Organophosphate poisoning

Summary

In this episode of MK's Medical Review, Dr. Moses Kazeefu provides an in-depth exploration of organophosphate and carbamate poisoning. He discusses the symptoms, signs, and pathophysiology of these poisons, which are commonly found in insecticides and can cause severe intoxication. The video covers the toxicological effects of acetylcholine buildup, clinical features of poisoning, and how to diagnose and treat affected patients. Treatment strategies include atropine administration and oxime use to reactivate acetylcholinesterase. Dr. Kazeefu also emphasizes the importance of timely intervention and monitoring to prevent respiratory failure and other complications.

Takeaways

• 😀 Organophosphate and carbamate poisoning are commonly found in insecticides and are responsible for over 1,000 deaths annually in developing countries.
• 😀 Poisoning can occur through ingestion, inhalation, and dermal absorption, as these chemicals are lipophilic and can accumulate in body fat over time.
• 😀 Organophosphates and carbamates inhibit the enzyme acetylcholinesterase, causing an accumulation of acetylcholine at nerve endings, leading to overstimulation of the nervous system.
• 😀 Muscarinic receptors (M1 to M5) and nicotinic receptors (NN and NM) are affected in organophosphate poisoning, resulting in a variety of symptoms based on their location in the body.
• 😀 Symptoms of poisoning include anxiety, restlessness, nausea, vomiting, abdominal cramps, diarrhea, sweating, and bradycardia (slow heart rate).
• 😀 Nicotinic effects include muscle fasciculation, weakness, and flaccid paralysis, particularly of respiratory muscles.
• 😀 Diagnosis of organophosphate poisoning is based on clinical history, physical examination, and testing erythrocyte cholinesterase activity, which is decreased in symptomatic patients.
• 😀 Treatment involves stabilizing the patient’s airway, administering atropine to counteract muscarinic effects, and using oximes like pralidoxime to reactivate acetylcholinesterase.
• 😀 Atropine is given in increasing doses (2-5 mg) until the patient shows signs of atropinization, including dry skin, dilated pupils, and an increased heart rate.
• 😀 Additional supportive treatments include oxygen therapy, intravenous fluids, and monitoring vital signs, while removing contaminated clothing and washing the patient are essential first steps.
• 😀 A rare but severe complication is delayed polyneuropathy, which can occur days after exposure and is caused by the aging of inhibited enzymes in peripheral nerves.

Q & A

What are the primary sources of organophosphates and carbamates that cause poisoning?

Organophosphates and carbamates are primarily found in insecticides, which are a common source of poisoning. These compounds can be ingested, inhaled, or absorbed through the skin, leading to intoxication.

How do organophosphates and carbamates affect the body at a biochemical level?

Organophosphates and carbamates inhibit the enzyme acetylcholinesterase, which is responsible for breaking down acetylcholine. This leads to an accumulation of acetylcholine at various cholinergic endings, including the neuromuscular junction, causing overstimulation of both muscarinic and nicotinic receptors.

What are the routes through which organophosphates can enter the body?

Organophosphates can enter the body through ingestion, inhalation, and dermal absorption. The compounds are lipophilic, meaning they can accumulate in fat tissue and cause symptoms to persist for extended periods.

What is the role of acetylcholine and acetylcholinesterase in normal body function?

Acetylcholine is a neurotransmitter that facilitates communication between neurons and between neurons and muscles. Acetylcholinesterase is the enzyme responsible for breaking down acetylcholine after it has transmitted its signal, thus terminating the action of acetylcholine at various synapses.

What is the significance of muscarinic and nicotinic receptors in organophosphate poisoning?

Muscarinic and nicotinic receptors are activated by the accumulation of acetylcholine due to acetylcholinesterase inhibition. This overstimulation leads to a variety of symptoms such as bradycardia, muscle fasciculations, respiratory issues, and pupil constriction (miosis).

What are the typical clinical features of organophosphate poisoning?

Clinical features include anxiety, restlessness, headache, nausea, vomiting, diarrhea, muscle fasciculations, bradycardia, miosis, hypersalivation, lacrimation, and urinary or fecal incontinence. Respiratory failure due to bronchorrhea and pulmonary edema can also occur.

How do you diagnose organophosphate poisoning?

Diagnosis is based on clinical history and physical examination. Blood tests can measure erythrocyte cholinesterase activity, which is typically reduced in poisoning cases. Other tests may include plasma cholinesterase activity, full blood count, and electrolytes to rule out other conditions.

What are the main treatment approaches for organophosphate poisoning?

Treatment involves securing the airway, providing oxygen, and removing contaminated clothing. Atropine is administered to counteract the effects of acetylcholine accumulation, with dosages adjusted to achieve atropinization, indicated by symptoms like pupil dilation and increased heart rate. In severe cases, oximes like pralidoxime may be used to reactivate acetylcholinesterase.

What is atropinization and how is it monitored in organophosphate poisoning treatment?

Atropinization refers to the therapeutic effect of atropine where the patient’s symptoms, such as bradycardia and miosis, are reversed. This is monitored by observing signs such as pupil dilation, increased heart rate, and skin dryness.

Why is organophosphate poisoning particularly common in developing countries?

Organophosphate poisoning is common in developing countries due to the widespread use of insecticides in agriculture and limited access to safety measures. Additionally, such poisons are often used in suicide attempts, especially among individuals facing emotional distress.