Regional and local anaesthesia

• Regional and local anaesthesia blocks pain by reversibly blocking voltage-gated sodium channels in nerve fibres, so action potentials cannot propagate; sensation returns when the drug diffuses away.
• Most agents used today are amides. They differ in onset, potency, duration and safety: lidocaine is the common short/medium agent, bupivacaine and ropivacaine are longer acting, and prilocaine is useful but can cause methaemoglobinaemia.
• Doses are weight-based and must be calculated deliberately for every patient; intravascular injection, overdose and rapid absorption from vascular sites are the main causes of local anaesthetic systemic toxicity.
• Spinal (intrathecal) anaesthesia works fast, with a dense block and small dose in the cerebrospinal fluid; epidural anaesthesia uses a larger dose in the extradural space and can be continued for hours or days through a catheter.
• Complications are uncommon but include hypotension, urinary retention, post-dural puncture headache, infection, bleeding (important in anticoagulated patients), nerve injury and local anaesthetic systemic toxicity.

By the end of this page you should be able to:

1. Explain in simple terms how a local anaesthetic blocks a nerve and why some agents act faster or last longer than others.
2. Calculate and limit a safe total dose of common local anaesthetics, including the effect of adding adrenaline (epinephrine).
3. Recognise local anaesthetic systemic toxicity early, explain the role of intravenous lipid emulsion, and outline the immediate management.
4. Compare spinal and epidural anaesthesia for onset, density, haemodynamic effects, complications and uses.
5. List the common peripheral and fascial plane blocks, their indications and the nerves they anaesthetise.
6. Outline evidence-based aseptic precautions for neuraxial and other regional techniques.

Regional and local anaesthesia is the set of techniques in which a local anaesthetic is placed close to the nerve or spinal cord so that a defined region of the body becomes numb. The effects are produced locally and reversibly; the patient may remain awake. For a medical student the most useful way to understand the subject is as three layers: the pharmacology of the drug, the anatomy of its placement, and the vigilance required to avoid systemic toxicity. This page covers all three, with the guideline sources named in the references: the third ASRA practice advisory on local anaesthetic systemic toxicity (2020 executive summary quoted and used in the case report above), the Brazilian Society of Anesthesiology (SBA) 2020 regional anesthesia safety update, StatPearls on local anaesthetic toxicity, and a 2026 Royal College of Anaesthetists endorsed consensus on asepsis for spinal anaesthesia.

Local anaesthetics are weak bases. A useful fraction is unionised at tissue pH and crosses the lipid nerve membrane; once inside the axon the drug gains a proton and binds to the intracellular side of voltage-gated sodium channels in their open or inactivated states. Repeated action potentials keep more channels in the drug-bound state, so high-frequency firing stops before ordinary traffic; this is use-dependent block. When enough channels in a single fibre are blocked, that fibre cannot conduct an action potential and the region beyond it goes numb.

Two physicochemical properties explain much of clinical practice:

• Onset. A lower pKa means more drug is unionised at physiological pH (about 7.4), so more crosses the membrane and the block starts sooner. Lidocaine (pKa 7.9) is faster than bupivacaine (pKa 8.1), even though both work well.
• Duration. Higher lipid solubility and stronger protein binding keep the drug in the nerve membrane and reduce its systemic disappearance. Bupivacaine and ropivacaine are longer acting than lidocaine; vasoconstrictors such as adrenaline prolong block further by slowing vascular uptake.

Local anaesthetics are traditionally divided into two chemical families.

• Amides (lidocaine, bupivacaine, levobupivacaine, ropivacaine, mepivacaine, prilocaine) are metabolised in the liver. They are the standard agents for spinal, epidural and nerve block work.
• Esters (procaine, tetracaine, benzocaine, cocaine) are hydrolysed by plasma pseudocholinesterase. They are used mainly topically; true allergy is more common with esters and their para-aminobenzoic acid (PABA) metabolites than with amides. In practice, a stated allergy to a local anaesthetic is usually to an ester or to a preservative or antioxidant in the solution, not to the amide itself.

