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Cited by 136Poisoning and overdose treatmentsCassava research and cyanidePlant-based Medicinal Research

Cyanide poisoning: pathophysiology and treatment recommendations

Beasley, D. M. G., Glass, W. I.·1998·Occupational Medicine
DOI 10.1093/occmed/48.7.427
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Abstract

This paper aims to assess and compare currently available antidotes for cyanide poisoning. Such evaluation, however, is difficult. Thus, extrapolation from the results of animal studies has potential pitfalls, as significant inter-species differences in response may exist, and these experiments often involve administration of toxin and antidote almost simultaneously, rather than incorporating a more realistic time delay before initiation of treatment. Direct inference from human case reports is also problematic; either because of uncertainties over the exposure levels involved (and hence the likely outcome without treatment), or because of difficulties in identifying the specific contribution of a particular antidote within the overall treatment regimen. Certainly an effort to compare the relative efficacy of cyanide antidotes produces equivocal findings, with no single regimen clearly standing out. Indeed, factors such as the risks of antidote toxicity to various individuals and other practical issues, may be more important considerations. There is therefore no single treatment regimen which is best for all situations. Besides individual risk factors for antidote toxicity, the nature of the exposure and hence its likely severity, the evolving clinical features and the number of persons involved and their proximity to hospital facilities, all need to be considered. Clinically mild poisoning may be treated by rest, oxygen and amyl nitrite. Intravenous antidotes are indicated for moderate poisoning. Where the diagnosis is uncertain, sodium thiosulphate may be the first choice. With severe poisoning, an additional agent is required. Given the various risks with methaemoglobin formers or with unselective use of kelocyanor, hydroxocobalamin may be preferred from a purely risk-benefit perspective. However the former alternatives will likely remain important.

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Crossref · 10.1093/occmed/48.7.427

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  • Sodium nitrite mediated metHb formation is slower than other cyanide antidotes (e.g. 4-dimethylaminophenol) and has lead to the notion that the cardiovascular effects of nitrite may also be protective against cyanide mediated increases in central venous pressure.

    “However, sodium nitrite mediated metHb formation is slower than other cyanide antidotes (e.g. 4-dimethylaminophenol) and has lead to the notion that the cardiovascular effects of nitrite may also be protective against cyanide mediated increases in central venous pressure [135].”

    From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [135]

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Authors
Beasley, D. M. G., & Glass, W. I.
Affiliations
University of Otago (NZ)
Corresponding author
Beasley, D. M. G.
Venue
Occupational Medicine
Publisher
Oxford University Press (OUP)
Published
1998
Volume
48
Issue
7
Pages
427-431
ISSN
  • 0962-7480 (ISSN-L)
  • 1471-8405
DOI
10.1093/occmed/48.7.427
OpenAlex
W2112076511
Cited by
136
References
20
Citations by year
2026: 1 · 2025: 4 · 2024: 4 · 2023: 10 · 2022: 6 · 2021: 11 · 2020: 5 · 2019: 9 · 2018: 5 · 2017: 3 · 2016: 6 · 2015: 8 · 2014: 2 · 2013: 6 · 2012: 7
FWCI
1.81
Type
journal article
Language
en
Open access
closed
Locations
  • Occupational Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Emergency Medicine › Poisoning and overdose treatments
  • Life Sciences › Agricultural and Biological Sciences › Plant Science › Cassava research and cyanide
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Plant-based Medicinal Research
Keywords
cyanide poisoning, cyanide antidote, sodium thiosulfate, hydroxocobalamin, amyl nitrite, methemoglobinemia, pathophysiology, treatment guidelines, animal-to-human extrapolation
MeSH terms
Antidotes, Cobalt, Cyanides, Humans, Methemoglobin, Oxidative Phosphorylation, Thiosulfate Sulfurtransferase

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