Failure Anesthesia

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SAAD DENTAL STUDENT PRIZE RUNNER-UP

Reasons for failed localanaesthesia in dentistryand their management

Local anaesthesia (LA) is a common yet importantprocedure in dentistry. LA can be defined as:The loss of sensation in a circumscribed area of the bodyby a depression of excitation in peripheral nerve endingsor by inhibition of the conduction process in peripheralnerves9

Local anaesthesia causes loss of all sensory modalities,of which the blocking of pain is desired during dentalsurgery. It acts peripherally and involves no loss ofconsciousness.

Local anaesthesia is produced by drugs called localanaesthetics, e.g. lignocaine and bupivacaine. The target

for these drugs is the fast sodium (Na+) channel in nerveaxons. When charged, the local anaesthetic moleculebinds to a phenylalanine residue on helix 6 of the Na +channel, blocking the pore and preventing the passage ofNa+ions through the channel. The interaction also causesa conformational change in the channel to its inactivatedstate, also preventing flux of Na+.

This action reduces depolarisation and upstroke of anaction potential; the nerve is blocked at a site and doesnot propagate action potentials to the central nervoussystem (CNS). Sensory modalities are not consciously

interpreted. All significant, clinically used localanaesthetics work by a hydrophilic pathway.

The two main techniques used in dental LA are infiltrationsand regional nerve blocks. Infiltrations are where LA isdeposited at the apex of the tooth to be operated on, withthe needle penetrating the oral mucosa and advancingtowards the apex. The deposited LA is left to diffusethrough the alveolar bone to achieve pulpal anaesthesia.

Regional nerve block anaesthesia is when localanaesthetic is applied to a named anatomical nerve (distalto the operative site) by injection. The nerve is blockedand therefore its receptive field is anaesthetised. Receptivefields can involve the oral mucosa, the periodontiumand several teeth, e.g. inferior alveolar/dental (ID) nerve

block. Clinical uses include restorations of multiple teethand oral surgery procedures.Local anaesthesia does not usually fail, but the incidenceof failure is significant. U.S dental practitionersadminister 4,000,000 local anaesthetic injectionsannually; failure rate of analgesia is estimated at 5-15%.17

The above statistic represents a large number of people.Failure of local anaesthesia may seem strange, as we aredealing with a molecular interaction that we assumewould work every time. Some causes of failure concern

the molecular interaction, but most causes are totallyindependent of a successful drug interaction.

Good pain control is essential in dental surgery; failure toachieve complete anaesthesia of the site will lead to painand stress with anxiety caused to both dentist and patient,with loss of the patient s confidence in addition. Thepurpose of this essay is to describe the main causes oflocal anaesthetic failure and to suggest some ways for theclinician to manage the various situations of failure thatmay occur.

Causes of failure of local anaesthesia will now be assessed

under a number of headings.

1. OPERATOR-DEPENDENT FAILURE

Factors in this category have no physiological/pharmacological basis but are the most common causeof failure, almost always with inexperienced operators.Incorrect positioning of the needle, e.g. during an IDblock, could involve depositing LA solution too near inthe medial pterygoid muscle or too far into the parotidgland, thus missing the target. Failure to touch bone atthe right location and depth will not ensure that the ID

nerve has been targeted successfully. Local anaesthetic canbe injected intravascularly with the entire drug being carried

REASONS FOR FAILED

LOCAL ANAESTHESIA

IN DENTISTRY

By Adam Radford, Student DentistBristol Dental Hospital


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away from the target site. If injection speed is too fast thenlocal anaesthetic will spray, not accumulating at the target.

With infiltrations, poor localisation of the tooth apex isa major problem; for example, failure to inject at the truedepth of the sulcus and depositing the LA solution intothe cheek will result in poor pulpal anaesthesia.

2. PHARMACOLOGICAL FAILURE

This situation occurs rarely and could be due to the LAdrug being out of date or not strong enough to achieveeffective anaesthesia. But pharmacological failure usually

concerns vasoconstrictors.

