Clinical Tips, Endodontic LA, General Updates

The Endospot Episode 1 | Preventing Local Anesthetic Failure in Endodontics

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Problems with Local Anaesthesia?

In this, post, we discuss practical techniques for preventing failure of LA for endodontics, especially when dealing with irreversible pulpitis. Listren to the audio file below:

Preventing Local Anesthetic Failure in Endodontics

For the new and updated podcast, go to the podcast page.

References referred to in this podcast:

Meta Analyisis on Artciaine V lidocaine:
KATYAL V. 2010. The efficacy and safety of articaine versus lignocaine in dental treatments: A meta-analysis.  J dent: 38: 307-317

Intraossesous Injections:
READER A, NUSSTEIN J. 2002. Local anesthesia for endodontic pain. Endodontic Topics: 3: 14–30

Use of Articaine for buccal infiltration:
MATTHEWS R, DRUM M, READER A, NUSSTEIN J, BECK M. 2009. Articaine for Supplemental Buccal Mandibular Infiltration Anesthesia in Patients with Irreversible Pulpitis When the Inferior Alveolar Nerve Block Fails. J Endod: 35(3): 343-346
AGGARWAL V, JAIN A, KABI D. 2009. Anesthetic Efficacy of Supplemental Buccal and Lingual Infiltrations of Articaine and Lidocaine after an Inferior Alveolar Nerve Block in Patients with Irreversible Pulpitis. J Endod: 35(7). 925-929

PSA Block Link –
Information on the PSA Nerve: http://en.wikipedia.org/wiki/Posterior_superior_alveolar_nerve
Video: You Tube Video on the PSA Nerve Block

Show Transcript:
Welcome to the Endospot Episode 1.
In today’s podcast I’ll be discussing my techniques for managing local anaesthetic failure and specifically how to manage teeth diagnosed with irreversible pulpitis.

On the site we have references and show notes for this episode, so head to www.endospot.com and remember you can sign up and receive the Endospot blog posts directly into your inbox.

So let’s get on with the podcast.

On the topic of failed LA, it’s important to recognise situations where complete anaesthesia is likely to be difficult to obtain. In general terms, the mandibular molar teeth are the most difficult to anaesthetise, and this is where you’re likely suffer the most failures.
The issue with mandibular molar teeth is compounded where we have an irreversible pulpitis. The inflamed pulp is always going to more difficult to anaesthetise. You’ll often have a slightly distressed patient in this situation, so it’s important to get it as right the first time. Once you’ve begun treatment on an anxious patient and they’ve suffered a level of pain due to failed LA, it can be quite difficult to win back their faith in you.

Now it’s certainly my experience that where the pulpitis has been long standing and is becoming more and more acute, this will be the most difficult tooth to get numb. A good example might be a case of cracked tooth syndrome where the tooth has been manageably painful to bite for months, but is now becoming more and more sensitive to thermal stimuli and spontaneous pain has begun to occur. I suggest you hit these ones with every trick in the book.

Abscessed teeth don’t normally represent a huge problem for anaesthesia in terms of being able to instrument the canals, but sometimes the surrounding tissues will be difficult to anesthetise and the patient will still respond to things like pressure. One caveat here though. Just because you’ve made a diagnosis of abscess, don’t assume that there is no vital tissue in the canal. Some vital tissue can remain in the canal even in the presence of pus and swelling, and attempting to debride this canal can result in high levels of pain. So, I always assume the worst when dealing with patients in pain and provide complete anaesthesia

In my previous last post, I covered the reasons for LA failure in pulpitis cases, so if you want more details and references, go to the blog post at endospot.com and review those there. The main points that are worth considering though, are that a numb lip after IANB does not necessarily equal pulpal anaesthesia. This is the case even when dealing with an uninflamed pulp, but is especially so where you are dealing with an inflamed pulp. Research generally tells us that if we are dealing with an irreversible pulpitis and we give an IAN block which is apparently successful as the patient’s lip is numb, then , we’ll still only be successful in completely anaesthetising the tooth nerve about 55% of the time. Now, that’s obviously unacceptable, so we’re going to need to use supplementary LA for these cases.

The second point to note is that LA takes time to work. Again, research tells us that in 19-27% of cases, complete anaesthesia doesn’t occur until 15 minutes after the injection. So, next time your LA fails, it may simply be that the LA hasn’t had time to work. Supplemental techniques such as the PDL and intraosseous injection tend to work much faster than IADB, and should have you removing that inflamed pulp much faster.

