No hard feelings
When administering an IDB, the needle should be advanced slowly. If bone is contacted too firmly, a microscopic barb can be created at the end of the needle that then tears the tissue as the needle is withdrawn.
Patients taking warfarin are at particular risk of haematomas. There is anecdotal evidence of airway compromise as a result of massive deep haematomas in such patients.
In 2005, Brewer wrote an article on this subject and indicated that local anaesthesia was a procedure that required no check of INR prior to its administration. He made no distinction between infiltration and block anaesthesia. However, Perry and colleagues in 2007 described both infiltration and block anaesthesia as potentially invasive along with treatments such as extraction. They advised an INR check of less than 3.0 before performing an IDB and advised that the IDB be given cautiously with an aspirating syringe.
The latest poster guidance from the National Patient Safety Agency (2009) gives a list of treatments where the INR does not need to be checked and a list of treatments where it should be checked as less than 4.0 within 72 hours beforehand. Local anaesthesia is on neither list! However, on the poster’s flow chart, there are recommendations that for those treatments where the INR needs to be checked, the local anaesthetic used should contain a vasoconstrictor; that, where possible, an infiltration, intraligamentary or mental block should be given and an IDB should only be given if there is no alternative and should be administered slowly using an aspirating technique.
This all leaves me unsure as to whether routine restorative dentistry under IDB anaesthesia does or does not require a pre-op check of the INR. Could someone reading this article please advise?
Given that roughly five to 7.5 cartridges of the commonly available dental local anaesthetic agents can be given safely to a healthy adult, overdose by this mechanism should be very rare indeed. Care should be taken in patients with chronic cardiac, renal or hepatic disease and in children where the maximum doses should be halved.
Systemic toxicity is much more likely to occur as a result of a rapid intravenous/intravascular injection, especially of a local anaesthetic containing adrenaline. The patient tends to turn very pale, feels anxious and nauseous and is aware of an unpleasant tachycardia. This can be a stressful experience for both the dentist and the patient. It is important that the patient is not labelled ‘allergic’ to local anaesthetic as a result of an intravascular injection. Prevention of this problem should be possible by using an aspirating syringe, advancing the needle through the tissues slowly and by injecting slowly. My experience is that the Astra aspirating syringe used with the so-called self-aspirating anaesthetic cartridges is the best aspirating system. Forced into an alternative when there was an acute shortage of local anaesthetic a few years ago, I have found that the genuine Aspiject syringe used with conventional cartridges is also very good. I find other ‘own-brand’ copies of this syringe are unreliable in my hands.
If a positive aspirate does occur (and it is usually but not exclusively with an IDB), then it is clearly necessary to move the tip of the needle until aspiration is negative before injecting. Sometimes the vessel moves with the needle initially and so it may be necessary to move the needle a fair distance before aspiration is negative. Repeated positive aspirates result in a band of pink solution at the top of the cartridge, which can then make it impossible to decide on whether the ensuing aspirates are positive or negative. In this situation, it may be necessary to switch to a new cartridge and start again, especially if treating a medically compromised patient.
Unfortunately, it is possible to get a false negative aspirate and produce an overdose reaction despite good technique. This is probably because the lumen of the needle is apposed to the wall of the vessel. For this reason, and given that dentistry is hard enough without unexpected medical emergencies, I now routinely use a non-adrenaline containing local anaesthetic agent for my IDBs. Until I could no longer get supplies of it, I used ‘Citanest’ with felypressin. Now I use 3 per cent plain mepivacaine (‘Scandonest’). This has a low pKa, which should theoretically facilitate entry into nerve cells, and the lack of vasoconstrictor should result in a more rapid resolution of lip and tongue numbness, especially useful in children. I have never experienced any problems associated with inadequate duration of anaesthesia of this agent. Inadvertent intravascular injection of this agent appears to give no problems other than failure of anaesthesia.
Consideration should be given to avoiding an adrenaline-containing local anaesthetic on patients with unstable angina, uncontrolled arrhythmias or a recent (less than one month) history of myocardial infarction.
These almost always occur at the higher end of the maximum allowable local anaesthetic doses and there is unlikely to be a problem as long as no more than two cartridges are used.
It has recently been recommended that a drug history be taken at the beginning of each patient visit.
At the doses used in dentistry, it is unlikely that the local anaesthetic agent itself will cause a drug interaction. Rather, it is the adrenaline component that has to be considered. (There is no documentation of felypressin interacting with other drugs). Additionally, systemic absorption of adrenaline and thus a drug interaction is very limited unless an intravascular injection occurs.
