Naropin Overdosage

Acute Systemic Toxicity: Systemic toxic reactions primarily involve the central nervous system (CNS) and the cardiovascular system (CVS). Such reactions are caused by high blood concentration of a local anaesthetic, which may appear due to (accidental) intravascular injection, overdose or exceptionally rapid absorption from highly vascularized areas (see Precautions).
CNS reactions are similar for all amide local anaesthetics, while cardiac reactions are more dependent on the drug, both quantitatively and qualitatively.
Accidental intravascular injections of local anaesthetics may cause immediate (within seconds to a few minutes) systemic toxic reactions. In the event of overdose, systemic toxicity appears later (15-60 minutes after injection) due to the slower increase in local anaesthetic blood concentration.
Central nervous system toxicity is a graded response with symptoms and signs of escalating severity. The first symptoms are usually lightheadedness, circumolar paraesthesia, numbness of the tongue, hyperacusis, tinnitus, and visual disturbances. Dysarthria, muscular twitching or tremors are more serious and precede the onset of generalized convulsions. These signs must not be mistaken for neurotic behaviour. Unconsciousness and grand mal convulsions may follow, which may last from a few seconds to several minutes. Hypoxia and hypercarbia occur rapidly during convulsions due to the increased muscular activity, together with the interference with respiration. In severe cases, apnoea may occur. The acidosis increases and extends the toxic effects of local anaesthetics.
Recovery follows the redistribution of the local anaesthetic drug from the CNS and subsequent metabolism and excretion. Recovery may be rapid unless large amounts of the drug have been injected.
Cardiovascular toxicity indicates a more severe situation and is 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 benzodiazepines or barbiturates. Hypotension, bradycardia, arrhythmia and even cardiac arrest may occur as a result of high systemic concentrations of local anaesthetics.
Treatment of Acute Systemic Toxicity: If signs of acute systemic toxicity appear, injection of the local anaesthetic should be stopped immediately.
In the event of convulsions, treatment will be required. The objectives of treatment are to maintain oxygenation, stop the convulsions and support the circulation. Oxygen must be given and ventilation assisted, when necessary (mask and bag or tracheal intubation). An anticonvulsant should be given i.v. if the convulsions do not stop spontaneously in 15-20 seconds. Thiopentone sodium 1-3 mg/kg i.v. will abort the convulsions rapidly. Alternatively diazepam 0.1 mg/kg i.v. may be used, although its action will be slow. Prolonged convulsions may jeopardize the patient's ventilation and oxygenation. If so, injection of a muscle relaxant (e.g. succinylcholine 1 mg/kg) will rapidly stop the convulsions so that ventilation and oxygentation can be controlled. Endotracheal intubation must be considered in such situations.
If cardiovascular depression is evident (hypotension, bradycardia), ephedrine 5-10 mg i.v. should be given and this dose should be repeated, if necessary, after 2-3 minutes.
Should circulatory arrest occur, immediate cardiopulmonary resuscitation should be instituted. Optimal oxygenation and ventilation and circulatory support as well as treatment of acidosis are of vital importance.
Should cardiac arrest occur, prolonged resuscitative efforts may be required to improve the possibility of a successful outcome.