Management overview for cocaine poisoning

Cocaine is a recreational stimulant drug with local anaesthetic properties. The effects of cocaine originate from the parent drug and its many metabolites. ‘Blow’, ‘charlie’ or ‘snow’ are common street names for cocaine. Forms include:

• ‘street’ cocaine (‘coke’)—usually a powder that can be snorted, or administered orally or intravenously
• ‘crack’ cocaine (‘freebase’)—a crystalline form that can be smoked or injected.

Effects of cocaine are due to sodium channel blockade and monoamine reuptake inhibition. Sodium channel blockade causes its local anaesthetic effect and delayed myocardial conduction (QRS widening). Monoamine reuptake inhibition increases dopamine, noradrenaline and serotonin concentrations, which cause sympathomimetic (stimulant) effects.

Cocaine toxicity affects many body systems with medical, surgical and psychiatric complications. Toxicity is mainly due to the drug’s sympathomimetic effects or from adulterants in the formulation. Effects of cocaine are similar to the effects of amfetamines, but at toxic doses cocaine has a greater risk of seizures and arrhythmias.

Cocaine promotes thrombogenesis by affecting platelet aggregation, and also causes endothelial changes, which together with vasospasm, can cause complications in any vascular bed.

If cocaine is taken with alcohol, a unique cocaine metabolite, cocaethylene, is produced. This has similar effects to cocaine but a prolonged duration of action.

Management of cocaine poisoning is as for sympathomimetic toxidrome. The aims of treatment are to:

• gain rapid control of severe agitation
• identify and aggressively treat severe hyperthermia
• identify and treat cardiovascular complications.

Initial resuscitation with attention to airway, breathing and circulation may be required in severe cases of cocaine poisoning. Benzodiazepines are the preferred treatment for tachycardia, hypertension, hyperthermia, agitation and seizures.