AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Background

Hydrogen sulfide (H₂S) is a colorless gas that reeks of rotten eggs. H₂S poisoning is a rarity, mainly observed in industrial settings. Emergency physicians must be aware of the presentation and management of H₂S poisoning because rapid identification and treatment is essential for recovery.

Pathophysiology

Significant H₂S poisoning usually occurs by inhalation. Local irritant effects, along with arrest of cellular respiration, may follow. H₂S forms a complex bond to iron causing inhibition of mitochondrial cytochrome oxidase (iron-containing protein), thereby arresting aerobic metabolism in an effect similar to cyanide toxicity.

As a cellular poison, H₂S affects all organs, particularly the nervous system. The spectrum of illness depends on the concentration and duration of exposure, with high concentrations (>800 ppm or >1200 mg/m³) causing sudden death.

Mortality/Morbidity

• Low-level exposures usually produce local eye and mucous membrane irritation, while high-level exposures rapidly produce fatal systemic toxicity.
• Exposures of 700-800 ppm or greater usually result in death.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

History

The presence of H₂S usually is apparent because of the characteristic rotten egg smell. However, concentrations above 150 ppm may overwhelm the olfactory nerve so that the victim may have no warning of exposure. Exposures are subdivided into low-, high-, and very high-level categories.

• Low-level exposure often is more chronic in nature and usually is seen in industrial settings. Chronic low-level exposure results primarily in irritation to mucous membranes and the respiratory system. Patients exposed to continuous low-level concentrations or after acute exposure to the very high concentrations of hydrogen sulfide can lose their ability to smell/detect the gas even though it is still present in the environment (olfactory fatigue/paralysis).
• • Headaches
  • Asthenia
  • Bronchitis
• High-level exposures result in more neurologic and pulmonary symptoms.
• • Cough
  • Dyspnea
  • Vertigo
  • Confusion
  • Nausea and vomiting
  • Possible loss of consciousness
  • Hemoptysis
• Very high concentrations lead to cardiorespiratory arrest because of brainstem toxicity.
• • Myocardial infarction
  • Seizure
  • Cardiopulmonary arrest

Physical

• Low-level exposure most often affects the mucous membranes and may show the following few physical signs:
• • Conjunctivitis
  • Green-gray line on gingiva
  • Wheezing
• High-level exposure may elicit the following signs:
• • Tremulousness
  • Agitation
  • Cyanosis
  • Pulmonary edema (may present with acute respiratory distress syndrome [ARDS])

Causes

• H₂S most often is encountered as a byproduct of the petroleum, viscose rayon, rubber, and mining industries.
• Organic decomposition of sulfur compounds in sewers, barns, ships' holds, and sulfur springs also produces H₂S.
• The petroleum industry is responsible for most cases of H₂S toxicity in North America.

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Other Problems to be Considered

Methemoglobinemia
Acute lung injury (ALI)

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Lab Studies

• Arterial blood gas
• • Arterial blood gas (ABG) usually reveals a marked uncompensated metabolic acidosis. Acidosis is associated with an elevation in serum lactate level.
  • Oxygen tension (pO₂) and calculated oxygen saturation are within the reference range unless the patient has concomitant pulmonary edema.
  • As with other hemoglobinopathies, however, measured oxygen saturation often is low and indicates a saturation gap.
  • Venous blood gas may indicate abnormally high oxygen tension (because of decreased oxygen utilization) resulting in a decrease in the PO₂ gradient between arterial and venous blood.
  • H₂S toxicity may be associated with carboxyhemoglobin or methemoglobinemia, depending on the source of H₂S and coexposure.

Imaging Studies

• Chest radiography
• • Chest radiographic findings initially may be normal, but up to 20% of patients present with pulmonary edema.
  • ARDS is viewed as a complication in H₂S poisoning.
• CT scan or MRI of the head: Often only delayed findings, such as basal ganglia lesions, are found.

Other Tests

• ECG may reveal ischemia or infarction patterns.
• Sulfide (unstable metabolite) and thiosulfate blood levels rarely are available (especially on short notice) and may be elevated in cases of significant exposure. However, with significant acute exposure due to respiratory paralysis, the amount of actually absorbed hydrogen sulfide can be lower in comparison to low-level chronic exposure.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Prehospital Care

• Initial treatment requires immediate removal of the victim from the contaminated area into a ventilated/fresh-air environment. Prehospital care providers should take hazardous materials precautions with respirator devices to avoid serious exposure.
• In severe cases, intubation may be necessary for ventilatory support and airway protection.
• Gain intravenous access or initiate other initial supportive care as necessary.
• Search the patient's pockets for discolored copper coins, which can be an early diagnostic clue.

