Hydrogen Sulfide Poisoning
By Richard A. Harrigan, MD
The following is a summary of a case reported in the medical literature1 that nicely illustrates the potential for the dramatic presentation of hydrogen sulfide poisoning.
During excavation of a construction pit in the wetlands just off the Atlantic coast, workers noted the odor of rotten eggs. While evacuating the premises, one worker went back into the pit to retrieve equipment and was rendered unconscious within seconds, as was the second worker who descended into the pit to rescue him. Similarly, a series of police officers and other workers, moments after attempting to rescue the others, collapsed one after vomiting blood.
Victims of the exposure reported headache, dizziness, nausea, vomiting, dyspnea, and cough. Burning discomfort of the chest, along with throat and eye irritation, were described. Victims were noted to have erythema of the conjunctiva and pharynx; corneal abrasions were noted in those suffering the most severe exposures. Overall, 37 people received ED evaluation and treatment, of whom six were admitted. The first worker presented with a Glasgow Coma Scale score of 3 and ultimately was left with significant neurocognitive disability, despite aggressive inpatient treatment for more than two weeks. The first police officer on the scene was the only fatality; he was pronounced dead at the excavation site.
Overview
Hydrogen sulfide (H2S) is unusual in that it acts as both a respiratory irritant and a chemical asphyxiant making it a veritable "double threat"as a toxin. It can be found in both industrial and natural settings, the latter resulting from the decomposition of proteins found in sewage and manure. Exposures have been reported in a variety of settings: mines, sewers, pulp mills, silos, oil refineries 2-6even in a cast room drain containing calcium sulfite plaster sludge when sulfuric acid was added7and after exposure to a tank yielding fumes from cooling roofing asphalt.8 A colorless gas, H2S is heavier than air, and thus tends to pool at the bottom of containers.4 Classically, it carries the odor of rotten eggs, but this potential warning sign is unreliable; at higher concentrations, olfactory fatigue occurs and the victim may cease to smell the gas.1,2,4
Toxicity
H2S is readily absorbed by mucous membranes, and thus exerts its irritant effects on the eyes, oronasopharynx, and pulmonary bed. These irritant effects, which are usually seen at lower concentrations, are evident in the case above; at high levels of exposure, noncardiogenic pulmonary edema may occur.1,2,4,5,8 The chemical asphyxiant properties have earned it the alias "knock-down gas," a phenomenon that was also evident in this case. Chemical asphyxia, which usually occurs at higher concentrations, may manifest itself with symptoms of nausea, vomiting, dizziness, confusion, ataxia, obtundation, seizures, coma, and cardiovascular collapse. If the exposure is severe enough, a progression is not seen; rather, the "knock-down" presentation may occur.
A large case series from the gas-and-oil producing Canadian province of Alberta provides data on 221 exposures to H2S.5 Most exposures necessitating hospitalization occurred in enclosed spaces, whereas those occurring in the open air were less problematic. More than 75% of exposures occurred in gas production facilities or well-pumping stations. The overall fatality rate was 6%. The central nervous system was the predominant organ system affected, yet the lungs were also frequently affected; rates of ventilatory support and pulmonary edema were significant. Although three-quarters of all victims lost consciousness after exposure to H2S, there were few neurologic sequelae, leading the authors to postulate that aggressive supportive care may well lead to complete recovery in those victims that survive. Delayed neurologic sequelae can occur, however; whether they are due to cerebral hypoxia or a direct toxic effect of H2S is unclear.1,4
Pathophysiology
The irritant effect is attributable to the formation of sodium sulfide when the toxin comes in contact with mucous membranes.4 As a chemical asphyxiant, H2S behaves similarly to cyanide. Cellular respiration is inhibited by the binding of H2S to the ferric moiety of cytochrome oxidase, leading to anaerobic metabolism and tissue hypoxia. With cyanide, this bond is less readily reversible than it is with H2S. The substance is principally detoxified via oxidation to form thiosulfate, which is measurable in the serumyet the assay is not available emergently, and thus will not assist in the real-time diagnosis of H2S poisoning.1,4 The diagnosis is made inferentially: the smell of rotten eggs, the catastrophic "knock-down" presentation, the combination of irritant (red eyes and throat, possibly pulmonary edema) and chemical asphyxiant effects (an elevated anion gap metabolic acidosis, an elevated lactate level) are all suggestive of H2S poisoning.
