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You are here: Home / 14. Toxicology / Hydrocarbons and Volatile Inhalants

Hydrocarbons and Volatile Inhalants

July 14, 2011 by CrashMaster

 

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 they’re not dead, they’re 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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Filed Under: 14. Toxicology


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