Adrenaline (epinephrine) in concentrations between 1:100,000 and 1:200,000 is the commonest vasoconstrictor. It reduces systemic absorption, prolongs the block and improves surgical conditions. Two safety points matter: ^[1]

• In healthy digits and most common comorbidities, modern dilute adrenaline used for digital or infiltration blocks has not been associated with digital infarction in large series; the reduction in perfusion is brief and reversible.^[1]
• At end-arterial sites (digits, nasal tip, ear, penis) where perfusion is already critically reduced (severe Raynaud disease, Buerger disease, critical limb ischaemia), adrenaline should generally be avoided, and plain lidocaine or proximal blocks used instead.^[1]

If prolonged blanching does occur, phentolamine (a non-selective alpha-blocker) can be infiltrated locally at about 1 to 5 mg (reconstituted to 1 mg per mL) to reverse vasospasm.^[1]

Every dose must be calculated, and the volume on the syringe checked again before injection. The figures below are approximate maximum single doses for healthy adults with normal hepatic and cardiac function, receiving standard infiltrative anaesthesia. Children, frail patients and those with liver or cardiac disease need lower totals; tumescent (very dilute) anaesthesia has its own, higher, limits because of the dilution.^[1]

Two practical habits keep dosing safe: inject slowly in small increments with frequent aspiration, and keep a running tally of every milligram given, because doses add across sites and a previous dose (including an infusion) still counts. A body weight in kilograms multiplied by the mg/kg ceiling gives that individual's limit.

Systemic absorption depends heavily on where the drug is placed. Highly vascular sites (intercostal, truncal blocks, mucosa, epidural) produce higher peak concentrations than skin infiltration. Barrier-deficient skin (burns, ulcers, eczema) behaves like an amplifier: topical and infiltrative agents reach the circulation faster, so concentrations should be reduced or a different technique chosen.^[1]

LAST is a toxic syndrome produced when enough local anaesthetic reaches the circulation to affect the central nervous system and heart. It is rare (about 0.03% of peripheral nerve blocks, or 0.27 episodes per 1000 blocks) but is the complication that all clinicians using regional techniques must be prepared to manage.^[2]

The classic sequence is excitation followed by depression, and it is a bedside diagnosis, because plasma levels are rarely available in time.

• Early central nervous system signs. Circumoral numbness, metallic taste, lightheadedness, tinnitus, visual disturbance, dysarthria, agitation, muscle twitching.
• Seizures, then loss of consciousness and respiratory depression.
• Cardiovascular effects. Conduction abnormalities, hypotension, ventricular arrhythmias and, in severe cases, cardiac arrest. Bupivacaine is particularly cardiotoxic: ventricular arrhythmias and arrest can occur with few warning signs.^[4]

Onset is usually rapid after intravascular injection, but may be delayed with gradual absorption, continuous infusions or sustained-release formulations. A patient who becomes drowsy, tinnitus or seizes shortly after a block has LAST until proven otherwise. Anaphylaxis, seizure disorder, stroke and other causes must be excluded, but treatment should not wait.^[2] StatPearls summarises it as a rare but potentially life-threatening adverse reaction caused by excessive circulating concentrations of a local anaesthetic.^[4]

• Intravascular injection (accidental bolus or catheter migration).
• Excessive total dose or repeated (accumulator) doses.
• Highly vascular injection sites and inflamed or barrier-deficient skin.
• Reduced hepatic clearance, low protein binding or extremes of age; elderly physiology narrows the margin.
• Drug interactions that slow clearance (CYP inhibition) or lower the seizure threshold.

