Local Anaesthesia Milan Chande

Composition u  Local anaesthetic agent : Lidocaine HCL 2% (20 mg/ml

u  Vasoconstrictor: Adrenaline 1:80,000 (0.012 mg)

u  Reducing Agent: Sodium Metabisulphite  0.5 mg - This act's as a preservative for the vasoconstrictor.

u  Preservative: Methylparaben 0.1% (1mg)

u  Isotonic Solution: Sodium Chloride 6 mg

u  Fungicide: Thymol

u  Vehicle: Ringer’s Solution - Minimises discomfort during injection

u  Diluting Agent: Distilled water

u  To adjust pH: Sodium Hydroxide

u  Nitrogen Bubble: 1-2mm in diameter and is present to prevent Oxygen from being trapped in the cartridge and potentially destroying the Vasopressor or vasoconstrictor

Types of Local Anaesthetics

Local Anaesthetic's

used in Dentistry

Amides Esters

Amides

u Metabolised in the liver

u Heat - Stable, therefore can be autoclaved

u  Stronger bond than esters, therefore more stable in solution

u  Storage time is also greater than esters

u  Less allergy reactions compared to esters

Lidocaine 

u  The most common used local anaesthetic agent used in Dentistry

u  Available as a 2% solution

u Gives pulpal anaesthesia for 1.5h

u  Altered soft tissue sensation for upto 3h

u  Also available as a topical cream for use before insertion of needle for local anaesthesia

Mepivacaine

Supplied in two formulations in the UK:

u  As a 2% solution with 1:100,000 epinephrine

u  As a 3% plain solution

u  Short acting LA advocated for restorative work.

u Hasn't really caught on due to lidocaine being cheaper and as effective

Prilocaine

Is supplied in two different forms in the UK

u  As a 3% solution in combination with the synthetic polypeptide vasoconstrictor felypressin

u  Also available as a plain 4% solution

u  Similar but slightly less duration compared to lidocaine

u  May cause methemoglobinemia in excess

u  Methemoglobinemia is higher than normal presence of methemglobin, which is the oxidised form of haemoglobin.They have a reduced oxygen affinity.  This reduces the ability of red blood cells to provide oxygen to tissues.

Bupivacaine

u  Available in 0.5% solution

u  Available with or without adrenaline

u  Effective for 6h without adrenaline and 8h with adrenaline

u  Long - acting Local Anaesthetic agent

u Useful for post operative analgesia

Articaine

u  Available as a 4% solution

u  As effective as lidocaine

u  Ability to diffuse through bone is better

u  Shorter acting compared to lidocaine

u Greater pulpal anaesthesia

u Not to be used in ID Blocks due to cases of permanent altered sensation after it's use.

Controversy around the use of Articaine in Inferior Alveolar Nerve Blocks 

u  Haas and Lennon published an article in 1993 suggesting the link between using a 4% solution and increased numbers of people getting paresthesia.

u  Controversy exists due to the fact that no clinical evidence has ever been able to replicate there findings.

u  A theory has come out to suggest why the use of articaine causes more paresthesia compared to lidocaine.

u  Articaine is usually used as a second choice of local anaesthetic agent, when lidocaine did not work.

u  The operator therefore tries to more anatomically be more accurate with the placement of the needle the second time around. This is more likely to cause damage to the nerve.

u  Evidence shows that injury to the ID nerve and haematoma's around it are causing the paresthesia.

u  It is still recommended not to use Articaine for ID Blocks.

Esters

u  Were the first pharmaceutical agents used to provide local anaesthesia in dentistry

u  Weaker bond compared to amide's, therefore not as soluble in solution

u  Not heat stable, therefore can not be autoclaved

u  Metabolised in the plasma (Except cocaine) by pseudocholinesterase

u  Para-aminobenzoate (PABA) is a metabolite responsible for the increased allergic reaction seen when using ester local anaesthetic's .

Procaine

u  It was the first injectable man made local anaesthetic

u  It's predecessor cocaine had problems as it was very addictive

u  Procaine solved this problem, as it was not addictive nor did it provide any sense of euphoria. 

u  It was not used in Dentistry anymore, due to the vast array of amide's available on the market.

Interestingly, Procaine was the primary ingredient used to make Gerovital H3, an anti - ageing treatment in the 1960's. It was eventually banned as clinical trials showed the efficacy of the treatment to be zero. 

