Overview
Why the Patient Becomes Wet, Weak, and Hypoxic
Organophosphate insecticides inhibit acetylcholinesterase, the enzyme that normally clears acetylcholine from synapses.
Organophosphate insecticides inhibit acetylcholinesterase, the enzyme that normally clears acetylcholine from synapses. Acetylcholine then continues stimulating receptors after the signal should have ended. The result is a cholinergic toxidrome: excessive parasympathetic activity at muscarinic receptors and excessive stimulation at nicotinic receptors. Muscarinic findings are often remembered with SLUDGEM: salivation, lacrimation, urination, defecation, gastrointestinal cramping, emesis, and miosis. At the bedside, the most dangerous muscarinic findings are the wet chest and slow circulation: bronchorrhea, bronchospasm, bradycardia, and hypotension. Nicotinic effects explain why a patient can become progressively weak even while secretions are being treated. Fasciculations may appear first, followed by weakness and possible paralysis of the respiratory muscles. Respiratory failure can therefore come from three directions at once: airways narrowed by bronchospasm, alveoli flooded with secretions, and inadequate ventilation from neuromuscular weakness. An experienced nurse notices the combination rather than any single sign: a patient who is pinpoint, drenched in secretions, wheezing or gurgling, and becoming weak has a cholinergic emergency until proven otherwise.