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Toxicity, Hydrogen Sulfide

Sujal Mandavia, MD, FRCP(C), FACEP, Clinical Assistant Professor of Emergency Medicine, USC, Department of Emergency Medicine, Cedars-Sinai Medical Center, Los Angeles County-University of Southern California Medical Center

Updated: Mar 24, 2009

Introduction

Background

Hydrogen sulfide (H₂ S) is a colorless gas that has strong odor of rotten eggs. H₂ S poisoning is a rarity, mainly observed in industrial settings. Emergency physicians must be aware of the presentation and management of H₂ S poisoning because rapid identification and treatment is essential for recovery.

Pathophysiology

Significant H₂ S poisoning usually occurs by inhalation. Local irritant effects, along with arrest of cellular respiration, may follow. H₂ S forms a complex bond to the ferric moiety causing inhibition of mitochondrial cytochrome oxidase (iron-containing protein), thereby arresting aerobic metabolism in an effect similar to cyanide toxicity. Very high lipid solubility allows it to penetrate easily through biologic membranes. 

As a cellular poison, H₂ S affects all organs, particularly the CNS and pulmonary system. The spectrum of illness depends on the concentration and duration of exposure, with high concentrations (>700 ppm or >975 mg/m³) causing sudden death possibly due to hydrogen sulfide effect on the brainstem respiratory center.

Frequency

United States

According to the 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System, 1134 single exposures and 13 fatal outcomes were reported.¹

It is very important to realize that 25% of fatalities usually involve rescuers, professionals, or bystanders.²

Mortality/Morbidity

• Low-level exposures of hydrogen sulfide usually produce local eye and mucous membrane irritation, while high-level exposures rapidly produce fatal systemic toxicity.
• Exposures of 700-800 ppm or greater can cause loss of consciousness and cardiopulmonary arrest.

Sex

Because hydrogen sulfide exposures predominantly occur in industrial exposures, it is conceivable that the majority of patients will be middle-aged men.

Age

If exposed to hydrogen sulfide, children are more vulnerable than adults.

Clinical

History

The presence of H₂ S 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 can be 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 of hydrogen sulfide 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 of hydrogen sulfide 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
  • Sudden loss of consciousness ("knockdown") 
  • Seizure
  • Cardiopulmonary arrest

Physical

• Low-level exposure of hydrogen sulfide most often affects the mucous membranes and may show the following few physical signs:
  • Conjunctivitis (even at levels of only 4 ppm)
  • Pharyngitis
  • Green-gray line on gingiva
  • Wheezing
• High-level exposure of hydrogen sulfide may elicit the following signs:
  • Bradycardia
  • Tremulousness
  • Agitation
  • Cyanosis
  • Acute lung injury (may present with acute respiratory distress syndrome [ARDS])

Causes

• H₂ S most often is encountered as a byproduct of the petroleum, viscose rayon, rubber, and mining industries.
• Organic decomposition of sulfur compounds in sewers, barns, liquid manure pits, ships' holds, and sulfur springs also produces H₂ S.
• The petroleum industry is responsible for most cases of H₂ S toxicity in North America.
• In nature, hydrogen sulfide can be found in caves, sulfur springs, underground deposits of natural gas, or as result of volcanic eruptions.
• Hydrogen sulfide has recently been implicated in suicides in Japan.³

Differential Diagnoses

Lactic Acidosis
Smoke Inhalation
Toxicity, Carbon Monoxide
Toxicity, Cyanide
Toxicity, Hydrocarbons

Other Problems to Be Considered

Methemoglobinemia
Acute lung injury (ALI)

Workup

Laboratory 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.
  • H₂ S toxicity may be associated with carboxyhemoglobin or methemoglobinemia, depending on the source of H₂ S and coexposure.

Imaging Studies

• Chest radiography
  • Chest radiographic findings initially may be normal, but up to 20% of patients present with evidence of acute lung injury.
  • ARDS is viewed as a complication in H₂ S 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.
• Measurement of sulfide and thiosulfate levels are more appropriate for the evaluation of low-level chronic exposures.

Treatment

Prehospital Care

• Initial treatment of hydrogen sulfide exposure 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 (SCBA) 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.
• Protected rescue personnel can measure environmental concentration of hydrogen sulfide providing initial clue to the diagnosis.

Emergency Department Care

High-flow (100%) oxygen is the mainstay of therapy for hydrogen sulfide poisoning.

• Supportive therapy includes aggressive ventilation and possible use of positive pressure ventilation for the patients with evidence of acute lung injury.
• IV fluids and vasopressors should be administered to hypotensive patients.
• Correction of acidosis based on ABG and serum lactate values is indicated.
• 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

Treatment of hydrogen sulfide (H₂ S) poisoning is based on the creation of methemoglobinemia.

Nitrites

Nitrite administration leads to formation of methemoglobinemia. H₂ S has a much greater affinity for methemoglobin than for cellular cytochromes, leading to lower metabolic toxicity.

Sodium nitrite

Initial DOC in hydrogen sulfide poisoning.

