Organophosphate Poisoning Classification
Organophosphate poisoning is classified into three distinct temporal syndromes based on time of symptom onset: acute cholinergic crisis (within 24 hours), intermediate syndrome (24 hours to 2 weeks), and delayed polyneuropathy (beyond 2 weeks). 1, 2
Time-Based Classification System
Acute Cholinergic Crisis (Within 24 Hours)
Muscarinic manifestations include the classic SLUDGE syndrome: salivation, lacrimation, urination, defecation, gastric cramps, and emesis, along with bronchorrhea, bronchospasm, bradycardia, and miosis (constricted pupils). 3, 1, 4
Nicotinic manifestations present as muscle fasciculations, weakness, and potentially respiratory failure due to diaphragmatic paralysis. 3, 5
Central nervous system effects include altered mental status, seizures, agitation, and coma. 5, 1
This acute phase results from irreversible inhibition of acetylcholinesterase enzyme, causing acetylcholine accumulation at synapses and excessive stimulation of both muscarinic and nicotinic receptors. 3, 4
Intermediate Syndrome (24 Hours to 2 Weeks)
Proximal muscle weakness develops after resolution of the initial cholinergic crisis, typically appearing 24-96 hours post-exposure, even as late as 4 days after acute exposure. 6, 2
This syndrome manifests as a myasthenic-like presentation with respiratory muscle weakness requiring prolonged mechanical ventilation. 5, 2
Critical pitfall: Cholinesterase levels cannot predict the development of intermediate syndrome, so clinical vigilance is essential during this window. 7
Delayed Polyneuropathy (Beyond 2 Weeks)
Peripheral neuropathies emerge 1-3 weeks after exposure, presenting as distal sensorimotor deficits. 7, 5
Neuropsychiatric abnormalities and extrapyramidal disorders may persist for months to years, including cognitive deficits, memory impairment, attention problems, and mood disorders. 7, 5
These late effects involve mechanisms independent of cholinesterase inhibition, including neuroinflammation and disruption of dopaminergic and glutamatergic neurotransmission. 7
Alternative Classification Approaches
Receptor-Based Classification
Peripheral muscarinic effects: Excessive glandular secretions, bronchospasm, bradycardia, miosis, urination, and defecation. 1, 4
Peripheral nicotinic effects: Muscle fasciculations, weakness, paralysis, and tachycardia (from sympathetic ganglia stimulation). 1, 4
Central nervous system effects: Seizures, altered consciousness, respiratory depression, and autonomic instability. 1, 4
Organ-System Classification
Cardiovascular manifestations: Bradycardia (muscarinic) or tachycardia (nicotinic), arrhythmias, and hemodynamic instability. 1, 2
Respiratory manifestations: Bronchorrhea, bronchospasm, respiratory muscle weakness, and respiratory failure requiring intubation. 1, 4
Neurological manifestations: Altered mental status, seizures, fasciculations, weakness, and delayed neuropathy. 1, 4
Rare complications: Acute pancreatitis, hepatic dysfunction, myonecrosis, and rhabdomyolysis with subsequent renal damage. 6, 2, 8
Clinical Severity Grading
Severity Assessment Parameters
Mild poisoning: Muscarinic symptoms without respiratory compromise or significant nicotinic effects. 1
Moderate poisoning: Bronchorrhea requiring atropine, fasciculations, and mild respiratory distress. 1
Severe poisoning: Respiratory failure requiring intubation, seizures, altered consciousness, or cardiovascular instability requiring aggressive atropinization (typically 10-20 mg atropine in first 2-3 hours). 6, 1
Key Clinical Distinctions
Organophosphates versus carbamates: Organophosphates cause permanent "aging" of the acetylcholinesterase enzyme through covalent bonding, while carbamates spontaneously dissociate and cause reversible inhibition. 6, 7
Diagnostic confirmation: Red blood cell cholinesterase activity <50% of normal confirms significant exposure, but treatment must never be delayed awaiting laboratory results—clinical symptoms drive all therapeutic decisions. 7
The time-based classification system is most clinically useful because it alerts providers to delayed complications that may occur after initial stabilization, preventing premature discharge and ensuring appropriate monitoring duration of at least 48-72 hours. 6, 1