A vasoconstrictor (usually adrenaline) is used alongsidelocal anaesthetics. It acts to constrict local bloodvessels, reducing bleeding and prolonging the time ofaction of the LA drug. If a vasoconstrictor was contra-indicated (e.g. in cases involving severe arrhythmias orosteoradionecrosis of the jaw) then the efficacy of thelocal anaesthetic may be reduced as it may be washedaway rapidly and its elimination through diffusioninto blood vessels may be increased. The duration ofanaesthesia will therefore be significantly reduced when

using plain solutions, and such solutions may therefore failto provide complete anaesthesia for the whole procedure.

Finally, there are two types of LA drugs available: ester-linked and amide-linked. Esters are metabolised locally byplasma and tissue esterases, while amides are metabolisedin the liver. Esters therefore have a shorter half-life andduration of action. For this reason, ester LA drugs such asProcaine may again fail to provide complete anaesthesiafor the whole procedure.

3. PSYCHOLOGICAL FAILURE

Fear, phobia or anxiety will increase the patients painthreshold. This will often present clinically as the patientinterpreting pressure or cold air from instruments aspain, even with a successful nerve block or infiltrationanaesthesia10.

4. ANATOMICAL VARIATION

This refers to the variable positioning of foraminae (andtherefore nerve trunks) between patients. For example,the mandibular foramen is commonly more superior inposition than usual10, resulting in local anaesthetic being

deposited below the nerve trunk with no regional blockobtained. The mental foramen is also variable in position,

which could account for some mental-incisive nerveblock failures. Wong and Jacobsen17reported problemsin achieving a correctly positioned block in patients withwide, flaring mandibles, bulky musculature and excessiveadipose tissue.

For maxillary buccal infiltrations the zygomatic buttressmay act as a diffusion barrier when LA is deposited at theapices of first molars. For posterior mandibular infiltrationsthe thick and dense cortical bone of the mandible also actsas a diffusion barrier for LA.

Failure of topical LA on the palatal soft tissues occurs

because the tissues are orthokeratinised and again act as adiffusion barrier, unlike the non-keratinised buccal tissues.

5. ACCESSORY NERVE SUPPLY

Normally, specific areas of the mouth are innervated bydesignated nerves. Accessory nerve supply refers to thesituation where these areas in the mouth are innervatedby additional branches of nerve trunks that are primarilyinvolved with the innervation of other structures. Herewe are mainly concerned with tooth pulpal fibres thatoriginate from accessory nerve trunks. Accessory nerve

supply is a major cause of LA failure, as accessory nervetrunks are not anaesthetised in a specific nerve block.Many people have researched accessory nerve supply, andsome accepted theories are outlined below. First are theipsilateral connections.

5.1 Palatal nervesIt has been accepted that the pulpal supply of the uppermolars may originate from the greater palatine nerve, andof upper incisors from the nasopalatine nerve10, causingfailure of the posterior, anterior and superior alveolarnerve blocks respectively.

5.2 Lingual nerveP. P. Robinson12found that in 10 out of 12 anaesthetisedcats, anterior mandibular teeth were supplied byipsilateral and one by contralateral lingual nerve fibres.He suggested that the lingual nerve accessed tooth pulpthrough accessory foraminae in the lingual cortex of themandible. In another study by R. N. Sutton15it was foundthat 265/300 human cadaver mandibles contained manysmall accessory foraminae, commonly lingually. Rood13believed that the lingual nerve was responsible for twofailures out of 334 ID blocks. It is suggested, then, thatthe lingual nerve is responsible for accessory supply to

anterior mandible teeth in humans with access throughaccessory foraminae.