Benzocaine

u  Available as a topical local anaesthetic

u  Available as a 20% ointment

u Used regularly on children to anaesthetise the mucosa before placement of the dental needle

u  It is available in flavours such as bubble gum which why it is used in children instead of topical applications of lidocaine

Cocaine

u  The first anaesthetic that was used in dentistry. u  It is what all present day local anaesthetic agents are

derived from u  Not used in Dentistry any more due to it's addictive

properties

u  Interestingly, Benzocaine powder is used to dilute down cocaine sold illegally on streets. A growing number of criminals are aware of the dental uses of benzocaine. Therefore could target dental practices.

Types of Vasoconstrictors

u  Epinephrine - It is a naturally occcuring hormone that is added to local anaesthetic agents. It prolong's the length of anaesthesia, gives better pulpal anaesthesia and also provides haemorrhage control.

u  Felypressin - Reduces local blood flow by causing vascular smooth muscles to contract. It has a similar action to vasopressin. It's activity is more marked in veins than arteries, therefore provides poorer control of haemorrhaging. It is also contraindicated in pregnancy as it may induce contractions. 

Mechanism of Action

u  When a local anaesthetic is injected, the solution is hydrophillic in nature and diffuses across the plasma membrane.

u  Local anaesthetic 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.

u  The local anaesthetic drug creates a blockade in the sodium channels.

u  When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited.

u  This action is reversible and time dependent on the type of local anaesthetic used and the use of a vasoconstrictor.

Overdose and Toxic Effects of Local Anaesthetic

u  Safe dosage for lidocaine? 1 cartridge per 10kg of body mass.

u  Toxicity can occur when the local anaesthetic agent is given in excessive doses or is given intravascularly.

u  Systemic problems can occur if toxic dose’s are administered.

u  Central Nervous System is altered giving symptoms such as tinnitus, metalic taste in mouth and tingling feeling around the mouth.

u  Advanced symptoms could include seizures, coma’s and respiratory arrest.

u  Management includes placing the patient into a recovery position and calling the emergency services as soon as possible. Prepare to carry out CPR if necessary.

u  Lipid Emulsion therapy is now becoming more used in the world. First successful report was in 2006. The patient is injected with a lipid emulsion, which should then act as a sink, for the toxic levels of the local anaesthetic agents to come into.

Refereneces

u  Permanent nerve damage from inferior alveolar nerve blocks--an update to include articaine.Pogrel MA. (Available at http://www.ncbi.nlm.nih.gov/pubmed/17612365)

u  Morphological changes of peripheral nerves following intraneural injection of local anesthetic.Dtsch Zahnarztl Z. (Available at http://www.ncbi.nlm.nih.gov/pubmed/1817900)

u  21 year retrospective study of reports of paresthesia following local anesthetic administration.Haas DA, Lennon D. (Available at http://www.ncbi.nlm.nih.gov/pubmed/7736335)

Pain Diagnosis Milan Chande

What is pain?

u  Unpleasant sensory and emotional experience associated with actual or potential damage, or described in terms of such damage.

u  Trauma, surgery and inflammatory disease cause a reaction at the site of tissue disruption or damage, and a physiological response throughout the body. The damage to the tissue results in the release or production of a mass of chemicals, which react with each other and on nerve endings. When these chemicals have stimulated the nerve endings, signals travel to the dorsal horn of the spinal cord and then up to the cortex of the brain, where perception of the pain takes place.

Pain History

u Site - Where is it?

u  Onset - When did it start

u  Character - Describe the pain, Sharp/Dull/Throbbing?

u  Radiation - Localised to one place or move from the place? 

u  Associating factors - Hot/Cold/Sweet Stimuli?

u  Time - Always there or comes and goes?

u  Exacerbating factors - Anything make it better or worse? Medications??

u  Severity - Score out of 10? Does it affect your sleep?

Special Investigations

u  Radiographs

u  Sensibility testing using ethyl chloride

u  Sensibility testing using hot gutta percha

u  Vitality  testing using Doppler Flowmetry

u  TTP testing using blunt end of dental mirror

u  Computed Tomography

u MRI Scan's

A delta fibres u When stimulated, these nerves transmit quickly and

result in the instant reflex response that causes rapid withdrawal of the tissue from the source of damage.

u  The fibres travel to the dorsal horn of the spinal cord and terminates mainly in lamina 1, before decussating and travelling to the thalamus and somatosensory areas.

C Fibres u  These fibres carry impulses more slowly than A

delta fibres and are associated with “second pain”, the dull, burning, aching, throbbing pain felt over a wide area.

u  The C fibres generally follow the same pathway as the A delta fibres but terminate over a wide area in the brain stem. No fibres project to the somatosensory cortex of the brain.

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