Pesticides Poisoning Quiz: Organophosphates & Carbamates

Pesticides Poisoning (Organophosphates & Carbamates)

• Learning Objectives: Students should understand the circumstances, toxicokinetics, mechanism, clinical picture, and treatment of organophosphorus compound (OPC) poisoning, and compare it with carbamate poisoning. Pearls and pitfalls concerning OPC poisoning are also key.

Circumstances of Poisoning

• Accidental: Poisoning occurs during pesticide handling (manufacturing, spraying), drinking contaminated water or food, or co-ingesting OPCs with cocaine.
• Suicidal: OPC poisoning is a common method for suicide due to ease of access and rapid lethality.
• Homicidal: Rare, potentially due to the distinctive "garlic" odor of OPCs.

Toxicokinetics of OPCs

• Absorption: OPCs are rapidly absorbed via respiratory, gastrointestinal, conjunctiva, dermal, and mucous membrane routes, with respiratory absorption being the fastest. Absorption is enhanced by broken skin or high environmental temperatures.
• Distribution: OPCs distribute throughout the body and cross the blood-brain barrier; they are highly lipid-soluble and can accumulate in fatty tissues, which can lead to prolonged toxicity.
• Metabolism: OPCs are mainly metabolized in the liver by cytochrome P-450 enzymes.
• Excretion: OPCs are excreted through urine and stool.

Mechanism of OPC Toxicity

• Cholinesterase Inhibition: OPCs irreversibly inhibit cholinesterase, an enzyme crucial for breaking down acetylcholine (Ach), resulting in its accumulation. The build-up causes initial stimulation of postganglionic parasympathetic nerve endings, autonomic ganglia, and neuromuscular junctions, followed by depression of impulse transmission.
• Consequences: The cholinergic syndrome (DUMBELLS) and nicotinic effects are symptomatic of cholinesterase inhibition.

Clinical Picture of OPC Poisoning

• Muscarinic Effects (DUMBELLS): Diarrhea, Urination, Miosis, Bradycardia, Bronchospasm, Lacrimation, and Excessive secretions (sweating, salivation).
• Nicotinic Effects: Prolonged QT interval (PVT), torsades de pointes, diaphoresis, hypertension, tachycardia, skeletal muscle fasciculations, weakness, paralysis, and respiratory arrest.
• CNS Effects: Anxiety, insomnia, confusion, ataxia, coma, seizures (more common in children), and respiratory and circulatory depression.

Treatment of OPC Poisoning

• Emergency & Supportive Measures (ABC): Airway and breathing management, frequent suctioning, respiratory support, intubation (if needed), control of fluid loss, and treatment of seizures (using diazepam or phenobarbital).
• Decontamination: Avoid further exposure. Gastric decontamination may not be beneficial due to rapid absorption; prevent contact with skin or contaminated clothes and items. Use soap and water, then ethyl alcohol for thorough cleaning.
• Physiological Antidotes:
• Atropine: A competitive Ach antagonist, reversing muscarinic and CNS effects, but not nicotinic effects. Dosage and duration of action vary depending on toxicity level. Side effects/high doses include peripheral anticholinergic effects (tachycardia, flushed skin, mydriasis, urine retention, hallucination).
• Oximes: Reactivate cholinesterase, detoxify OPC molecules. Correct nicotinic manifestations. Used in cases of suspected or confirmed poisoning, or with significant atropine requirement or neuromuscular weakness. Specifically, obidoxime (toxogonin) used outside the USA.

Carbamate Poisoning

• Difference: Carbamates are acetylcholinesterase inhibitors similar to OPCs but have a shorter duration of action; binding is reversible.
• Clinical Picture: Similiar to OPCs, but less severe and shorter-lasting manifestations. Lower risk of CNS manifestations compared to OPC, because carbamates have poorer BBB penetration.
• Treatment: Oximes are generally not indicated because the carbamate effects resolve spontaneously.

Pearls & Pitfalls

• Prognosis: Quickly recognized and treated OPC poisoning typically has a good outcome. Untreated cases may lead to respiratory failure and potentially, death within 24 hours.
• Observation: Delayed onset symptoms are possible, especially with fat-soluble agents. Patients require observation (12–24 hours, to account for delayed onset).
• Return to Work: Farmers and workers may not return to work until levels of cholinesterase (CHE) return to over 75% normal.
• Intubation: If intubation is needed, avoid succinylcholine and mivacurium, as these are metabolized by pseudocholinesterase which can prolong paralysis by over 24 hours.

Test your knowledge on the circumstances, toxicokinetics, and treatment of organophosphate compound poisoning as well as carbamate poisoning. Understand the differences in clinical presentations and learn about the potential pitfalls in managing these conditions.