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5.3 Mylohyoid nerveThe mylohyoid nerve is considered to be a commonsource of accessory nerve supply. Wilson et al.16discovered that in 16 out of 37 (43%) of human cadaversthe mylohyoid nerve continued beyond the mylohyoidmuscle and entered the lingual aspect of the mandiblethrough accessory foraminae. It was also found that themylohyoid nerve branched from interior alveolar at amean distance of 14.7 mm superior to the mandibularforamen. This was higher than previously thought.Local anaesthetics work at the nodes of Ranvier and itwas discovered that three nodes of Ranvier had to beblocked in order to prevent action potential propagation

and block the nerve1. It was proposed by Wilson et al.16that the mylohyoid nerve may exist only as a very smallsegment in the pterygomandibular space, with too fewnodes of Ranvier to be sufficiently anaesthetised duringan ID block, and that the nerves higher branching pointwould also prevent it being blocked as local anaestheticmay not diffuse this far up the pterygomandibular space.The mylohyoid nerve is likely to account for some failuresof total anaesthesia of anterior mandibular teeth withan ID block. Wilson suggested that this evidence couldexplain the increased success rate of the Gow-Gates block(where local anaesthetic is deposited higher, at the neck

of the condyle, and is likely to block inferior alveolar,mylohyoid, long buccal and lingual nerves (and manypossible accessory nerves). The Gow-Gates block hasbeen demonstrated to have a 96% success rate, comparedwith 65% for the inferior alveolar block6.

All theories are backed up by Frommer et al.5whodemonstrated (histologically) that the mylohyoid nervecontained sensory fibres, i.e. it was not a pure motornerve.

5.4 Long buccal nerveThis nerve is believed to supply posterior, mandibular

teeth in some cases10. This theory is supported by Rood13,who demonstrated that the buccal infiltrations resolved72 out of 79 failed ID blocks, and Sutton15, who proposedthat the long buccal nerve could enter the mandiblethrough external surface accessory formina and thatbuccal infiltrations resolved failed local anaesthesia herein many of his patients.

5.5 Facial nerveThe mandibular branch of the facial nerve was shown indissections by Sutton15to lie close to the mental foramen.This led Sutton to suggest, based on the previous work

by Farache and Alonso4

, that the facial nerve can enter themandible here and supply the pulps of the teeth.

5.6 Upper cervical nervesThese nerves are thought by many to supply pulpalafferents to some of the mandibular teeth. Sutton15found in dissections that cervical nerves ran close to themandible and proposed that they could enter buccallythrough accessory forminae. Supply from these nervescould explain a failed Gow-Gates block.

5.7 Auriculotemporal nerveThe role of accessory supply to mandibular teeth by thisnerve was reviewed by Heasman and Beynon7. Theyexplained that auriculotemporal nerve branches may enteraccessory forminae high on the coronoid process and

condyle of the mandible.

5.8 Bilateral supplyThis is common for mandibular central incisors:innervation of these teeth commonly arrives from itsipsilateral as well as its contralateral inferior alveolarnerve, crossing the midline symphysis.

In a study by Yonchak et al.18, 38 patients were given(randomly) unilateral or bilateral ID blocks over twovisits. The pulps of teeth 1 to 3 were tested afterwards.In conclusion, the bilateral ID block had a success rate of

66% compared with 39% for a unilateral nerve block fora lower central incisor. Greater success was also reportedfor teeth 2 and 3. Bilateral supply is a likely cause offailure of an ipsilateral ID block to anaesthetise anteriormandibular teeth.

6. PRESENCE OF ACUTE INFLAMMATION

It is well recognised that local anaesthesia readily fails inthe presence of acute inflammation. This is commonlydue to a pH decrease (to 5 or 6) in inflamed tissue,associated with mediators of inflammation (Figure 2).

THE TISSUE PH IS A MAJOR FACTOR IN THE RATIO OF CHARGED TO

UNCHARGED LOCAL ANAESTHETIC MOLECULES CALCULATED BY THE

HENDERSON-HASSELBALCH EQUATION, I.E.:

PKA PH = LOG [LAH+]

[LA]

A DECREASE IN PH RESULTS IN AN INCREASE IN THE AMOUNT OF

CHARGED MOLECULES PRESENT, WHICH REDUCES THE AMOUNT

OF LOCAL ANAESTHETIC MOLECULES PENETRATING THE NERVE

MEMBRANE AND INTERACTING WITH THE TARGET. THE NERVE WILL

NOT BE SUFFICIENTLY BLOCKED.

