Hydrogen sulfide inhalation injury can be life threatening. The toxic gas is produced, sometimes unexpectedly, from a wide variety of sources. Because its mechanism of toxicity is similar to that of cyanide, hydrogen sulfide poisoning is commonly treated with the nitrite component of the cyanide antidote kit. In this case report, hyperbaric oxygen was successfully used to treat hydrogen sulfide intoxication. Further evaluation of hyperbaric oxygen therapy as adjunctive treatment of hydrogen sulfide poisoning is recommended.

Hydrogen sulfide is a potent lethal gas. Supportive care, nitrite therapy and hyperbaric oxygen are the treatment modalities reported in the literature in cases of hydrogen sulfide exposure. We describe an industrial exposure in which 6 workers inhaled high concentrations of hydrogen sulfide when they entered a closed spreader tank partially filled with liquid swine manure. Five of the 6 lost consciousness, and 2 were agitated and poorly responsive on arrival to the emergency department despite having already received high-flow oxygen for nearly 1 hour. These 2 patients received nitrite therapy followed by orotracheal intubation and hyperbaric oxygen. All patients were discharged home without sequelae after short stays in hospital. The emergency management of hydrogen sulfide exposure is briefly reviewed.

RATIONALE: The toxicity of H2S has been attributed to its ability to inhibit cytochrome c oxidase in a similar manner to HCN. However, the successful use of methemoglobin for the treatment of HCN poisoning was not successful for H2S poisonings even though the ferric heme group of methemoglobin scavenges H2S. Thus, we speculated that other mechanisms contribute to H2S induced cytotoxicity. Experimental procedure. Hepatocyte isolation and viability and enzyme activities were measured as described by Moldeus et al. (1978), and Steen et al. (2001). RESULTS: Incubation of isolated hepatocytes with NaHS solutions (a H2S source) resulted in glutathione (GSH) depletion. Moreover, GSH depletion was also observed in TRIS-HCl buffer (pH 6.0) treated with NaHS. Several ferric chelators (desferoxamime and DETAPAC) and antioxidant enzymes (superoxide dismutase [SOD] and catalase) prevented cell-free and hepatocyte GSH depletion. GSH-depleted hepatocytes were very susceptible to NaHS cytotoxicity, indicating that GSH detoxified NaHS or H2S in cells. Cytotoxicity was also partly prevented by desferoxamine and DETAPC, but it was increased by ferric EDTA or EDTA. Cell-free oxygen consumption experiments in TRIS-HCl buffer showed that NaHS autoxidation formed hydrogen peroxide and was prevented by DETAPC but increased by EDTA. We hypothesize that H2S can reduce intracellular bound ferric iron to form unbound ferrous iron, which activates iron. Additionally, H2S can increase the hepatocyte formation of reactive oxygen species (ROS) (known to occur with electron transport chain). H2S cytotoxicity therefore also involves a reactive sulfur species, which depletes GSH and activates oxygen to form ROS.