Makindo Medical Notes

Cholinergic crisis is a life-threatening condition caused by overstimulation of acetylcholine (ACh) receptors, often seen in organophosphate toxicity or excessive treatment for myasthenia gravis.

About

• Occurs due to overstimulation of central and peripheral ACh receptors, particularly nicotinic and muscarinic receptors.
• Results from excessive accumulation of ACh at neuromuscular junctions and muscarinic receptors due to inhibition of acetylcholinesterase, leading to a cholinergic crisis.

Aetiology

• Results from decreased breakdown of ACh due to acetylcholinesterase inhibition.
• Exposure to nerve agents, such as sarin, soman, tabun, and VX.
• Organophosphates found in insecticides and pesticides (e.g., malathion, parathion).
• Carbamate pesticides, including agents like aldicarb and carbaryl.
• Overdose or excessive use of acetylcholinesterase inhibitors in treating myasthenia gravis.

Nerve Agents Overview

Nerve agents are highly toxic chemicals initially developed as chemical warfare agents. They irreversibly inhibit acetylcholinesterase, leading to severe cholinergic effects. Common nerve agents include:

• Sarin (GB): A fast-acting, volatile liquid that readily evaporates into a toxic gas, causing symptoms within seconds to minutes.
• Soman (GD): A more persistent nerve agent that is highly toxic even in low concentrations, with rapid onset of symptoms and prolonged effects.
• Tabun (GA): The first synthesized nerve agent, less volatile than sarin, and highly toxic with both liquid and vapor exposures.
• VX: An extremely potent nerve agent with high persistence in the environment. It is a thick, oily liquid that poses a contact hazard and is considered one of the deadliest known nerve agents.

Clinical Features

• Excessive muscarinic effects: Nausea, vomiting, diarrhoea, excessive salivation, and sweating.
• Respiratory distress: Bronchial secretions, bronchospasm, miosis (constricted pupils), bradycardia, or tachycardia.
• Flaccid paralysis: Weakness or paralysis of muscles, respiratory failure due to muscle weakness.
• Severe cardiovascular and respiratory symptoms: Copious salivation, bronchial secretions, bradycardia, and miosis.
• Death may occur due to respiratory paralysis, pulmonary edema, or cardiac arrest.

Investigations

• Full Blood Count (FBC), Urea & Electrolytes (U&E), Arterial Blood Gas (ABG), and Lactate levels.
• Chest X-ray (CXR) and Electrocardiogram (ECG) to monitor for respiratory or cardiac complications.

Management

• Decontamination: In cases of nerve agent exposure, ensure healthcare providers avoid skin-to-skin contamination, and remove contaminated clothing and wash the skin with soap and water.
• Supportive care: Maintain ABCs (Airway, Breathing, Circulation) and administer high-flow oxygen as needed. Tracheostomy may be considered in severe cases of respiratory failure.
• Secretions management: Use bronchial aspiration and postural drainage to manage excessive secretions.
• Antimuscarinic treatment: Administer IV atropine (1-4 mg) for muscarinic symptoms, with additional doses every 5 to 30 minutes as needed until symptoms improve.
• Avoid atropine overdose: Overdosage can lead to complications like tenacious secretions or bronchial plugs.
• Pralidoxime (2-PAM): Used to reactivate acetylcholinesterase in cases of organophosphate or nerve agent poisoning.
• Intubation and ventilation: Required if the patient does not improve with atropine and pralidoxime.