Figure 2


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This theory may explain failure of infiltration anaesthesiabut it does not explain failure of nerve blocks where localanaesthetic is deposited away from the site of infection.

Hyperaemia during acute inflammation will causewashing of local anaesthetic from the system andincreased elimination via diffusion into local bloodvessels10. The theory can only explain failure of infiltrationanaesthesia.

Hyperalgesia is when the threshold of nociceptiveneurones to noxious stimuli is decreased, both in andaround the site of insult. Excessive discharge from these

nerves results from the weakest of noxious stimuli. Thiswas demonstrated by Rood and Pateromichelakis14, whoapplied artificial inflammation to sciatic nerves in rats.There was an increased rate of firing and action potentialamplitude for the inflamed nerves opposed to the controlnerves, suggesting hyperalgesia. Rood concluded that asolution to hyperalgesia is to use a stronger concentrationof drug (5% lignocaine with adrenaline), which willsufficiently block hyperalgesic nerves.

Brown2applied artificial inflammation to saphenousnerves in rats. He discovered, after a time period of

several hours, the action potential amplitude of theinflamed nerves increased on average by 11.1%, asopposed to the control nerves. This would reducelocal anaesthetic efficacy in decreasing the upstrokeof an action potential. He proposed that a time delaywas required for certain inflammatory mediators to besynthesised and that these worked to increase their nerveaxons permeability to sodium ions, thus increasing theaction potential amplitude.

Management of failed local

anaesthesia1. MANAGEMENT OF OPERATOR-DEPENDENT

FAILURE

This usually involves the clinician reviewing his or herknowledge of anatomy and/or clinical injection technique.In the event of difficulties in locating the mandibularforamen an OPG radiograph may be useful for location10.Correct syringe aspiration prior to injection will usuallyprevent an intravascular injection. A slow injectiontechnique and a massage of the injected area will help to

maximise the localisation of the LA drug to the site ofinterest during infiltration anaesthesia.

2. MANAGEMENT OF PSYCHOLOGICALFAILURE

A calm and reassuring manner on the part of the clinicianis appropriate in most situations. However, in cases ofmore severe anxiety, IV sedation, e.g. with midazolam,can be used to good effect. Dental phobias requiretreatment under GA or referral to a specialist phobiaclinic.

3. MANAGEMENT OF PHARMACOLOGICALFAILURE

Firstly, the clinician should always check the expiry dateof the LA drug.

If a stronger drug is needed, then 5% lidocaine withadrenaline is usually effective, or articaine can be usedfor its excellent diffusion properties. When adrenalineis contra-indicated then Citanest (3% Prilocaine + 0.03IU/ml Felypressin) is very effective. When forced to use aplain LA solution then Scandonest (3% Mepivacaine) isthe most effective. Ester LA drugs should be avoided atall costs.

4. MANAGEMENT OF ANATOMICALVARIATION

An OPG can be used to locate the mental andmandibular foraminae. Infiltrations mesial and distal tothe zygomatic buttress will overcome its effect as a barrier.Posterior mandibular infiltrations should be conductedwith articaine because of its excellent diffusion properties.

5. MANAGEMENT OF ACCESSORY NERVESUPPLY

In the maxilla, greater palatine/nasopalatine nerve

blocks can be used to stop possible accessory supply. Inthe mandible, additional buccal and lingual infiltrationsfollowing an ID block can be used to combat accessorysupply.

During an ID block the lingual nerve should be deliberatelyanaesthetised in order to eliminate any possible accessorysupply, especially in oral surgery procedures. Alternatively aGow-Gates block, which deposits LA higher at the neckof the condyle, can be used to block long buccal, infralveolar,mylohyoid and lingual nerves and thus significantlyreduce the risk of their accessory supply10. In difficult

cases, intraligamentary anaesthesia with articaine is veryeffective, or intrapulpal LA if permitted.