As to which type of LA you should use, this will to a certain extent come down to personal preference, and obviously the medical profile of the patient. In general terms though, I would recommend using articaine. There’s been plenty of research in recent years devoted to articaine with some conflicting results. But, a recent meta-analysis concluded that articaine was more effective than lidocaine for anaesthetising mandibular molars. The article is by an Australian and so refers to lignocaine, but I assure you it’s the same drug.
So now I’ll go through my standard technique for dealing with hot pulps. Wherever not contraindicated, I’ll prescribe ibuprofen as soon as possible prior to treatment. There is some evidence that this alone may assist in achieving complete anaesthesia in inflamed pulps, but even if it doesn’t let’s remember that  these patients are presenting with pain, and therefore are at risk for post-operative pain. In this case, Ibuprofen (unless contraindicated) would be part of my pain management regime anyway.

When faced with a hot mandibular molar, I’ll start with a regular IAN Block and follow this with a buccal and lingual infiltration. The buccal infiltration ensures that a rubber dam clamp can be placed comfortably, but more importantly, I think that combining the block of the nerve with the local infiltration simply means that we have two sites along the nerve trunk that are blocked and this will lead to improved anaesthesia. This makes a lot of sense to me and is backed up by a number of studies which show that in cases of irreversible pulpitis, the infiltration significantly improves success rates. These studies have also shown the improved effect of articaine over lidocaine for this purpose.

After the buccal and lingual infiltrations, we take a minute’s break to ensure they are active and then move onto the PDL injection. There are a number of specialised equipment kits for PDL injections available, but they can be done successfully with a standard syringe. The first step is to bend the needle with some haemostats so that you are able to place pressure on the needle as it is forced into the PDL. The needle is inserted into the gingival crevice and with the bevel facing away from the root surface. Press hard and inject for 10s. There should be back pressure, if there isn’t, then the solutions wont’ be forced through the cribriform plate into the cancellous space and won’t be effective. I’ll perform the PDL injection at the four corners of the tooth.

The PDL injection is not really a PDL injection. I mentioned that the solution is forced into the cancellous space and as such It’s really an intraosseous injection. Therefore, there may be cardiovascular effects and this should be taken into account when selecting the LA. If an adrenaline containing LA is contraindicated, then you can use a non-adrenaline containing LA for this purpose.

The rate of onset of a PDL injection is fast, but the duration is short compared to IAN block, so at this point I’ll get a rubber dam on to the tooth and start access almost immediately. Once the pulp space is penetrated, and if vital tissue is found, then I’ll perform an intrapulpal injection. This injection relies on backpressure, so can only be used if only a small perforation is made into the pulp chamber.
For maxillary molars, I’ll start with a buccal and palatal infiltration, injecting most of the cartridge bucally. The palatal injection allows the rubber dam clamp to be placed comfortably, but might also anaesthetise the palatal root where a buccal infiltration could fail. After this, I perform a posterior superior alveolar block. I’ve placed a link in the show notes so you can have a look at this technique if you’re not familiar with it. I think that in the same way that the buccal infiltration in the mandible works with the IAN block to improve anaesthesia by blocking two points along the nerve trunk, combining a SPAN block with infiltrations should do the same. I then move onto PDL injections and perform an intrapulpal once the pulp chamber is entered.

The vast majority of cases, these procedures will allow you to enter the pulp space and remove most of the inflamed pulp tissue. If you are unable to even enter the pulp space, then your only real option is to perform an intraosseous injection. This does require specialised equipment. A good review of this technique can be found in the endodontic topics article referred to in the show notes. If you are comfortable with intraosseous injections, then these can be substituted for the PDL injections in the standard routine. My practical experience though is that if you follow the techniques described you really should have a very high level of success.

One point to note though is that infiltrations and PDL injections won’t make up for a failed IANB, so if there is any doubt that the block has been successful, then it’s worth repeating the block. If you want to be certain, it might make sense for you to perform the block and then wait until there are significant signs of lip and tongue anaesthesia before going onto the infiltrations and PDL injections. Obviously these injections can cause lip numbness also and so can mask a failed IAN block.

After entering the pulp chamber, you may find that you can remove some or most of the pulp tissue but attempting to pass a file to length in the canal elicits pain. In this case, I don’t see any reason to persist as the process of removing the bulk of the pulp tissue will result in resolution of the patient’s symptoms. I’ll dress the tooth with a corticosteroid containing dressing such as ledermix or odontopaste and send the patient home with assurances that the symptoms will resolve and the tooth will be easier to treat at the subsequent visit as the inflammation in the pulp will have resolved greatly. If you persist when complete anaesthesia isn’t achieved, you’re likely to put your patient and yourself through a lot of unnecessary pain, and the patient will be sure to be more anxious and will probably be one of those people that for the rest of their life tells their friends how agonising root canal treatment is.

So that is my routine for dealing with hot pulps. I’m aware there will be many different techniques out there and I’d love to hear some feedback. For those listeners who are just beginning their career, I’d recommend getting into the habit of using block and infiltration anaesthesia for all endodontic cases, and adding the PDL and intrapulpal injections when required.