Treatment
Initial on-site treatment revolves around removal of the victim from the site of exposure; however, as this unfortunate case vividly illustrates, the rescuers must protect themselves. Self-contained breathing apparatuses and life lines must be employed by rescuers.1,8 The mainstay of treatment is aggressive supportive care; indeed, the victim may simply respond well to ventilatory assistance with oxygen. Beyond these two tenets of care, however, controversy exists regarding the efficacy of other treatment modalities. Toxicologic similarities to cyanide have led to the use of sodium nitrite in H2S poisoning. Nitrites generate methemoglobin, which in turn more avidly binds H2S than does cytochrome oxidase, leading to the formation of sulfmethemoglobin. Anecdotal reports have shown mixed efficacy, and it is possible that if nitrites do work, they may work by other mechanisms than the formation of methemoglobin.1,8 The sodium thiosulfate component of the cyanide kit is clearly of no benefit in cases of H2S poisoning; this compound serves as a sulfur donor to the liver enzyme rhodanese (which converts cyanomethemoglobin to thiocyanate in cases of cyanide detoxification) and is irrelevant in cases of H2S toxicity.1,8 As in cases of sodium nitrite administration for cyanide poisoning, the emergency physician must be aware of two significant side-effects of this substance: potential life-threatening hypotension secondary to overly-rapid intravenous infusion, and the possibility of significant impairment of oxygen-carrying capacity due to creation of methemoglobinemia.8
Hyperbaric oxygen therapy has been reported to be beneficial in cases of severe H2S toxicity.3,6 In both cases, the victims had failed to respond to aggressive supportive care and had exhibited an unsatisfactory response to nitrite therapy. Both patients experienced significant improvement after repeated treatments with hyperbaric oxygen, demonstrating only minor neurocognitive impairment upon discharge. Postulated therapeutic mechanisms for hyperbaric oxygen therapy include improvement of tissue oxygenation in the presence of pulmonary edema, enhanced oxidation of sulfides and sulfur leading to detoxification, and inhibition of H2S binding with cytochrome oxidase, thus salvaging oxidative phosphorylation and cellular respiration.4
The number of cases of significant H2S poisoning is too small to allow for a clinical trial to evaluate the efficacy of either hyperbaric oxygen or sodium nitrate therapy; the clinician should decide on the benefit of such therapy in consultation with a toxicologist on a case-by-case basis.
Summary
H2S is a potentially devastating toxin that has the ability to cause significant morbidity and mortality. It causes both irritant effects to mucous membranes and systemic toxicity through its chemical asphyxiant properties. Most exposures occur in an industrial setting, but exposure may occur in a natural environment also. The characteristic odor of rotten eggs is often, but not invariably, present. Effective management focuses on safe removal of the victim from the site of exposure and aggressive supportive therapy in the ED. Interventions such as administration of sodium nitrite and use of hyperbaric oxygen therapy are controversial but may be helpful in severe cases not responding to supportive care.
References
1. Snyder JW, et al. Occupational fatality and persistent neurological sequelae after mass exposure to hydrogen sulfide. Am J Emerg Med 1995;13:199-203.
2. Reiffenstein RJ, et al. Toxicology of hydrogen sulfide. Ann Rev Pharmacol Toxicol 1992;109-134.
3. Whitcraft DD, et al. Hydrogen sulfide poisoning treated with hyperbaric oxygen. J Emerg Med 1985;3:23-25.
4. Kerns II WP, Kirk MA. Cyanide and hydrogen sulfide. In: Goldfrank LR, et al, eds. Goldfrank’s Toxicologic Emergencies. 5th ed. Norwalk, CT: Appleton & Lange; 1994:1215-1227.
5. Burnett WW, et al. Hydrogen sulfide poisoning: Review of five years’ experience. Can Med Assoc J 1977;117:1277-1280.
6. Smilkstein MJ, et al. Hyperbaric oxygen therapy for severe hydrogen sulfide poisoning. J Emerg Med 1985;3:27-30.
7. Peters JW, et al. Hydrogen sulfide poisoning in a hospital setting. JAMA 1981;246:1588-1589.
8. Hoidal CR, et al. Hydrogen sulfide poisoning from toxic inhalations of roofing asphalt fumes. Ann Emerg Med 1986;15:826-830.
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