How should acute chlormequat poisoning be managed?

Management of Acute Chlormequat Poisoning

Immediate Recognition and Stabilization

Chlormequat poisoning produces a cholinergic crisis that can cause death within one hour of ingestion, requiring immediate aggressive atropinization and intensive supportive care. 1, 2

• Recognize that chlormequat acts directly on nicotinic and muscarinic receptors (not through cholinesterase inhibition), producing symptoms identical to organophosphate poisoning including salivation, diaphoresis, bradycardia, visual disturbances, bronchorrhea, bronchospasm, and seizures. 1, 2
• Secure the airway immediately, as rapid progression to respiratory failure, pulmonary edema, and cardiovascular collapse occurs within the first hour. 1, 2
• Intubate early if the patient shows any signs of altered mental status, respiratory distress, or excessive secretions that compromise airway patency. 1

Atropine Administration Protocol

Administer atropine aggressively using the same dosing strategy as for nerve agent or organophosphate poisoning, starting with 2 mg IV for adults (0.02 mg/kg for children) and repeating every 5-10 minutes until full muscarinic antagonism is achieved. 3

• Titrate atropine to reverse bronchorrhea, bronchospasm, bradycardia, and hypotension—not to pupil size. 3, 4
• Expect to use cumulative doses of 10-20 mg in the first 2-3 hours, with some patients requiring up to 50 mg in 24 hours before achieving adequate control of cholinergic symptoms. 3
• Continue atropine administration as clinically necessary based on persistent signs of cholinergic toxicity. 3

Cardiovascular Support

• Treat severe bradycardia with atropine as the first-line agent. 3, 4
• Recognize that ventricular fibrillation progressing to asystole is a documented cause of death in chlormequat poisoning. 1
• Provide aggressive fluid resuscitation for hypotension, followed by vasopressor support (preferably norepinephrine or dopamine) if hypotension persists despite adequate volume replacement. 3
• Monitor continuously for cardiac arrhythmias and be prepared for advanced cardiac life support measures. 1

Seizure Management

• Administer benzodiazepines (midazolam 0.05-0.1 mg/kg IV or diazepam 0.2 mg/kg IV) in fractionated doses for seizure control. 3
• Repeat dosing as needed to achieve adequate seizure suppression and reduce resistance to mechanical ventilation. 3

Decontamination Considerations

• Remove all contaminated clothing and decontaminate skin with copious water immediately to prevent continued dermal absorption. 5, 4
• Do not induce vomiting due to the rapid onset of CNS depression and high aspiration risk. 5, 6
• Consider activated charcoal only if the patient presents within 1 hour of ingestion, is fully conscious, and can protect their airway—though its efficacy in chlormequat poisoning is uncertain. 7, 6

Critical Pitfalls to Avoid

• Do not underestimate the lethality of chlormequat poisoning—death can occur within one hour, and the case fatality rate approaches 43% in reported series. 2
• Do not withhold atropine due to concerns about tachycardia or mydriasis; these are therapeutic endpoints, not contraindications. 3
• Do not delay intubation in patients with significant ingestions, as pulmonary edema develops rapidly. 1
• Contact poison control immediately for real-time guidance, as chlormequat poisoning is uncommon and easily confused with organophosphate toxicity. 5, 4

Monitoring and Supportive Care

• Provide intensive monitoring in an ICU setting with continuous cardiac monitoring, pulse oximetry, and frequent reassessment of respiratory status. 1, 2
• Monitor for development of acute renal failure and provide renal replacement therapy if indicated. 1
• Treat hyperthermia aggressively with external cooling if present. 5
• Maintain adequate oxygenation but avoid excessive supplemental oxygen, as this may theoretically worsen oxidative injury (though this is extrapolated from paraquat data and not specifically studied in chlormequat). 8, 9