Local Anaesthetic Systemic Toxicity

Definition & Cause

Local anaesthetic systemic toxicity (last) is the toxic effect of an excessive plasma concentration of local anaesthetic, from an overdose (exceeding the safe dose) or, more dangerously, accidental intravascular injection. It primarily affects the central nervous system and the cardiovascular system, and can be fatal.

Clinical Features (progressive)

Toxicity is dose-related and progressive. Early/CNS: circumoral and tongue numbness/tingling, a metallic taste, tinnitus, light-headedness, visual disturbance, slurred speech and agitation — progressing to muscle twitching and convulsions, then CNS depression (drowsiness, coma, respiratory arrest). Cardiovascular (later, more serious): hypotension, arrhythmias, conduction block and cardiovascular collapse — bupivacaine being especially prone to refractory cardiac arrest.

Management

Stop injecting and call for help. Manage ABC: secure the airway, give 100% oxygen, and control convulsions (benzodiazepine). Treat cardiovascular collapse with standard resuscitation (but prolonged CPR may be needed). The specific antidote is intravenous lipid emulsion (‘Intralipid’ / lipid rescue) — a bolus followed by an infusion — which ‘soaks up’ the lipophilic drug from the tissues. Avoid or reduce certain drugs (e.g. Use small adrenaline doses) as advised in last protocols.

Prevention

Last is largely preventable: calculate and stay within the maximum dose, aspirate before injecting (to detect intravascular placement), inject slowly in small increments while talking to the patient, use a test dose (often with adrenaline) for large blocks, and use ultrasound guidance where available.

Timing & Vigilance

The presentation of local anaesthetic systemic toxicity varies with how the toxic level arose: an accidental intravascular injection produces sudden, dramatic features within seconds to a minute, often beginning with seizures or collapse, whereas an overdose absorbed from the tissues produces a more gradual onset over minutes as the plasma level climbs, typically heralded by the early neurological warning signs. This is why the injecting clinician talks to the patient throughout a large block, watching for the earliest symptoms, and why monitoring is continued for a period after injection — the peak plasma level from tissue absorption may not be reached until some minutes have passed.

Cardiac Features & Bupivacaine

While the neurological features usually appear first, it is the cardiovascular effects that make local anaesthetic toxicity lethal, and these are worst with bupivacaine, which binds cardiac sodium channels avidly and dissociates from them slowly so that arrhythmias and myocardial depression can be profound and resistant to standard resuscitation. The picture ranges from hypertension and tachycardia early, through bradycardia and conduction block, to ventricular arrhythmias and asystole, and because recovery of the heart depends on the drug leaving the channels, resuscitation may need to be sustained for a long time — which is exactly the situation in which intravenous lipid emulsion, by drawing the drug out of the tissues, can be life-saving.

CNS signs precede cardiac toxicity — except with bupivacaine.

• Last: toxic plasma LA level from overdose or intravascular injection; affects CNS & CVS; can be fatal.
• CNS first: perioral tingling, metallic taste, tinnitus → convulsions → CNS depression.
• CVS later/serious: arrhythmias, collapse (bupivacaine especially refractory).
• Manage: stop, ABC, O₂, control seizures, resuscitate; give IV lipid emulsion (Intralipid) early.
• Prevent: stay within max dose, aspirate, inject slowly in increments, test dose, ultrasound.