Basics
Description
- Prototypical volatile hydrocarbon
- Clear, colorless liquid with sweet odor
Etiology
- Abused for its euphoric effect
- Occupational exposures
- Used as organic solvent found in:
- Oil paints and stains
- Paint thinners
- Glues, inks, dyes, correction fluid
- Coolants
- Petroleum products
- Aerosolized household products
- Degreasers
- Production and use of gasoline is largest source of exposure
- Prevalent in adolescent age group:
- Inexpensive "high " ¯ with readily available sources
- Many psychosocial problems
- May develop chronic neurologic dysfunction
- Mechanism:
- Rapidly absorbed by inhalation
- Readily crosses blood " “brain barrier, reaching high concentrations in brain
- May sensitize myocardium to dysrhythmogenic effect of catecholamines
- Inhibits myocardial voltage-gated sodium channels and inward rectifying potassium channels
- Alveolar excretion and liver metabolism
- Methods of intoxication:
- Sniffing: Simple inhalation of substance directly from container
- Huffing: Vapors inhaled through cloth saturated with substance
- Bagging: Vapors inhaled from bag containing substance
- Toxic range:
- 100 ppm: Impairment of psychomotor and perceptual performance
- 500 " “800 ppm: Headache, drowsiness, nausea, weakness, and confusion, potential lethal ranges
- >800 ppm: Convulsions, ataxia, staggering gait
- 10,000 " “30,000 ppm: Anesthesia within 1 min
Diagnosis
Signs and Symptoms
- Acute:
- Neurologic:
- Depression
- Euphoria
- Ataxia
- Dizziness
- Seizures
- Cardiac:
- Pulmonary:
- Chemical pneumonitis
- Pulmonary edema
- Electrolytes:
- Hypokalemia
- Hypocalcemia
- Hyperchloremic metabolic acidosis, likely from hippuric acid metabolite
- GI:
- Abdominal pain
- Nausea, vomiting
- Hematemesis
- Renal:
- Distal renal tubular acidosis
- Hematuria
- Proteinuria
- Musculoskeletal:
- Chronic:
- Neurologic:
- Peripheral neuropathy (diffuse demyelination)
- Leukoencephalopathy
- Cerebral/cerebellar atrophy
- Optic atrophy
- Dementia
- Cognitive/neurobehavioral abnormalities
- Cardiac:
- Dysrhythmias
- Dilated cardiomyopathy
- Renal:
- Distal renal tubular acidosis
- Renal failure
- Fanconi syndrome
- Musculoskeletal:
- Psychiatric:
- Fetal solvent syndrome reported from mothers who chronically abused toluene while pregnant, resembles fetal alcohol syndrome
- Infant more likely premature, low birth weight, microcephaly, and developmental delay
History
- Detailed history of sniffing, huffing, bagging, or other abuse of paints/solvents
- Occupational exposures
Physical Exam
- Presence of agent on lips, nose, or clothes (metallic paint has highest concentration)
- Perioral eczematous dermatitis from chronic huffing or bagging
- Odor of agents
Essential Workup
- Detailed physical exam
- CXR for suspected pneumonitis
Diagnosis Tests & Interpretation
Lab
- Electrolytes, BUN, creatinine, glucose:
- Hypokalemia
- Normal or high anion gap metabolic acidosis
- Hyperchloremia
- Impaired renal function
- Severe hypocalcemia/hypophosphatemia
- Urinalysis:
- Check for myoglobin (rhabdomyolysis)
- Hematuria and protein often present
- Creatinine kinase if suspect rhabdomyolysis
- Alcohol level " ”often coingestant
- Liver enzymes, prothrombin time (PT), partial thromboplastin time (PTT), INR, as may cause hepatotoxicity
- Urine for hippuric acid (metabolite of toluene):
- Confirms exposure but does not correlate with systemic effects
- Serum levels only detectable for short time after exposure
Imaging
- EKG:
- For atrial and ventricular dysrhythmias
- CXR:
- Indicated if dyspnea or low oxygen saturation
- Chemical pneumonitis
- CT head:
- For altered mental status/chronic exposure
- Cerebral/cerebellar atrophy, white matter hypodensity
Diagnostic Procedures/Surgery
CSF often unremarkable but may be indicated for altered mental status to rule out other etiologies ‚
Differential Diagnosis
- Alcohol intoxication
- Other hydrocarbon abuse
- Other inhalants (nitrous oxide, difluoroethane, butane, etc.)
