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Local anaesthetics and local anaesthetic systemic toxicity (LAST)
Local anaesthetics block sodium channels; a high dose or an intravascular injection causes brain signs first and then cardiac collapse — and the specific treatment is 20% lipid emulsion.
Why it matters in the exam
The exam asks about the maximal doses of lidocaine and bupivacaine, the difference between esters and amides (allergy, metabolism), the order of the toxicity signs, and the treatment of LAST — including the lipid emulsion dose and what not to give during resuscitation. Other questions deal with methaemoglobinaemia after prilocaine or benzocaine and with why local anaesthesia fails in inflamed tissue.
The speed of absorption depends on the injection site: it is highest after intercostal injection, followed by caudal and epidural, then the brachial plexus, and lowest after subcutaneous injection. Adrenaline adds duration, reduces absorption and serves as a marker of intravascular injection. A low pKa close to physiological speeds onset, lipid solubility raises potency, and protein binding prolongs duration. Bupivacaine is especially cardiotoxic, so cardiac collapse can appear with almost no preceding brain signs.
Good prevention avoids most cases: calculating the maximal dose by weight before injecting, aspirating before every dose, injecting slowly in small increments, using ultrasound, and adrenaline as a marker of intravascular injection. Remember that toxicity can appear even half an hour or more later, when the drug is absorbed from a site rich in vessels, so the patient is observed after the block. Wherever blocks are performed, a treatment kit with lipid emulsion must be available. Higher-risk groups are older patients, cardiac patients, patients with liver disease and pregnant women, and in them the dose is reduced and observation is closer.
Key points
- Maximal dose: lidocaine 4.5 mg/kg (7 mg/kg with adrenaline); bupivacaine 2.5 mg/kg.
- Order of toxicity: brain signs, then the heart; with bupivacaine the heart can come first.
- 20% lipid emulsion: 1.5 mL/kg bolus, then 0.25 mL/kg/min.
- In resuscitation: small doses of adrenaline, no vasopressin and no lidocaine.
- Prilocaine and benzocaine cause methaemoglobinaemia — methylene blue.
Summary table
| Agent | Class | Maximal dose | Exam point |
|---|---|---|---|
| Lidocaine | Amide | 4.5 mg/kg; with adrenaline 7 mg/kg | Also an antiarrhythmic |
| Bupivacaine | Amide | 2.5 mg/kg | The most cardiotoxic; forbidden for IV regional (Bier) |
| Ropivacaine | Amide | 3 mg/kg | Less cardiotoxic; less motor block |
| Chloroprocaine, tetracaine, benzocaine | Esters | — | Broken down by pseudocholinesterase; PABA — allergy |
| Prilocaine, benzocaine | — | — | Methaemoglobinaemia; treated with methylene blue |
In the full version for subscribers
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- 5 review cards
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Sources
- ASRA Practice Advisory / Checklist for Treatment of Local Anesthetic Systemic Toxicity, 2020 — Management of LAST
- Miller's Anesthesia, 9th edition (2020) — Local Anesthetics
- Morgan & Mikhail's Clinical Anesthesiology, 7th edition (2022) — Local Anesthetics
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-02. The text may contain errors; when in doubt, check the source.