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