Emergency Department Care

High-flow (100%) oxygen is the mainstay of therapy.

• Based on the similarities in cyanide and hydrogen sulfide toxicity, induced methemoglobinemia may be used for the treatment of hydrogen sulfide toxicity. Methemoglobin acts as a scavenger, and it is more attractive to hydrogen sulfide than cytochrome oxidase. Administer 10 mL of 3% sodium nitrite intravenously over 2-4 minutes (adult dose). Obtain methemoglobin level 30 minutes after administration of antidote.
• Patients with persistent neurologic findings should be considered for hyperbaric oxygen therapy (HBO). Anecdotal reports indicate a salutary effect.

Consultations

Consultation with the local hyperbaric chamber facility may be necessary for patients who are unresponsive to nitrites.

MEDICATION

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Treatment of H₂S poisoning is based on the creation of methemoglobinemia.

Drug Category: Nitrites

Nitrite administration leads to formation of methemoglobinemia. H₂S has a much greater affinity for methemoglobin than for cellular cytochromes, leading to lower metabolic toxicity.

Drug Category: Bronchodilators

These agents are effective in reversing acute bronchospasm of allergic or irritant origin through combined alpha-adrenergic and beta-adrenergic agonist action.

An additional option in the management of persistent bronchospasm involves anticholinergics. These agents block action of acetylcholine at parasympathetic sites in bronchial smooth muscle, causing bronchodilation.

FOLLOW-UP

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Further Inpatient Care

• Admit patient to the ICU for any significant exposure (ie, other than chronic low-level exposure with mucous membrane irritation).
• Consider hyperbaric oxygen for patients who are unresponsive to intravenous nitrites or who have delayed neurologic sequelae.
• If possible, consult with or admit patient to a medical toxicologist.

Transfer

• Transfer the patient if hyperbaric treatment is required but unavailable at the present facility.

Complications

• Acute respiratory distress syndrome
• Acute myocardial infarction
• Delayed neuropsychiatric sequelae

Prognosis

• Occurrence of long-term neurologic sequelae is unknown but appears to be linked to longer sublethal exposures.
• Paradoxically, high-concentration exposures may have no long-term effects.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

• Gregorakos L, Dimopoulos G, Liberi S, Antipas G. Hydrogen sulfide poisoning: management and complications. Angiology. Dec 1995;46(12):1123-31. [Medline].
• Hall AH, Rumack BH. Hydrogen sulfide poisoning: an antidotal role for sodium nitrite?. Vet Hum Toxicol. Jun 1997;39(3):152-4. [Medline].
• Hessel PA, Herbert FA, Melenka LS, et al. Lung health in relation to hydrogen sulfide exposure in oil and gas workers in Alberta, Canada. Am J Ind Med. May 1997;31(5):554-7. [Medline].
• Kilburn KH, Warshaw RH. Hydrogen sulfide and reduced-sulfur gases adversely affect neurophysiological functions. Toxicol Ind Health. Mar-Apr 1995;11(2):185-97. [Medline].
• Milby TH, Baselt RC. Hydrogen sulfide poisoning: clarification of some controversial issues. Am J Ind Med. Feb 1999;35(2):192-5. [Medline].
• Richardson DB. Respiratory effects of chronic hydrogen sulfide exposure. Am J Ind Med. Jul 1995;28(1):99-108. [Medline].
• Smilkstein MJ, Bronstein AC, Pickett HM, Rumack BH. Hyperbaric oxygen therapy for severe hydrogen sulfide poisoning. J Emerg Med. 1985;3(1):27-30. [Medline].
• Snyder JW, Safir EF, Summerville GP, Middleberg RA. Occupational fatality and persistent neurological sequelae after mass exposure to hydrogen sulfide. Am J Emerg Med. Mar 1995;13(2):199-203. [Medline].
• Watt MM, Watt SJ, Seaton A. Episode of toxic gas exposure in sewer workers. Occup Environ Med. Apr 1997;54(4):277-80. [Medline].
• Whitcraft DD, Bailey TD, Hart GB. Hydrogen sulfide poisoning treated with hyperbaric oxygen. J Emerg Med. 1985;3(1):23-5. [Medline].

Article Last Updated: Mar 13, 2007