The management is supportive and immediate; the centrepiece is intravenous lipid emulsion. Guidelines based on the 2020 ASRA practice advisory recommend a 20% lipid emulsion bolus of 1.5 mL/kg over one minute, followed by a continuous infusion of 0.25 mL/kg/min for 30 minutes.^[2] The post-stabilisation observation window in current guidance is 12 to 24 hours, particularly after lipid emulsion, to detect delayed or biphasic toxicity.^[2]

Lipid emulsion is thought to act mainly as a "lipid sink", sequestering lipophilic local anaesthetic molecules away from critical tissues and into an intravascular lipid phase, with additional benefits on cardiac metabolism. It is recommended as first-line therapy for LAST by ASRA and, in UK practice, by the Association of Anaesthetists of Great Britain and Ireland.^[2] If lipid is unavailable, aggressive support and resuscitation still offer the best chance.

Both are neuraxial techniques: drug is placed near the spinal cord. Their differences determine when each is chosen.

• Spinal (intrathecal) anaesthesia. A small dose of hyperbaric (or isobaric) solution is injected through a fine needle into the cerebrospinal fluid in the subarachnoid space. Onset is rapid (minutes), the block is dense and reliable, and the dose is small, so systemic toxicity is unlikely. The main haemodynamic effect is a fall in blood pressure from sympathetic block, which is more pronounced the higher the level. The single-shot technique cannot be topped up.
• Epidural anaesthesia. A larger dose is placed through a needle (or catheter) into the epidural space outside the dura. Onset is slower and the block is more segmental; it can be prolonged with a catheter for hours or days, which is valuable in labour, postoperative analgesia and major surgery. Hypotension is usually less abrupt than with spinal, but the total drug dose is larger, so vigilance for systemic toxicity still matters.

Clinically:

1. Surgery below the umbilicus (caesarean section, hip or knee replacement, prostate surgery) and short procedures suit spinal anaesthesia well.
2. Labour analgesia uses low-dose epidural (often with opioid) so the mother keeps motor function.
3. Thoracic or high abdominal surgery is an indication for thoracic epidural or a fascial plane block rather than spinal, because a high intrathecal block risks cardiorespiratory compromise.
4. Single-shot spinal is contraindicated in the presence of raised intracranial pressure, infection near the insertion site, or true coagulopathy or therapeutic anticoagulation; epidural placement also carries bleeding risk. Always follow the current anticoagulant guidance for neuraxial procedures.

Asepsis is essential for both. The 2026 consensus endorsed by the Royal College of Anaesthetists states that meticulous skin decontamination of clinician and patient, a head covering, sterile gloves, sterile drapes and a fresh surgical facemask should be considered mandatory in all cases; routine sterile gowns are not considered mandatory for uncomplicated single-shot spinal anaesthesia.^[5]

• Hypotension from sympathetic block, most prominent with spinal; prevented and treated with fluids and vasopressors (ephedrine or phenylephrine) and lateral tilt in pregnancy.
• High or total spinal block (too high a sensory level) can cause respiratory weakness and cardiovascular collapse; it is a rare but serious emergency.
• Post-dural puncture headache, caused by cerebrospinal fluid leak through a dural hole. Risk is much higher after large-gauge cutting (Quincke) needles and lower with fine pencil-point (Whitacre, Sprotte) needles and good technique. It usually presents 24 to 72 hours after the block, worsens on sitting up and improves lying flat; a blood patch may be required for persistent cases.
• Urinary retention, from sacral blockade.
• Bleeding or haematoma near the canal. This is rare but catastrophic; it is why neuraxial techniques must respect current guidance on antiplatelet and anticoagulant drugs.
• Infection: meningitis or epidural abscess. The SBA 2020 update, drawing on the Royal College of Anaesthetists 3rd National Audit Project (NAP3), estimates the risk of major infectious complications of neuraxial anaesthesia at about 1 in 40,000 cases (15 epidural abscesses and 3 meningitis cases in 700,000 blocks), with epidural techniques carrying a higher complication rate than spinal.^[3]
• Neurological injury: transient patchy sensory changes are not uncommon; severe permanent injury is very rare.
• Local anaesthetic systemic toxicity, less likely with spinal (small dose) but always possible with epidural or accidental intravascular injection.

