Journal of The Korean Society of Clinical Toxicology

Two Cases of Comatose Patients Presenting after Exposure to Hydrogen Sulfide Gas: Hyun-Ho Ryu, Byeong-Guk Lee, Kyung-Woon Jeung, Tag Heo, Yong-Il Min; J Korean Soc Clin Toxicol. 2009;7(1):26-31. Published online June 30, 2009

Abstract PDF: Hydrogen sulfide is a by-product of decayed organic material and is ubiquitously found as an ingredient of manufacturing reagents or as an undesirable by-product of the manufacturing or industrial processing. Hydrogen sulfide is a chemical asphyxiant and interferes with cytochrome oxidase and aerobic metabolism. It has thus been deemed an important cause of work-related sudden death. This gas is particularly insidious due to the unpredictability of its presence and concentration and its neurotoxicity at relatively low concentrations, causing olfactory nerve paralysis and loss of the warning odor. Here, we report two cases of comatose patients presenting after accidental exposure to hydrogen sulfide gas.

A Case of Acute Hydrogen Sulfide Intoxication Caused Rapid Loss of Consciousness: Jung-Hwan Ahn, Yoon-Seok Jung; J Korean Soc Clin Toxicol. 2004;2(2):147-150. Published online December 31, 2004

Abstract PDF: Hydrogen sulfide is a colorless, and malodorous 'rotten eggs' gas that results from the decay of organic material. It is a byproduct of industry and agriculture. The mechanism of its toxicity is primarily related to inhibition of oxidative phosphorylation, which causes a decrease in available cellular energy. Because there is no rapid method of detection that is of clinical diagnostic use, management decisions must be made based on history, clinical presentation, and diagnostic tests that imply hydrogen sulfide's presence. Although there is some anecdotal evidence to suggest that the early use of hyperbaric oxygen is beneficial, supportive care remains the mainstay of therapy. We describe an occupational exposure to hydrogen sulfide gas in 51-year-old man. While cleaning the sewage of pigs. he became unconscious. When he arrived in the emergency department, he had irritability and confused mentality. The typical smell of rotten eggs on clothing and exhaled air were enough to be considered to be exposed to hydrogen sulfide. Hyperbaric oxygen therapy was performed. He had a recovery to normal function.

Hydrogen Sulfide Poisoning: Young-Hee Choi, Byung-Kuk Nam, Hyo-Kyung Kim, Ji-Kang Park, Eun-Seog Hong, Yang-Ho Kim; J Korean Soc Clin Toxicol. 2004;2(1):31-36. Published online June 30, 2004

Abstract PDF: Three workers, field operators in lubricating oil processing of petroleum refinery industry were found unconscious by other worker. One of them who were exposed to an high concentration of H2S was presented with Glasgow Coma Score of 5, severe hypoxemia on arterial blood gas analysis, normal chest radiography, and normal blood pressure. On hospital day 7, his mental state became clear, and neurologic examination showed quadriparesis, profound spasticity, increased tendon reflexes, abnormal Babinski response, and bradykinesia. He was also found to have decreased memory, attention deficits and blunted affect which suggest general cognitive dysfunction, which improved soon. MRI scan showed abnormal signals in both basal ganglia and motor cortex, compatible with clinical findings of motor dysfunction. Neuropsychologic testing showed deficits of cognitive functions. SPECT showed markedly decreased cortical perfusion in frontotemporoparietal area with deep white matter. Another case was recovered completely, but the other expired the next day.

Chemical Asphyxiants - Cyanides and Hydrogen Sulfides: Yang Ho Kim, Young Hee Choi, Choong Ryeol Lee, Ji Ho Lee, Cheolln Yoo, Hun Lee; J Korean Soc Clin Toxicol. 2003;1(1):12-20. Published online June 30, 2003

Abstract PDF: Cyanides and hydrogen sulfide ($H_2S$) are major chemical asphyxiants. They have common mechanism of action which inhibit cellular respiration and induce histotoxic hypoxia. They do not generate ATP, and all processes dependent on ATP are stopped. No extraction of $O_2$ from blood decreases AV $O_2$ differences, and the shift to anaerobic glycolysis brings about lactic acidosis with high anion gap. The mainstay of the treatment is rapid treatment with appropriate use of antidotes. However, there are several differences between cyanides and $H_2S$. First, $H_2S$ is not metabolized by enzymes such as thiosulfate. Thus thiosulfate does not play any role in treatment of $H_2S$. Second, $H_2S$ is a more potent inhibitor of cytochrome aa3 than cyanide. Third, $H_2S$ induces more divergent neurologic sequele than cyanide. Finally, $H_2S$ is not absorbed via skin.

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