Overview

1. Sedation, anticholinergic and cardiotoxity are possible depending on dose and whether older (sedating) or newer (non-sedating) generation of antihistmines.

Toxic mechanism

1. Competitive inhibition at H1 receptors. Sedating AH are lipophilic and cross BBB, they also block M1, & 5HT receptors. Non-sedating AH are less lipophilic and H1 selective, although OD may selectivity and still cause CNS sedation. Cardiac Na & K channel blockade occurs in large/massive OD.

Toxicokinetics

1. Well abs. Lipophilic with large Vd (Sedating AH), or small Vd (Non-sedating). Variable liver met. Variable T½.

Clinical features

1. CNS depression/sedation: minor with non-sedating AH
2. Anticholinergic toxidrome: minor with non-sedating AH
3. Seizures: rare – only really a risk with sedating AH

CVS

1. HR
2. Hypotension 2º to NaBlockade rare after massive OD of sedating AH.
3. QTc 2º to KBlockade rare after large OD of non-sedating AH.

Investigations

1. Screening: serial ECG, paracetamol, BSL

Risk assessment

1. Large OD may CVS toxicity otherwise sedation/anticholinergic effects more likely with sedating AH. Children may gate anticholinergic delirium.

Management

Resus

1. Rarely required but should be cardiac monitored for 6h (12h non-sedating).

Supportive Care

1. Treat seizures with BDZs.
2. For QRS/NaBlockade: Sodium bicarbonate 1–2mmol/kg boluses over 1–2min.
3. For QTc: MgSO4, isoprenaline or overdrive pacing.
4. Antidote: Physostigmine if severe anticholinergic delirium unresponsive to BDZ.

Disposition

1. If asymptomatic and normal ECG at 6hr d/c else admit. If sig. delirium/sedation or dysrhythmia HDU/ICU.