Local anaesthesia

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Local anaesthesia refers to deliberate blockage of nerve fibres to remove sensation from a part of the body without affecting consciousness. This can be achieved in a number of ways, but most commonly, local anaesthetic drugs are infiltrated near the required nerves.

Local anaesthesia can be divided into several conceptual categories:

  • Infiltration of local anaesthetic directly into an area of skin or tissue- this is known as local infiltration.
  • Infiltration of local anaesthetic around a peripheral nerve or plexus, proximal to the desired site of action (such as a limb)- this is known as a regional block (sometimes field block).
  • Infiltration of local anaesthetic around the spinal cord or cauda equina- this is known as a neuraxial block (and includes epidural and spinal anaesthesia, and tends to provide anaesthesia of the lower part of the body.
  • Local anaesthetics can be directly applied to skin or mucous membranes, such as those of the eye, nose or pharynx- this is known as topical anaesthesia.


Helpful tips

  • Local anaesthetic drugs can be dangerous if administered incorrectly. If you are not sure what you are doing, ask a senior colleague or anaesthetist for advice (or direct supervision).
  • It is good practice to become familiar with only one or two drugs at first. Lidocaine is a good all-rounder for all sorts of short procedures. Even experienced anaesthetists will usually use only two or three local anaesthetics routinely.
  • Almost all procedures involving needles are rendered more comfortable by a bleb of local anaesthetic first. The notion of "it's two jags instead of just one" is nonsense propounded by people who cannot give local infiltration properly. If this is in doubt, ask a colleague to insert a 14G cannula into you. A comfortable patient is far more likely to keep still, and to be forgiving if you fail.
  • Be familiar with the maximum safe dosage for your patient and do not exceed it.

Methods to reduce pain on injection:

  • Use the finest needle you can
  • Inject slowly
  • Warm the anaesthetic solution to body temperature beforehand (e.g. in your pocket for 15 mins)

For venous cannulation, use a 2ml syringe and a short orange needle (25G, 1cm long). 1% lidocaine is fine (2% is not noticeably better). Hold the syringe in your dominant hand, in such a way that you can inject one-handed (there are several ways to do this effectively). Swab the skin with alcohol. Insert the bevel of the needle just under the skin exactly where you want to place the cannula. Aspiration is not necessary. Inject a tiny bleb of local (e.g. 0.1ml)into the skin- this is intradermal infiltration. It works instantly. (Subcutaneous infiltration requires more volume, takes longer to work, and may obscure the vein). The final result resembles a nettle sting- a pale lump in the skin 2-3mm diameter. When cannulating, place the cannula directly through the centre of this bleb.

This technique is an effective starting point for deeper infiltration, when a larger needle can then be inserted through the bleb.

Historical perspective

The earliest local anaesthetic drug discovered was cocaine. In addition to its local anaesthetic properties, cocaine also has CNS stimulant effects due to its properties as an uptake-1 inhibitor. Cocaine, an alkaloid from the leaves of the coca plant (Erythroxylon coca) of the Peruvian Andes, is also a powerful (albeit indirect) vasoconstrictor, which makes it useful when applied topically in surgery of the eye or nose.

Cocaine was isolated in 1860 by Niemann, and introduced into practice by Karl Koller, a Viennese surgeon, who used it topically in ophthalmic surgery (it is well absorbed topically). In 1884 he recommended it to his friend Sigmund Freud as a decongestant to treat his troublesome nasal polyps. Freud was very impressed with cocaine's stimulant properties and became a regular user himself. Koller went on to become a celebrated ophthalmic surgeon.

The dangers and addictive properties of cocaine led researchers to search for a substance which possessed the numbing effect of cocaine without the problematic effects. In 1905, the first synthetic local anaesthetic drug, procaine (an ester, whose trade name is Novocain) was produced by Einhorn. Tinkering with the molecule gave different variants such as amethocaine, which is still in use.

The first amide drug was lidocaine (formerly lignocaine), introduced by Lofgren in 1943, which was followed by prilocaine in 1959, bupivacaine (whose trade name is Marcaine) in 1964 and ropivacaine in 1997.

Most recently, purified active enantiomers of anaesthetic drugs, such as levobupivacaine have also been introduced. These purport to offer increased safety over the racemic preparation.



All local anaesthetics are pharmacological agents which temporarily block fast sodium channels in excitable tissues (which includes nerve fibres, skeletal muscle and cardiac muscle).

