Hydrogen sulfide toxicity: Difference between revisions
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==General Information== | |||
*Colorless, flammable gas | |||
==General Information | *Encountered in following industries: oil, gas, organic decomposition (sewer and manure), roofing asphalt tanks | ||
*Most common fatal gas exposure | |||
Colorless, flammable gas | *“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> | |||
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 | |||
==Mechanisms of toxicity== | |||
*Highly lipid soluble | *Highly lipid soluble | ||
*Disrupts oxidative phosphorylation by inhibiting cytochrome oxidase aa3 (toxicity through cellular asphyxia and impairs ATP production) => lactate accumulation and metabolic acidosis | *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 | *Causes hyperpolarization of potassium-mediated channels in neurons | ||
*Potentiates neuronal inhibitory mechanisms | *Potentiates neuronal inhibitory mechanisms | ||
*Alters brain neurotransmitter content and release | *Alters brain neurotransmitter content and release | ||
==Symptoms | ==Symptoms== | ||
*Respiratory: dyspnea, cyanosis, hemoptysis, rales, delayed pulmonary edema | *Respiratory: dyspnea, cyanosis, hemoptysis, rales, delayed pulmonary edema | ||
*Ophthalmic: conjunctivitis, corneal ulceration, corneal scarring | *Ophthalmic: conjunctivitis, corneal ulceration, corneal scarring | ||
*Central nervous system: headache, weakness, disequilibrium, intention tremor, muscle rigidity, loss of consciousness, seizures, coma | *Central nervous system: headache, weakness, disequilibrium, intention tremor, muscle rigidity, loss of consciousness, seizures, coma | ||
*Gastrointestinal: green-gray line on gingiva, nausea, vomiting | *Gastrointestinal: green-gray line on gingiva, nausea, vomiting | ||
*Cardiovascular: [[chest pain]], [[bradycardia]] | |||
*Cardiovascular: chest pain, bradycardia | |||
*Neuropsychiatric: amnesia, lack of insight, disorientation, delirium, dementia | *Neuropsychiatric: amnesia, lack of insight, disorientation, delirium, dementia | ||
*Death | *Death | ||
==Differential Diagnosis:== | ==Differential Diagnosis:== | ||
*[[Carbon Monoxide]] Toxicity | |||
*[[Cyanide]] Toxicity | |||
*[[Hydrocarbons]] Toxicity | |||
*Smoke Inhalation Injury | |||
==Diagnosis== | |||
==Diagnosis | |||
*No single test to verify exposure or levels | *No single test to verify exposure or levels | ||
*[[ABG|ABG Interpretation]]: metabolic acidosis and normal oxygen saturation (unless pulmonary edema present) | |||
*ABG: metabolic acidosis and normal oxygen saturation (unless pulmonary edema present) | |||
*Elevated lactate | *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== | |||
==Treatment | |||
*Removal from source | *Removal from source | ||
*100% oxygen | *100% oxygen | ||
*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) | ||
| Line 71: | Line 42: | ||
**Adult dose: 10 mL | **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)</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 | |||
*Admission, likely to MICU | *Admission, likely to MICU | ||
*Toxicology consult | *Toxicology consult | ||
==Sources | ==Sources== | ||
<references/> | <references/> | ||
[[Category:Tox]] | [[Category:Tox]] | ||
Revision as of 02:42, 15 September 2014
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)
- 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)</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
- Admission, likely to MICU
- Toxicology consult