Xylocaine W/ Adrenaline Overdosage

Symptoms: Acute emergencies associated with the use of local anaesthetics are generally related to high plasma levels or to unintended subarachnoid injection of the local anaesthetic solution (see Precautions and Adverse Reactions).
With accidental intravascular injections, the toxic effect will be obvious within 1-3 min. With overdosage, peak plasma concentrations may not be reached for 20-30 min depending on the site of injection and toxic signs will be delayed. Toxic reactions mainly involve the CNS and cardiovascular system.
In children, early signs of local anaesthetic toxicity may be difficult to detect in cases where the block is given during general anaesthesia.
Acute Toxicity: CNS toxicity is a graded response with symptoms and signs of escalating severity. The 1st symptoms are circumoral paraesthesia, numbness of the tongue, lightheadedness, hyperacusis and tinnitus. Visual disturbance and muscular tremors are more serious and precede the onset of generalised convulsions. These signs must not be mistaken for neurotic behaviour.
Unconsciousness and grand mal convulsions may follow. These may last from a few seconds to several minutes. Hypoxia and hypercarbia occur rapidly following convulsions due to the increased muscular activity, together with the interference with normal respiration and loss of the airway. In severe cases, apnoea may occur. Acidosis increases the toxic effects of local anaesthetics.
Recovery is due to re-distribution of the local anaesthetic drug from the CNS and metabolism. Recovery may be rapid unless large amounts of the drug have been injected.
Cardiovascular toxicity indicates a more severe situation. Hypotension, bradycardia, decreased cardiac output, heart block, arrhythmia and even ventricular arrhythmias, ventricular fibrillation and cardiac arrest may occur as a result of huge systemic concentrations of local anaesthetics.
Cardiovascular toxic effects are generally preceded by signs of toxicity in the CNS, unless the patient is receiving a general anaesthetic or is heavily sedated with drugs eg, a benzodiazepine or a barbiturate. In rare cases, cardiac arrest has occurred without prodromal CNS effects.
Treatment: If signs of acute systemic toxicity appear, injection of the local anaesthetic should be stopped immediately. If convulsions occur, then immediate attention is required for the maintenance of a patent airway and assisted or controlled ventilation with oxygen, via a positive airway pressure delivery system mask. Adequacy of the circulation should then be evaluated, bearing in mind that drugs used to treat convulsions depress the circulation when administered IV.
Should convulsions persist despite adequate respiratory support, and if the status of the circulation permits, appropriate anticonvulsant medication eg, an ultrashort-acting barbiturate (eg, thiopentone) or a benzodiazepine (eg, diazepam) may be administered IV. The clinician should be familiar with these anticonvulsant drugs prior to use of local anaesthetics.
Suxamethonium will stop the muscle convulsions rapidly but will require tracheal intubation and controlled ventilation, and should only be used by those familiar with procedures.
If ventricular fibrillation or cardiac arrest occurs, effective cardiovascular resuscitation treatment must be instituted and maintained for a prolonged period if necessary. Optimal oxygenation and ventilation, and circulatory support as well as treatment of acidosis are of vital importance.
If cardiovascular depression occurs (hypotension, bradycardia), appropriate treatment with IV fluids, vasopressor, chronotropic and/or inotropic agents should be considered. Children should be given doses commensurate with age and weight.
Dialysis is of negligible value in the treatment of acute overdosage with lignocaine.
To counteract the pressor effects of adrenaline, use rapidly-acting vasodilators eg, nitrates or α-blocking agents.
For treatment of reactions caused by adrenaline, consult standard textbooks.