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. 2010 Dec;40(4):213-7.

Severe hydrogen sulphide poisoning treated with 4-dimethylaminophenol and hyperbaric oxygen

Affiliations
  • PMID: 23111938

Severe hydrogen sulphide poisoning treated with 4-dimethylaminophenol and hyperbaric oxygen

Joerg Lindenmann et al. Diving Hyperb Med. 2010 Dec.

Abstract

INTRODUCTION Hydrogen sulphide (H2S) is a highly toxic gas which originates mainly during breakdown of organic matter under anaerobic conditions. After inhalation, H2S binds to mitochondrial respiratory enzymes preventing oxidative phosphorylation, thereby causing reversible inhibition of aerobic metabolism and cellular anoxia. The use of hyperbaric oxygen therapy (HBOT) for H2S poisoning remains controversial, but has a similar underlying rationale to that in carbon monoxide poisoning.

Methods: A retrospective review of patients with severe H2S intoxication who presented during 2006 and 2007 was carried out. Ten victims of severe occupational H2S poisoning were identified, of whom four died at the site of the accident. Two further patients required cardiopulmonary resuscitation at the site of the accident and the remaining four all received 100% oxygen followed by endotracheal intubation and artificial ventilation prior to hospital admission. In these six cases, 4-dimethylaminophenol was administered on admission as an antidote, followed immediately by HBOT using the schedule otherwise used in carbon monoxide intoxication.

Clinical outcome: The two patients who required cardiopulmonary resuscitation at the site of exposure died of cerebral ischaemia or pulmonary oedema on the first and seventh days after the accident respectively. The remaining four patients recovered without any neurological sequelae and were discharged for outpatient care after a median of nine days (range 8-12 days). No antidote-related adverse effects could be detected. Acid-base status and oxygenation improved and methaemoglobin fell with the first HBOT in all six cases.

Conclusion: In severe H2S intoxication, supportive HBOT may play a useful role in improving oxygenation and acid-base status quickly and counteracting the decrement in oxygen carriage caused by methaemoglobinaemia due to antidote administration.

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