Management of acute emergencies and traumatic dental injuries

Principles of management of pain

The most fulfilling aspect of endodontic treatment is the opportunity to care for the patient in pain. Acute dental pain is notoriously difficult to cope with for most patients, particularly that of pulpal origin. They will arrive in a distressed state, being anxious and irritable having had disturbed sleep, eating patterns. Their psychological demeanor may be defensive, aggressive, blaming or even dulled through fatigue and dosing on medication.

Successful management of pain is:

1. preceded by sharp diagnostic and psychological insight complemented by a confident manner

2. accompanied by effective and efficient treatment execution, including adequate anaesthesia and analgesia

3. succeeded (hopefully) by patient gratitude and loyalty; and a personally enhanced reputation for the dentist.

For effective practice development, there is no greater pathway than caring for patients in acute pain. The investment required is a moral, human, compassionate, patient and confident approach, coupled with understanding of the biology of the problem, as well as insight about pharmacological armamentaria.

The majority of patients attending the dentist in pain suffer from the acute consequences of pulpal or periradicular disease (Table 10.1), but the dentist must beware of confounding factors.

Table 10.1

Prevalence of acute orofacial or dental pain

Population	Prevalence of acute orofacial or dental pain	Comments
USA (National Health Interview Survey, 1989)	14% (acute orofacial pain in the past 6 months)	Most common causes: caries & periodontal disease
UK (Adult Dental Health Survey, 2009)	26% (dental pain)	Most cases were associated with gross caries & sepsis
Toronto, Canada (Locker & Grushka, 1987)	29% (teeth with cold/hot); 14% (toothache) in the past 4 weeks	50% of cases reported severe symptoms
Sao Paulo, Brazil (age 12, 15 adolescents) (2010)	26% (dental pain)	Most cases were associated with untreated caries or endodontic treatment need
Hong Kong, China (1222 18+ Chinese speaking people in 2006)	28% (tooth sensitivity); 13% (toothache)

The clinician’s aim in providing emergency care is to control the infection and inflammation by removing the cause of the problem. However, the response to the underlying injury will endure for the period of time it takes for the triggered biological mechanisms to switch off. During this latent period, pharmacological means may be intelligently employed to help control the lingering pain until the unpleasant experience subsides naturally through innate physiological mechanisms. There are strong psychological elements to pain control as evidenced by placebo effects, hence, a biologically robust strategy, accompanied by effective surgical execution and a firm, confident manner is paramount.

Diagnostic accuracy

Patients presenting in a dental practice suffering from orofacial pain must be viewed from a broad diagnostic perspective. The cognitive and material tools possessed by dentists naturally sway their management towards dental intervention but non-dental factors can mimic dental pain too. This is due in part to convergence of peripheral neural pathways in the central nervous system and in part to the patients’ inability to articulate their experience in a meaningful way to the dentist. Dentists should therefore be aware of the common causes of misdiagnosis. These include non-odontogenic inflammation, vascular, musculoskeletal, neurological, and systemic or psychogenic problems (see Chapter 16). Temporomandibular joint (TMJ) and muscular pain from the masseter, lateral pterygoid and temporalis muscles may refer pain to the maxillary or mandibular molars, premolars or even anterior teeth on occasion. Such a condition may be more appropriately managed with reassurance, explanation, reduction in muscle and joint load, stretching exercises, heat/cold therapy and lastly, the use of an occlusal acrylic splint may help (Figs 10.1, 10.2).

Fig. 10.1 Splint therapy for TMJ dysfunction

Fig. 10.2 Palatal view of occlusal splint

It is also worth bearing in mind that patients who have been suffering long-standing pain may have a reduced threshold of pain perception as a result of central or peripheral sensitization. The zone of sensitization may be restricted close to the origin of the problem or expanded to various distances from it. It is worth, therefore, exploring and mapping zones of hyperalgesia (heightened response to noxious stimuli) and allodynia (heightened response to non-noxious stimuli), lest detected local tenderness is in fact part of this phenomenon. Sensitization may be evident in patients with a history of chronic pain, TMJ dysfunction, fibromyalgia and whiplash injury.

