Hydrogen sulfide toxicity: Difference between revisions
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*Can give nitrite component of cyanide antidote kit (do NOT give the thiosulfate portion): | *Can give nitrite component of cyanide antidote kit (do NOT give the thiosulfate portion): | ||
**Theoretically increasing methemoglobin formation in blood will cause conversion of sulfide to sulfmethemoglonin (less toxic) | **Theoretically increasing methemoglobin formation in blood will cause conversion of sulfide to sulfmethemoglonin (less toxic) | ||
**Sodium nitrite (3% NaNO2) IV over 2-4 minutes | **Amyl nitrite | ||
**Sodium nitrite (3% NaNO2) IV over 2-4 minutes; adult dose 10 mL | |||
**Obtain methemoglobin level 30 minutes after dose (desired level < 30%) | **Obtain methemoglobin level 30 minutes after dose (desired level < 30%) | ||
*Hyperbaric oxygen therapy (though not proven to have any benefit)< | *Hyperbaric oxygen therapy (though not proven to have any benefit)<ref>Goldfrank et. al. Hydrogen Sulfide Poisoning. In: Goldfrank et. al. Goldfrank’s Toxicologic Emergencies. New York, NY: McGraw Hill. 2002. 1504-1507. </ref> | ||
==Disposition== | ==Disposition== | ||
Revision as of 20:33, 13 February 2016
General Information
- Colorless, flammable gas
- Encountered in following industries: oil, gas, organic decomposition (sewer and manure), roofing asphalt tanks
- Most common fatal gas exposure
- “Rotten egg” smell which diminishes with high concentrations or prolonged low concentration exposure
- Often used in suicide attempts: acidic detergent (toilet bowl cleaner) is mixed with bath salts or pesticides</ref>Tintinalli et. al. Hydrogen Sulfide. In: Tintinalli et. al. Emergency Medicine A Comprehensive Study Guide. New York, NY: McGraw Hill. 2011. 1320.</ref>
Mechanisms of toxicity
- Highly lipid soluble
- Disrupts oxidative phosphorylation by inhibiting cytochrome oxidase aa3 (toxicity through cellular asphyxia and impairs ATP production) => lactate accumulation and metabolic acidosis
- Causes hyperpolarization of potassium-mediated channels in neurons
- Potentiates neuronal inhibitory mechanisms
- Alters brain neurotransmitter content and release
Symptoms
- Respiratory: dyspnea, cyanosis, hemoptysis, rales, delayed pulmonary edema
- Ophthalmic: conjunctivitis, corneal ulceration, corneal scarring
- Central nervous system: headache, weakness, disequilibrium, intention tremor, muscle rigidity, loss of consciousness, seizures, coma
- Gastrointestinal: green-gray line on gingiva, nausea, vomiting
- Cardiovascular: chest pain, bradycardia
- Neuropsychiatric: amnesia, lack of insight, disorientation, delirium, dementia
- Death
Differential Diagnosis:
- Carbon Monoxide Toxicity
- Cyanide Toxicity
- Hydrocarbons Toxicity
- Smoke Inhalation Injury
Diagnosis
- No single test to verify exposure or levels
- ABG Interpretation: metabolic acidosis and normal oxygen saturation (unless pulmonary edema present)
- Elevated lactate
- Discolored copper coins found on patient may be helpful in diagnosis</ref>Gresham, C. Hydrogen Sulfide Poisoning. Medscape: http://emedicine.medscape.com/article/815139-overview. Updated Jan 27, 2014. Accessed Aug 8, 2014.</ref>
Treatment
- Removal from source
- 100% oxygen
- Can give nitrite component of cyanide antidote kit (do NOT give the thiosulfate portion):
- Theoretically increasing methemoglobin formation in blood will cause conversion of sulfide to sulfmethemoglonin (less toxic)
- Amyl nitrite
- Sodium nitrite (3% NaNO2) IV over 2-4 minutes; adult dose 10 mL
- Obtain methemoglobin level 30 minutes after dose (desired level < 30%)
- Hyperbaric oxygen therapy (though not proven to have any benefit)[1]
Disposition
- Admission, likely to MICU
- Toxicology consult
Sources
- ↑ Goldfrank et. al. Hydrogen Sulfide Poisoning. In: Goldfrank et. al. Goldfrank’s Toxicologic Emergencies. New York, NY: McGraw Hill. 2002. 1504-1507.