Cognisance is required if a patient is taking one of the following: non-selective beta-blockers – e.g. propranolol, sotalol, nadolol (can cause unchecked alpha effects including life-threatening rise in blood pressure); non-potassium sparing diuretics – e.g. furosemide, bendroflumethiazide (can cause hypokalaemia and arrhythmias); tricyclic antidepressants – e.g. amitriptyline, imipramine (can cause adrenaline toxicity); atomoxetine used to treat ADHD (similar risks to tricyclics); dopaminergics – e.g. entacapone (can cause adrenaline toxicity); serotonin and noradrenaline reuptake inhibitors – e.g. duloxetine, venlafaxine and phenothiazines – e.g. chlorpromazine (may produce severe prolonged hypotension or hypertension). An adrenaline-containing local anaesthetic should not be used in a patient who has taken a drug with sympathomimetic properties – e.g. cocaine, cannabis, amphetamines within the last 24 hours.
A recent article in Dental Update shows that this is more than a theoretical consideration even in the modern era of disposable needles. Fracture usually occurs at the hub of a narrow/30 gauge needle. Prevention of this problem includes making sure the injection is administered painlessly so that there is no risk of sudden patient movement. One should avoid repeated use of the same needle; avoid pre-bending the needle; always withdraw a needle along its long axis; only move a needle medially or laterally within the tissue if its tip is just below the surface and never insert a needle right up to its hub. This suggests that a short needle should not be used for an IDB. A haemostat should always be handy at the chairside just in case a needle ever fractures.
Allergy to modern amide dental local anaesthetic agents is extremely rare. The most likely allergen is the metabisulphite antioxidant preservative agent, which is only required in vasoconstrictor-containing anaesthetics. Thus, in an emergency, a plain local anaesthetic can be given.
Many patients who say they are allergic to local anaesthetic give a history that suggests a previous intravascular injection. Past reports to the CSM suggestive of genuine allergy have included facial swelling, breathlessness and skin rash. Patients giving this sort of history should be referred for patch testing or equivalent. For patients who are latex allergic, it is now possible to get latex-free local anaesthetic cartridges (e.g. Septanest and Citanest).
Some patients appear to be supersensitive to the adrenaline component of dental local anaesthetics and experience prolonged tachycardia in response to these drugs even when there has been no apparent intravascular injection. A plain local anaesthetic should be used in such patients.
This is less common than an intravenous injection and can usually be avoided by moving the needle if undue resistance to injection is felt and by injecting slowly. Intra-arterial injection may produce discomfort and a localised area of skin blanching. In its more extreme form, it may cause visual disturbances, hearing disturbances and hemiparesis of the body.
An adrenaline-containing local anaesthetic should not be used on a patient who has received head and neck radiotherapy due to the risk of osteoradionecrosis.
Recently it has been suggested that an adrenaline-containing local anaesthetic should not be used by the intra-ligamentary route in a patient who has received bisphosphonates. The latest Greater Glasgow and Clyde bisphosphonate protocol does not make mention of this, although this is a rapidly evolving area.
Prolonged impairment of sensation
This is more likely to affect the lingual nerve than the inferior alveolar nerve possibly due to structural differences between the two. I am not aware of other branches of the trigeminal nerve being disrupted by dental local anaesthetics (e.g. mental nerve).
Prolonged impairment of sensation is more likely the more concentrated the anaesthetic agent. Thus, the risk is about one in 1.2 million injections for two per cent and three per cent solutions and one in 400,000 injections for four per cent solutions. As articaine is supplied as a four per cent solution, and as there is no evidence that articaine is superior to other solutions when it comes to block injections, articaine should not be used for an IDB.
Aside from neurotoxicity of the anaesthetic agent, nerve damage can also arise from direct needle trauma. If significant resistance is felt during injection, the needle should be moved until normal resistance is felt. Similarly, if a patient feels an ‘electric shock’ sensation during an injection, the needle should be moved slightly before continuing. A note should be made of this occurrence in the clinical records. Having said that, only 15 per cent of patients who experience an electric shock sensation subsequently suffer prolonged impairment and 57 per cent of patients suffering from prolonged impairment had no ‘electric shock’. About 80 per cent of cases of prolonged impairment of sensation resolve within two weeks and almost all resolve within eight weeks. Impairment beyond eight weeks is likely to be permanent.
It has been estimated that every dentist, during a career, will have at least one patient who experiences permanent nerve damage following an IDB and that there is no way to prevent it happening or to treat it if it does.
The reader is referred to other texts for this important issue. Written protocols are essential and consideration should be given to needle guards, Ultra Safety Plus syringes and the dentist having sole responsibility for assembling and dismantling the syringe.
An adrenaline-containing local anaesthetic should not be used on a patient with unstable angina, an uncontrolled arrhythmia or with a history of a myocardial infarction within the last month.
The gold standard for record keeping as it relates to use of local anaesthetic should include the following:
- Site/ sites of injections
- Type of injection – infiltration/block etc
- Agent used and concentration
- Quantity used – ml or number/concentration of cartridge(s).
- Record any difficulties and how they were managed
- Record if local anaesthetic not used
When referring a patient to a hygienist, a clear prescription should be provided for any local anaesthetic to be used and this should be signed by the dentist.
The author would like to thank Lesley Smith for her advice on bisphosphonates and Andrew Hadden for his help with medicolegal considerations.
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