Hydrogen sulfide toxicity: Difference between revisions
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==Background== | |||
===General Information=== | |||
==General Information | *Colorless, flammable gas | ||
*Encountered in following industries: oil, gas, organic decomposition (sewer and manure), roofing asphalt tanks | |||
Colorless, flammable gas | *Most common fatal gas exposure | ||
*“Rotten egg” smell which diminishes with high concentrations or prolonged low concentration exposure | |||
Encountered in following industries: oil, gas, organic decomposition (sewer and manure), roofing asphalt tanks | *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=== | |||
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 | ||
== | ==Clinical Features== | ||
*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== | ||
{{Toxic gas exposure DDX}} | |||
==Evaluation== | |||
*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 | *Discolored copper coins found on patient may be helpful in diagnosis | ||
== | ==Management== | ||
*Removal from source | *Removal from source | ||
*100% oxygen | *100% oxygen | ||
*[[Hydroxocobalamin]] (Cyanokit) | |||
**5 g over 15 min to start, followed by a second dose PRN | |||
**If given as early as possible, has been shown in animal models to prevent PEA<ref>Haouzi P et al. High-dose hydroxocobalamin administered after H2S exposure counteracts sulfide-poisoning-induced cardiac depression in sheep. Clin Toxicol (Phila). 2015 Jan;53(1):28-36.</ref> | |||
**[[Cobinamide]], a vitamin B12 analog, shows promise as first line for H2S toxicity<ref>Jiang J et al. Hydrogen Sulfide—Mechanisms of Toxicity and Development of an Antidote. Nature. Scientific Reports 6, Article number: 20831 (2016).</ref><ref>Brenner M et al. The vitamin B12 analog cobinamide is an effective hydrogen sulfide antidote in a lethal rabbit model. Clin Toxicol (Phila). 2014 Jun;52(5):490-7.</ref> | |||
*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)<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 | ||
== | ==References== | ||
<references/> | <references/> | ||
[[Category: | [[Category:Toxicology]] | ||
Latest revision as of 11:10, 25 September 2021
Background
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[1]
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
Clinical Features
- 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
Toxic gas exposure
- Carbon monoxide toxicity
- Chemical weapons
- Cyanide toxicity
- Hydrocarbon toxicity
- Hydrogen sulfide toxicity
- Inhalant abuse
- Methane toxicity
- Smoke inhalation injury
- Ethylene dibromide toxicity
Evaluation
- 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
Management
- Removal from source
- 100% oxygen
- Hydroxocobalamin (Cyanokit)
- 5 g over 15 min to start, followed by a second dose PRN
- If given as early as possible, has been shown in animal models to prevent PEA[2]
- Cobinamide, a vitamin B12 analog, shows promise as first line for H2S toxicity[3][4]
- 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)[5]
Disposition
- Admission, likely to MICU
- Toxicology consult
References
- ↑ Tintinalli et. al. Hydrogen Sulfide. In: Tintinalli et. al. Emergency Medicine A Comprehensive Study Guide. New York, NY: McGraw Hill. 2011. 1320.
- ↑ Haouzi P et al. High-dose hydroxocobalamin administered after H2S exposure counteracts sulfide-poisoning-induced cardiac depression in sheep. Clin Toxicol (Phila). 2015 Jan;53(1):28-36.
- ↑ Jiang J et al. Hydrogen Sulfide—Mechanisms of Toxicity and Development of an Antidote. Nature. Scientific Reports 6, Article number: 20831 (2016).
- ↑ Brenner M et al. The vitamin B12 analog cobinamide is an effective hydrogen sulfide antidote in a lethal rabbit model. Clin Toxicol (Phila). 2014 Jun;52(5):490-7.
- ↑ Goldfrank et. al. Hydrogen Sulfide Poisoning. In: Goldfrank et. al. Goldfrank’s Toxicologic Emergencies. New York, NY: McGraw Hill. 2002. 1504-1507.