Marcaine 0.5% Adrenaline Overdosage

Symptoms: Acute systemic toxicity: Systemic toxic reactions include the central nervous system and the cardiovascular system. Such reactions are caused by a high concentration of local anaesthetic in the blood, which can occur as a result of accidental intravascular injection, overdose, or unusually rapid absorption from richly vascularised tissues (see also Precautions).
CNS symptoms are similar for all local anaesthetics of the amide type, while cardiac symptoms differ for different drugs, both quantitatively and qualitatively.
Accidental intravascular injections of local anaesthetics can cause immediate system-toxic reactions (within seconds to a few minutes). Signs of systemic 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.
CNS toxicity occurs gradually, with symptoms and reactions of escalating severity. The first symptoms are usually light-headedness, circumoral paraesthesia, numbness of the tongue, hyperacusis, tinnitus and visual disturbances. Difficulty in articulating, muscle twitching or tremor are more serious and precede generalised convulsions. These signs must not be interpreted as neurotic behaviour. Unconsciousness and grand mal seizures may follow and may last from a few seconds to several minutes. Hypoxia and hypercapnia occur rapidly during the seizures due to the increased muscular activity and inadequate ventilation. In severe cases apnoea may occur. Acidosis increases the toxic effects of local anaesthetics. Recovery is due to the metabolism and distribution of the local anaesthetic away from the central nervous system. This takes place rapidly unless very large amounts of the drug have been injected.
Cardiovascular effects generally cause a more serious situation and are usually preceded by signs of CNS toxicity, which can, however, be masked by general anaesthesia or heavy sedation with drugs such as benzodiazepines or barbiturates. A fall in blood pressure, bradycardia, arrhythmia and even cardiac arrest can occur as a result of high systemic concentrations of local anaesthetics. Cardiovascular toxic effects are often related to depression of the conduction system in the heart and myocardium, leading to reduced cardiac output, hypotension, AV block, bradycardia and sometimes ventricular arrhythmias including ventricular tachycardia, ventricular fibrillation and cardiac arrest. These states are often preceded by signs of severe CNS toxicity, e.g. in the form of convulsions, but in rare cases cardiac arrest has occurred without prodromal CNS effects. After a very rapid intravenous bolus injection, such a high blood concentration of bupivacaine can be reached in the coronary vessels that an effect on the circulation occurs alone or before effects on the CNS. With this mechanism, myocardial depression can then occur even as a first symptom of intoxication.
As children often develop greater blocks only after anaesthesia is begun, particular alertness to early signs of intoxication is required in this group.
Systemic effects of adrenaline must also be taken into account in cases of overdose.
Treatment: In the event of total spinal block optimal ventilation should be secured (free airways, oxygen, if necessary intubation and assisted ventilation). In the event of hypotension/bradycardia a vasopressor with inotropic effect should be administered.
If signs of acute systemic toxicity occur the administration of local anaesthetics must be stopped immediately and CNS symptoms (convulsion, CNS depression) must promptly be treated with appropriate airway/respiratory support and the administration of anticonvulsant drugs.
If circulatory shock occurs, (hypotension, bradycardia), appropriate treatment with intravenous fluids, vasopressors, inotropic substances and/or other lipid emulsions should be considered. Children must be given doses in proportion to their age and bodyweight for treatment of systemic toxicity.
In the event of circulatory arrest, 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, a successful outcome may require prolonged resuscitative efforts.