Blockage of the sodium channels prevents action potentials from being transmitted along the axon of the nerve, and hence signals such as pain (but also temperature, touch, vibration and proprioception). It is also the cause of toxicity of local anaesthetic drugs (which are toxic to the heart and brain, both structures being rich in fast sodium channels).

Local anaesthetics block the sodium channel from the inside, which means that, in order to be effective, they must diffuse across the cell membrane (in their un-ionised form), and then become ionised in the cytoplasm in order to block the sodium channel. The pKa of each agent is important, as this determines the equilibrium between the ionised and unionised forms.[1]

The resting membrane potential of the axon is unaffected by the action of the local anaesthetic.

LogoKeyPointsBox.pngLocal anaesthetic drugs work very poorly in acidic environments, such as around abscesses

All local anaesthetic agents are weak bases. Acidic environments favour the ionised form. However, the charged ionised form cannot diffuse through the lipid bilayer of neurones. Consequently, local anaesthetic drugs are far less effective in acidic environments, e.g. in inflamed tissue (therefore do a nerve or field block proximal to an abscess rather than infiltrate it).


Cocaine aside, the structure of local anaesthetic drugs is comparatively consistent. Each has an aromatic (lipophilic) "head", a body (intermediate chain), which consists of an ester or amide bond, and a hydrophilic "tail" (which contains a secondary or tertiary amine group).

The intermediate chain gives important determinants of properties such as duration of action, site of metabolism and potential for allergic response.

Local anaesthetic drugs may be classified on the basis of their central bond into amides and esters.

Ester drugs include procaine and amethocaine, which are commonly used for topical administration. Esters are relatively unstable in solution, poorly protein-bound in plasma, and are short-acting, undergoing hydrolysis by plasma cholinesterase to PABA (para-amino benzoic acid), which can provoke allergic reactions including anaphylaxis (see below). Most ester drugs are achiral.

Amide drugs include lidocaine and bupivacaine, which are extremely commonly used for local, regional and neuraxial blocks. Amides are much more stable, highly protein-bound, metabolised in the liver, and allergic reactions are extremely rare (see below). Most amide drugs (with the exception of lidocaine) are chiral.


Local anaesthetic drugs tend to be poorly soluble in water and are therefore usually presented as their hydrochloride salts. These in turn are dissolved in a modified Ringer's lactate solution. The final product is usually weakly acidic (pH 4-5.5).

Additives may include:

LogoWarningBox4.pngSolutions containing preservatives should never be used intrathecally.
  • Preservatives such as parabens to extend the shelf life.
Info bulb.pngConventional teaching and wisdom suggests that using adrenaline-containing local anaesthetic on appendages risks ischaemia from vasoconstriction of end arteries. Digital ischaemia from modern preparations is lacking and one literature review suggests that previously reported adverse sequelae may be associated with technique and poorly-formulated solutions.[2]. Some people including at least one doctor have held an Adrenaline self-injector pen wrong way round, and filled their thumb-tip with Adrenaline. It isn't nice but they have not dropped off.
  • Vasoconstrictors to extend the duration of action.
Classically adrenaline was used, but increasingly synthetic vasopressin derivatives such as octapressin or felypressin may be added.
  • 8% dextrose to increase baricity of the solution for intrathecal administration.

Pharmacological Properties

The properties of any local anaesthetic drug are determined by three essential features:

