Aggressive treatment, outcome and long time neurologic and pulmonary complications of lethal hydrogen sulphide (H2S) intoxication

Hydrogen sulphide poisoning can occur in industrial/occupational (oil refining, viscose rayon manufacturing, vulcanization of rubber, hydrochloric acid in farm wells, leather industry, sewage cleaning, roofing asphalt tanks, etc), recreational (cleaning of hot spring reservoirs, caves, sulfur springs, etc), or hospital (plaster of Paris, etc) settings. The first reports date from the 17th century where city sewage cleaners were found dead in the vicinity of the sewers. At a concentration of 0–25 ppm H2S has a specific odour of rotten eggs. This odour is an unreliable marker since at higher concentrations (> 100 ppm) the gas rapidly causes paralysis of (the olfactory system resulting in anosmia. At concentrations > 50 ppm symptoms are characterized by mucositis (conjunctivitis, upper airway irritation), nausea and dizziness, at > 200 ppm pulmonary edema can occur, at > 500 ppm neurologic problems arise (agitation, seizures followed by coma), at > 1000 ppm sudden death can occur. Main target organs are the central nervous system (CNS) and the respiratory system. Acute high dose intoxication mainly results in CNS problems whereas chronic lower dose intoxication results in acute lung injury (ALI) or acute pulmonary edema, the latter carrying a worse prognosis. There is still a great controversy in the literature about the best treatment and little is known about long time CNS and pulmonary complications in survivors.