Sudden sniffing death syndrome<\/a> 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\u0092re not dead, they\u0092re 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??)<\/p>\n <\/p>\n
Nitrous Oxide (Whippets, Laughing Gas)<\/p>\n
Nanging is the term for use<\/p>\n
Can get asphyxia or metheglobinemia<\/p>\n
Long term abuse leads to myeloneuropathy or megaloblastic anemia both from decreased B12<\/p>\n
Amyl Nitrite (Poppers)<\/p>\n
can induce methemoglobinemia<\/p>\n
vasodilator peripheral and cerebral<\/p>\n
deaths are usually from anoxia<\/p>\n
chronic users get B12 depletion<\/p>\n
<\/h4>\nHalogenated Hydrocarbons (trichloroethylene, trichloroethane)<\/h4>\n
Correction fluid and freon<\/p>\n
Sudden death due to catecholamine sensitization of the heart.\u00a0 May need b blockers<\/p>\n
Lungs (Bronchospasm, hypoxia), CNS (Brain damage), Heart (Sensitizes to catecholamines)<\/p>\n
Low viscosity=toxicity<\/p>\n
Aspiration is facilitated by low viscosity, passes right down trachea.\u00a0 Also dangerous are low surface tension and low viscosity, as allows inhalation and quicker spread to entire lungs.<\/p>\n
Radiographic changes 30 minutes post-exposure<\/p>\n
Avoid catecholamines unless absolutely necessary<\/p>\n
Do not lavage b\/c non-toxic to gi but aspiration=death<\/p>\n
Camphor causes seizures<\/p>\n
Halogenated-liver and dysrhythmias, needs gi decontamination<\/p>\n
Aromatics-bone marrow cancer<\/p>\n
Metals<\/p>\n
Pesticides<\/p>\n
Gasoline<\/h4>\n
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)<\/em><\/p>\nToluene<\/h4>\n
Glue or spray paint<\/p>\n
mixed met. Acidosis from RTA c hypokalemia, Urine pH>5.5<\/p>\n
and hippuric acid is a metabolite of toluene giving anion gap<\/p>\n
Can lead to cerebellar ataxia and end organ damage to all organs<\/p>\n
Methylene Chloride<\/h4>\n
In paint strippers and wax removers<\/p>\n
and aerosols<\/p>\n
Metabolized in the liver to CO<\/p>\n
<\/p>\n
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).<\/p>\n
Chloral Hydrate<\/h4>\n
the pediatric sedative has the same risk profile as sniffer\/huffers<\/p>\n
add to ETOH and you have a Mickey Finn<\/em>, the classic knockout drops<\/p>\n <\/p>\n
<\/p>\n
Unintentional Hydrocarbon Ingestions<\/h3>\n
Hydrocarbons are organic compounds derived from sources such as animal fats, plant oils, petroleum and<\/p>\n
natural gas. They are found in a wide variety of household products. Toxicity depends on their physical<\/p>\n
(viscosity, volatility) and chemical (aliphatic, aromatic, halogenated) properties. Aliphatic hydrocarbons (i.e.<\/p>\n
petroleum distillates) such as lamp oil, gasoline, kerosene and furniture polish are not readily absorbed from<\/p>\n
the GI tract and do not cause serious systemic toxicity unless aspirated. Aspiration risk increases as viscosity<\/p>\n
decreases. As little as one milliliter can penetrate deep into the bronchopulmonary tree when aspirated and<\/p>\n
directly destroy the lung tissue leading to inflammation, shock, cardiopulmonary collapse and death. Aromatic<\/p>\n
and halogenated hydrocarbons (e.g. benzene, toluene, xylene, tetrachloroethane) can pose significant risk of<\/p>\n
systemic toxicity resulting in neurological, cardiac, gastrointestinal, hepatic and renal toxicity.<\/p>\n
Following unintentional ingestion of aliphatic hydrocarbons, the majority of patients remain asymptomatic.<\/p>\n
These patients can be closely observed at home for 6 hours post ingestion. All patients with initial symptoms<\/p>\n
suggesting aspiration (e.g. vomiting or persistent coughing and choking) should be referred to an ED. Tachypnea,<\/p>\n
rales, rhonchi, bronchospasm, and signs of respiratory distress may quickly follow. CNS depression can<\/p>\n
occur secondary to hypoxia.<\/p>\n
Gastric emptying should be avoided for aliphatic hydrocarbons as it increases the risk of aspiration. GI decontamination<\/p>\n
may be recommended for other hydrocarbons or if the hydrocarbon contains a toxic substance<\/p>\n
(e.g. insecticides, heavy metal). A chest x-ray should be obtained at 6 hours after ingestion; earlier x-rays may<\/p>\n
be negative as it takes time for changes to evolve. Patients who are asymptomatic at 6 hours and have normal<\/p>\n
radiographs can be discharged home. If, at 6 hours, symptoms continue and\/or the chest Xray is abnormal,<\/p>\n
consider admission for further observation and treatment. Monitor ABGs, pulse oximetry and pulmonary function<\/p>\n
tests in symptomatic patients. Therapy with oxygen, bronchodilators, intubation and ventilation should be<\/p>\n
provided as needed. There is no basis for prophylactic antibiotic and\/or steroid treatment for hydrocarbon<\/p>\n
pneumonitis. (From Maryland ToxLine)<\/p>\n
<\/p>\n
<\/p>\n
|\u00a0\u00a0 \u00a0\u00a0 |\u00a0\u00a0 \u00a0\u00a0 |<\/p>\n","protected":false},"excerpt":{"rendered":"
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