A powerpoint presentation with details on the current state of local anaesthetics available for Dentistry in the UK.

1. Local Anaesthesia
Milan Chande

2. 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

3. Types of Local Anaesthetics
Local
Anaesthetic's
used in Dentistry
Amides Esters

4. 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

5. 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

6. 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

7. 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.

8. 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

9. 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.

10. 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.

11. 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 .

12. 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.

13. 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

14. 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.

15. 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.

16. 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.

18. 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.

19. 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)

20. Pain Diagnosis
Milan Chande

21. 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.

22. 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?

24. 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

25. 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.

26. 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.

28. Thank you for listening