Regional & Neuraxial Anaesthesia

📘 1 · Miller's Anesthesia — Neuraxial Anaesthesia

Principles, Anatomy & Physiology

"Neuraxial blockade produces surgical anaesthesia by depositing local anaesthetic around the spinal nerve roots. Its physiological signature is a sympathetic block that extends two or more dermatomes above the sensory level, producing vasodilatation and hypotension; the higher the block, the greater the cardiovascular and respiratory consequences. Understanding this sympathectomy — and treating it promptly — is the core skill of safe neuraxial practice."

Synthesised from Miller's Anesthesia, 9th Ed — Spinal, Epidural & Caudal Anaesthesia.

🧬 Anatomy & the three block types

Landmarks: Tuffier's line (top of iliac crests) ≈ L4; the spinal cord ends at L1–L2 in adults, so spinals are placed at L3/4 or below to avoid cord injury.
Layers (midline): skin → supraspinous → interspinous → ligamentum flavum → (epidural space) → dura → arachnoid → CSF.
Differential block: sympathetic (highest) > sensory > motor (lowest) — the sympathetic level sits ~2 segments above sensory.

⚖️ Benefits vs the trade-off

Neuraxial and regional techniques provide excellent analgesia, reduce opioid use, blunt the surgical stress response, allow an awake patient (e.g. Caesarean section) and lower the risk of respiratory complications and (for some operations) VTE. The trade-off is sympathectomy-driven hypotension, the risk of a high/total spinal, and — rarely but seriously — vertebral canal haematoma or abscess and LAST. Every regional technique demands full monitoring, IV access, and resuscitation drugs/lipid emulsion immediately available.

📗 2 · Barash / Stoelting Pharmacology — Local Anaesthetics

Local-Anaesthetic Pharmacology

"Local anaesthetics block the voltage-gated sodium channel from within the axon, preventing propagation of the action potential. Potency tracks lipid solubility, duration tracks protein binding, and speed of onset tracks the pKa relative to tissue pH — which is why local anaesthetics work poorly in the acidic environment of infected tissue. Toxicity, like potency, rises with lipid solubility: bupivacaine is the most cardiotoxic of the common agents."

Synthesised from Stoelting's Pharmacology & Physiology in Anesthetic Practice; Barash — Clinical Anesthesia.

🔑 Structure–activity in one glance

Amides (lidocaine, bupivacaine, ropivacaine, prilocaine — "two i's" in the name) — hepatic metabolism; esters (procaine, chloroprocaine, tetracaine, cocaine) — plasma cholinesterase, allergy risk via PABA.
Potency ↑ with lipid solubility; duration ↑ with protein binding; onset faster with lower pKa (more un-ionised drug at tissue pH).
Adrenaline added to prolong duration, reduce systemic absorption/peak levels and mark intravascular injection — never with adrenaline in end-artery territories (digits, penis).

Agent	Max dose (approx.)	Onset / duration	Notes
Lidocaine	3 mg/kg (7 mg/kg with adrenaline)	Fast / short–intermediate	Versatile; topical/infiltration/nerve block
Bupivacaine	2 mg/kg	Slow / long	Most cardiotoxic — avoid IV; workhorse for spinal (heavy 0.5%)
Ropivacaine	3 mg/kg	Slow / long	Less cardiotoxic than bupivacaine; more motor-sparing
Prilocaine	6 mg/kg	Fast / intermediate	Least toxic amide; methaemoglobinaemia at high dose
2-Chloroprocaine	~11 mg/kg	Very fast / very short	Ester; rapid plasma hydrolysis; short day-case spinals

📙 3 · Morgan/Mikhail — Techniques Compared

Spinal vs Epidural vs CSE

Spinal (subarachnoid)

Small dose into CSF below L2; single shot
Fast, dense, reliable block
Low LA dose → minimal LAST risk
Hypotension can be rapid; fixed duration; PDPH risk (use pencil-point needle)

Epidural

Larger LA volume into epidural space; catheter → titratable & prolongable
Slower onset, segmental block; good for labour & post-op analgesia
Higher LA dose → real LAST risk; risk of accidental dural puncture

Combined spinal–epidural (CSE)

Rapid spinal + catheter flexibility
Useful for labour, prolonged/lower-limb surgery

Peripheral nerve / plane blocks

Ultrasound-guided; brachial plexus, femoral/adductor canal, TAP, ESP, PECS
Excellent opioid-sparing analgesia; watch cumulative LA dose (LAST)

💧 Managing neuraxial hypotension

Caused by the sympathetic block (venodilation → ↓ preload; arterial dilation → ↓ SVR). Treat: left-lateral tilt/uterine displacement in pregnancy, a vasopressor (phenylephrine first-line in obstetrics; ephedrine if bradycardic), fluid co-loading, and atropine for bradycardia. Prophylactic phenylephrine infusion is standard for spinal Caesarean section.

