Indirect view of palate where 4% articaine with 1:80,000 adrenaline was administered. Sloughing following vasoconstrictor induced ischemia is a more likely reason than the anesthetic per se
Of note also that with long maxillary teeth, e.g., some canines, failure to achieve anaesthesia may be due the fact that the anaesthetic has not been delivered sufficiently close enough to the apex of the tooth.
With many maxillary teeth, infection and inflammation are in the area where an injection would normally be made. Effectiveness of a local anaesthetic solution is pH dependant. For a local anaesthetic solution to work effectively, the pH should be closer to physiological levels. Infected tissues usually have a lower pH. Thus, if local anaesthesia is delivered to a site that is inflamed or infected, its effectiveness may be severely diminished. The use of block injections, particularly an infraorbital block, is often necessary in these events.
Ophthalmic complications of maxillary injections and inferior alveolar nerve block can occur. Most of the reported cases are from single injections and due to inadvertent intravascular injections. If these do occur, it is important to reassure the patient about the transient nature of the problem and cover the eye until the corneal reflex returns. The patient should be escorted home and not drive until vision returns completely to normal. Ophthalmic advice should be sought if symptoms persist for more than 6 hours.
3.4 Complications of Local Anaesthesia and Endodontic Treatment
3.4.1 Possible Mechanism of LA Nerve Injury
3.4.2 Damage to the IANB
Any damage to sensory nerve tissue may cause a mixture of anaesthesia (numbness), paraesthesia (altered sensation which is not painful), dysaesthesia (altered sensation which is uncomfortable/painful) and neuropathic pain. Neuropathy in the orofacial region must be taken seriously and the cause established, as there are some serious conditions that need to be eliminated if a cause is not obvious . Often there is a history that helps determine the origin. Sensory deficits should be mapped on the face so that an estimate can be made of resolution or expansion of the deficit. Any patient with an expanding area of paraesthesia for which a cause has not been established should be referred for specialist evaluation. Amongst other things, paraesthesia can result from trauma, nerve injury, surgery, infections and prolonged reactions to local anaesthesia, viruses, malignancy or serious pathoses. If a dental cause is suspected, patients require reassurance, careful documentation and follow-up.
Unilateral paraesthesia and facial paralysis can occur in a misdirected block where local anaesthetic solution is deposited in the parotid gland. It usually occurs when the depth of needle penetration is nearly to the hub of a long needle. It is more likely to happen when the ramus of the mandible is flared laterally making it difficult for the operator to ‘hit the bone’. The unilateral paralysis of facial muscles is reversible. This resolves over hours. The patient needs to be reassured, and the eye has to be protected until the blink reflex returns, as corneal reflex is often lost.
184.108.40.206 Neurological Injuries Resulting from Untreated Periapical Infections
It is not uncommon in endodontic practice to encounter patients with apical periodontitis of endodontic origin leading to sensory impairment of the inferior alveolar or mental nerve. This invariably resolves with the reduction in inflammation and local swelling. A number of authors have reviewed and documented clinical cases of neurological disorder with paraesthesia and hypaesthesia of the mental nerve resulting as a sequel of apical periodontitis of a mandibular second premolar and second molar teeth [40–42].
220.127.116.11 Motor Nerve Palsy Due to Endodontic Treatment
18.104.22.168 Paraesthesia and Pain Associated with Endodontically Related Nerve Injuries
Endodontic treatment of premolar and mandibular teeth has the potential to damage the inferior alveolar nerve via direct trauma, pressure or neurotoxicity. Trigeminal nerve injury is the most problematic consequence of dental surgical procedures with major medicolegal implications . While incidence of lingual nerve injury has remained static over many years, the incidence of inferior alveolar nerve injury has increased; the latter likely being due to implant surgery and endodontic therapy .
Persistence of any peripheral sensory nerve injury depends on the mechanisms, the severity of the injury, the increased age of the patient, the time elapsed since the injury and the proximity of the injury to the cell body (the more proximal lesions are having a worse prognosis). Most sensory nerve injuries related to dentistry are permanent. LA-induced nerve injuries have nearly 80% likelihood of recovery. Many authors recommend referral of injuries before 4 months , but this may be too late for many endodontically related peripheral sensory nerve injuries. Inferior alveolar nerve injuries related to endodontic treatment, particularly where there is extrusion of filling material, require immediate attention with permanency likely after 24–30 h . After 3 months, permanent central and peripheral changes occur within the nervous system subsequent to such injury, and they are unlikely to respond to surgical intervention .
