Hydrogen sulfide toxicity: Difference between revisions

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==Background==
==Background==
#Colorless, flammable gas w/ rotten egg odor
===General Information===
#Encountered in oil/gas industries, natural product of decomposition (e.g. septic tank)
*Colorless, flammable gas
#Mechanism of toxicity is similar to CN (disruption of aerobic metabolism)
*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


==Clinical Features==
==Clinical Features==
#One of the few chemical asphyxiants that also possesses irritative properities
*Respiratory: dyspnea, cyanosis, hemoptysis, rales, delayed pulmonary edema
##Respiratory, ocular irritation
*Ophthalmic: conjunctivitis, corneal ulceration, corneal scarring
#High conc exposure may result in LOC, sz, and death after only a few breaths
*Central nervous system: headache, weakness, disequilibrium, intention tremor, muscle rigidity, loss of consciousness, seizures, coma
##Delayed pulm edema and corneal destruction should be anticipated w/ massive exposures
*Gastrointestinal: green-gray line on gingiva, nausea, vomiting
*Cardiovascular: [[chest pain]], [[bradycardia]]
*Neuropsychiatric: amnesia, lack of insight, disorientation, delirium, dementia
*Death


==Treatment==
==Differential Diagnosis==
#Decontamination of skin/eyes
{{Toxic gas exposure DDX}}
#O2 100% NRB
#Consider giving nitrite component of CN kit (do not give thiosulfate portion)
##Low level MetHb may enhance conversion of sulfide to less toxic sulfmethemoglobin


==Source==
==Evaluation==
Tintinalli
*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


[[Category:Tox]]
==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]]

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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