. Incidence of use
tripled between 1983 and 1993 [6] , peaking in 1995, and then showed a steady decline until 2002. Since
that time, incidence has gradually increased [2] . Unlike other drugs of abuse, male and female adolescents
have a similar rate of inhalant abuse [5] . In the past, Native American children were at higher risk for
inhalant abuse [7,8] . However, rates of abuse have fallen steadily since 1985 and are now at levels
comparable to the general population. Education on prevention and treatment is thought to be
responsible for this trend [9] . A slightly higher incidence of inhalant abuse in rural communities continues
to be noted [10] .

Numerous studies have demonstrated significant mental health and behavioral co-morbidities among
patients who are inhalant abusers. They are more likely to have an episode of major depression [5,11,12] ,
suicidality [13] , conduct disorder [11] , and are at an increased risk for future drug abuse problems [14] .

MECHANISM OF ACTION — Volatile hydrocarbons and nitrous oxide have a similar mechanism of action.
Like ethanol and other inhalational anesthetic agents, they are highly lipid soluble. They are rapidly
absorbed across the pulmonary bed into the bloodstream and are distributed throughout the body [15] .
Neurons, which have a high lipid content, are particularly susceptible to the solvent properties of these
compounds [16,17] .

These inhalants act as central nervous system (CNS) depressants. CNS depression is thought to be
mediated by alteration of neuronal membrane function at glutamate or gamma amino butyric acid
receptors [18-20] .

These inhalants produce an effect within seconds that typically lasts 15 to 45 minutes. There have been
rare cases of prolonged symptoms when large quantities have been inhaled [21] . Initial euphoria is
followed by lethargy. Judgment and coordination are impaired [22] . Intoxication is maintained through
repeated use. Symptoms of tolerance to the effects of inhalants and physiologic withdrawal have been
described [1] .

Nitrites produce their pleasurable effects by intense vasodilation which produces a sensation of heat and
warmth. Absorption is rapid across the pulmonary bed leading to onset of hypotension and reflex
tachycardia within seconds of inhalation. Effects are brief, lasting less than five minutes. Nitrites are also
used to enhance sexual pleasure by prolonging penile erection and promoting anal sphincter relaxation.

TECHNIQUES (SNIFFING, HUFFING, or BAGGING) — In the United States, the most frequently used
inhalants include glue, shoe polish, or toluene (30.3 percent); gasoline or lighter fluid (24.9 percent);
nitrous oxide or "whippits" (24.9 percent); and spray paints (23.4 percent) [5] . Each of these substances
may contain more than one toxic compound (show table 1) [1] .

Inhalants may be sniffed directly from a container or sprayed directly on to a heated surface to enhance
vaporization ("sniffing") [23] . Volatile liquid substances also may be inhaled from a saturated cloth that is
held under the nose or near the mouth ("huffing"), or from a bag that is placed over the mouth, nose, or
head ("bagging"). The risk of asphyxia is increased with bagging because the partial pressure of
hydrocarbon displaces oxygen in the alveoli. The possibility of a suicide attempt should be considered in an
individual who "bags" inhalants, particularly when the bag is placed over the head [24] . The concentration
of the inhaled substance increases from sniffing, to huffing, to bagging.

Nitrous oxide is abused most commonly as "whippits". These are small, cylindrical metal bulbs with a
pierceable end that contains compressed nitrous oxide, which are meant for use as a propellant for
whipped cream makers. When misused, the end is pierced with a "cracker" and the escaping gas is
captured in a balloon and then inhaled. Nitrous oxide can also be sniffed from whipped cream canisters.

The desired effects of inhalant abuse include euphoria, lightheadedness, and a general state of intoxication
similar to that produced by alcohol or marijuana. The effects usually last for only 15 to 30 minutes, but can
be sustained by continuous or repeated use [25] .

RECOGNITION OF INHALANT ABUSE — Inhalant abuse frequently goes undetected. Clues to inhalant abuse
include chemical odors on the breath, skin, or clothes, and empty solvent containers or bags, rags, or gauze
in the child's possession or trash [24] . "Glue-sniffer's rash" is an eczematoid dermatitis with erythema,
inflammatory changes, and pruritus that occurs in the perioral area and extends to the midface. It is caused
by the drying effects of hydrocarbons [26] . Symptoms and signs of inhalant use are listed in the table
(show table 2).