  • Lipid solubility determines potency, and is expressed as the heptane-buffer partition coefficient.
  • Protein binding determines duration of action, and is expressed as a percentage.
  • Dissociation constant (pKa) determines speed of onset and is expressed as a figure.
Local Anaesthetic Agents
Name Type Onset Duration Max. Dose (with adr) Common preparations Other forms Comments
Lidocaine Amide Rapid Intermediate 3mg/kg (7mg/kg) 1%, 2% EMLA, gel, 4% solution Good all-rounder. Ideal for short procedures.
Bupivacaine (Marcaine™) Amide Slow Long 2mg/kg 0.25%, 0.5% Hyperbaric ('Heavy') for spinal use. Lasts twice as long as lidocaine. Ideal for blocks, spinals, epidurals. Less suitable for infiltration.
Levobupivacaine (Chirocaine™) Amide Slow Long 2mg/kg 0.25%, 0.5% 0.75% Active enantiomer of bupivacaine, considered to be safer. Doses are same as racemic preparation.
Ropivacaine (Naropin™) Amide Slow Long 3.5mg/kg 0.75%, 1% 0.2% Less potent and toxic than bupivacaine but otherwise behaves similarly.
Prilocaine (Citanest™) Amide Intermediate Intermediate 6mg/kg (8mg/kg) 1%, 2% EMLA Preferred for Bier's blocks. Can cause methaemoglobinaemia.
Mepivacaine Amide Rapid Intermediate 4-7mg/kg Restricted to dentistry in UK.
Articaine Amide Rapid Intermediate Restricted to dentistry in UK; good penetration through bone.
Etidocaine Amide Rapid Intermediate 8mg/kg 1.5% Not in use in the UK.
Cocaine Ester Rapid Short 1.5mg/kg (topical) 10% (spray) High abuse potential; still used in ENT surgery.
Procaine (Novocain™) Ester Slow Short 10-14 mg/kg 2% Obsolete agent in UK.
Tetracaine (Amethocaine) Ester Slow Long 1.0-1.5 mg/kg 4% gel Ametop, eye drops Good topical absorption.
Oxybuprocaine (Benoxinate) Ester Rapid Intermediate 0.4% Eye drops only.
Proxymetacaine Ester Rapid Intermediate 0.5% Eye drops only.
Chloroprocaine Ester Rapid Short 15mg/kg Not in use in the UK.
Benzocaine Ester Rapid Short Throat lozenges and mucosal topical preparations only.

Non-pharmacological methods

Info bulb.pngIn the Russian campaign, Baron Larry - surgeon to Napoleon's army - noted that wounded men who had lain in the snow for some time did not feel pain in their chilled limbs.

There are non-pharmacological agents, e.g. ethyl chloride which work by chilling the tissue (due to rapid evapouration of this volatile organic compound). It has a limited role in local anaesthesia as duration of action is brief and it works only superficially.


LogoWarningBox4.pngBupivacaine and ropivacaine should absolutely never be used for Bier's blocks.

There are numerous applications of local anaesthesia:

Additionally, many drugs which have local anaesthetic properties are anti-arrhythmic (class I in the Vaughan Williams antiarrhythmic classification), such as flecainide.

Toxicity and Reactions

Toxicity may result from excessive absorption of the agent. Other reactions may be due to the effects of other chemicals in the product, or more rarely, allergy.

Reducing Toxicity

Vasoconstricting agents such as adrenaline reduce clearance of the local anaesthetic agent increasing the maximum allowable dose and the duration of the effect.


Decreases depolarisation in cardiac tissue.

LogoKeyPointsBox.pngThe heart is likely to stop in asystole

Features of Toxicity

LogoWarningBox4.pngIn the event of toxicity:
  • ABC
  • May requires intubation and ventilation
  • Fluids for hypotension
  • Symptomatic treatment of seizures



Info bulb.pngRemoving the highly lipid-soluble local anaesthetic into a lipid emulsion has been suggested and experimented with. The Intralipid parenteral feeding preparation is the obvious one to try. See lipid rescue


Given how often local anaesthetic agents are used, side effects are rare. Some reactions may simply be autonomic events related to stress. Other reactions may be due to other chemicals in the product including parabens, sulphites and neomycin.

True type 1 hypersensitivity has been described in the ester group, but only very rarely in the amide group. Cross-sensitivity is common among members of the ester group, but rarely between the groups or among the amides. Patch testing and intradermal skin prick testing can be done (although they may give discordant results). If a preservative containing product is used for testing, then it is obviously difficult to determine whether the anaesthetic agent itself is the culprit. Adrenaline containing products should be avoided for testing as reactions may be impaired. If these tests are negative, then a blinded subcutaneous test dose might be considered the final test. [3]

Practical Aspects

LogoKeyPointsBox.pngTo convert percentage to mg per ml, multiply the percentage of solution by 10

Calculating Total Dose

Most local anaesthetic solutions are expressed as weight per volume percentage. Therefore, in 1% of lidocaine there is:

    1g in 100ml
1000mg in 100ml
  10mg in   1ml


LogoKeyPointsBox.pngWhen injecting local anaesthetic, always aspirate to avoid inadvertent intra-vascular administration.

Use small needle initially (e.g. orange 25G needle).

A dental syringe (e.g. 27G) has a very fine needle and can be less painful to inject.

(Reducing pain on injection)