Updated: Feb 5, 2008
Inhalant-related psychiatric disorders are a heterogenous group of illnesses caused by the abuse of solvents, glues, paint, fuels, or other volatile substances.
Although huffing, as it is commonly referred to, has existed since ancient times, it has regained popularity in recent years. The resurgence of this newfound phenomenon is believed to be due to a number of variables (eg, low cost, availability, peer influence, rapid mood-elevating quality), which have made this potentially fatal activity popular among many young people today. A relationship may exist between inhalant use and an increased risk of frequent drinking, binge-type drinking, smoking, and the use of other drugs, making inhalant-related disorders a new public health problem deserving of more attention.
Because most of the products used in huffing are legal household products, they are easily accessible and are relatively inexpensive to obtain. Most recent reports state that nearly 1000 such products are available to huffers every day. Some of the most common products used for inhaling are spray paint (containing butane, lead, or propane), permanent markers, correction fluid (eg, Liquid Paper, Wite-Out), glue (containing toluene or ethyl acetate), lighter fluid (containing butane or isopropane), hairspray (containing butane or propane), propane, gasoline (containing lead), kerosene, and nitrous oxide from a balloon. Because of the increase in awareness of the potential dangers caused by sniffing or inhaling, laws have been established that prohibit the sale of certain products to minors; however, enforcing these laws is difficult.
Generally, adolescents practice huffing; however, younger children and young adults also engage in this potentially fatal act. Huffing involves placing the volatile substance (most commonly some type of chemical, eg, butane found in spray paint, acetone found in nail polish remover) on a rag or in a closed container (eg, soda can, plastic bag [termed "bagging"]), placing the rag over the nose and mouth, and breathing deeply to cause mood-altering effects.
The inhalation of these substances can cause permanent organ damage and death. Huffing is a problem in the United States and abroad, and it accounts for a large portion of emergency department visits. Diagnosis of inhalant-related psychiatric disorders is based on Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-Text Revision (DSM-IV-TR)1 or International Classification of Diseases, 10th Revision criteria.
Although studies have shown that inhalant abuse has been difficult to diagnose, treatment efforts for inhalant-related psychiatric disorders may be promising. Treatment consists of psychotherapy (eg, 12-step programs similar to Alcoholics Anonymous, cognitive behavior therapy, rational-emotive therapy) and pharmacotherapy. Early intervention may play a key role because engagement in this activity may lead to the use of other drugs.
Inhalants are CNS depressants (similar to alcohol) and are thought to influence gamma-aminobutyric acid (GABA), although the exact mechanism has yet to be determined. No evidence associates inhalants with the opiate system; N -methyl-D-aspartate may play a role.
Medical effects
Psychiatric effects
The psychiatric effects of inhalant abuse include impaired judgment, confusion, fright, hyperactivity, anxiety, acute psychosis, increased violence and aggressive behavior, depression, organic brain syndrome (ie, coarse tremor, staggering gait, speech problems, thought disorder), abuse, tolerance and dependence, hallucinations, decreased intelligence quotient, intoxication, mood disorder, dementia, and withdrawal. Inhalant abuse also affects social, educational, and economic status. In addition, persons who abuse inhalants are more likely to be involved in accidents (eg, falls, burns, frostbite). Importantly, note that the number of planned suicides in persons with inhalant-related psychiatric disorders is equal to the number of planned suicides in persons with other psychiatric illnesses; however, the number of unplanned suicides is dramatically higher in children and adolescents who engage in huffing.
Of the population, 6% have tried huffing once and 1% are current users. According to statistics gathered by the National Inhalant Prevention Coalition, ". . . by the time a student reaches the eighth grade, 1 in 5 will have used inhalants."2 Inhalants account for 1% of substance-induced death. Huffing is more common in rural versus inner-city adolescents, although exact numbers are difficult to determine.
Incidents occur worldwide, but determining exact numbers is difficult.
Inhalants work quickly by passing through the nasal cavity and entering the lungs, bloodstream, and brain, all in a matter of seconds. The chemical vapors of the inhalants are dissolved into the fatty tissues of the brain. The results of inhalant abuse affect virtually every organ and function of the body, including the brain, heart, lungs, kidneys, muscle, bone marrow, and peripheral and central nervous systems, to name a few. Persons who abuse inhalants long-term may become permanently disabled, losing their ability to walk, talk, and think. The possible damage depends on the chemical used, the frequency with which it is used, and the amount used.
Persons who abuse inhalants predominantly are white; however, studies have found minority involvement in subcultures of American and Canadian Indians and in Hispanic persons with low-income status. Inhalant use is more common in rural and suburban areas than in urban areas.