TOXICITY AND CLINICAL FINDINGS BY AGENT — Although the vast majority of children who abuse volatile
inhalant substances do not seek or require medical attention, inhalant abuse is potentially life-threatening.
Death may result from asphyxia, suffocation, choking on vomitus, careless or dangerous behavior in
potentially dangerous settings, and sudden sniffing death [27,28] seen with hydrocarbon abuse, especially
halogenated hydrocarbons. Diagnosis of inhalant abuse is primarily based on history or circumstance (eg,
patient found unresponsive with toxic inhalant or inhalant apparatus nearby). (See "Techniques (sniffing,
huffing, or bagging)" above).

Hydrocarbons — Household products abused as inhalants typically contain a mixture of hydrocarbons.

They are categorized by structure: aliphatic, aromatic, and halogenated. (See "Hydrocarbon poisoning").

Aliphatic compounds are straight-chain compounds and include butane, propane, kerosene, and mineral
seal oil. Gasoline is a mixture of aliphatic hydrocarbons that also may contain other substances such as
xylene, toluene, benzene, naphthalene, or lead [15,29] .

Aromatic hydrocarbons are cyclic compounds containing a benzene ring and are used as industrial
solvents; benzene, toluene, and xylene are encountered most commonly. Toluene is found in a large
number of household products including glues, adhesives, acrylic paints, paint thinners, and automotive
products [15] .

Halogenated hydrocarbons include fluorinated hydrocarbons (freons) and chlorinated hydrocarbons

(carbon tetrachloride, trichloroethylene, trichloroethane). They are used as solvents, degreasers, and spot
removers, and in the dry cleaning industry. Freons are widely used as refrigerants and in fire extinguishers
[30-32] .

The most important toxicities are cardiac and neurological, although hydrocarbons are toxic to essentially
all body systems. Certain agents are more closely associated with a particular toxicity.

CNS effects — Acute CNS effects include slurred speech, ataxia, disorientation, headache, hallucinations,
agitation, violent behavior, and seizures [6,27,33-35] . Generalized CNS depression may involve the
respiratory centers of the brain, rarely causing respiratory arrest and death [36] . Toluene intoxication can
cause temporary or progressive cerebellar dysfunction and cranial neuropathies [1,6] .

The long-term CNS effects are equally worrisome and include neurocognitive impairment, cerebellar
dysfunction, and peripheral neuropathy [24,37] . The neurologic findings may be related to loss of brain
mass or abnormal perfusion. Computed tomography (CT) and magnetic resonance imaging (MRI) of
inhalant users demonstrates loss of brain mass and degeneration of white matter, respectively [38-40] .
Single photon emission computed tomography (SPECT) in long-term inhalant users demonstrates abnormal
perfusion [41] .

Abuse of gasoline can lead to persistent peripheral neuropathy and myopathy with myoglobinuria and
creatine kinase elevation [42-45] . In addition, Parkinsonism can be caused by octane-enhancing additives
[46] , and lead poisoning may occur if lead-containing gasoline is inhaled. (See "Childhood lead poisoning:
Clinical manifestations and diagnosis").

Cardiovascular effects — Arrhythmias, myocarditis, or myocardial infarction may rarely occur with acute or
chronic use [7,47] . Chronic heavy use of toluene has been reported to result in a statistically significant
increase in QT dispersal, a marker for sudden death in a variety of clinical conditions [48] .

