Tricyclic antidepressant (TCA) poisoning remains a major cause of morbidity and mortality. Deliberate self-poisoning may lead to the rapid onset of CNS and cardiovascular toxicity. Prompt intubation, hyperventilation and sodium bicarbonate administration at the first evidence of severe toxicity is life-saving.
| Table 3.75.1: Dose-related risk assessments: Tricyclic antidepressants | |
| Dose | Effect |
| <5 mg/kg | Minimal symptoms |
| 5-10 mg/kg | Drowsiness and mild anticholinergic effects Major toxicity not expected |
| >10 mg/kg | Potential for all major effects (coma, hypotension, seizures, cardiac dysrhythmias) to occur within 2-4 hours of ingestion Anticholinergic effects likely but often masked by coma |
| >30 mg/kg | Severe toxicity with pH-dependent cardiotoxicity and coma expected to last > 24 hours |
References
- Bateman ND. Tricyclic antidepressant poisoning: central nervous system effects and management. Toxicological Reviews 2005; 24(3): 181-186.
- Bradberry SM, Thanacoody HKR, Watt BE et al. Management of the cardiovascular complications of tricyclic antidepressant toxicity- role of sodium bicarbonate. Toxicological Reviews 2005; 24(3): 195-204.
- Liebelt EL, Francis PD, Woolf AD. ECG lead aVR versus QRS interval in predicting seizures and arrhythmias in acute tricyclic antidepressant toxicity. Annals of Emergency Medicine 1995; 26(2): 195-201.
- Heard K, Cain BS, Dart RC, Cairns CB. Tricyclic antidepressants directly depress human myocardial mechanical function independent of effects on the conduction system. Academic Emergency Medicine 2001; 8(12):1122-1127.
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