Management overview for local anaesthetic poisoning
Local anaesthetic drugs available in Australia for medical or dental use are articaine, benzocaine, bupivacaine, cinchocaine, cocaine, levobupivacaine, lidocaine, mepivacaine, oxybuprocaine, prilocaine, proxymetacaine, ropivacaine and tetracaine (amethocaine).
Cocaine is more often used as a recreational stimulant than a local anaesthetic. For management of cocaine poisoning, see here.
Local anaesthetic poisoning usually involves parenteral use and is the result of a dosing error, inadvertent intravascular or spinal administration, or equipment failure during a Bier block1. Poisoning can also occur after topical use. Most parenteral and topical poisonings occur in a clinical setting. Ingestion by adults rarely results in toxicity because local anaesthetics have a large hepatic first-pass effect; children have a greater risk of toxicity after ingestion.
If toxicity does occur, it has a rapid evolution and resolution. Peak toxicity is directly related to peak serum concentration, and is determined by the route of exposure and whether the local anaesthetic has been coformulated with adrenaline (epinephrine)2. Toxicity can occur within minutes of intravascular administration, or hours after regional administration of local anaesthetic with adrenaline.
Severe toxicity is characterised by cardiovascular collapse and seizures. Methaemoglobinaemia is an important complication of some local anaesthetics, but is not the process driving the cardiovascular collapse and seizures associated with severe acute toxicity.
Management priorities for severe local anaesthetic toxicity include resuscitation and serum alkalinisation.