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MDV: Accidental intravascular injections of local anaesthetics can cause immediate system-toxic reactions (within seconds to a few minutes). Signs of system toxicity in cases of overdose occur later (15-60 minutes after injection) due to a slower increase in the concentration of local anaesthetic in the blood (see Adverse Reactions).
Toxicity: Oral administration: Less than 50 mg seems not impose any risk for toddlers. 75 mg to a 2 years old child caused a mild, 100 mg to a 5 months old child cause serious, 300 + 300 mg within 4 hours to a 3½ years old child caused serious to very serious, 400-500 mg to a 2 year old child and 1 g during 12 hours to a 1 year old child caused very serious intoxication. 600 mg to an adult caused mild, 2 g to an adult caused moderate intoxication.
Parenteral administration: 50 mg intravenously to a 1 month old child caused very severe intoxication. 200-400 mg infiltration to an adult caused serious, 500 mg to an 80 year old patient and 1 g intravenously to adults caused very severe intoxication.
Topical administration: 8.6-17.2 mg/kg BW to toddlers when used on burn injured skin caused serious intoxication.
Symptoms: First CNS excitation, later CNS depression. When exposed for large doses the first symptom can be rapidly developing seizures. Agitation, dizziness, visual disturbances, perioral paresthesia, nausea. Later ataxia, auditory disturbances, euphoria, confusion, speech difficulties, paleness, sweating, tremor, seizures, coma, apnoea. Different kinds of arrhythmias especially bradycardial arrhythmias but also if exposed to large doses ventricular tachycardia, ventricular fibrillation, QRS prolongation, atrio-ventricular block. Cardiac failure, hypotension (rare cases of methaemoglobinaemia are described).
Treatment: If oral exposure, active charcoal. (Provoking vomiting may be hazardous due to anaesthesia of the mucous membrane and the risk for seizures in the early phase.
If ventricular lavage is indicated, this should be done with a ventricular tube after tracheal intubation.)
Seizures are treated with diazepam. Oxygen.
If needed tracheal intubation and controlled respiration (if needed hyperventilation). Bradycardia is treated with atropine. Circulatory deterioration is treated with fluids administrated intravenously, dobutamine and if needed epinephrine (initially 0.05 microgram/kg BW/min, to be increased if needed by 0.05 microgram/kg BW/min each 10 minutes), in more severe cases guided by haemodynamic monitoring. Ephedrine may also be tried. If circulatory arrest, resuscitation efforts for several hours may be indicated.
Polyamp: 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 ADVERSE REACTIONS and PRECAUTIONS).
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 central nervous and cardiovascular systems.
In children, early signs of local anaesthetic toxicity may be difficult to detect in cases where the block is given during general anaesthesia.
Symptoms of acute toxicity: Central nervous system toxicity is a graded response with symptoms and signs of escalating severity. The first symptoms are circumoral paraesthesia, numbness of the tongue, light-headedness, 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 redistribution of the local anaesthetic drug from the central nervous system 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 central nervous system, unless the patient is receiving a general anaesthetic or is heavily sedated with drugs such as a benzodiazepine or a barbiturate. In rare cases, cardiac arrest has occurred without prodromal CNS effects.
Treatment of overdosage: 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 intravenously.
Should convulsions persist despite adequate respiratory support, and if the status of the circulation permits, appropriate anticonvulsant medication such as an ultra-short acting barbiturate (e.g. thiopentone) or a benzodiazepine (e.g. 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 these 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 intravenous 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.
