Clinical presentation

Clinical effects of TCA poisoning are apparent within 2 hours after ingestion, and most serious effects or complications occur within 6 hours after ingestion. Consult a clinical toxicologist early.

If patients remain asymptomatic 6 hours after ingesting TCAs, they are unlikely to develop clinical effects of poisoning.

Effects of TCA toxicity are worse in the presence of metabolic and respiratory acidosis. Altered conscious state, respiratory depression and seizures all contribute to acidosis, and can therefore exacerbate the risk of life-threatening complications.

Effects of TCA poisoning include:

• central nervous system (CNS) effects
  • rapidly decreasing level of consciousness, respiratory depression and coma in moderate to severe poisoning
  • seizures in severe poisoning (associated with QRS widening)
• cardiovascular effects
  • hypotension due to alpha-adrenoceptor blockade and myocardial depression
  • sinus tachycardia due to alpha-adrenoceptor blockade and anticholinergic effect
  • sodium channel blockade, QRS widening, arrhythmias (see Electrocardiographic changes)
• anticholinergic toxidrome
  • mydriasis, warm dry skin, sinus tachycardia, dry mouth
  • urinary retention and reduced bowel sounds
  • anticholinergic delirium that can persist beyond 24 to 48 hours following recovery from severe toxicity; as sedation wears off, delirium becomes more apparent.