"Sudden sniffing death" where a patient has cardiovascular collapse associated with inhalation of volatile
compound has been reported with all classes of hydrocarbon, but is most commonly seen in children who
abuse halogenated hydrocarbons [28,49] . Although a rare event, it is unpredictable and can occur in first
time users. Commonly, it follows exertion or masturbation, both of which lead to increased catecholamine
release [28,50] . It is thought to be due to sensitization of the myocardium to catecholamines that is
possibly accentuated by hypoxia associated with inhalant abuse [1,26,28,36] .
Other effects Pulmonary effects - Hypoxia may result from displacement of oxygen in the alveoli,
particularly with butane, isobutane, propane, and nitrous oxide [33] , or suffocation when the patient huffs
using a plastic bag. Pneumonitis with surfactant dysfunction, bronchospasm, or noncardiogenic or
hemorrhagic pulmonary edema may occur [26,30,47,51] . Exposure to fluorocarbon may cause a reactive
airway syndrome similar to asthma [52] . Pneumothorax may occur if gas is inhaled directly from a
pressurized tank [24] . (See "Spontaneous pneumothorax in children"). Gastrointestinal effects - The
gastrointestinal effects of inhalant use include nausea, vomiting, and abdominal cramps [33,47] . Anorexia
and loss of weight may occur with chronic abuse [24] . Chlorinated solvents such as trichloroethylene and
1,1,1-trichloroethane are hepatotoxic [53] . Renal effects - Volatile substance use may cause metabolic
acidosis, urinary calculi, and glomerulonephritis [4,13,20,33] . Toluene, in particular, causes metabolic
acidosis with profound potassium and phosphate wasting [54,55] . (See "Causes of hypokalemia", section
on Nonreabsorbable anions). Hematologic effects - Inhalant abuse, particularly chronic abuse of benzene,
may cause aplastic anemia and malignancy (eg, leukemia, lymphoma, multiple myeloma) [24,53,56-58] .
Inhalation of methylene chloride (dichloromethane), which is metabolized to carbon monoxide, can result
in a clinically important carboxyhemoglobin level [59] Dermatologic effects - "Glue-sniffer's rash" is an
eczematoid dermatitis with erythema, inflammatory changes, and pruritus that occurs in the perioral area
and extends to the midface. It is caused by the drying effects of hydrocarbons [26] . Burns may occur when
a flammable inhalant ignites. Musculoskeletal effects - Heavy toluene abuse is associated with generalized
muscular weakness (often to the point of quadriparesis) and is typically accompanied by metabolic
acidosis, profound hypokalemia, hypophosphatemia, rhabdomyolysis, and elevated creatine kinase. These
metabolic abnormalities are caused primarily by the conversion of toluene to hippuric acid, with the
subsequent rapid excretion of hippurate in the urine [60] . (See "The Δ anion gap/Δ HCO3 in metabolic
acidosis"). Pregnancy and postnatal effects - Inhalant use during pregnancy may increase the risk of
spontaneous abortion, premature delivery, or fetal malformation [61-63] . Toluene, in particular, is
associated with oral clefts, micrognathia, microcephaly, growth deficiency, and developmental delay [64] .
Infants born to mothers who used inhalants during pregnancy may have symptoms of withdrawal [65] .
Miscellaneous - Trauma can result from falls, drowning, or motor vehicle accidents during the period of
intoxication [66,67] .

Nitrous oxide — Nitrous oxide (NO) is used as a propellant in canisters of whipping cream, as a power
booster in automobiles and motorcycles, and as a sedative/amnestic agent for painful medical and dental
procedures. It usually is inhaled from a balloon [22] . Neurologic, hematologic, and reproductive toxicity
may result from exposure to NO. Neurologic effects — Neurologic toxicity is well documented in patients
who abuse NO. Abuse is associated with a myriad of neurological findings including polyneuropathy [25,68-
70] , ataxia [69,71,72] , and psychosis [71,73] . Neurotoxicity is potentially reversible with B12
supplementation and abstinence from NO.

The neurotoxicty of NO is due to its effects on vitamin B12. Vitamin B12 is a coenzyme of methionine
synthase. Nitrous oxide converts vitamin B12 from the active monovalent form to the inactive bivalent
form thereby causing an irreversible inhibition of methionine synthase. Methionine synthase is a
ubiquitous cytosolic enzyme that plays a crucial role in the generation of methyl groups for the synthesis of
DNA, RNA, and myelin, among other products. The clinical effects are similar to pernicious anemia [74] .
Nitrous oxide is known to precipitate vitamin B12 deficiency when used on a chronic basis or acutely in
patients with marginal stores of vitamin B12 such as the elderly or malnourished [72] . Hematologic effects
- NO has the potential for causing megaloblastic anemia on the basis of its interaction with B12. This has
not been reported in patients who abuse NO, although it has been noted when NO was used as an
anesthetic agent [75,76] . Reproductive effects - Given NO effects on Vitamin B12 and methionine
synthase, it is plausible to assume that NO may have reproductive health risks. Animal studies have
demonstrated fetotoxicity with prolonged exposure to NO. Human studies are difficult to interpret given
the number of confounding variables [20] . However, a study of occupationally exposed healthcare workers
has demonstrated a dose-dependent correlation between NO exposure and DNA damage [77] . Pulmonary
effects - Pneumothorax may occur if gas is inhaled directly from a pressurized tank [24,78] . (See
"Spontaneous pneumothorax in children").

