Reduced GCS, miosis and tachycardia is almost pathognomonic of olanzapine overdose in the western world.
Sedation, ataxia, miosis (unlike the mydriasis commonly seen with anticholinergics), fluctuating mental status.
Clinical features should manifest within 2 – 4 hours and may last 48 hours (coma usually lasts 24 – 48 hours).
Delayed extrapyramidal effects can occur in children days later.
Children: the toxic dose is unclear but symptoms are likely to develop when >0.5 mg/kg have been ingested.
Can be managed with benzodiazepines (varying doses in the textbooks, easy method is 0.1mg/kg IV for lorazepam (max 4mg) / midazolam (max 10mg) / diazepam (max 10mg).
Check the patient is not in a dysrhythmia.
Seizures (rare)/agitation: IV benzodiazepines incrementally dosed every 5 minutes to effect.
Hypotension: Give 10 – 20 ml/kg of IV crystalloid, if response is not adequate start noradrenaline ( adrenaline is contraindicated due to paradoxical hypotension from beta 2 mediated vasodilatation). Noradrenaline dose: 0.15mg/kg in 50ml D5W at 1-10ml/hr (0.05 – 0.5 mcg/kg/min).
Reduced GCS: Prompt intubation and ventilation.
Hepatic metabolism to inactive water-soluble metabolites.
Large volume of distribution 10-20 L/kg.
This causes an anticholinergic effect (muscarinic receptors) in overdose and drowsiness (histamine receptor blockade). Olanzapine antagonises the mesolimbic dopamine (D2), serotonin, histamine the muscarninic M1 and peripheral alpha 1 receptors. Olanzapine like queitiapine has a predictable dose-dependent CNS depression. Widely used in Australasia and therefore a fairly common presentation to the emergency department. Olanzapine is a second generation atypical antipsychotic.
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