Most modern blocks are performed under ultrasound, which has improved accuracy and reduced volumes. Typical examples:

For each block, aspiration before every increment, slow injection, and fractionated dosing are the habits that prevent accidents. Adrenaline-containing solutions are common for blocks (to prolong duration and flatten systemic uptake), but the end-arterial site caution above still applies.

• Discuss site, expected numbness, failure rates and complications; remember that regional techniques sometimes fail completely or partially and a backup plan must exist.
• For neuraxial work, RCoA-endorsed consensus emphasises hand hygiene, mask, sterile gloves, sterile drapes and skin preparation; needle and catheter asepsis matter more than gown use.^[5]
• For patients with ulcers, eczema or fragile skin, prefer dilute infiltration or tumescent techniques over high-strength topicals.^[1]
• In low-resource settings, careful needle technique, aspiration, conservative dosing and basic monitoring (pulse oximetry, blood pressure, level checking) produce safe spinal anaesthesia; dilute, weight-calculated doses are safer than memorised volumes.
• StatPearls recommends keeping in mind the classic early warning signs of toxicity (circumoral numbness, metallic taste, tinnitus, dizziness), because urgent treatment of LAST starts with recognition, not with a laboratory result.^[4]

• Local anaesthetics block voltage-gated sodium channels; both unionised fraction (onset) and lipid solubility/protein binding (duration) determine clinical behaviour.
• Amides are metabolised in the liver; esters in plasma. Most severe allergy is to esters or preservatives, not amides.
• Lidocaine is the standard 4.5–5 mg/kg agent (7 mg/kg with adrenaline), bupivacaine 2.0–2.5 mg/kg (3.0 mg/kg with adrenaline), ropivacaine and mepivacaine 3.0 mg/kg and 5–6 mg/kg respectively; never exceed ceilings and add doses across sites. ^[1]
• Spinal anaesthesia is fast, dense and uses a small intrathecal dose; epidural is slower, segmental and can be continued via catheter.
• Local anaesthetic systemic toxicity presents with early central nervous system signs followed by seizures and, potentially, cardiovascular collapse; bupivacaine is the most cardiotoxic.
• Current 2020 ASRA-based guidance recommends 20% lipid emulsion 1.5 mL/kg bolus then 0.25 mL/kg/min for 30 minutes, with 12 to 24 hours of observation.
• End-arterial sites are safe with dilute adrenaline in most patients but adrenaline should be avoided in critical ischaemia, Buerger disease and severe Raynaud disease.
• Post-dural puncture headache, hypotension and urinary retention are the commonest spinal complications; infection risk is roughly 1 in 40,000 (NAP3) and is higher after epidural than spinal techniques.
• Blocks are safer with ultrasound, aspiration between increments, slow injection and fractionated dosing.
• All references are cited above in the front matter; no separate references section appears in the body, as MedGrasp convention requires.

• A single-shot spinal uses a small drug volume and is well suited where monitoring is limited, provided aseptic technique, aspiration, fractionated dosing and blood pressure monitoring are observed.
• If an ultrasound is unavailable, surface landmarks and careful technique still permit safe femoral, axillary and ankle blocks; keep volumes conservative and always respect the maximum dose.
• For skin ulcers and burns, use dilute infiltration rather than high-strength topical agents.

• Airway management and anaesthesia monitoring
• Peripheral nerve injury and neuropathic pain
• Haemostasis, anticoagulation and neuraxial techniques
• Acute pain management and postoperative analgesia
• Pharmacology of intravenous anaesthetic and analgesic drugs
• Consent and perioperative care of day-case surgery

Review status: pending. Last verified: 2026-10-31.