Although long-term inhalant use is more common in males than in females, experimental use is equally common in males and females.
Experimental use of inhalants normally occurs in late childhood and early adolescence (age 9-13 y). Long-term use appears during early and late adolescence (age 12-17 y). Inhalants are commonly the first substance used before the onset of substance (eg, tobacco, alcohol, marijuana, cocaine) abuse occurs. Inhalant abuse among younger children and adults is less frequent, although it does occur.
Persons who abuse inhalants commonly share characteristics that may help identify them as users. While taking the patient's history, determine their diagnosis based on the DSM-IV-TR criteria for inhalant abuse, inhalant dependence, inhalant intoxication, substance intoxication delirium, substance-induced persistent dementia, substance-induced psychotic disorder, substance-induced mood disorder, substance-induced anxiety disorder, and inhalant-related disorder not otherwise specified (NOS). Pay close attention to the signs and symptoms commonly associated with persons who abuse inhalants (see below). Inquire about other drugs of abuse and a family history of drug and alcohol abuse or addiction. The diagnosis is based solely on the history and a very high index of suspicion.
Much speculation exists on the cause of inhalant abuse. Its popularity appears to be based on the fact that the substances are easily accessible to young people. The products used are fairly easy to hide, fairly inexpensive, easily attainable, and, for the most part, legal. Therefore, inhalants are readily becoming the drugs of choice. Many adolescents are becoming interested in the instant gratification huffing offers, while others engage in huffing merely because their friends are doing it. However, one subgroup of young people who abuse inhalants do so because they have seen their parents or older siblings abuse illegal drugs, and these young people have decided that huffing is the activity they choose to begin their drug use and addiction.
Anxiety Disorders
Delirium
Depression
Stimulants
Because substance-induced psychiatric disorders resemble the primary mental disorders (ie, major depression, generalized anxiety disorder), these should be considered in the differential diagnosis.
Other disorders to consider include the following:Findings may include evidence of heavy metal damage to specific organs, such as that caused by lead in gasoline and paint, and inflammation, rhabdomyolysis, brain atrophy, and renal tubular acidosis.
If psychosis or delirium is present, use an antipsychotic such as risperidone or haloperidol and/or an anticonvulsant such as carbamazepine. Avoid benzodiazepines because they may worsen respiratory depression.
Reduce psychosis and aggressive behavior. All antipsychotics may be equally efficacious, but their adverse effect profiles are different. The atypical antipsychotics such as risperidone, olanzapine, quetiapine, and ziprasidone have an advantage in the adverse effect profile, especially with their lower risk to cause adverse extrapyramidal effects and tardive dyskinesia.
Indicated for psychosis, also to treat motor and vocal tics in children and adults.
0.5-5 mg PO bid; 2-5 mg IM q4-8h
<3 years: Not established
3-12 years (15-40 kg): 0.05-0.15 mg/kg/d PO
>12 years: Administer as in adults
May increase TCA serum concentrations and hypotensive action of antihypertensive agents; phenobarbital or carbamazepine may decrease effects; coadministration with anticholinergics may increase intraocular pressure; encephalopathylike syndrome associated with concurrent administration of lithium
Documented hypersensitivity; narrow-angle glaucoma; bone marrow suppression; severe cardiac or liver disease; severe hypotension; subcortical brain damage
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Severe neurotoxicity manifesting as rigidity or inability to walk or talk may occur in patients with thyrotoxicosis also receiving antipsychotics; if IV/IM, watch for hypotension; caution in diagnosed CNS depression or cardiac disease; if history of seizures, benefits must outweigh risks; significant increase in body temperature may indicate intolerance to antipsychotics (discontinue if it occurs); elevates prolactin levels
Binds to dopamine D2 receptor with 20-times lower affinity than 5-HT2–receptor affinity. Improves negative symptoms of psychoses and reduces incidence of adverse extrapyramidal effects.
0.25-6 mg/d PO qd/bid
Not established
Coadministration with carbamazepine may decrease effects; may inhibit effects of levodopa; clozapine may increase levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Orthostatic hypotension, seizures, dysphagia, hyperprolactinemia, cognitive and motor impairment, priapism, and rare thrombotic thrombocytopenic purpura may occur
Usually used to treat seizures but have been used for treatment of manic-depressive symptoms and behavioral agitation. Other anticonvulsants such as valproic acid (Depakene) or divalproex sodium (Depakote) may also be as effective as carbamazepine.