🇮🇳 Indian Context

Subarachnoid (spinal) block with heavy bupivacaine is the workhorse for Caesarean section and lower-limb/urological/lower-abdominal surgery across India — cheap, reliable and avoiding a general anaesthetic in an often un-fasted, higher-aspiration-risk population. Ensure 20% lipid emulsion (Intralipid) is stocked wherever regional anaesthesia is performed, along with a displayed LAST protocol. Use pencil-point (Whitacre/Sprotte) needles to reduce PDPH, which matters greatly for young obstetric patients.

📋 4 · Guidelines — Neuraxial Blocks & Anticoagulation

Anticoagulation & Contraindications

Absolute & relative contraindications

Absolute: patient refusal, local infection at the site, raised intracranial pressure, true LA allergy, uncorrected coagulopathy/therapeutic anticoagulation, uncorrected hypovolaemia/shock.
Relative: systemic sepsis, fixed cardiac output states (severe aortic/mitral stenosis — a fall in SVR is dangerous), certain neurological disease, anatomical/spinal abnormality.

Timing around anticoagulants — neuraxial & catheter removal ASRA / AAGBI

Selected intervals before a neuraxial block (and before removing an epidural catheter):
• Prophylactic LMWH — 12 h; therapeutic LMWH — 24 h.
• Unfractionated heparin (prophylactic SC) — 4–6 h & normal coagulation.
• Warfarin — stopped with INR ≤1.4.
• Clopidogrel — 7 days; ticagrelor — 5 days; prasugrel — 7–10 days.
• DOACs (e.g. rivaroxaban/apixaban) — ~72 h (drug- and renal-dependent).
Restart anticoagulants only after an appropriate delay following block/catheter removal. Aspirin alone is not a contraindication. When in doubt, follow the current ASRA/AAGBI tables exactly — timing prevents vertebral canal haematoma.

🚨 5 · Local Anaesthetic Systemic Toxicity (LAST)

LAST & Lipid Emulsion Rescue

🚨 Recognise LAST

Early/CNS: peri-oral tingling, tinnitus, metallic taste, agitation, confusion → seizures → coma. Cardiovascular (later, or first with bupivacaine): hypertension/tachycardia then bradycardia, conduction block, ventricular arrhythmias and cardiac arrest. Suspect it with any collapse or neurology soon after an LA injection — onset may be delayed up to ~30–60 min.

🧯 Immediate management (ASRA 2020 / AAGBI)

Stop injecting LA; call for help; ABC — secure airway, 100% O₂, prevent hypoxia/acidosis (they worsen toxicity).
Control seizures — benzodiazepine (avoid large doses of propofol in the unstable patient).
Give 20% lipid emulsion (Intralipid): bolus 1.5 mL/kg over 1 min, then infusion 15 mL/kg/h; repeat bolus (×1–2) and double the infusion rate for persistent instability; maximum ~12 mL/kg.
If cardiac arrest: standard ALS with modifications — expect a prolonged resuscitation, use small adrenaline doses (≤1 µg/kg), avoid vasopressin, calcium-channel/β-blockers and lidocaine; consider cardiopulmonary bypass/ECMO if available.
Monitor for ≥4–6 h (or longer after arrest); report to the LipidRescue registry.

🛡 Prevention beats rescue

Use the lowest effective dose and calculate the maximum by weight; aspirate before injecting and inject in fractionated aliquots; use ultrasound guidance; consider an adrenaline-containing test dose to detect intravascular placement; and be most cautious with bupivacaine and in the elderly, small, or cardiac patient.

🗺 6 · Complications Flowchart

Recognising & Treating Complications

High / total spinal

Rapidly rising block: arm weakness, difficulty breathing, hypotension, bradycardia → apnoea & unconsciousness
Treat: ABC, intubate & ventilate, vasopressors, fluids, atropine; support until the block recedes

Hypotension & bradycardia

Sympathectomy → vasopressor (phenylephrine/ephedrine), fluid, tilt; atropine for bradycardia; adrenaline if severe

Post-dural-puncture headache (PDPH)

Postural (worse sitting/standing), fronto-occipital, ± neck stiffness/photophobia, days after dural puncture
Treat: conservative (analgesia, fluids, caffeine); epidural blood patch if severe/persistent. Prevent with pencil-point needles

Vertebral canal haematoma / abscess

Red flags: severe back pain, a block that is dense/prolonged or progressing, new weakness, bladder/bowel dysfunction
Urgent MRI + neurosurgery — decompression within ~8 h preserves cord function. A neurological emergency

LAST

Peri-oral tingling/seizures/arrhythmia after LA → stop, ABC, 100% O₂, 20% lipid emulsion, modified ALS (see §5)

⚠️ 7 · Common Mistakes

Common Mistakes in Regional Anaesthesia

❌ Mistake 1 — No lipid emulsion / no LAST plan in the room

Regional anaesthesia without immediate access to 20% lipid emulsion, resuscitation drugs and a displayed protocol is unsafe. Every location performing blocks must stock them and rehearse the drill.

