Citation

Hulse EJ, Davies JOJ, Simpson AJ, Sciuto AM, Eddleston M. Am. J. Respir. Crit. Care Med. 2014; 190(12): 1342-1354.

Affiliation

Pharmacology, Toxicology and Therapeutics, Centre for Cardiovascular Sciences, University of Edinburgh, Edinburgh, United Kingdom ; elspeth_uk@hotmail.com.

Copyright

(Copyright © 2014, American Thoracic Society)

DOI

10.1164/rccm.201406-1150CI

PMID

25419614

Abstract

Organophosphorus (OP) compound poisoning is a major global public health problem. Acute OP insecticide self-poisoning kills over 200,000 people every year, the majority from self-harm in rural Asia. Highly toxic OP nerve agents (e.g. sarin) are a significant current terrorist threat as shown by attacks in Damascus during 2013. These anticholinesterase compounds are classically considered to cause an acute cholinergic syndrome with decreased consciousness, respiratory failure, and in the case of insecticides a delayed intermediate syndrome that requires prolonged ventilation. Acute respiratory failure, by central and peripheral mechanisms, is the primary cause of death in most cases. However, pre-clinical and clinical research over the last two decades has indicated a more complex picture of respiratory complications following OP insecticide poisoning, including onset of delayed neuromuscular junction (NMJ) dysfunction during the cholinergic syndrome, aspiration causing pneumonia and acute respiratory distress syndrome, and the involvement of solvents in OP toxicity. The treatment of OP poisoning has not changed over the last 50 years. However, a better understanding of the multiple respiratory complications of OP poisoning offers additional therapeutic opportunities.

Language: en