Systemic and localised adverse effects of local anaesthetic drugs usua
lly occur because of excessive dosage, rapid absorption or inadvertent
intravascular injection. Small children are more prone than adults to
methaemoglobinaemia, and the combination of sulfonamides and prilocai
ne, even when correctly administered, should be avoided in this age gr
oup. The incidence of true allergy to local anaesthetics is rare. All
local anaesthetics can cause CNS toxicity and cardiovascular toxicity
if their plasma concentrations are increased by accidental intravenous
injection or an absolute overdose, Excitation of the CNS may be manif
ested by numbness of the tongue and perioral area, and restlessness, w
hich may progress to seizures, respiratory failure and coma. Bupivacai
ne is the local anaesthetic most frequently associated with seizures,
Treatment of CNS toxicity includes maintaining adequate ventilation an
d oxygenation, and controlling seizures with the administration of thi
opental sodium or benzodiazepines. Cardiovascular toxicity generally b
egins after signs of CNS toxicity have occurred. Bupivacaine and etido
caine appear to be more cardiotoxic than most other commonly used loca
l anaesthetics. Sudden onset of profound bradycardia and asystole duri
ng neuraxial blockade is of great concern and the mechanism(s) remains
largely unknown. Treatment of cardiovascular toxicity depends on the
severity of effects. Cardiac arrest caused by local anaesthetics shoul
d be treated with cardiopulmonary resuscitation procedures, but bupiva
caine-induced dysrhythmias may be refractory to treatment. Many recent
reports of permanent neurological complications involved patients who
had received continuous spinal anaesthesia through a microcatheter. I
njection of local anaesthetic through microcatheters and possibly smal
l-gauge spinal needles results in poor CSF mixing and accumulation of
high concentrations of local anaesthetic in the areas of the lumbosacr
al nerve roots. In contrast to bupivacaine, the hyperbaric lidocaine (
lignocaine) formulation carries a substantial risk of neurotoxicity wh
en given intrathecally. Drugs altering plasma cholinesterase activity
have the potential to decrease hydrolysis of ester-type local anaesthe
tics. Drugs inhibiting hepatic microsomal enzymes, such as cimetidine,
may allow the accumulation of unexpectedly high (possibly toxic) bloo
d concentrations of lidocaine. Reduction of hepatic blood flow by drug
s or hypotension will decrease the hepatic clearance of amide local an
aesthetics. Special caution must be exercised in patients taking digox
in, calcium antagonists and/or beta-blockers.