1. INTRODUCTION
Organophosphate poisoning is a common prevalent emergency care problem
found in Nepal due to its easy access and widespread availability of
insecticides and pesticides among farmers.1,2Approximately, case fatality rate of treated OP poisoning is 5-20% in
developing countries in Asia and 7.4% in Nepal.3,4Exposure may occur through inhalation, ingestion, or dermal contact. The
severity of the symptoms depends on the amount ingested, route of
absorption, and rate of metabolic breakdown of the insecticide. The
pathophysiology of OP insecticide is the irreversible inhibition of
enzyme acetylcholinesterase (AchE) which breaks down neurotransmitter
acetylcholine found in both peripheral and central nervous system,
followed by overstimulation of muscarinic and nicotinic receptors
resulting in cholinergic toxidrome.5,6 Figure 1.
Pathophysiology of OP poisoning.6
In Nepal, the grading of OP poisoning is based on the Peradeniya
Organophosphorus Poisoning (POP) scale. Parameters such as pupil size,
respiratory rate, heart rate, fasciculations, level of consciousness
(LOC), and seizures are used to rate the poisoning as mild, moderate, or
severe.3,7 Treatment begins with decontamination,
airway control and oxygenation. The mainstays of pharmacological therapy
include atropine, pralidoxime (2-PAM), and diazepam. Initial management
must focus on adequate use of atropine and optimising oxygenation prior
to the use of atropine is recommended to minimise the potential for
dysrhythmias.8