Aggressive management of seizures, noncardiogenic pulmonary edema, and acidosis should proceed as per standard protocols. Symptomatic patients with a normal examination, normal baseline laboratory measurements and a normal chest x-ray should be observed in a monitored setting for 4 to 24 hours. A sulfur odor on the patient or emanating from freshly-drawn blood, or darkly stained coins from the patient's pocket may arouse clinical suspicion of H 2 S exposure in a patient presenting with altered mental status. Serum sulfide and thiosulfate concentrations may have diagnostic and prognostic value but are not routinely available. The use of nitrites in acute exposure to high H 2 S levels is controversial.
Efficacy is limited to anecdotal reports.
The mechanism of action of nitrites may be related to induction of methemoglobin which has a higher affinity for H 2 S than cytochrome oxidase, vasodilatory changes in microcirculation, and a direct inhibitory effect of the H 2 S-cytochrome oxidase interaction. HBO therapy, when available, should be considered for severe toxicity with persistent symptoms such as acidosis, altered mental status, or life threatening dysrhythmias. Further studies to elucidate the toxic mechanism of action of H 2 S, the long term sequelae and benefit of current available therapy as well as new therapies are ongoing. Intensive neurologic and neuropsychiatric testing of H 2 S exposure survivors is strongly recommended. Prevention Companies and workers at risk should be made aware of the dangers of H 2 S. Exhaust ventilation should be used when applicable.