Successful management of acute collective hydrogen sulfide exposure

Objective: H2S is a highly lipophilic, toxic and irritant gas, usually formed from bacterial breakdown of organic material in the absence of oxygen, such as in swamps and sewers; a process commonly known as anaerobic digestion (1). H2S toxicodynamic consists, similarly to cyanide, in interrupting oxidative phosphorylation by inhibition of cytochrome a3 oxidase, thus producing cytotoxic hypoxemia, decreasing ATP production and enhancing anaerobic metabolism (2). Moreover, H2S activates guanylate cyclase increasing the intracellular concentration of cGMP, inducing vasodilation (3). Case series: In May 2014 two sewer employees experienced acute inhalation exposure to H2S. Both of them collapsed within one minute in attempt to help each other without protective equipment. Because of acute respiratory failure, both patients were intubated on-scene and mechanical ventilation started. On Emergency Department arrival the patients presented a GCS score of 3 and were hemodynamically stable. Both patients showed signs of tissue hypoxia with “arterialized” venous blood (venous blood partial pO2 99.9 and 90.1 mmHg, respectively). Both patients were admitted to Intensive Care Unit mechanically ventilated and invasive monitored. In order to create a false substrate to bind the toxic hydrosulfide anion and to obtain a detoxification, sodium nitrite was administered. Nitrite-induced methaemoglobin, by competitively binding the toxic hydrosulfide anion, presumably reactivated and protected cytochrome oxidase thus improving patient's recovery by enhancing aerobic metabolism. Methaemoglobinaemia was closely monitored and restoration of respiratory physiological values gradually occurred. No focal neurological dysfunctions were found and the patients were discharged after 15 days of hospitalization. Conclusion: H2S is an extremely toxic gas and severe exposure manifestations are life-threatening. Severe cases of sulfide poisoning could be treated with nitrite-induced methemoglobinemia in addition to vigorous supportive care and, in the future, with inhibitors of guanylate cyclase (i.e. methylene blue) thus reducing the decrease in blood pressure.