Nitrites — Alkyl nitrites (amyl, butyl, and isobutyl nitrites) have been used and abused for nearly 150 years
[79] . Amyl nitrite is available by prescription for treatment of angina pectoris and as part of the "cyanide
kit" for treatment of cyanide toxicity. It is available in glass ampule encased in a woven absorbent covering.
The ampule is broken or "popped" and the covering held close to the nose and inhaled. Butyl and isobutyl
nitrites (also known as "Rush" and "Climax") are used as room deodorizers, particularly for locker rooms.
They also are sold as "liquid incense." They were banned by the Anti-Drug Abuse Act of 1988, but are still
available illegally, as are isopropyl and cyclohexyl nitrites [79] . They are typically sniffed directly from the
container.

Inhalation of nitrate causes smooth muscle relaxation resulting in peripheral vasodilatation, flushing, and
hypotension with reflex tachycardia. Dilation of cerebral blood vessels causes an increase in intracranial
pressure (the "rush" reportedly experienced by users), headache, nausea, and syncope. Skin irritation,
tracheobronchitis, and allergic reactions with wheezing and pruritus may occur [80,81] .

Inhalation of nitrite may cause acute acquired methemoglobinemia, although this toxicity is much more
common after oral ingestions [79,82] . (See "Extrinsic nonautoimmune hemolytic anemia due to drugs and
toxins", section on Nitrites). Patients with acute acquired methemoglobinemia are symptomatic because
the acute impairment of oxygen delivery to tissues does not allow sufficient time for compensatory
mechanisms. Early symptoms include headache, fatigue, dyspnea, and lethargy. At higher methemoglobin
levels (eg, greater than 70 percent), respiratory depression, altered consciousness, shock, seizures, and
death may occur [15,79,83,84] .

In addition, nitrite vapors are highly flammable, and serious burn injuries can occur if the substance comes
into contact with a candle, cigarette, or other open flame.

ANCILLARY STUDIES — All patients with inhalant intoxication should have the following performed: Pulse
oximetry Electrocardiogram and continuous cardiac monitoring for arrhythmias Urine screen for drugs of
abuse

In addition, the following may be performed, especially in adolescents suspected of chronic abuse [16] :
Complete blood count to evaluate for bone marrow suppression (benzene abuse) Serum electrolytes to
identify hypokalemia and metabolic acidosis (toluene abuse) Liver enzymes (AST [aspartate
aminotransferase] and ALT [alanine aminotransferase], blood urea nitrogen, and serum creatinine to
detect liver or renal impairment (halogenated hydrocarbons) Urine rapid dipstick and microscopic
urinalysis to assess for renal tubular acidosis (chronic toluene use) or findings consistent with interstitial
nephritis (halogenated hydrocarbons). (See "Overview of renal tubular acidosis").

Methemoglobin levels should be obtained if nitrite abuse is suspected or if clinical features of

methemoglobinemia are evident (eg, chocolate brown venous blood or cyanosis that does not resolve with
supplemental oxygen). (See "Clinical features, diagnosis, and treatment of methemoglobinemia", section
on Clinical features).

A venous blood lead level is appropriate in patients in whom volatile abuse using leaded gasoline is
suspected.

A chest radiograph should be obtained in patients with hypoxemia, rales, or respiratory distress.
Abnormalities on chest radiograph may develop as late as 24 hours after exposure in symptomatic patients
[26] . They include increased bronchovascular markings, bibasilar and perihilar infiltrates, and
pneumatoceles [26] .
Although exposure to some hydrocarbons may be confirmed by detection of urinary metabolites (eg,
tricholorethanol after chlorinated hydrocarbon exposure, 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. Thus, the diagnosis of hydrocarbon exposure is based on clinical features.