Used to treat epilepsy and trigeminal neuralgia.
200-600 mg PO bid; 800-1200 mg/d maintenance
<6 years: 10-20 mg/kg/d PO bid; <35 mg/kg/d maintenance
6-12 years: 100 mg PO bid; 400-800 mg/d maintenance
>12 years: Administer as in adults
Do not coadminister with MAOIs; cimetidine may increase toxicity, especially if taken in first 4 wk of therapy; grapefruit juice, danazol, isoniazid, cimetidine, fluoxetine, erythromycin, and phenelzine increase plasma levels; phenytoin, alprazolam, clonazepam, primidone, and phenobarbital decrease levels
Decreases levels of imipramine, phenothiazines, haloperidol, ritonavir, contraceptives, risperidone, thiothixene, corticosteroids, doxycycline, trazodone, and amitriptyline; increases plasma levels of diltiazem and verapamil; can reduce its own level by autoinduction; coadministration with clozapine further increases bone marrow toxicity and resulting agranulocytosis
Documented hypersensitivity; administration of MAOIs within 14 d; history of liver disease and blood dyscrasias
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Very small but significant risk of agranulocytosis or aplastic anemia; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness; caution in mixed seizure disorders and cardiac, renal, liver, or hematological problems; report any indications of blood dyscrasias (eg, easy bruising, sore throats, fever, rash)
Although mechanism of action is not established, activity may be related to increased brain levels of GABA or enhanced GABA action. Valproate also may potentiate postsynaptic GABA responses, affect potassium channel, or have a direct membrane-stabilizing effect.
Has proven effectiveness in treating and preventing mania. Classified as a mood stabilizer and can be used alone or in combination with lithium. Useful in treating patients with rapid-cycling bipolar disorders and has been used to treat aggressive or behavioral disorders. A combination of valproic acid and valproate (ie, divalproex [Depakote]) has been effective in treating persons in manic phase, with a success rate of 49%.
10-20 mg/kg/d PO divided bid; may gradually titrate upward by 5-10 mg/kg/d at weekly intervals; not to exceed 30-60 mg/kg/d
Administer as in adults
Coadministration with cimetidine, salicylates, felbamate, and erythromycin may increase toxicity; rifampin may significantly reduce valproate levels; in pediatric patients, protein binding and metabolism of valproate decrease when taken concomitantly with salicylates; coadministration with carbamazepine may result in variable changes of carbamazepine concentrations with possible loss of seizure control; valproate may increase diazepam and ethosuximide toxicity (monitor closely); valproate may increase phenobarbital and phenytoin levels while either one may decrease valproate levels; valproate may displace warfarin from protein binding sites (monitor coagulation tests); may increase zidovudine levels in HIV seropositive patients
Documented hypersensitivity; hepatic disease/dysfunction; hyperammonemic encephalopathy and urea cycle disorders
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Thrombocytopenia and abnormal coagulation parameters have occurred; the risk of thrombocytopenia increases significantly at total trough valproate plasma concentrations > 110 mcg/mL in females and 135 mcg/mL in males; at periodic intervals and prior to surgery determine platelet counts and bleeding time before initiating therapy; reduce dose or discontinue therapy if hemorrhage, bruising or a hemostasis/coagulation disorder occur; hyperammonemia may occur, resulting in hepatotoxicity; monitor patients closely for appearance of malaise, weakness, facial edema, anorexia, jaundice, and vomiting; may cause drowsiness
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huffing, sniffing, bagging, volatile substance abuse, substance abuse, drug abuse, drug-induced psychosis, inhalant abuse, inhalant dependence, inhalant intoxication, substance intoxication delirium, substance-induced anxiety disorder, inhalant-related disorder NOS, inhalant-related disorder not otherwise specified, substance-induced psychotic disorder, depression, general anxiety disorder, sudden sniffing death syndrome
Guy E Brannon, MD, Associate Clinical Professor of Psychiatry, Louisiana State University Health Sciences Center; Director, Adult Psychiatry Unit, Chemical Dependency Unit, Clinical Research, Brentwood Behavior Health Company
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Barry I Liskow, MD, Vice Chairman, Director Psychiatry Residency Program, Professor, Department of Psychiatry, University of Kansas Medical School
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Iqbal Ahmed, MBBS, Professor, Department of Psychiatry, John A Burns School of Medicine, University of Hawaii
Iqbal Ahmed, MBBS is a member of the following medical societies: Academy of Psychosomatic Medicine, American Association for Geriatric Psychiatry, American Neuropsychiatric Association, and American Psychiatric Association
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Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
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