Pesticides Poisoning: Organophosphates & Carbamates

Pesticides Poisoning (Organophosphates & Carbamates)

• Organophosphate (OPC) poisoning encompasses accidental, suicidal, and homicidal exposures.
• Accidental exposure frequently involves handling insecticides or consuming contaminated food or water.
• Cocaine users may co-ingest OP pesticides, prolonging the drug's effect.
• Suicidal use of OP pesticides is common due to their ready availability and lethality.
• Homicidal use is rare, often due to a distinctive odor.

Learning Objectives

• Students should understand the circumstances of OPC poisoning.
• Students should know the toxicokinetics and mechanism of OPC poisoning, including the clinical presentation.
• Students should learn about the treatment of OPC poisoning cases.
• Students should understand the difference between OPC and carbamate poisoning.
• Students should be familiar with pearls and pitfalls in OPC poisoning cases.

Circumstances of Poisoning

• Accidental: Exposure during insecticide handling (manufacturing, spraying), consuming contaminated food or water.
• Suicidal: Common method of suicide, easily obtained, rapid death.
• Homicidal: Rare, characterized by detecting a distinctive odor.

Toxicokinetics of OPCs

• Absorption: Rapid absorption through various routes, including respiratory, gastrointestinal, conjunctival, and dermal. Broken skin and high environmental temperatures increase absorption.
• Distribution: Widespread distribution throughout the body, including crossing the blood-brain barrier. High lipid solubility leads to storage in fat tissue, potentially causing prolonged toxicity.
• Metabolism: Primarily metabolized in the liver by cytochrome P-450 system.
• Excretion: Eliminated through urine and stool.

Mechanism of OPC Toxicity

• Cholinesterase Inhibition: OPs inhibit cholinesterase, the enzyme responsible for breaking down acetylcholine. This leads to an accumulation of acetylcholine, triggering initial stimulation followed by depression of nerve impulse transmission.
• Postganglionic Parasympathetic Nerve Endings: This includes muscarinic receptors.
• Autonomic Ganglia and Neuromuscular Junctions: Includes nicotinic receptors.
• Central Nervous System (CNS): Also affected by the inhibition.

Clinical Picture of OPC Poisoning

• Muscarinic Effects (DUMBELLS): Classic cholinergic syndrome, including diarrhea, nausea, vomiting, urination, defecation, miosis, bradycardia, hypotension, bronchospasm, wheezing, cyanosis, lacrimation, increased secretions.
• Nicotinic Effects: Prolonged QT interval, ventricular tachycardia, diaphoresis, elevated blood pressure, tachycardia, skeletal muscle fasciculations, weakness, paralysis, respiratory arrest,.
• CNS Effects: Anxiety, insomnia, confusion, ataxia, coma, seizures (more common in children), Cheyne-Stokes respiration, and circulatory depression.

Treatment of OPC Poisoning

• I. Emergency & Supportive Measures: Airway and breathing management, frequent suctioning, respiratory support, intubation if needed for ventilatory support. Control of other symptoms or complications.
• II. Decontamination: Limited benefit due to rapid absorption; avoid ipecac, gastric lavage only for recent ingestion, activated charcoal may be used in co-ingestion cases. Dermal decontamination involves removing clothes and washing with soap and water, then ethyl alcohol.
• III. Enhanced Elimination: For eye exposure, copious irrigation with water or saline, followed by ophthalmologist consultation.
• IV. Physiological Antidotes (Atropine): Competitive antagonist of acetylcholine at muscarinic and CNS receptors. Reverses only muscarinic and CNS effects, not nicotinic effects. Dosage adjusted for age and toxicity severity.
• IV. Physiological Antidotes (Oximes): Reactivate cholinesterase; more effective against nicotinic effects than muscarinic.

Carbamate Poisoning

• Carbamate insecticides are acetylcholinesterase inhibitors, but their toxic effects last for a shorter duration than OPs.
• Carbamate-cholinesterase binding is reversible.
• Clinical picture of carbamate poisoning is similar to OPC poisoning, but less severe and shorter in duration.

Pearls & Pitfalls

• Prompt recognition and treatment of OPC poisoning is crucial for a good prognosis.
• Delayed-onset symptoms warrant continuous observation.
• Workers should not return to work if their cholinesterase levels are below 75% of normal.
• Intubation may prolong paralysis if succinylcholine or mivacurium are used.

This quiz focuses on the critical aspects of Organophosphate (OP) poisoning, including its causes, clinical effects, and treatment options. Students will learn to differentiate between organophosphate and carbamate poisoning, as well as understand toxicokinetics and the circumstances leading to these toxic exposures. The quiz also addresses common misconceptions and challenges in managing OP poisoning cases.