DIFFERENTIAL DIAGNOSIS — Many other toxins may cause altered mental status or cardiac arrhythmias in
overdose. Often characteristic clinical findings can help differentiate these from inhalant abuse (show table
3). (See "Approach to the child with occult toxic exposure").

When hydrocarbons are inhaled, the characteristic sweet solvent odor of halogenated hydrocarbons or the
"glue" odor of toluene may be detectable on the breath.

TREATMENT — Management of acute inhalant intoxication is supportive. Maintenance of cardiorespiratory

function and removal of the child from the source of the toxin (eg, bottle, rag or bag, or contaminated
clothing) are of primary importance.

Supportive care — Supplemental 100 percent oxygen by a nonrebreather face mask is administered to
treat hypoxia. Airway and breathing - Respiratory depression often responds transiently to tactile
stimulation of the patient. However, clinicians should proceed with endotracheal intubation and
mechanical ventilation if there is any doubt about the patient's ability to breathe adequately on their own
or if pulmonary aspiration poses a significant risk. Circulation - Children with ventricular arrhythmias
should receive countershock treatment according to standard protocols (show algorithm 1 and show
algorithm 2). (See "Defibrillation and cardioversion in children (including automatic external
defibrillation)").

Children who have inhaled halogenated hydrocarbons may develop ventricular arrhythmias in response to
parenterally administered epinephrine or other catecholamines (eg, norepinephrine) because these
treatments can precipitate or worsen arrhythmias in the irritable myocardium [47,58] . In contrast,
amiodarone has been successfully used to treat fluorocarbon-induced ventricular fibrillation [85] . We
suggest that these patients receive intravenous amiodarone (5 mg per kilogram) or lidocaine (1 mg per
kilogram) instead of catecholamines.

Antidotes — Specific antidotes may be necessary to treat methemoglobinemia caused by nitrite exposure
or lead toxicity due to inhalation of leaded gasoline: Patients with methemoglobinemia who are
symptomatic should be treated with high-dose oxygen and intravenous methylene blue. (See "Clinical
features, diagnosis, and treatment of methemoglobinemia", section on Acquired methemoglobinemia).
Lead toxicity may require chelation therapy, depending on the results of lead levels obtained from whole
blood. (See "Childhood lead poisoning: Treatment").

Psychiatric care — Acutely, patients with findings of inhalation abuse should undergo screening for
depression and suicidality [13] .

Long-term management includes referral for addiction treatment and a formal period of detoxification if
indicated [24] . Chronic complications of abuse may resolve if the patient remains drug-free. Polydrug use
and coexisting psychopathology are common occurrences, complicating the treatment of these children.
Residential treatment may improve outcome. Systematic data comparing different approaches to
treatment are lacking [1] .

Disposition — Patients with significant toxicity marked by central nervous system findings (eg, coma,
seizures) or cardiac arrhythmias warrant hospital admission to a unit with pediatric critical care capability.
Children who receive treatment for methemoglobinemia or lead toxicity may also require admission
depending on the degree of toxicity.

Children who express suicidal thoughts need urgent psychiatric evaluation for possible admission to a
mental health facility.

Patients who are asymptomatic in the emergency department or have mild symptoms (eg, lethargy) that
quickly resolve may be discharged home as long as appropriate mental health and primary care follow-up
are assured.

PREVENTION — The American Academy of Pediatrics encourages pediatricians to increase their awareness
of the clinical features and complications of inhalant abuse and to promote education about the health
hazards of inhalants to children, adolescents, parents, teachers, and vendors of volatile substances [27] .

The Massachusetts Department of Public Health has developed a suggested action plan for prevention of
inhalant abuse (www.state.ma.us/dph/inhalant). Their suggestions include the following: Review
purchases of school supplies and substitute water-based products for solvent-based products whenever
possible. Explain that the school is looking for ways to reduce indoor air pollution. Describing solvent-based
products as inhalants or drugs may arouse the curiosity of students. Closely monitor the use of solvent-
based products and gases; in schools, such products should be checked out and in. Provide information to
school faculty, staff, and nurses. Educate parents about the dangers of inhalant abuse. Review the
appropriate use and consequences of misuse of solvents and gases whenever these products are used (eg,
vocational programs, science, art). Develop a plan of action to treat students who use inhalants.

