Sniffing: directly from can
Bagging: from plastic bag, i.e. potato chip bag
Huffing: sprayed onto rag
Sudden sniffing death syndrome is, ahem, sudden death after huffing an inhalant, thought to be due to a catecholamine surge from a huffer who is startled or just got caught. Apparently if theyre not dead, theyre incredibly tachycardic (perhaps pulseless VT), and the treatment is actually beta blockers to try to stop the catecholamine surge. Certainly counter-intuitive. (From the Central Line??)
Nitrous Oxide (Whippets, Laughing Gas)
Nanging is the term for use
Can get asphyxia or metheglobinemia
Long term abuse leads to myeloneuropathy or megaloblastic anemia both from decreased B12
Amyl Nitrite (Poppers)
can induce methemoglobinemia
vasodilator peripheral and cerebral
deaths are usually from anoxia
chronic users get B12 depletion
Halogenated Hydrocarbons (trichloroethylene, trichloroethane)
Correction fluid and freon
Sudden death due to catecholamine sensitization of the heart. May need b blockers
Lungs (Bronchospasm, hypoxia), CNS (Brain damage), Heart (Sensitizes to catecholamines)
Low viscosity=toxicity
Aspiration is facilitated by low viscosity, passes right down trachea. Also dangerous are low surface tension and low viscosity, as allows inhalation and quicker spread to entire lungs.
Radiographic changes 30 minutes post-exposure
Avoid catecholamines unless absolutely necessary
Do not lavage b/c non-toxic to gi but aspiration=death
Camphor causes seizures
Halogenated-liver and dysrhythmias, needs gi decontamination
Aromatics-bone marrow cancer
Metals
Pesticides
Gasoline
Abuse of gasoline usually involves inhalation directly from a can or glass jar. Intoxication occurs after 10-20 breaths and lasts for 3-5 hours. Intoxication is frequently accompanied by nausea and vomiting, which increases the risk of aspiration during the inebriated state. Where “leaded” gas is still available, lead toxicity can occur. The primary additive is tetraethyl lead. Tetraethyl lead and its metabolites are extremely neurotoxic and can produce a syndrome of ataxia, tremor, and encephalopathy in chronic users. (EM Reports)
Toluene
Glue or spray paint
mixed met. Acidosis from RTA c hypokalemia, Urine pH>5.5
and hippuric acid is a metabolite of toluene giving anion gap
Can lead to cerebellar ataxia and end organ damage to all organs
Methylene Chloride
In paint strippers and wax removers
and aerosols
Metabolized in the liver to CO
Methylene chloride, a solvent found in paint remover and aerosol propellants, is a source of significant toxicity after inhalation exposure due tp carbon monoxide (Emerg Med Clin N Am, Vol. 22, pg. 987).
Chloral Hydrate
the pediatric sedative has the same risk profile as sniffer/huffers
add to ETOH and you have a Mickey Finn, the classic knockout drops
Unintentional Hydrocarbon Ingestions
Hydrocarbons are organic compounds derived from sources such as animal fats, plant oils, petroleum and
natural gas. They are found in a wide variety of household products. Toxicity depends on their physical
(viscosity, volatility) and chemical (aliphatic, aromatic, halogenated) properties. Aliphatic hydrocarbons (i.e.
petroleum distillates) such as lamp oil, gasoline, kerosene and furniture polish are not readily absorbed from
the GI tract and do not cause serious systemic toxicity unless aspirated. Aspiration risk increases as viscosity
decreases. As little as one milliliter can penetrate deep into the bronchopulmonary tree when aspirated and
directly destroy the lung tissue leading to inflammation, shock, cardiopulmonary collapse and death. Aromatic
and halogenated hydrocarbons (e.g. benzene, toluene, xylene, tetrachloroethane) can pose significant risk of
systemic toxicity resulting in neurological, cardiac, gastrointestinal, hepatic and renal toxicity.
Following unintentional ingestion of aliphatic hydrocarbons, the majority of patients remain asymptomatic.
These patients can be closely observed at home for 6 hours post ingestion. All patients with initial symptoms
suggesting aspiration (e.g. vomiting or persistent coughing and choking) should be referred to an ED. Tachypnea,
rales, rhonchi, bronchospasm, and signs of respiratory distress may quickly follow. CNS depression can
occur secondary to hypoxia.
Gastric emptying should be avoided for aliphatic hydrocarbons as it increases the risk of aspiration. GI decontamination
may be recommended for other hydrocarbons or if the hydrocarbon contains a toxic substance
(e.g. insecticides, heavy metal). A chest x-ray should be obtained at 6 hours after ingestion; earlier x-rays may
be negative as it takes time for changes to evolve. Patients who are asymptomatic at 6 hours and have normal
radiographs can be discharged home. If, at 6 hours, symptoms continue and/or the chest Xray is abnormal,
consider admission for further observation and treatment. Monitor ABGs, pulse oximetry and pulmonary function
tests in symptomatic patients. Therapy with oxygen, bronchodilators, intubation and ventilation should be
provided as needed. There is no basis for prophylactic antibiotic and/or steroid treatment for hydrocarbon
pneumonitis. (From Maryland ToxLine)
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