Adverse experiences following administration of lignocaine are similar in nature to those observed with other amide local anaesthetic agents. These adverse experiences are in general, dose-related and may result from high plasma levels caused by excessive dosage or rapid absorption, or may result from a hypersensitivity, idiosyncrasy or diminished tolerance on the part of the patient.
Serious adverse experiences are generally systemic in nature. The following types are those most commonly reported: Central Nervous System: CNS manifestations are excitatory and/or depressant and may be characterised by lightheadedness, nervousness, apprehension, euphoria, confusion, dizziness, drowsiness, tinnitus, hyperacusis, blurred vision, vomiting, sensations of heat, cold or numbness, twitching, tremors, convulsions, unconsciousness, respiratory depression and/or arrest, agitation, difficulty in swallowing, paraesthesia circumoral, numbness of the tongue and slurred speech.
The excitatory manifestations may be very brief or may not occur at all, in which case the first manifestation of toxicity may be drowsiness merging into unconsciousness and respiratory arrest. Drowsiness following administration of lignocaine is usually an early sign of a high blood level of the drug and may occur as a result of rapid absorption. In unconscious patients, circulatory collapse should be watched for as CNS effects may not be apparent, as an early manifestation of toxicity may in some cases progress to frank convulsions and ultimately lead to respiratory depression and/or arrest. It is crucial to have resuscitative equipment and anticonvulsant drugs available to manage such patients (see Treatment under Overdosage).
Cardiovascular manifestations are usually depressant and are characterised by bradycardia, hypotension and cardiovascular collapse, which may lead to cardiac arrest.
Cardiac arrhythmias and hypertension have also been observed. Methaemoglobinaemia can occur following IV administration.
Cardiovascular toxic effects are generally preceded by signs of toxicity in the CNS, unless the patient is receiving a general anaesthetic or heavily sedated with drugs eg, benzodiazepine or a barbiturate. In rare cases, cardiac arrest has occurred without prodromal CNS effects.
In children, early signs of local anaesthetic toxicity may be difficult to detect in cases where the block is given during general anaesthesia.
Regional anaesthesia may lead to maternal hypotension.
Allergic reactions are characterised by cutaneous lesions, urticaria, oedema or anaphylactoid reactions/shock.
Allergy to amide-type local anaesthetics is rare.
The detection of sensitivity by skin testing is of doubtful value.
The incidences of adverse reactions associated with the use of local anaesthetics may be related to the total dose of local anaesthetic administered and are also dependent on the particular drug used, the route of administration and the physical status of the patient.
Neurological reactions following regional nerve blocks have included persistent numbness, paraesthesia and other sensory disturbances.
In a prospective review of 10,440 patients who received lignocaine for spinal anaesthesia, the incidences were reported to be about 3% each for positional headaches, hypotension and backache; 2% for shivering; and <1% each for peripheral nerve symptoms, nausea, respiratory inadequacy and double vision. Many of these observations may be related to local anaesthetic techniques, with or without a contribution from the local anaesthetic.
In the practice of caudal or lumbar epidural block, occasional unintentional penetration of the subarachnoid space by the catheter may occur. Subsequent adverse effects may depend partially on the amount of drug administered subdurally.
These may include spinal block of varying magnitude (including total spinal block), hypotension secondary to spinal block, loss of bladder and bowel control and loss of perineal sensation and sexual function. Persistent motor, sensory and/or autonomic (sphincter control) deficit of some lower spinal segments with slow recovery (several months) or incomplete recovery have been reported in rare instances when caudal or lumbar epidural block has been attempted. Backache and headache have also been noted following use of these anaesthetic procedures.
Peripheral nerve injury and arachnoiditis have been observed.