The IAN is at risk from a variety of endodontic procedures. The IAN is contained within a bony canal, predisposing it to ischemia, trauma and subsequent injury in relation to dental procedures. This may explain the higher incidence of permanent damage for inferior alveolar nerve injuries compared with lingual nerve injuries . Inferior alveolar nerve injury during endodontic treatment can result from local anaesthetic accidents, from irrigant extrusion and from over instrumentation or overfilling, in all cases resulting in one or a combination of mechanical injury, haemorrhagic, ischaemic or chemical injury to the nerve.
There are relatively few detailed reports on nerve injuries resulting from endodontic treatment . The largest series of endodontic-related trigeminal nerve injuries included 61 patients reviewed over an 8-year period , with most of these patients presenting with persistent pain. There are relatively few reports of persistent pain subsequent to endodontic procedures . In a recent study of 216 patients with trigeminal nerve injuries related to dentistry, 70% are reported to have chronic neuropathic post-traumatic pain .
Neuropathic pain (NP) syndromes are chronic pain disorders that develop after a lesion involving the peripheral or central nervous structures that are normally involved in signalling pain. The characteristics of NP differ substantially from those of other chronic pain states, i.e. chronic nociceptive pain, which develops while the nervous system that is involved in pain processing is intact. Apart from the existence of negative somatosensory signs (deficit in function), there are other features that are characteristic of neuropathic conditions (allodynia, hyperalgesia and hyperpathia) . Paraesthesia is typically described by patients as bothersome but not painful. Furthermore, NP states require different therapeutic approaches such as anticonvulsants, which are not effective in nociceptive pain .
Thus symptoms experienced by patients with post-traumatic neuropathy of the trigeminal nerve can range from next to no symptoms, such as minimal anaesthesia in a small area to devastating effects on the patient’s quality of life .
22.214.171.124 Local Anaesthesia-Related Neuropathy During Endo Procedures
As stated earlier, local anaesthesia is often complex in endodontics as the patients often experience difficulty in achieving analgesia. Patients undergoing endodontic treatment often have multiple injections and may be more at risk of local anaesthetic-related nerve injuries . More recently the incidence of nerve injury in relation to IANBs has been calculated as 1:609,000 but with a reported increase in injury rate when 4% anaesthetic agents are used . These LA injuries are associated with a 34–70% incidence of neuropathic pain, which is lower when compared with endodontic-related nerve injuries. Recovery is reported to take place at 8 weeks for 85–94% of cases .
LA injuries may have a better prognosis than nerve injuries resulting from endodontic treatment. In both cases, the nerve injury may be physical (compression due to epineural or perineural haemorrhage or extruded material) or chemical (haemorrhage or local anaesthetic or endodontic compound contents). There may be elements of direct mechanical trauma, which generally would be worse in endodontically caused nerve injuries.
Intraoperatively all clinicians should document unusual patient reactions occurring during application of local analgesic blocks (such as sharp pain or an electrical shock-like sensation), and multiple blocks should be avoided if possible as they may also increase the risk of local anaesthetic-related nerve injuries.
3.4.3 Assessment of Trigeminal Nerve Injuries
The emphasis in trigeminal neuro-functional studies has been on using conventional mechanical tests, which are subjective. Due to the variability in methodology and reporting, they are of limited value for inter-study comparisons and little clinical significance in relation to a patient’s pain and functionality. Recently several investigators have recommended the use of the patient’s report alone , in combination with subjective and objective neurosensory tests  or utilising quality of life questionnaires (OHIP 14–31) for a more holistic approach for the assessment of patients with trigeminal nerve injury . In this way hopefully to make studies easier to compare.
3.4.4 Management of Neuropathy Related to Endodontics
Differentiation between the possible causes of nerve injury, whether it is of local anaesthetic, periapical inflammation  or endodontically origin, is difficult. An accurate diagnosis is dependent on a thorough history and specific identification of the neuropathic area distribution. On occasions the use of adjunctive antibiotics or NSAIDS and paracetamol may enable the clinician to exclude inflammatory or infection-related pain as against post-traumatic NP.