- Methanol
- Ethylene glycol
- Salicylate
- Heavy metal exposure
- Guillain " “Barre syndrome
- Metabolic abnormalities
Treatment
Pre-Hospital
- Rapid onset of toxicity
- Death possible with sudden cardiac dysrhythmias (sudden sniffing death), often from catecholamine surge (e.g., eluding police)
- Topical decontamination as needed
- Forced emesis is not indicated:
- Decreased level of consciousness may lead to aspiration.
Initial Stabilization/Therapy
- ABCs
- Supplemental oxygen
- Cardiac monitor
- 0.9% NS IV access
- Naloxone, thiamine, and check glucose if altered mental status
Ed Treatment/Procedures
- Treat cardiac dysrhythmias in standard fashion:
- Consider ˇ ²-blocker for tachydysrhythmias.
- Monitor respiratory status with pulse oximetry, CXR, and ABG if significant inhalation.
- Steroids not recommended for pneumonitis.
- Correct metabolic abnormalities:
- Potassium
- Calcium
- Phosphate
- Acidosis resolves with IV fluids.
- If rhabdomyolysis, maintain high urine output.
- Gastric decontamination for oral ingestion rarely useful and may cause harm:
- Charcoal does not bind hydrocarbons well and stomach distention may predispose to vomiting and aspiration.
Medication
- Dextrose: D50W, 1 amp: 50 mL or 25 g (peds: D25W, 2 " “4 mL/kg) IV
- Naloxone (Narcan): 2 mg (peds: 0.1 mg/kg) IV or IM initial dose
- Thiamine (vitamin B1): 100 mg (peds: 50 mg) IV or IM
Follow-Up
Disposition
Admission Criteria
- Altered mental status
- Dysrhythmias
- Hepatic dysfunction
- Renal failure
- Rhabdomyolysis
- Severe metabolic derangements
- Refractory hypokalemia
Discharge Criteria
After 4 " “6 hr of observation: ‚
- Mental status at baseline
- No evidence of cardiac, metabolic, or neurologic derangement
Follow-Up Recommendations
- Psychiatry referral for intentional/repeated ingestions and addiction counseling
- Cessation of use is most important intervention
Pearls and Pitfalls
- Myocardial sensitization to catecholamines:
- Possibility of sudden dysrhythmia/death
- Cardiac dysrhythmias have poor prognosis
- Monitor and replete electrolyte abnormalities.
Additional Reading
- Bowen ‚ SE, Hannigan ‚ JH. Developmental toxicity of prenatal exposure to toluene. AAPS J. 2006;8:E419 " “E424.
- Filley ‚ CM, Halliday ‚ W, Kleinschmidt-Demasters ‚ BK. The effects of toluene on the central nervous system. J Neuropathol Exp Neurol. 2004;63:1 " “12.
- Long ‚ H. Inhalants. In: Goldfrank ‚ LR, ed. Goldfranks Toxicologic Emergencies. 9th ed. New York, NY: McGraw-Hill; 2011:1157 " “1165.
- Tang ‚ HL, Chu ‚ KH, Cheuk ‚ A, et al. Renal tubular acidosis and severe hypophosphataemia due to toluene inhalation. Hong Kong Med J. 2005;11(1):50 " “53.
- Yucel ‚ M, Takagi ‚ M, Walterfang ‚ M, et al. Toluene misuse and long-term harms: A systematic review of the neuropsychological and neuroimaging literature. Neurosci Biobehav Rev. 2008;32:910 " “926.
The author would like to provide special thanks to the author of the prior edition, Matthew Valento. ‚
Codes
ICD9
- 305.90 Other, mixed, or unspecified drug abuse, unspecified use
- 982.0 Toxic effect of benzene and homologues
ICD10
- F18.10 Inhalant abuse, uncomplicated
- F18.120 Inhalant abuse with intoxication, uncomplicated
- T52.2X1A Toxic effect of homologues of benzene, accidental (unintentional), initial encounter
- T52.2X4A Toxic effect of homologues of benzene, undetermined, initial encounter
SNOMED
- 212821000 Toxic effect of homologues of benzene (disorder)
- 70340006 inhalant abuse (disorder)
- 445931006 Poisoning by fumes (disorder)
- 216671002 Accidental poisoning by petroleum solvents (disorder)