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Emergency and Acute Medicine – Tricyclic Antidepressant (TCA) Poisoning
Tricyclic antidepressant (TCA) poisoning is a life-threatening toxicologic emergency characterized by rapid clinical deterioration, primarily due to cardiac sodium channel blockade (a quinidine-like effect). Additional mechanisms include inhibition of norepinephrine reuptake, α-adrenergic blockade, and anticholinergic effects. Compared to TCAs, selective serotonin reuptake inhibitors (SSRIs) have a much wider safety margin and less cardiovascular toxicity, while serotonin–norepinephrine reuptake inhibitors (SNRIs), such as venlafaxine, may still cause seizures and dysrhythmias.
Common TCAs involved include amitriptyline, nortriptyline, imipramine, and doxepin. Toxicity can develop quickly after ingestion, and even initially well-appearing patients may deteriorate suddenly with seizures, arrhythmias, or coma.
Clinical manifestations affect multiple systems. In the central nervous system, patients may exhibit either stimulation (agitation, tremor, fasciculations, seizures) or depression (drowsiness, lethargy, coma). Seizures are particularly dangerous, as resulting acidemia worsens cardiotoxicity. Cardiovascular findings are the hallmark and include early sinus tachycardia due to anticholinergic and norepinephrine effects, followed by potential hypotension and late bradycardia from catecholamine depletion. ECG abnormalities are critical: QRS widening greater than 100 ms is associated with seizures, and greater than 160 ms predicts ventricular dysrhythmias. A characteristic finding is a prominent R wave in lead aVR (>3 mm), reflecting rightward terminal QRS axis deviation.
Anticholinergic effects such as dilated pupils, decreased bowel sounds, and urinary retention may occur but are less prominent than cardiac toxicity.
Evaluation centers on rapid recognition and cardiac monitoring. An ECG is the most important diagnostic tool and should be obtained immediately and repeated as needed. Continuous cardiac monitoring is essential. Laboratory tests include electrolytes, renal function, glucose, arterial blood gas, and toxicology screening to assess for coingestants. Serum TCA levels are not useful for guiding management, as they correlate poorly with severity.
Management requires aggressive and early intervention. Initial stabilization follows airway, breathing, and circulation principles, with a low threshold for intubation in patients with altered mental status. Intravenous fluids and oxygen are administered, and cardiac monitoring is continuous.
The cornerstone of treatment is sodium bicarbonate therapy. Indications include QRS widening greater than 100–120 ms or any evidence of cardiac toxicity. Boluses of sodium bicarbonate (1–2 mEq/kg) are given and repeated as needed, with the goal of narrowing the QRS and maintaining an arterial pH of 7.45–7.5. Hyperventilation may assist in achieving this alkalinization. If needed, a bicarbonate infusion can be started.
Dysrhythmias are treated with sodium bicarbonate first; lidocaine may be used as a second-line agent. Class IA and IC antiarrhythmics (e.g., procainamide) and physostigmine are contraindicated, as they can worsen toxicity. Hypotension is managed with IV fluids, and if refractory, norepinephrine is the preferred vasopressor due to its α-agonist effects.
Seizures are treated with benzodiazepines such as diazepam or lorazepam, followed by phenobarbital if needed. Refractory seizures may require neuromuscular paralysis and airway control.
Decontamination with activated charcoal is appropriate if the patient presents early and the airway is protected. Gastric lavage may be considered within 1 hour of ingestion in severe cases. Ipecac is contraindicated due to the risk of aspiration. Flumazenil should not be used, especially in mixed overdoses, as it may precipitate seizures.
Patients require close observation and disposition decisions depend on clinical status. Symptomatic patients, those with ECG abnormalities, altered mental status, seizures, or persistent tachycardia beyond 6 hours should be admitted, often to an intensive care setting. Asymptomatic patients with a normal ECG after 6 hours of observation may be considered for discharge, provided psychiatric evaluation is completed if the ingestion was intentional.
Key clinical points include recognizing that TCA poisoning can deteriorate rapidly, making early ECG monitoring essential. QRS widening is a critical marker of toxicity, and prompt treatment with sodium bicarbonate can be lifesaving.
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