Hydrogen sulfide toxicity: Difference between revisions

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==Sources:==
==Sources:==


Tintinalli et. al. Hydrogen Sulfide. In: Tintinalli et. al. Emergency Medicine A Comprehensive Study Guide. New York, NY: McGraw Hill. 2010.  
Tintinalli et. al. Hydrogen Sulfide. In: Tintinalli et. al. Emergency Medicine A Comprehensive Study Guide. New York, NY: McGraw Hill. 2011. 1320.


Goldfrank et. al. Hydrogen Sulfide Poisoning. In: Goldfrank et. al. Goldfrank’s Toxicologic Emergencies. New York, NY: McGraw Hill. 2002. 1504-1507.  
Goldfrank et. al. Hydrogen Sulfide Poisoning. In: Goldfrank et. al. Goldfrank’s Toxicologic Emergencies. New York, NY: McGraw Hill. 2002. 1504-1507.  

Revision as of 14:52, 12 August 2014

Hydrogen Sulfide Poisoning. Catherine Neal, MD and Alex Koyfman, MD. Department of Emergency Medicine, UT Southwestern Medical Center / Parkland Memorial Hospital, Dallas, Texas, USA

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

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

Hydrocarbon Toxicity

Smoke Inhalation Injury

Diagnosis:

  • No single test to verify exposure or levels
  • ABG: metabolic acidosis and normal oxygen saturation (unless pulmonary edema present)
  • Elevated lactate
  • Discolored copper coins found on patient may be helpful in diagnosis

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)

Disposition:

  • Admission, likely to MICU
  • Toxicology consult

Sources:

Tintinalli et. al. Hydrogen Sulfide. In: Tintinalli et. al. Emergency Medicine A Comprehensive Study Guide. New York, NY: McGraw Hill. 2011. 1320.

Goldfrank et. al. Hydrogen Sulfide Poisoning. In: Goldfrank et. al. Goldfrank’s Toxicologic Emergencies. New York, NY: McGraw Hill. 2002. 1504-1507.

Gresham, C. Hydrogen Sulfide Poisoning. Medscape: http://emedicine.medscape.com/article/815139-overview. Updated Jan 27, 2014. Accessed Aug 8, 2014.

Source