Steroids: Step-down 5-day course of prednisolone, oral 50 mg, 40 mg, 30 mg, 20 mg and10 mg for 5 days
NSAIDs: Ibuprofen oral 400–600 mg 6 hourly
Vitamin B complex
Patients who report severe electric-like pain (though it is not a definite sign) following the administration of an IANB should be followed up . What is important, however, is to inform all patients of the risks of problems that may result from IANB, however slight the risk, beforehand and do everything in your power to minimise the risks. Such as minimising repeat blocks and using supplementary techniques.
Block anaesthesia: Consider first whether block anaesthesia is really required. By avoiding IANBs there is less risk of injury to the lingual and inferior alveolar nerves, which though rare, is debilitating to the patients and has no cure. Infiltrations provide more localised and shorter lasting anaesthesia which is of benefit to the patients. This technique requires less skill and less discomfort for the patient during the injection and avoids unnecessary lingual anaesthesia after dental treatment. Recent studies [9, 59–62] have suggested that infiltration of 4% articaine in the mandibular molar region can result in anaesthesia of the lower first molar that is in most cases as effective as an inferior dental block.
Concentration of LA: Any increased concentration of any agent leads to increased neural neurotoxicity .
Volume of LA: There is no evidence to support the suggestion that increased volumes of solution result in more nerve damage, but as all chemicals are neurotoxic, it is dependent upon the proximity to the nerve, concentration, neural damage and additional volumes that add to potential neurotoxicity.
Multiple injections: Second or subsequent injections that impede directly on or in neural tissue may not be associated with the usual ‘funny bone’ neuralgic pain. Thus the patient does not self-protect as effectively possibly rendering the nerves more at risk of direct damage. Alternatives to block injections may be indicated.
Type of LA agent: Bupivacaine is the most neurotoxic of all LA agents.
Type of vasoconstrictor: The role of vasoconstrictor in nerve damage is unknown.
Sedated or anaesthetised patients: There is no evidence to support unresponsive patients are prone to nerve injury as they are less likely to protect themselves when the IDB needle encroaches too close to the nerve.
Lack of LA aspiration: There is no evidence to support that aspiration during an IANB results in lower persistent neuropathies though it is always advisable.
Patient factors: Patient factors include age (>50 years of age), migraines, patients with existing neuropathic pain conditions (fibromyalgia) and those predisposed to developing peripheral neuropathy.
Escoda-Francoli et al.  described a case of endodontic treatment of a permanent right mandibular first molar in which the sealer cement overextended in large amounts and damaged the right inferior alveolar nerve. The condition reverted a few months after the surgical removal of the material. There are several reports of nerve injury in relation to over instrumentation and overfilling [67, 68]. Endodontic retreatment for inferior alveolar nerve injury was also reported by Yatsuhashi et al. . Gatot and Tovi  recommended steroid therapy for early postoperative neuritis. More recently Grotz et al.  described the management of 11 patients with endodontic-associated neuropathy. They similarly reported that the neurological findings were dominated by hypaesthesia and dysaesthesia with 50% of patients reporting pain. Initial X-rays showed root filling material in the area of the mandibular canal. Nine cases were treated with apicectomy and decompression of the nerve; in two cases, extraction of the tooth was necessary. Only one patient reported persistent pain after surgery. Both Scolozzi et al.  and Brkic et al.  describe a limited series of patients successfully treated with surgical decompression (removal of material within the canal or apicecting the tooth) resulting in resolution of the endodontically related nerve injury. As stated earlier, patients must be assessed on a case-by-case basis, but immediate surgical exploration and débridement may provide satisfactory results.
If the neuropathy is longer standing and the patient has chronic pain, then post-traumatic neuropathy must be diagnosed and appropriate treatment prescribed. Most patients accept a full explanation and reassurance for their symptoms. Many patients can find the explanation for their neuropathic pain symptoms very helpful. Antibiotics may be prescribed to exclude apical infection. NSAIDs and paracetamol will also exclude inflammatory pain, but neuropathic pain due to post-traumatic nerve injury will not respond to these medications.
Oshima et al.  reported that 16 patients of 271 patients presenting with chronic orofacial pain were diagnosed with chronic neuropathic tooth pain subsequent to endodontic retreatment. Most of these patients were treated for maxillary teeth, and 70% of the patients responded to tricyclic antidepressant therapy which highlights the importance of establishing whether the patient has neuropathic pain to start with. A recent Cochrane review highlights the lack of robust evidence in managing trigeminal nerve injuries . Recommendations for treatment of trigeminal neuropathic pain are also well described by Truelove .