Intravenous regional anaesthesia (IVRA) is a useful method of providing analgesia for minor surgical procedures. The local anaesthetic agent is injected into a vein of a limb that has been previously exsanguinated and occluded by a tourniquet. The site of action is probably the unmyelinated nerve fibres, reached by retrograde spread in the vascular bed. The onset of action is almost immediate.

Lignocaine or prilocaine are commonly used and systemic blood levels of these agents are unlikely to be significant if the tourniquet is released more than 15 min after injection.

Bupivacaine and etidocaine should never be used for IVRA! They are significantly protein bound and once the tourniquet is released there is a risk of cardiotoxicity. Several deaths have been reported during IVRA with bupivacaine.

 
Toxicity of Local Anaesthetic Agents

Local anaesthetic agents are relatively free from side effects if they are administered in an appropriate dosage and in the correct anatomical location. However, systemic and localised toxic reactions may occur, usually from the accidental intravascular or intrathecal injection, or the administration of an excessive dose of the local anaesthetic agent. Systemic reactions to local anaesthetics involve primarily the central nervous system (CNS) and the cardiovascular system.

The initial symptoms of CNS toxicity involve feelings of light- headedness, dizziness and circumoral paraesthesia which may precede visual and/or auditory disturbances such as difficulty focusing and tinnitus (ringing in the ears). Other subjective CNS symptoms include disorientation and feelings of drowsiness. Objective signs of CNS toxicity are usually excitatory in nature and include shivering, muscular twitching and tremors initially involving muscles of the face and distal parts of the extremities. Ultimately, generalised convulsions of a tonic-clonic nature occur. If a sufficiently large dose, or rapid intravenous injection of local anaesthetic is given, the initial signs of excitation may progress very rapidly to generalised CNS depression and coma. Respiratory depression may result in respiratory arrest. CNS toxicity is exacerbated by hypercarbia and acidosis.

Extremely high concentrations of local anaesthetics depress spontaneous pacemaker activity in the sinus node resulting in sinus bradycardia and sinus arrest. They also exert a dose - dependent negative inotropic action on isolated cardiac tissue. The more potent local anaesthetics depress cardiac contractility at lower concentrations than the less potent drugs.

Local anaesthetic agents appear to exert a biphasic effect on peripheral vascular smooth muscle. In lower doses they may increase peripheral vascular resistance, and in higher doses, reduce it. Cocaine is the only anaesthetic that causes vasoconstriction consistently because of its ability to inhibit the re-uptake of noradrenaline by storage granules at the synapse. The excess concentration of free circulating noradrenaline is responsible for the vasoconstriction associated with the use of cocaine. In general, a direct relationship exists between the anaesthetic potency and cardiovascular depressant potential of the various agents. The more potent drugs e.g. bupivacaine and etidocaine, have been reported to cause rapid and profound cardiovascular depression in some patients following accidental intravascular injection. Severe cardiac arrhythmias such as resistant ventricular fibrillation may occur.

 
Management of Acute Toxicity

The airway is maintained and oxygen administered by facemask, using artificial ventilation if apnoea occurs. Convulsions should be treated with anticonvulsant drugs such as thiopentone (150-250mg I.V.) or diazepam (10-20 mg I.V.) repeated as necessary. Profound hypotension and brady -arrhythmias should be treated with intravenous atropine (0.5-1.5mg) and colloid or crystalloid infusions as plasma expanders may be necessary. Occasionally adrenaline may be required for severe hypotension or bradycardia.

In patients with ventricular fibrillation due to bupivacaine toxicity, cardiopulmonary resuscitation should be continued for at least 60mins. Bretyllium may facilitate cardioversion.

 
Practical Use of Local Anaesthetic Agents

Example 1

A 70 kg male is scheduled for axillary block. The anaesthetist decides to use 30 mls of solution. He only has 2% plain lignocaine available. What should he do?

• A 2% solution contains 20mg/ml lignocaine. The toxic dose of lignocaine is 3mg/kg without adrenaline added and 7mg/kg with adrenaline.

• The maximum safe dose of lignocaine for this patient is 210mg without and 490 mg with adrenaline.

• 30mls of 2% plain lignocaine gives 600mg. The anaesthetist must therefore dilute the lignocaine and add adrenaline to it.

• 20 mls of 2% plain lignocaine contains 400 mg lignocaine which can be made up to a 30 ml solution with 10 mls N. Saline.

• The adrenaline is 1:1000 i.e. 1mg/ml and he requires 1:200,000 i.e. 5 microgram/ml. Therefore for every 20mls of local anaesthetic solution he should add 0.1ml of 1:1000 solution; a total of 0.15mls for his 30ml mixture.

A 6 year old child weighing 20kg is scheduled for hernia repair. The anaesthetist wishes to supplement general anaesthesia with an ilioinguinal block. He only has 0.5% plain bupivacaine. What should he do? Ideally he would wish to use at least 10mls of solution. The maximum dose of bupivacaine which can be given is 2mg/kg ie. 40mg.

• 10 ml of 0.5% solution should be diluted with 10ml normal saline to give 20ml 0.25% solution. 10 ml of this solution should be used to produce an ilioinguinal block.

This article contained links to the following additional information:

Table 1 - Upper dose limits for commonly used local anaesthetics.
Table 2 - Pharmacological effects & clinical uses of local anaesthetics.

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