Local Anaesthesia


Mechanism of Action

  • All local anesthetics are membrane stabilizing drugs; they reversibly decrease the rate of depolarization and repolarization of excitable membranes (like nociceptors).
  • Local anesthetic drugs act mainly by inhibiting sodium influx through sodium-specific ion channels in the neuronal cell membrane, in particular the so-called voltage-gated sodium channels. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited.
  • Local anesthetics are weak bases and are usually formulated as the hydrochloride salt to render them water-soluble.
  • All nerve fibers are sensitive to local anesthetics, but generally, those with a smaller diameter tend to be more sensitive than larger fibers.
  • Local anesthetics block conduction in the following order: small myelinated axons (e.g. those carrying nociceptive impulses), non-myelinated axons, then large myelinated axons. Thus, a differential block can be achieved (i.e. pain sensation is blocked more readily than other sensory modalities).

Localised Toxicity

  • A cause of local toxicity is allergic reaction to para-aminobenzoic acid (PABA). These reactions range from urticaria to anaphylaxis.
  • PABA is a metabolic product of the degradation of Ester class of local anaesthetics, such as procaine (Novocaine), benzocaine, and, to a lesser degree, amide class anaesthetics such as lidocaine, and prilocaine. It is also a metabolic by-product of methylparaben, a preservative in multi-dose vials of lidocaine. When allergic response to injected anesthetics does occur, it is most likely due to the ester class local anesthetics. The amide class of local anesthetics is far less likely to produce allergic reaction.

Systemic Toxicity

  • Systemic toxicity of anesthetics involves the central nervous system (CNS), the cardiovascular system, and the immune system.
  • Methemoglobinemia is a process where iron in hemoglobin is altered, reducing its oxygen-carrying capability, which produces cyanosis and symptoms of hypoxia. Benzocaine, lidocaine, and prilocaine all produce this effect, especially benzocaine.
  • Cardiovascular effects are primarily those of direct myocardial depression and bradycardia, which may lead to cardiovascular collapse.
  • Systemic toxic reactions to locally administered anaesthetics are progressive as the level of the anaesthetic agent in the blood rises.
  • Initial symptoms such as a ringing in the ears (tinnitus), a metallic taste in the mouth, or tingling or numbness of the mouth.
  • Advanced symptoms include motor twitching in the periphery followed by grand mal seizures, coma, and eventually respiratory arrest. At extremely high levels, cardiac arrhythmia or hypotension and cardiovascular collapse occur.


  • Intravenous lipid emulsions may be useful for cardiotoxicity however the evidence at this point is still limited. This treatment is termed lipid rescue. This method of toxicity treatment was invented by Dr. Guy Weinberg in 1998, and had not been widely used until after the first published successful rescue in 2006. Since then more than a dozen case reports have been published.
  • Though most reports to date have used Intralipid, a commonly available intravenous lipid emulsion, other emulsions, such as Liposyn and Medialipid have also been shown to be effective.


  • Lignocaine 1%  (1g in 100mL = 10mg in 1mL)
    • Short acting = approximately 40 mins without adrenaline and 2 to 6 hours with adrenaline
    • Suitable for most simple wound closures
    • Maximal dose:
      • Without adrenaline = 3mg/kg (so for average 70kg, can use 21mL)
      • With adrenaline = 7mg/kg (average 70kg = 49mL)
        • Adrenaline NOT to be used on areas of terminal blood supply ie fingers, nose, penis, toes, ears as adrenaline causes vasoconstriction
  • Can be made more comfortable to use if:
    • Use smallest needle possible: 25 gauge
    • Inject slowly
    • Inject through surface of wound subdermally instead of piercing the skin
    • Work from anesthetised area
    • Warm to body temperature
    • Add 1ml NaHCO3 4.2% to 10mls of lignocaine (to buffer the acidic nature of the lignocaine, which is thought to cause the burning sensation)


  • Used where prolonged analgesia is required, such as in partially amputated finger (in a finger block), awaiting plastics review / admission
  • Naropin (Ropivicaine HCL 0.75% – 150mg in 20mLs; 75mg in 10mLs)
    • Maximal dose 3mg/kg = (which equates to 28mLs for average 70kg)
  • Marcain (Bupivicaine 0.25%; 25mg in 10mLs)
    • Maximal dose both with and without adrenaline = 2mg/kg = 0.8mls/kg (which equates to 40mls in an average 70kg)


  • Wound Infiltration
    • Inject into both sides of wound – inject into subdermal tissue from middle of wound to all 4 edges, withdrawing needle as you inject.
    • Aim to create a bubble underneath the skin
  • Nerve Blocks
    • Less wound edge distortion
    • Less total Local Anaesthetic required
    • Slower onset
  • Digital Nerve Block
    • Inject 2mls lignocaine without adrenaline through dorsal aspect of hand/ foot on both left and right sides of digit
  • Bier’s Block
    • Commonly used for distal radial fractures.
    • A specialised blood pressure cuff is inflated to a level 100mmHg higher than usual systolic blood pressure until the radial pulse is absent.
    • A local anaesthetic, usually prilocaine is injected into a cannula in the dorsum of the hand (inserted as far distal as possible)