Conditions · Emergency medicine and toxicology

Local anaesthetic systemic toxicity (LAST) !

A rare, life-threatening reaction when a local anaesthetic reaches high blood levels. It affects the brain (seizures) and the heart (arrhythmias, arrest).

Updated 2026-11-01

Structures involved

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Why it happens

What it is

Local anaesthetic systemic toxicity (LAST) happens when a local anaesthetic such as lidocaine or bupivacaine reaches toxic levels in the blood, usually after accidental intravascular injection or absorption from a highly vascular site. It first affects the central nervous system and then the heart, and can cause cardiac arrest that is hard to reverse. Lipid emulsion is the specific treatment.

Who gets it

Rare but feared complication of regional anaesthesia, nerve blocks, tumescent liposuction, dental and dermatological procedures and airway topicalisation. It is relevant wherever procedures with large volumes of local anaesthetic are done, including outpatient cosmetic surgery, which is common in Colombia.

Causes

Accidental intravascular injection during a nerve block or epidural
Absorption of large doses from vascular sites (intercostal, paracervical, airway, tumescent infiltration)
Cumulative dose from repeated injections or continuous infusions
Use of long-acting, more cardiotoxic agents such as bupivacaine

Risk factors

Extremes of age and low muscle mass
Heart disease, especially conduction disorders and heart failure
Liver disease (reduced amide metabolism)
Pregnancy
Metabolic or respiratory acidosis and hypoxia

Pathophysiology

Local anaesthetics block voltage-gated sodium channels. The brain is affected at lower levels: inhibitory pathways are blocked first, causing excitation (perioral numbness, metallic taste, tinnitus, agitation, seizures), then generalised depression and coma. At higher levels, sodium-channel block in the heart slows conduction (widened QRS, PR prolongation), depresses contractility and causes bradycardia, ventricular arrhythmias and asystole. Bupivacaine binds cardiac channels tightly and dissociates slowly, making arrest especially resistant. Acidosis and hypoxia worsen toxicity.

Classification

Central nervous system only: prodrome, excitation, seizures, then depression
Combined CNS and cardiovascular toxicity
Isolated cardiovascular toxicity (can occur without warning, especially with bupivacaine or under sedation)
Immediate (intravascular injection) versus delayed (absorption, infusions)

Symptoms and signs

Numbness around the mouth and tongue, metallic taste
Tinnitus, dizziness, blurred vision
Agitation, confusion, muscle twitching
Seizures, then drowsiness and coma
Bradycardia, hypotension, wide-complex arrhythmias
Cardiac arrest

Diagnosis

Clinical: Clinical diagnosis based on timing after local anaesthetic administration and progression of CNS and cardiac signs; can appear within a minute or up to an hour later.
Tests: Continuous ECG, blood pressure and oxygen saturation; arterial blood gas for acidosis; drug levels are not needed for treatment decisions.
Imaging: Not required for diagnosis.

Differential diagnosis

Vasovagal reaction
Anaphylaxis
Epinephrine absorption (tachycardia, hypertension)
High or total spinal anaesthesia
Primary seizure disorder or stroke

Goal of treatment

Stop the injection, protect oxygenation, stop seizures, give lipid emulsion early and sustain circulation until the drug is redistributed.

Treatment

Acute: Stop injecting and call for help; airway management with 100% oxygen and avoid hypoventilation, because hypoxia and acidosis worsen toxicity.
Medical: Intravenous lipid emulsion at the first signs of serious toxicity; it draws the drug away from the heart and brain (lipid sink and shuttle). Benzodiazepines for seizures; avoid large doses of propofol in unstable patients.
Acute: Modified cardiac life support: smaller doses of epinephrine; avoid vasopressin, calcium-channel blockers, beta-blockers and other local anaesthetics (such as lidocaine) for arrhythmias. Prolonged CPR may be needed.
Procedure: Cardiopulmonary bypass or extracorporeal support if there is no response to lipid emulsion and resuscitation.
Follow-up: Monitor at least several hours after a CNS event and longer after cardiovascular instability, as toxicity can recur. Prevention: aspirate and inject in small increments, use ultrasound guidance, test doses with epinephrine and calculate the maximum dose.

Complications

Status epilepticus
Refractory ventricular arrhythmias and asystole
Hypoxic brain injury
Recurrent toxicity after initial recovery
Pancreatitis from large volumes of lipid emulsion

Prognosis

With rapid recognition and lipid emulsion, most patients survive without sequelae. Outcomes are worse in bupivacaine-related cardiac arrest, in office settings without lipid emulsion available, and when hypoxia and acidosis are not corrected.

Prevention

Lowest effective dose and volume, weight-based maximum dose calculation, incremental injection with aspiration, ultrasound-guided blocks, monitoring during and after the block, and lipid emulsion stocked wherever local anaesthetics are used in large amounts

Test yourself

Think of the answer, then tap the question to see it.

What are the early signs of local anaesthetic toxicity?

Perioral numbness, metallic taste, tinnitus, dizziness and agitation, before seizures and cardiac effects.

What is the specific treatment for LAST?

Intravenous lipid emulsion, given early, along with airway management and seizure control.

Which local anaesthetic is most cardiotoxic and why?

Bupivacaine, because it binds cardiac sodium channels tightly and dissociates slowly.

Which antiarrhythmic must be avoided in LAST?

Lidocaine (another local anaesthetic), along with vasopressin, calcium-channel blockers and beta-blockers.

Why are hypoxia and acidosis dangerous in LAST?

They increase the free fraction and cardiac binding of the local anaesthetic, worsening toxicity.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Lipid Emulsion for Treating Local Anesthetic Systemic Toxicity (International Journal of Medical Sciences, 2018); Checklist for Treatment of Local Anesthetic Systemic Toxicity (LAST) (American Society of Regional Anesthesia and Pain Medicine (ASRA Pain Medicine), 2020).

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