- Include the phenothiazines: chlorpromazine, fluphenazine, thioridazine (discontinued in Aus) and the butyrophenones: haloperidol & droperidol. These neuroleptics cause CNS depression, orthostatic hypoBP, anticholinergic effects in OD.
- Thioridizine was the most cardiotoxic.
- Main action is central D2 antagonism, but they have unwanted effects at other receptors (H1, GABA-A, M1, 1, 2, 5HT). They also have Na & K channel-blocking effects.
- Rapidly abs but more erratically in OD. 1st pass metabolism.- Cyt P450. Many have active metabolites and long elimination half-lives.
- Intoxication: within 2–4hrs.
- CNS depression: LOC, coma from large OD. Seizures & EPE uncommon.
- Anticholinergic effects: agitated delirium, urinary retention, HR, mydriasis, etc
- Cardiotoxicity: QRS, QTc, Torsade & other arrhythmias (mainly thioridazine)
- NB: Neuroleptic Malignant Syndrome occurs rarely in OD.
- Screening: BSL, ECG, paracetamol
- Other: Serial ECGs & cardiac monitoring for 6hrs, longer for thioridazine
- Only significant risk of cardiac toxicity with thioridazine, otherwise relatively low risk.
- Thioridazine coma & cardiotoxicity likely with OD >5g
- Torsade risk if QTc>500ms
- Chlorpromazine coma likely with OD >5g
- Resus: ABCs
- Fluid management for BP
- Treat NaBlockade with bicarbonate.
- Treat TdP by correcting hypoxia, hypoK and give MgSO4 or, if HR<100, give isoprenaline 1–10µg/min IV infusion or overdrive pace to 100–120bpm.
- Manage delirium with non-pharmacological & BDZ rather than physostigmine.
- Treat seizures with BDZ.
- Treat acute dystonic reactions (EPE) with benztropine ± BDZ.
- Activated charcoal indicated if intubated.
- If remain asymptomatic at 6hr post OD with normal ECG can be d/c.