Effective intraoperative pain control

Local analgesic agents and their actions

Difficulties can often be encountered in trying to secure analgesia in irreversibly inflamed pulps or where there is acute infection. Failure of analgesia may be operator dependent (poor technique, choice of technique and/or solution) or patient dependent (anatomical, pathological or psychological).

The most commonly used analgesic solution for most endodontic procedures is lignocaine with adrenaline (epinephrine) (Fig. 10.3). Providing the analgesic solution is given slowly with an aspirating technique, then the adrenaline (epinephrine) is not a problem in most patients.

Fig. 10.3 Xylocaine

The success rate for inferior alveolar block injections is over 90%. A practitioner who regularly fails with this method should reassess their technique. Although, it is generally considered that the sign of a successful block is a numb lip, all that this indicates is that the nerves to the soft tissues of the lip have been blocked; it does not necessarily infer pulpal analgesia. The presence of infection and inflammation can reduce the efficacy of analgesic solutions. In solution, the local analgesic exists in two ionic forms, an uncharged anion (RN) and a positively charged cation (RNH⁺). Both forms of the solution are required for analgesia.

RNH⁺ RN + H⁺

Inflammation lowers the tissue pH and, correspondingly, the amount of the base form of the analgesic available to penetrate the nerve membrane. Consequently, there is less of the ionized form within the nerve to achieve analgesia. In addition, nerves arising in inflamed tissue have altered resting potentials and decreased excitability thresholds. These changes are not restricted to the inflamed pulp but affect the entire neural membrane.

Articaine with adrenaline (epinephrine) (Fig. 10.4) has gained favour as a local analgesic solution to use where lignocaine appears to have failed. Articaine differs from lignocaine as it has a thiophene ring as its lipophilic component rather than a substituted aromatic ring. Studies show that it is no more effective as an analgesic agent than lignocaine. However, it does have an increased propensity to diffuse widely, which may allow it to block accessory innervations over a broader field. In addition, the different stereochemical structure may also account for its apparently higher success rate. Unfortunately, it is also associated with a higher frequency of persistent paraesthesia.

Fig. 10.4 Articaine

The use of long-acting anaesthetics may provide the patient pain relief while the postoperative analgesics start to act. Marcaine (0.5% bupivacaine with 1 : 200 000 epinephrine) when used as a regional block can give soft-tissue anaesthesia of 6–8 hours. Marcaine is not available in all countries in dental anaesthetic cartridges and, in some areas, is not licensed for dental use. Dental practitioners should satisfy themselves as to the local rules before administering it. Other preparations of bupivacaine are available, such as carbostesin (Fig. 10.5).

Fig. 10.5 Carbostesin

Local analgesic agent delivery

If an inferior alveolar block fails and a repeat attempt also fails, then an alternative technique should be considered. The Gow–Gates and the Akinosi techniques both attempt to anaesthetize the inferior alveolar nerve at a higher level. Both these methods are best reserved for cases where the conventional block fails as they can produce more complications than the standard approach – the higher the needle, the closer it is to the maxillary artery and the pterygoid plexus.

Gow–Gates technique

This is a true mandibular block injection that provides analgesia of all the sensory divisions of the mandibular nerve, including buccal, inferior alveolar, lingual and mylohyoid. The method relies upon the deposition of analgesic solution adjacent to the head of the mandibular condyle (Fig. 10.6). The patient has the mouth wide open and a line is imagined from the corner of the mouth to the intertragic notch; this is the plane of approach. The needle is introduced from the direction of the contralateral mandibular canine tooth and directed over the ipsilateral maxillary second molar (Fig. 10.7). The point of mucosal penetration is higher than for a conventional inferior dental block. The needle is advanced until bony contact is made with the head of the condyle, withdrawn slightly, aspiration performed, and a full cartridge of analgesic is delivered.