SUMMARY AND RECOMMENDATIONS — Inhalant abuse is common. Unlike nearly all other classes of
drugs, their use is most prevalent among younger adolescents with use peaking between 7th and 9th grade
among school children in the United States. (See "Epidemiology" above).

Abuse Volatile substances produce a rapid feeling of euphoria and inebriation because of their rapid
absorption through the pulmonary vascular bed and their lipophilic properties that allow for quick
deposition into the brain. (See "Mechanism of action" above). The most frequently used inhalants include
glue, shoe polish, or toluene; gasoline or lighter fluid; nitrous oxide or "whippits"; and spray paints. Each of
these substances may contain more than one toxic compound (show table 1). Common methods of abuse
involve sniffing, huffing, or bagging to concentrate the inhaled substance. (See "Epidemiology" above and
see "Techniques (sniffing, huffing, or bagging)" above).

Clinical findings — Inhalant abuse frequently goes undetected. Clues to inhalant abuse include chemical
odors on the breath, skin, or clothes and empty solvent containers or bags, rags, or gauze in the child's
possession or trash. Children may also display characteristic skin changes (eg, glue sniffer's rash) (show
table 2). (See "Recognition of inhalant abuse" above). Inhalant abuse is potentially life-threatening. Death
may result from asphyxia, suffocation, choking on vomitus, careless or dangerous behavior in potentially
dangerous settings, and sudden sniffing death seen with hydrocarbon abuse. (See "Toxicity and clinical
findings by agent" above). Cardiac arrhythmias and central nervous system dysfunction (inebriation,
agitation, seizures) are the most concerning acute toxic effects of volatile inhalants especially,
hydrocarbons. (See "Toxicity and clinical findings by agent" above). Additional findings or chronic toxicity
varies by agent including (see "Toxicity and clinical findings by agent" above):

- Methemoglobinemia (nitrites)
- Lead toxicity (leaded gasoline)
- Polyneuropathy and megaloblastic anemia (nitrous oxide)
- Muscle weakness, renal tubular acidosis (toluene)
- Carbon monoxide poisoning (methylene chloride)
Management Management of acute inhalant intoxication primarily consists of support of airway,
breathing, and circulation (see "Supportive care" above):

- Supplemental 100 percent oxygen by a nonrebreather face mask should be administered to treat
hypoxia.

- Clinicians should proceed with endotracheal intubation and mechanical ventilation if there is any
doubt about the patient's ability to breathe adequately on their own or if pulmonary aspiration poses a
significant risk.

- Children with ventricular arrhythmias should receive treatment according to standard protocols (show
algorithm 1 and show algorithm 2). (See "Defibrillation and cardioversion in children (including automatic
external defibrillation)").

- Children with cardiac arrhythmias caused by inhalation of halogenated hydrocarbons may have
worsening cardiovascular status in response to epinephrine or other catecholamines (eg, dopamine,
norepinephrine). We suggest that these patients receive intravenous amiodarone (5 mg per kilogram) or
lidocaine (1 mg per kilogram) instead of catecholamines (Grade 2C). Specific antidotes may be necessary to
treat methemoglobinemia caused by nitrite exposure or lead toxicity due to inhalation of leaded gasoline.
(See "Clinical features, diagnosis, and treatment of methemoglobinemia", section on Acquired
methemoglobinemia and see "Childhood lead poisoning: Treatment"). Acutely, patients with findings of
inhalation abuse should undergo screening for depression and suicidality. Long-term management includes
referral for addiction treatment and a formal period of detoxification if indicated. (See "Psychiatric care"
above).

ACKNOWLEDGMENT — We are saddened by the untimely death of Michael Shannon, MD, MPH, who
passed away in March 2009. UpToDate wishes to acknowledge Dr. Shannon's many contributions to
pediatric medicine and emergency medicine, in particular, his work as our section editor for pediatric
toxicology, and prior editorial work in pediatric resuscitation.

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