Organophosphate Poisoning

Organophosphates phosphorylate and inactivate acetylcholinesterase. Acetylcholine then accumulates at muscarinic receptors, nicotinic receptors in autonomic ganglia and the neuromuscular junction, and throughout the central nervous system. This produces several effects at once: - Muscarinic excess: salivation, lacrimation, sweating, bronchorrhoea, bronchospasm, miosis, vomiting, diarrhoea, urination, bradycardia, and sometimes atrioventricular block. - Nicotinic excess: fasciculations followed by muscle weakness or flaccid paralysis; autonomic ganglion stimulation can also produce tachycardia, hypertension, or other mixed cardiovascular findings. - Central nervous system toxicity: anxiety, confusion, seizures, coma, and abnormal respiratory drive. The bedside picture is the net result of these opposing receptor effects, so not every patient is bradycardic, sweaty, or miotic. A patient may have tachycardia despite marked muscarinic secretion, and normal pupils do not exclude poisoning. Respiratory failure is the immediate threat. Bronchorrhoea and bronchospasm obstruct oxygen movement, while weakness of the respiratory muscles reduces ventilation and the ability to clear secretions. Treating only one part of this combination leaves the patient at risk. The enzyme-inhibitor bond changes over time. Before aging, an oxime such as pralidoxime may reactivate acetylcholinesterase. After aging, the...