SUPERStudy: Organophosphate Poisoning
Introduction
Organophosphate poisoning is a potentially life-threatening condition caused by exposure to organophosphate (OP) compounds. These agents irreversibly inhibit acetylcholinesterase, leading to the accumulation of acetylcholine and overstimulation of cholinergic receptors.
Etiology
Sources:
- Agricultural pesticides (e.g., malathion, parathion).
- Chemical warfare agents (e.g., sarin, VX gas).
- Ophthalmologic agents for glaucoma (e.g., echothiophate, isoflurophate).
- Accidental exposure or suicidal ingestion.
Mechanism:
- Irreversible inhibition of acetylcholinesterase.
- Accumulation of acetylcholine causes overstimulation of muscarinic, nicotinic, and CNS receptors.
Epidemiology
- Prevalent in developing countries due to widespread agricultural use.
- Significant cause of morbidity and mortality, particularly in rural areas.
- Common in intentional poisonings (e.g., suicide attempts).
Pathophysiology
- Inhibition of Acetylcholinesterase: Prevents acetylcholine breakdown at synaptic junctions.
- Excess Acetylcholine: Leads to overstimulation of muscarinic, nicotinic, and CNS receptors.
Effects by Receptor Type:
- Muscarinic: Bronchoconstriction, bradycardia, increased secretions, miosis.
- Nicotinic: Muscle fasciculations, cramps, flaccid paralysis, tachycardia, hypertension.
- CNS: Seizures, confusion, coma, hallucinations, anxiety.
Clinical Manifestations
- Muscarinic Symptoms:
- SLUDGE-M:
- Salivation
- Lacrimation
- Urination
- Diarrhea
- Gastrointestinal upset
- Emesis
- Miosis
- Killer B’s: Bradycardia, Bronchorrhea, and Bronchospasm.
- Hypotension.
- SLUDGE-M:
- Nicotinic Symptoms:
- Muscle weakness, fasciculations, flaccid paralysis.
- Tachycardia and hypertension (due to adrenal stimulation).
- CNS Symptoms:
- Anxiety, confusion, delirium, seizures, coma.
Diagnosis
- Clinical Presentation: Characteristic symptoms (SLUDGE-M, muscle weakness, CNS involvement).
- Cholinesterase Activity:
- Plasma butyrylcholinesterase or pseudocholinesterase levels (decreased in acute poisoning).
- RBC acetylcholinesterase levels (gold standard).
- Confirmatory Tests: Detection of OP compounds in blood, urine, or gastric aspirate.
Treatment
- Emergency Stabilization:
- Airway protection and oxygenation.
- Intubation if respiratory failure occurs.
- Antidotes:
- Atropine: Blocks muscarinic effects (given until secretions dry up).
- Pralidoxime (2-PAM): Reactivates acetylcholinesterase (effective if administered early).
- Supportive Care:
- Decontamination: Remove clothing and wash skin thoroughly.
- Activated Charcoal: For ingestion cases.
- Benzodiazepines: For seizures.
Prognosis
- Mild Cases: Full recovery with prompt treatment.
- Severe Cases: High risk of death due to respiratory failure or multiorgan dysfunction.
- Long-term Effects: Chronic neurological sequelae in survivors of severe poisoning.
SUPERPoint
Organophosphate poisoning leads to a life-threatening cholinergic crisis characterized by muscarinic, nicotinic, and CNS symptoms, requiring rapid administration of atropine and pralidoxime.
SUPERFormula: Patient presents with muscarinic symptoms (SLUDGE-M: Salivation, Lacrimation, Urination, Diarrhea, Gastrointestinal upset, Emesis, Miosis) + Nicotinic symptoms (muscle fasciculations, weakness, respiratory paralysis) + CNS effects (confusion, seizures, coma) + is a farmer exposed to pesticide spraying or deliberate self-poisoning + irreversible acetylcholinesterase inhibition + Accumulation of acetylcholine + Diagnosis (clinical + low cholinesterase levels) + Treatment (Atropine for muscarinic symptoms + Pralidoxime to reactivate acetylcholinesterase + Decontamination + Supportive care) = Organophosphate Poisoning |
References:
Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill Education; 2020.