CNS Toxicity of local anaesthetics
Clive Collier
Injection of local anaesthetic into an epidural vein may lead to signs of CNS toxicity within 15 to 30 secs, depending on the dose and speed of injection (Table 36.2) (Chapter 36). The picture is of initial CNS stimulation followed by depression.

A relatively small dose (5 to 10ml lignocaine 1%) may cause ringing in the ears, a metallic taste in the mouth, numbness of the tongue, blurring of vision, drowsiness with decreased awareness, muscular twitching, restlessness and apprehension. With a larger dose, delirium may ensue and progress to grand mal convulsions (Table 36.6). Asphyxia may develop if the convulsions are not treated rapidly and adequately, leading to metabolic and respiratory acidosis with cardiac depression, and eventually fatal cardiac arrest (Table E.2). Some of the manifestations of cardiac toxicity may, in fact, be directly due to brain-stem toxicity (1) (Chapter 89).

The presence of added adrenaline in the local anaesthetic will usually lead to the immediate development of palpitations following intravenous injection, and this may be the first symptom.

The treatment of convulsions is aimed at maintaining the airway and oxygenation. Seizure activity can be controlled with diazepam or thiopentone (Table 36.5).

Toxicity arising from an excessive total dose of local anaesthetic in the epidural space usually produces similar signs and symptoms to those seen following intravascular injection but occurs after a delay of 5 to 20 minutes.

References:
1. HEAVNER JE. Cardiac dysrhythmias induced by infusion of local anesthetics into the lateral cerebral ventricle of rats. Anesthesia and Analgesia 1986; 65:133-138.