hydrogen sulphide gas poisoning

see also:

• toxicology

• hydrogen sulphide is a colourless, highly toxic gas, and thankfully poisonings are rare
• it may be produced in chemical reactions that are involved in rubber vulcanization, viscose rayon manufacturing, pesticide production and the action of acid drain cleaners with sulfur-containing sludge.
• poisonings generally occur:
  • in industrial settings such as mine sites
  • in areas of volcanic activity
  • in suicide attempts
• at low concentrations (0.02–0.13 ppm), it is readily recognised by its “rotten egg” odour
• at high concentrations (100–150 ppm), the olfactory nerve function becomes impaired and it thus becomes odorless

• reacts with moisture on mucous membranes to produce sodium sulfide, which is an irritant and thus many complain of sore eyes and throat
• its major toxicity derives from inhibition of cytochrome oxidase by binding to the ferric ion (Fe3+), leading to inhibition of oxidative phosphorylation and, hence, cellular hypoxia and anaerobic metabolism.
• also causes potassium channel-mediated hyperpolarization of neurones resulting in enhancement of inhibitory neuronal pathways
• it is normally detoxified to sulfate or thiosulfate by undergoing spontaneous oxidation catalysed by oxyhaemoglobin.
• oxygen also competes with hydrogen sulfide in binding to cytochrome oxidase
• hyperbaric oxygen assists with this at the tissue level and may also enhance sulfide detoxification by maximizing sulfide oxidation to sulfate or thiosulfate.

• immediate toxicity of hydrogen sulfide is reversible with removal from exposure and the administration of oxygen, thus cytochrome-bound sulfide is extremely low by the time of arrival to definitive care.
• diagnosis is primarily based upon history
• sulfhaemoglobin levels are poor reflections of sulfide levels
• irritable eyes, throat
• headache
• decreased mental state
• seizures
• neurologic injury
• Parkinsonism presumably due to reversible sulfide binding to the basal ganglia
• V-Q mismatch / pneumonitis / acute pulmonary oedema
• cardiopulmonary arrest
• several case reports of those who lost consciousness still had persistent neurological signs 5 years later including memory, cognitive and motor impairment.

• rescuers need to avoid exposure to the gas which can be an ongoing issue in confined spaces
  • may require protective clothing and breathing equipment
• victims with pulmonary or systemic symtoms should be given high flow oxygen to hasten detoxification process
• victims with irritated eyes should have the eyes irrigated

• general supportive care
• eye irrigation if irritable
• maintain high flow oxygen if symptomatic
• patients with serious toxicity such as decreased conscious state should be considered for:
  • intubation
  • ABG's, serum lactate as metabolic acidosis is common
  • hyperbaric oxygen (rat models of sulfide toxity had improved survival of 80% compared to 60% with 100% oxygen and to 25% survival of controls)
    • perhaps most patients with more than “mild toxicity” should be considered for early hyperbaric oxygen Rx¹⁾
  • iv sodium nitrite infusion although this remains controversial but did seem to further improve rat survival in sulfide poisoning as it causes methaemoglobinaemia which is then converted to sulfmethaemoglobin