❌ Mistake 2 — Exceeding the maximum LA dose

Always calculate the weight-based maximum, especially for infiltration and multiple/large-volume blocks where doses accumulate. Bupivacaine's low threshold and cardiotoxicity are unforgiving.

❌ Mistake 3 — Ignoring anticoagulation timing

Placing or removing a neuraxial catheter outside the ASRA/AAGBI intervals risks a devastating vertebral canal haematoma. Check the timing tables every time, for both insertion and removal.

❌ Mistake 4 — Missing spinal haematoma/abscess red flags

Attributing new leg weakness, severe back pain or bladder dysfunction to "residual block" delays MRI and decompression. An unexpectedly dense, prolonged or progressing block after neuraxial anaesthesia is a red flag until proven otherwise.

❌ Mistake 5 — Adrenaline-containing LA in an end-artery

Never use adrenaline-containing solutions for digital, penile or other end-artery blocks — ischaemic necrosis can follow.

❌ Mistake 6 — Treating spinal hypotension too slowly

Sympathectomy-driven hypotension in the pregnant or fixed-output patient can crash quickly. Anticipate it, co-load, and have vasopressors drawn up before performing the block.

❌ Mistake 7 — Sedating to hide a failing block instead of converting

Deep sedation to cover an inadequate regional block risks airway loss in an un-fasted patient. Recognise block failure and convert to general anaesthesia with a secured airway when needed.

🎓 8 · Exam Pearls — DrNB / MD / EDAIC

Exam Pearls

Q: How do local anaesthetics work, and what determines potency/onset/duration?
They block the intracellular voltage-gated Na⁺ channel. Potency ∝ lipid solubility; onset ∝ pKa (lower pKa → faster); duration ∝ protein binding.

Q: Why is bupivacaine dangerous IV?
High lipid solubility and avid, slowly-reversible Na⁺-channel binding make it the most cardiotoxic common LA — refractory ventricular arrhythmias and arrest. Ropivacaine is less cardiotoxic.

Q: Maximum doses of lidocaine and bupivacaine?
Lidocaine 3 mg/kg (7 with adrenaline); bupivacaine 2 mg/kg. Always weight-based, and lower in the frail/cardiac patient.

Q: Outline lipid rescue for LAST.
20% lipid emulsion 1.5 mL/kg bolus over 1 min, then 15 mL/kg/h; repeat bolus and double the rate if unstable (max ~12 mL/kg). Secure airway/100% O₂, control seizures, and give modified ALS with small adrenaline doses, avoiding vasopressin/lidocaine/Ca-blockers.

Q: Where does the cord end, and where do you place a spinal?
Conus at L1–L2 in adults; place spinals at L3/4 or below (Tuffier's line ≈ L4) to avoid cord injury.

Q: Why is neuraxial block associated with hypotension?
Sympathetic block (2+ segments above sensory) causes venodilation (↓ preload) and arterial dilation (↓ SVR); a high block also blocks the cardiac accelerators (T1–T4) → bradycardia.

Q: PDPH — features and definitive treatment?
Postural fronto-occipital headache after dural puncture, ± neck stiffness/photophobia/diplopia. Conservative measures first; epidural blood patch for severe/persistent cases. Pencil-point needles reduce incidence.

Q: LMWH timing before neuraxial block?
Prophylactic LMWH 12 h; therapeutic LMWH 24 h before the block/catheter removal — per ASRA/AAGBI. Aspirin alone is not a contraindication.

📚 9 · References

References

Neal JM, Barrington MJ, Fettiplace MR, et al. (ASRA). The Third ASRA Practice Advisory on Local Anesthetic Systemic Toxicity — 2020. Reg Anesth Pain Med. 2021;46:81–82 (and 2020 checklist).
Horlocker TT, Vandermeulen E, Kopp SL, et al. (ASRA). Regional Anesthesia in the Patient Receiving Antithrombotic or Thrombolytic Therapy (4th Ed). Reg Anesth Pain Med. 2018;43:263–309.
Association of Anaesthetists (AAGBI). Regional anaesthesia and patients with abnormalities of coagulation. Anaesthesia. 2013;68:966–972; and AAGBI LAST management guideline.
Gropper MA, et al. (eds). Miller's Anesthesia, 9th Edition. Spinal, Epidural & Caudal Anaesthesia; Local Anaesthetics. Elsevier; 2020.
Stoelting RK, Hillier SC. Pharmacology & Physiology in Anesthetic Practice, 6th Edition. Local Anaesthetics. Wolters Kluwer; 2021.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology, 6th Edition. Spinal, Epidural & Caudal Blocks. McGraw-Hill; 2018.