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Failed Anaesthesia
Clinical Tips, Endodontic LA, General Updates

The Endospot Guide to Understanding Local Anesthetic Failure

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Failed Anaesthesia

The patient with a hot pulp spells trouble when it come to anaesthesia

Every dentist has had the unfortunate experience of being unable to achieve anesthesia, especially when dealing with an irreversibly inflamed dental pulp. You find yourself filled with self-doubt and feeling helpless, especially where the patient has presented in pain and you feel you need to remove that inflamed pulp!

But, LA failure is a bit more complex than I think most of us realise. Most of the information that follows is taken from an excellent review of the topic by Ken Hargreaves & Karl Keiser, so grab that if you want in depth analysis (Hargreaves et al. 2002). I’m going to cover what I think is important for most of us.


There are a number of reasons for LA Failure, but the first thing I think we should consider is this:
1.    Complete pulpal anesthesia is not achieved 100% of the time in normal pulps;
2.    Complete pulpal anesthesia has a slower onset than most of us would expect .

The simple fact is that a well administered inferior alveolar nerve block does not provide complete pulpal anesthesia 100% of the time. Bou Dagher conducted IAN block on 30 subjects and achieved 100 numbness of the lip, but only 50-75% of these patients demonstrated complete molar anesthesia when measured by electric pulp tester (Bou Dagher 1997). For most dentists, the majority of LA is given for restorative procedures, and often, anesthesia may be sufficient to prepare a cavity for restoration without problem. I think this probably lulls us into a false sense of security as to how successful our techniques are.

The next point to make is that the onset of complete pulpal Anesthesia takes time, most commonly up to 15 minutes. It’s fair to say that we would often not wait that long before attempting a procedure. In studies, onset was longer than 15 minutes in 19-27% of cases and longer than 30 minutes in 8% of cases. Complete lip numbness occurred much faster, within 5-7 minutes.
On this topic, It has been shown that injecting a second cartridge of LA injected after an apparently successful IAN block does not improve the onset time (Vreeland et al. 1989). In those situations where we have an apparently failed IAN block (despite profound lip numbness), and we inject a second cartridge and we then achieve anesthesia, it’s probably just that we’ve allowed more time for the initial injection to work.

The key points here are:
1.    Lip numbness does not confirm pulpal anesthesia;
2.    Onset takes time
3.    IAN blocks are unreliable when it comes to achieving pulpal anesthesia even in uninflamed pulps

What happens when we have an inflamed pulp? Things are even more dire. Two studies that evaluated pulpal anesthesia after IAN where the pulp was inflamed reported an average of only 55%, despite 100% numbness of the lip (Cohen et al. 1993, Nusstein et al. 1998).
Theories on failure of LA

It is my recollection from reading textbooks at dental school that IAN blocks failed because of the increased pH in the region of an inflamed pulp which prevented dissociation from the acid form of the LA to the base form. The base form was then unable to diffuse across the cell membrane in order to block the sodium channel. This never sat well with me because I couldn’t understand why inflammation at the site of a lower canine tooth would affect the dissociation of an LA molecule deposited near the mandibular foramen.  The truth is that while this theory remains a possibility, it is unlikely that this is a real explanation for the failure of LA. Firstly, the change in pH in inflamed tissues is not large, and inflamed tissues possess a greater buffering ability than normal tissues. Secondly, any change in tissue pH is also likely to be very localised (Punnia-Moorthy, 1988).  So, given our clinical results of reduced anesthesia of mandibular teeth after IAN blocks, we can consider this explanation to have some, but probably limited clinical relevance.

The second reason I recall from dental school for failure of IAN blocks was accessory innervation from the myelohyoid nerve. The lingual, buccal and transverse cervical nerve have also been implicated, however there is limited evidence for these mechanisms. Potentially, however, they could contribute to LA failure.

A third possible method mentioned in the literature is resistance or tachyphylaxis. According to Kenneth Hargreaves (who by the way is an extraordinary speaker and you should make an effort to see him speak) there is little evidence for this, and I think we should be happy to take his word for it.

The next possible mechanism of failure of LA is through the increased blood flow that occurs in inflamed tissues. This could potentially result in increased removal of LA from a site. Again, this is likely to be a localised issue and should not affect regional block anesthesia. Theoretically, increasing the concentration of vasoconstrictor in LA should counteract this mode of failure, but to date there have been few studies (I couldn’t find any) comparing different concentrations of adrenaline in pulpitis cases. In normal pulps, the results have been a little contradictory with some studies showing equivalent results for different concentrations of adrenaline (Epinephrine). One study however has shown a dose dependant effect on onset and duration of infiltration anesthesia with 2% lidocaine and 1:200000, 1:100000 and 1:50000 adrenaline.