Fig. 10.6 Position of deposition of local anaesthetic solution for Gow–Gates technique for inferior dental block

Fig. 10.7 Gow–Gates technique for inferior dental block

Akinosi technique

This is a simpler technique than the Gow–Gates method and is sometimes known as the closed-mouth technique. The patient has the mouth closed and a 35 mm needle is used. The syringe is advanced parallel to the maxillary occlusal plane at the level of the maxillary mucogingival junction. The needle is advanced until the hub is level with the distal surface of the maxillary second molar (Fig. 10.8). At this point, a cartridge of analgesic solution is deposited. This technique does not rely on touching bone and this can be a disadvantage. However, the Akinosi technique allows provision of analgesia in a situation where all other methods of giving an inferior dental block would fail. Both motor and sensory analgesia are achieved allowing the patient to open the mouth.

Fig. 10.8 Akinosi technique for inferior dental block

Intraligamental injections

Intraligamental injections are used to deposit analgesic directly into the periodontal ligament space and a number of specialized syringes (Fig. 10.9) and small needles have been developed to facilitate this. The needle is inserted into the mesial gingival sulcus and in contact with the tooth (Fig. 10.10). The needle is supported by fingers and positioned with maximal penetration between the root and crestal alveolar bone. Pressure is slowly applied to the syringe handle for 20–30 seconds. Backpressure has to be developed for this technique to work and blanching of the soft tissues would be a sign of probable success. If analgesic solution flows readily out of the sulcus then analgesia will not be achieved. Pressure is necessary to force the solution into the marrow spaces to contact and block the dental nerves. The technique should be repeated on the distal and lingual surfaces of the involved tooth.

Fig. 10.9 Peripress for intraligamental injections

Fig. 10.10 Needle insertion for intraligamental injection

Effective postoperative pain control

Following the option of long-acting local anaesthetics, the next option is the use of systemically administered centrally or peripherally acting analgesics. A medical history needs to be taken to rule out possible drug hypersensitivity. Dental pain is generally of short duration with analgesics only being taken for 24–48 hours and it is unlikely, therefore, that unwanted effects would occur.

The relative efficacy of different analgesics is provided by the Oxford league table (Table 10.2). Aspirin is widely used. However, its efficacy is dose related, 1000–1200 mg four times per day providing greater analgesia than 500–600 mg four times per day. Non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, can also be used. Ibuprofen has been shown to be one of the most effective analgesics at reducing acute pain and its efficacy is also dose related; 400 mg four times per day appears to be the optimal dose but up to 800 mg delivers 100% efficacy, if there are no side effects. Paracetamol is often used by patients with sensitivity to aspirin and the other NSAIDs and can be efficacious in high dosage, but it does not have the same anti-inflammatory properties.

Table 10.2

The 2007 Oxford league table of analgesic efficacy

(www.jr2.ox.ac.uk/bandolier/booth/painpag/)

^*Numbers needed to treat (NNT) are calculated for the proportion of patients with at least 50% pain relief over 4–6 hours compared with placebo in randomized, double-blind, single-dose studies in patients with moderate to severe pain. Drugs were oral, unless specified, and doses are milligrams.

Peripherally acting analgesics are often provided in combination with a centrally acting analgesic, such as codeine. Evidence suggests that combined analgesics are more effective than the individual constituents alone.

Severe pain may be treated by the use of a NSAID and paracetamol in tandem. An initial dose of the NSAID can be given with paracetamol being taken 2–3 hours later. The NSAID can again be given 2 hours following this. The obvious risks are patients not understanding the drug regimen or using a proprietary analgesic with both an NSAID and paracetamol, and therefore possibly overdosing on the paracetamol.

Analgesics have been shown to be more beneficial if they are taken before severe pain occurs. Patients should be advised that the analgesics should be taken if they feel the onset of pain and possibly to continue with a regular dose after the pain has subsided for a period of time.

The mechanism of action of NSAID-like drugs is through the inhibition of cyclo-oxygenase, of which there are two types, COX₁ and COX₂. The former are constitutive and are present in stomach, kidneys and platelets; they are inhibited by the traditional NSAIDs. The latter are inducible and are synthesized in inflamed tissues. Side effects include cardiovascular or gastrointestinal problems. COX₂ inhibitors should have fewer side effects, such as gastrointestinal of kidney problems.