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To overcome bilateral supply, buccal and lingualinfiltrations can be used in the midline to block thecrossover supply.

6. MANAGEMENT OF ACUTE INFLAMMATION

In the event of persistent failure to obtain localanaesthesia with conventional techniques,intraligamentary local anaesthetic can be given usingarticaine, or a stronger solution of 5% lidocaine andadrenaline can be used in infiltrations to combathyperalgesia. Articaine is also effective in infiltrationshere because of its excellent diffusion properties.

In the event of absolute failure, treatment should stopand the patient should be discharged with a course ofantibiotics and ibuprofen to take to reduce or stop theinflammation/infection. The treatment can then beundergone at a later date.

In conclusion, total local analgesia is essential for dentaltreatment. Failure of this has effects on the patient,increasing pain, fear, anxiety and loss of confidence,and on the dentist, increasing stress in performing theprocedure. The failure of dental LA has many causes,

with much firm experimental evidence behind eachone. I believe that failure could arise from any of thefactors described above, possibly from combinationsof factors. To avoid failure of total local analgesia theoperator should increase knowledge and practice of therelevant surgical techniques, apply correct dosages, useradiographs to check for anatomical variations, considerthe use of anxiolytic drugs for anxious patients, useinfiltration techniques around the tooth concerned orconsider a Gow-Gates block if accessory nerve supply issuspected, and use antibiotics or a stronger solution oflocal anaesthetic in the case of acute inflammation.

BIBLIOGRAPHY1. Blair and Erlanger 1939.

2. Brown RD. The failure of local anaesthesia in acuteinflammation. Brit Dent J (1981),151,47-50.

3. Evers H, Haegerstam G. Introduction to dental localanaesthesia (1990). Dentsply Pharmaceutical.

4. Farache and Alonso 1969.

5. Frommer J, Mele FA, Monroe CW. The possible role

of the mylohyoid nerve in mandibular posterior toothsensation. JADA (1972). 85, July, 113-117.

6. Gow-Gates 1973.

7. Heasman PA, Beynon ADG. Clinical anatomy ofregional analgesia: An approach to failure. DentUpdate (1986). Nov-Dec Issue 469-476.

8. Kaufman E, Weinstein P, Milgrom P. Difficulties inachieving local anaesthesia. J Am Dent Assciation( JADA).(1984).108,205-208.

9. Meechan JG, Robb ND, Seymour RA. Pain andanxiety control for the conscious dental patient.(1998). Oxford University Press.

10. Meechan JG. How to overcome failed localanaesthesia. Brit Dent J (1999).186, 1, 15-20.

11. Meechan JG. Practical dental local anaesthesia.(2002). Quintessence.co.Ltd.

12. Robinson PP. An electrophysiological study of thepathways of pulpal nerves from mandibular teeth in

the cat. Arch Oral Biol (1980).25, 825-829.

13. Rood JP. The analgesia and innervation of mandibularteeth. Brit Dent J (1976).140,237-239.

14. Rood JP, Pateromichelakis S. Local anaestheticfailures due to an increase in sensory nerve impulsesfrom inflammatory sensitisation. J Dent (1982).10(3),201-206.

15. Sutton RN. The practical significance of mandibularaccessory foramina. Aust Dent J (1974); June; 167-173.

16. Wilson S, Johns P, Fuller PM. The inferior alveolarand mylohyoid nerves: an anatomic study andrelationship to local anaesthesia of the anteriormandibular teeth. JADA (1984).108, March, 350-352.

17. Wong MKS, Jacobsen PL. Reasons for localanaesthesia failures. JADA (1992).123. Jan. 69-73.

18. Yonchak T, Reader A, Beck M, Meyers WJ.Anaesthetic efficacy of unilateral and bilateral inferioralveolar nerve blocks to determine cross innervation inanterior teeth. Oral Surg Oral Med Oral Pathol Oral

Radiol Endod (2001).92(2),132-135.


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