Hydrogen sulfide toxicity: Difference between revisions

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HYDROGEN SULFIDE
==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<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


n pathophys identicle to cn except bond of h2s to cytochrome more rapidly reversible than cn.  Therefore, just need to remove pt from source and use standard resus measures to reverse h2s toxicity.
==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 DDX}}


HYDROGEN SULFIDE (septic tank)
==Evaluation==
*No single test to verify exposure or levels
*[[ABG|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


remove pt from source and use standard resus measures
==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<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):
**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)<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


==References==
<references/>


 
[[Category:Toxicology]]
[[Category:Tox]]

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

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

  1. ↑ Tintinalli et. al. Hydrogen Sulfide. In: Tintinalli et. al. Emergency Medicine A Comprehensive Study Guide. New York, NY: McGraw Hill. 2011. 1320.
  2. ↑ 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.
  3. ↑ Jiang J et al. Hydrogen Sulfide—Mechanisms of Toxicity and Development of an Antidote. Nature. Scientific Reports 6, Article number: 20831 (2016).
  4. ↑ 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.
  5. ↑ Goldfrank et. al. Hydrogen Sulfide Poisoning. In: Goldfrank et. al. Goldfrank’s Toxicologic Emergencies. New York, NY: McGraw Hill. 2002. 1504-1507.
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