Dosing

Adult

0.33 mL/kg of 3% solution slow IV push (2.5-5 mL/min) to maximum 10 mL

Pediatric

Administer as in adults

Interactions

Methylene blue counteracts methemoglobin formation

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May produce hypotension when administered intravenously in large doses or rapidly; high methemoglobin levels may exacerbate ischemia in patients with poor underlying cardiopulmonary reserve as they decrease oxygen-carrying capacity; adjust dose in severe anemia as outlined in package insert

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.

Albuterol sulfate (Ventolin, Proventil)

Beta agonist useful in treatment of bronchospasm refractory to epinephrine. Relaxes bronchial smooth muscle by acting on beta2 receptors with little effect on heart rate.

Dosing

Adult

2-4 mg/dose PO divided tid/qid; not to exceed 32 mg/d
Inhalant: 1-2 inhalations q4-6h; not to exceed 12 inhalations/d
Nebulizer: 0.5 mL (2.5 mg) of the 0.5% inhalation solution diluted in 1-2.5 mL of normal saline q4-6h; higher frequency may be used for intensive care patients

Pediatric

<2 years: Not established
2-6 years: 0.1-0.2 mg/kg/dose PO divided tid; not to exceed 12 mg/d
6-12 years: 2 mg/dose PO divided tid/qid; not to exceed 24 mg/d
>12 years: Administer as in adults
Inhalant dose for <12 years: Using a tube spacer, give 1-2 inhalations qid
Inhalant dose for >12 years: Administer as in adults
Nebulizer dose for <5 years: 0.25-0.5 mL (1.25-2.5 mg) of the 0.5% inhalation solution diluted in 1-2.5 mL of normal saline q4-6h in equally divided doses
Nebulizer dose for >5 years: Administer as in adults

Interactions

Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, and sympathomimetic agents

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hyperthyroidism, diabetes mellitus, and cardiovascular disorders

Follow-up

Further Inpatient Care

• Admit the 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.
• Perform a secondary survey to rule out traumatic injuries (7% of victims).
• If possible, consult with or admit the 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 from hydrogen sulfide exposure is unknown but appears to be linked to longer sublethal exposures.
• Paradoxically, high-concentration exposures of hydrogen sulfide may have no long-term effects.

Miscellaneous

Medicolegal Pitfalls

• Failure to establish the correct diagnosis and provide 100% oxygen
• Failure to protect oneself while entering exposed area during the rescue effort (SCBA protective equipment)
• Failure to provide trauma assessment and immobilization of unresponsive victims
• Failure to correct acidosis and hypovolemia
• Failure to institute antidote therapy in severely ill patients and to transport them to the HBO treatment

References

1. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Heard SE. 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th Annual Report. Clin Toxicol (Phila). Dec 2008;46(10):927-1057. [Medline].

2. Fuller DC, Suruda AJ. Occupationally related hydrogen sulfide deaths in the United States from 1984 to 1994. J Occup Environ Med. Sep 2000;42(9):939-42. [Medline].

3. Truscott A. Suicide fad threatens neighbours, rescuers. CMAJ. Aug 12 2008;179(4):312-3. [Medline].

4. Gregorakos L, Dimopoulos G, Liberi S, Antipas G. Hydrogen sulfide poisoning: management and complications. Angiology. Dec 1995;46(12):1123-31. [Medline].

5. Hall AH, Rumack BH. Hydrogen sulfide poisoning: an antidotal role for sodium nitrite?. Vet Hum Toxicol. Jun 1997;39(3):152-4. [Medline].

6. 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].

7. 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].

8. Milby TH, Baselt RC. Hydrogen sulfide poisoning: clarification of some controversial issues. Am J Ind Med. Feb 1999;35(2):192-5. [Medline].

9. Richardson DB. Respiratory effects of chronic hydrogen sulfide exposure. Am J Ind Med. Jul 1995;28(1):99-108. [Medline].

10. 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].

11. 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].

12. Watt MM, Watt SJ, Seaton A. Episode of toxic gas exposure in sewer workers. Occup Environ Med. Apr 1997;54(4):277-80. [Medline].

13. Whitcraft DD, Bailey TD, Hart GB. Hydrogen sulfide poisoning treated with hyperbaric oxygen. J Emerg Med. 1985;3(1):23-5. [Medline].

Keywords

hydrogen sulfide toxicity, hydrogen sulfide exposure, hydrogen sulfide poisoning, rotten egg odor, H₂ S toxicity, H₂ S poisoning, H₂ S, inhalation of hydrogen sulfide

Contributor Information and Disclosures

Author

Sujal Mandavia, MD, FRCP(C), FACEP, Clinical Assistant Professor of Emergency Medicine, USC, Department of Emergency Medicine, Cedars-Sinai Medical Center, Los Angeles County-University of Southern California Medical Center
Sujal Mandavia, MD, FRCP(C), FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

David C Lee, MD, Research Director, Department of Emergency Medicine, Associate Professor, North Shore University Hospital and New York University Medical School
David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

John G Benitez, MD, MPH, FACMT, FACPM, FAAEM, Associate Professor, Department of Medicine, Clinical Pharmacology Division, Vanderbilt University; Managing Director, Tennessee Poison Center
John G Benitez, MD, MPH, FACMT, FACPM, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

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