11.4 Principles of Local, Regional & General Anaesthesia
Key Takeaways
- Local Anaesthetics (LAs) are classified into Amides (Lidocaine, Bupivacaine, Ropivacaine - hepatic metabolism) and Esters (Procaine, Tetracaine, Cocaine - plasma cholinesterase metabolism), blocking voltage-gated Na+ channels.
- Local Anaesthetic Systemic Toxicity (LAST) presents with early CNS excitation (tinnitus, metallic taste, seizures) progressing to cardiovascular collapse; 20% Intravenous Lipid Emulsion (Intralipid) is the specific antidote.
- Spinal Anaesthesia (Subarachnoid Block) is performed at the L3-L4 or L4-L5 interspace below the conus medullaris (L1 in adults), penetrating dura mater into the subarachnoid space containing CSF.
- The Triad of General Anaesthesia comprises Hypnosis/Unconsciousness, Analgesia, and Muscle Relaxation; pre-operative airway evaluation utilizes the Mallampati Classification (Classes I-IV) to anticipate difficult endotracheal intubation.
- Malignant Hyperthermia is an autosomal dominant pharmacogenetic emergency triggered by volatile inhalational agents or Succinylcholine, presenting with unexplained hypercapnia, masseter rigidity, rapid temperature elevation, and rhabdomyolysis, treated immediately with IV Dantrolene.
Local Anaesthetics, Mechanism of Action & Systemic Toxicity (LAST)
Local Anaesthetics (LAs) reversibly block nerve impulse conduction along nerve axons by binding to the intracellular domain of voltage-gated sodium (Na+) channels, preventing Na+ influx and membrane depolarization.
Chemical Classification & Pharmacology
Local anaesthetic molecules consist of a lipophilic aromatic ring connected by an intermediate chain to a hydrophilic tertiary amine group. The nature of the intermediate linkage divides them into Amides and Esters:
- Amide Local Anaesthetics (contain an 'i' in the prefix before -caine: Lidocaine, Bupivacaine, Ropivacaine, Prilocaine, Etidocaine):
- Metabolized in the liver by cytochrome P450 enzymes.
- Low potential for hypersensitivity/allergic reactions.
- Ester Local Anaesthetics (Procaine, Chloroprocaine, Tetracaine, Cocaine, Benzocaine):
- Metabolized in the plasma by plasma pseudocholinesterase (butyrylcholinesterase).
- Higher risk of allergic reactions due to metabolic breakdown into para-aminobenzoic acid (PABA).
Clinical Pharmacological Profiles
| Local Anaesthetic Agent | Class | Onset of Action | Duration of Action | Max Single Dose (plain) | Max Dose with Adrenaline (1:200,000) | Primary Clinical Application |
|---|---|---|---|---|---|---|
| Lidocaine (Lignocaine) | Amide | Rapid (2-5 mins) | Intermediate (1-2 hrs) | 4.5 mg/kg (max 300 mg) | 7.0 mg/kg (max 500 mg) | Infiltration, nerve block, epidural, IV regional (Bier block), antiarrhythmic |
| Bupivacaine | Amide | Slow (15-20 mins) | Long (4-8 hrs) | 2.0 mg/kg (max 150 mg) | 2.5 mg/kg (max 225 mg) | Spinal, epidural, peripheral nerve block. High cardiotoxicity |
| Ropivacaine | Amide | Moderate (10-15 mins) | Long (4-8 hrs) | 3.0 mg/kg (max 200 mg) | 3.5 mg/kg (max 250 mg) | Epidural analgesia, nerve block (less cardiotoxic S-enantiomer of bupivacaine) |
| Prilocaine | Amide | Rapid | Intermediate | 6.0 mg/kg | 8.0 mg/kg | IV regional anaesthesia; causes Methemoglobinemia (treated with Methylene Blue) |
| Tetracaine | Ester | Slow | Long | 1.5 mg/kg | 2.0 mg/kg | Spinal anaesthesia, topical ophthalmic anaesthesia |
Role of Adrenaline Additive: Adding Adrenaline (1:200,000 dilution = 5 mcg/mL) causes local vasoconstriction, which slows systemic vascular absorption, decreases peak blood concentration, prolongs duration of anaesthesia, and reduces surgical bleeding. Contraindicated in end-artery appendages (fingers, toes, penis, nose, ears) due to risk of ischemic gangrene.
Local Anaesthetic Systemic Toxicity (LAST)
LAST occurs due to accidental intravascular injection or rapid systemic absorption of excessive LA doses. Bupivacaine is particularly cardiotoxic due to slow dissociation from cardiac Na+ channels during diastole.
Clinical Sequence of LAST
- Central Nervous System (CNS) Manifestations (Occurs first):
- Early (Excitatory): Circumoral numbness, metallic taste in mouth, tongue paresthesia, tinnitus, lightheadedness, restlessness, visual disturbances.
- Late (Inhibitory): Muscle twitching, generalized tonic-clonic seizures, sudden CNS depression, loss of consciousness, apnea.
- Cardiovascular System (CVS) Manifestations (High mortality):
- Hypertension and tachycardia progressing rapidly to severe myocardial depression, bradycardia, ventricular arrhythmias (ventricular fibrillation/tachycardia), and refractory cardiovascular collapse.
