TCA Toxicity
Background
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Multi-system effects due to:
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Blockade of cardiac fast sodium channels
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Antagonism of:
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Central & peripheral muscarinic acetylcholine receptors
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Peripheral α-1 adrenergic receptors
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Histamine (H1) receptors
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CNS GABA A receptors
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Greatest risk of seizure & arrhythmias occurs in first 6-8 hours of TCA ingestion
Considerations
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Emergency/full stomach
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Co-ingestants
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Life threatening multi-system effects:
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CNS: sedation, coma, seizures
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CVS: tachyardia, hypotension, myocardial dysfunction, lethal arrhythmias
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Anticholinergic toxidrome (red, hot, mydriasis, dry, delirium)
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Treatment
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Consult toxicology/ICU immediately
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Admit to monitored setting
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Intubate & hyperventilate (promotes alkalosis)
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Sedation with benzodiazepines & propofol (to ↑ seizure threshold)
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Gastric decontamination (if ingestion < 1hr & airway is protected)
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Hypotension: fluids & vasopressor (norepinephrine)
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QRS > 100 ms = high risk of arrhythmias & seizures:
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NaHCO3
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2-3 mEq/kg then 3 amps/L at 250 ml/hr or 2x maintenance
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Goals: QRS < 100, stable BP, sodium ~ 150, pH ~ 7.5
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3% NaCl if pH > 7.50 & persistent QRS elevation
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Arrhthmia treatment (VT/VF):
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Run ACLS/defibrillate
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Lidocaine 1 mg/kg
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MgSO4 if prolonged QTc or Torsades develops
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Amiodarone/procainamide contraindicated
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Seizures:
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Treat with midazolam
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Do NOT use phenytoin
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Intralipid for cardiac arrest or refractory hypotension
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ECMO as last resort
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Hemodialysis NOT effective
Contraindicated Therapies
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Anti-arrhythmic drugs:
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Class IA (e.g., procainamide) & class IC agents (e.g., flecainide) due to their inhibition of rapid sodium channels (similar to TCA effect)
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Class III agents (e.g., amiodarone) due to QTc prolonging effect
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Phenytoin
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Flumazenil: can induce seizures