OK, now we get into the important stuff – the real reasons why we have trouble convincing inflamed pulps to be quite while we operate on them. In the presence of inflammation, a number of changes occur to the actual nociceptors, or pain receptors. The receptors become both activated and sensitized. For example, when bradykinin is released, this will cause the neuron to fire, causing pain.
Sensitization of nociceptors occurs due to other inflammatory mediators, such as prostaglandin E2 (PGE2).  This results in the threshold for the nerve firing reducing. The result is that the nociceptors will activate with a much milder stimulus. It has been shown that both activation and sensitization result in a level of resistance to anesthetics (Rood et al. 1981).

Another thing that occurs in response to inflammation that might surprise you is nerve sprouting. Inflammatory mediators actually cause nerves to grow into the inflamed are and this has been shown to happen in human dental pulp (Byers et al. 1999). This simply means there are far more nociceptors to block and results in an increased receptive field. Check out work by Byers for some great microscope images showing the vast increase in nociceptors in inflamed rat pulps.

Inflammation also causes an increase in the production of proteins by nociceptors, such as substance P and calcitonin gene related peptide. These proteins play a role in the regulation of inflammation in the pulp, and may have some role to play in LA failure.
Another interesting concept relates to a specific type of sodium channel on neurons which is resistant to tetrodotoxin (TTX), funnily enough called the TTX-resistant sodium channel. These channels are less sensitive to lidocaine, about one quarter as sensitive as normal sodium channels and are present on human pulp nociceptors under normal conditions. Expose a nerve to PGE2, and their activity doubles (gold et al. 1996).  Therefore, this represents a mechanism whereby LA could fail. My thoughts are that the prostaglandin might only operate on these channels locally, and this theory might suffer from the same argument as the pH change theory, that is that it might only occur locally, so shouldn’t necessarily effect block anesthesia.

Central Nervous System (CNS) Sensitization may contribute to LA failure. When inflammation and pain occur for an extended period of time, this results in an increased excitability of the CNS. In basic terms this means that a lesser stimulus will result in a higher level of pain being experienced. Central sensitization is a blog post all by itself and as an endodontists, we are particularly careful of pain control in any patient who presents with a history of chronic pain. Hargreaves feels that the excited CNS may be responsible for otherwise innocuous stimulus presenting as anesthetic failure. For example, we may treat a patient who feels some minor discomfort but tolerates it for the procedure. In a patient who has been subject to central sensitisation, the discomfort may present as pain.

So there you go, and I hope this makes you feel a bit better the next time you can’t anaesthetize a “hot” pulp. It’s probably a bit more complicated than you previously thought, and it’s probably a bit less your fault than you previously felt. I’ll be discussing my methods for dealing with LA failure and inflamed pulps in a separate blog post.

BYERS MR, NARHI MVO. 1999. Dental injury models: Experimental tools for understanding neuro-inflammatory interactions and polymodal nociceptor functions. Crit Rev Oral Biol
Medical . 104–139.

BOU DAGHER F, YARED G, MACHTOU P. 1997. An evaluation of 2% lidocaine with different concentrations of epinephrine for inferior alveolar nerve block. J Endod. 23: 178–180.

COHEN HP, CHA BY, SPANGBERG LS. 1993. Endodontic anesthesia in mandibular molars: a clinical study. J Endod. 19: 370–373.
GOLD M, REICHLING D, SHUSTER M, LEVINE JD. 1996. Hyperalgesic agents increase a tetrodotoxin-resistant Na¹ current in nociceptors. Proc Nat Acad Sci: 93: 1108.

KENNETH M. HARGREAVES & KARL KEISER. 2002. Local anesthetic failure in endodontics:
Mechanisms and Management. Endodontic Topics 2002, 1, 26–39

KNOLL-KOHLER E, FORTSCH G. 1992. Pulpal anesthesia dependent on epinephrine dose in 2% lidocaine. Oral Surg Oral Med Oral Pathol. 73: 537–540.

NUSSTEIN J, READER A, NIST R, BECK M, MEYERS WJ. 1998. Anesthetic efficacy of the supplemental intraosseous injection of 2% lidocaine with 1: 100,000 epinephrine in irreversible pulpitis. J Endod. 24: 487–491.

PUNNIA-MOORTHY A. 1988. Buffering capacity of normal and inflamed tissues following the injection of local anesthetic solutions. Br J Anaesth. 6: 154–159.

ROOD JP, PATEROMICHELAKIS S. 1981. Inflammation and peripheral nerve sensitisation. Br J Oral Surg 19: 67–72.

VREELAND D, READER A, BECK M, MEYERS W, WEAVER J .1989. An evaluation of volumes and concentrations of lidocaine in human inferior alveolar nerve block. J Endod 1989: 15: 6–
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