Emergency LAST Protocol (Lipid Rescue)
- Stop LA Injection immediately and call for help.
- Secure Airway: Hyperventilate with 100% oxygen (hypercapnia and acidosis worsen LA toxicity).
- Control Seizures: Administer IV Benzodiazepines (Midazolam 1-2 mg or Lorazepam).
- ANTIDOTE: 20% Intravenous Lipid Emulsion (Intralipid):
- Initial Bolus: 1.5 mL/kg IV over 1 minute (~100 mL for 70 kg adult).
- Continuous Infusion: 0.25 mL/kg/min.
- Mechanism ("Lipid Sink Theory"): Lipophilic LA molecules partition out of cardiac/brain tissue into the circulating lipid plasma phase.
Neuraxial Blocks, General Anaesthesia & Airway Management
Neuraxial Anaesthesia: Spinal vs Epidural
Neuraxial blocks involve injecting local anaesthetic around the spinal cord sheath to produce sensory, motor, and autonomic blockade of the lower body.
| Clinical Parameter | Spinal Anaesthesia (Subarachnoid Block) | Epidural Anaesthesia |
|---|---|---|
| Anatomical Target Space | Subarachnoid space (mixes directly with Cerebrospinal Fluid CSF) | Epidural space (potential space between ligamentum flavum and dura mater) |
| Anatomical Level | Below L1/L2 termination of spinal cord (usually L3-L4 or L4-L5 interspace) | Lumbar, thoracic, or cervical level (spinal cord absent/present) |
| Dura Mater Puncture | Yes (dura and arachnoid punctured with fine needle - 25G/27G Quincke/Pencil-point) | No (dura remains intact; Tuohy needle used to identify space via Loss of Resistance) |
| Volume & Dose of LA | Very small volume (2.0 - 3.5 mL of 0.5% Hyperbaric Bupivacaine) | Large volume (15 - 20 mL of Lidocaine or Bupivacaine) |
| Onset of Block | Rapid (2 - 5 minutes) | Slow (15 - 20 minutes) |
| Post-Dural Puncture Headache (PDPH) | Risk present (occurs 24-48 hrs post-procedure due to CSF leak; treated with fluids, caffeine, or Epidural Blood Patch) | Absent unless accidental dural puncture occurs |
| Primary Clinical Uses | Lower abdominal, pelvic, urological, and lower limb surgeries | Labor analgesia, post-operative continuous catheter analgesia |
Triad of General Anaesthesia (GA)
General Anaesthesia requires three core components: Hypnosis/Amnesia (inhalational/IV hypnotics), Analgesia (opioids), and Muscle Relaxation (neuromuscular blockers).
Airway Assessment: Mallampati Classification
Evaluates patient sitting upright, mouth open fully, tongue protruded without phonation:
- Class I: Soft palate, fauces, uvula, anterior and posterior tonsillar pillars visible (Easy intubation).
- Class II: Soft palate, fauces, and portion of uvula visible.
- Class III: Soft palate and base of uvula visible.
- Class IV: Only hard palate visible; soft palate completely hidden (High risk of difficult intubation).
High-Yield Anaesthetic Emergencies
1. Malignant Hyperthermia (MH)
An autosomal dominant pharmacogenetic disorder of skeletal muscle calcium regulation caused by mutations in the Ryanodine Receptor gene (RYR1). Triggered by volatile inhalational anesthetics (Halothane, Isoflurane, Sevoflurane) or depolarizing muscle relaxant Succinylcholine.
- Pathophysiology: Uncontrolled efflux of calcium from sarcoplasmic reticulum causes sustained muscle contraction, hypermetabolism, hypercapnia, severe metabolic acidosis, hyperkalemia, hyperthermia (>40°C), and rhabdomyolysis.
- Earliest Clinical Sign: Unexplained rapid rise in end-tidal CO2 (ETCO2) and Masseter muscle spasm / rigidity after succinylcholine administration.
- Specific Antidote: Intravenous Dantrolene Sodium (initial dose 2.5 mg/kg IV stat, repeated up to 10 mg/kg). Mechanism: Inhibits calcium release from rhabdomyocyte sarcoplasmic reticulum.
2. Aspiration Pneumonitis (Mendelson's Syndrome)
Chemical pneumonitis caused by pulmonary aspiration of acidic gastric contents (volume >25 mL, pH <2.5) during induction or emergence from GA. Prevented by Rapid Sequence Induction (RSI) using Sellick's maneuver (cricoid pressure compressing esophagus against C6 vertebra until endotracheal tube cuff is inflated).
What is the specific intravenous antidote indicated for the emergency treatment of Local Anaesthetic Systemic Toxicity (LAST) and refractory cardiotoxicity caused by Bupivacaine?
At which anatomical interspace is a subarachnoid block (spinal anaesthesia) safest to perform in an adult patient to avoid damaging the spinal cord?
A 30-year-old male undergoing appendectomy under General Anaesthesia suddenly develops severe masseter muscle rigidity following succinylcholine administration, accompanied by a rapid rise in end-tidal CO2 (ETCO2) and temperature spiking to 40.5°C. What is the definitive pharmacological agent required immediately?
During pre-operative airway evaluation, a patient in sitting position with mouth fully open and tongue protruded displays visualization of only the hard palate, while the soft palate, uvula, and fauces are completely hidden. What is the Mallampati score for this patient?