Contraindications for aspirin include ulcers, asthma, diabetes, gout, influenza (Reye’s syndrome) and liver dysfunction. It is well to remember the possibility of drug interactions of NSAID-like drugs, which include: reduction of anti-high blood pressure effectiveness with ACE inhibitors, beta blockers, thiazide and loop diuretics; increased nephrotoxicity with cyclosporins; increased serum concentrations with hydantins and lithium; increased toxicity with methotrexate, increased blood pressure with sympathomimetics; and increased prothrombin time with anticoagulants.

Emergency scenarios

Endodontic emergencies may be divided by temporal association into preoperative, intraoperative and postoperative events, although the boundaries of this classification are not sacrosanct. Preoperative pain often predicts intraoperative and postoperative pain but other factors may also be involved.

Preoperative emergencies

Patients fall into two broad categories, those who are part of the practice and under regular or irregular review and those who have never attended the practice before and merely seek resolution of an urgent problem. The former group of patients will have available details of dental status and previous treatment, albeit with their recent history requiring updating; whereas the latter group requires a thorough investigation to determine the nature of the problem, as well as the level and type of service appropriate for their needs.

Inevitably, patients arrive seeking emergency treatment at a time inconvenient to the busy practitioner. However, it is essential that time is made to reach a proper diagnosis. Apart from the patient often not being able to locate the specific tooth causing the problem, there are a number of pathological entities that will mimic pain of odontogenic origin and, in these cases, endodontic procedures are obviously not indicated.

Identifiable endodontic emergencies fall into the following categories:

• pain of pulpal origin

• emergencies of periradicular origin

• emergencies resulting from traumatic injuries.

Emergencies of pulpal origin

Diagnosis

The innervation of the dental pulp consists of myelinated Aδ fibres and unmyelinated C fibres, which give rise to distinct types of pain sensations as discussed in Chapter 4. Pulpal pain is typically stimulated by hot or cold stimuli, however, it is important to be clear whether the pain has the sharp quality attributable to Aδ fibre stimulation or the dull aching, throbbing quality associated with pulpitis and C fibres. Many dentists confuse localizable dentine sensitivity with the unlocalizable pain of pulpal origin. Identification of the tooth is not helped by the perception of the patient, as to which tooth is the culprit; even dentists with toothache get it wrong. Pulpal pain only becomes localizable when the inflammation is advanced enough to involve the periapical tissues and the tooth becomes tender to touch or tap.

The dentist should seek all historical, clinical and radiographic clues to identify the cause. Sometimes, this will be obvious, such as secondary caries or crack (Figs 10.13, 10.14a) and, at other times, the patient may present with a quadrant of teeth with deep restorations (Fig. 10.15), all posing as potential candidates. It is not unheard of that, under such circumstances, several teeth end up with pulp extirpations. It is important to differentiate the causative tooth by using a combination of pulpal stimulation (uncomfortable as that may be) and selective, diagnostic local anaesthesia. There is no local anaesthetic technique that can be completely confined to one tooth but intraligamental anaesthesia affords a close possibility. The principle is to choose the most likely candidate but to anaesthetize from the mesial to distal and maxillary to mandibular. When the pain is abolished, the tooth is identified; effectiveness of anaesthesia may be tested by pulp testing.

Fig. 10.13 Irreversible pulpitis in mandibular first molar showing a widened periodontal ligament space around both apices

Fig. 10.14 (a) Vertical unrestorable fracture in maxillary molar (arrowed); (b) maxillary molar following extraction; (c) maxillary molar with separated fractured segment

Fig. 10.15 Teeth with deep restorations

The distinction between reversible and irreversible pulpitis is not clear-cut. In both cases, there may be pain stimulated by hot, cold or sweet stimuli, lingering for various periods of time as a dull ache, sometimes arising spontaneously and sometimes keeping the patient awake at night. At times, the pain may be so severe that the patient will find it intolerable, described as the worst imaginable pain and likened to being stabbed in the jaw with a red-hot poker or knife. The longer the episodes of lingering pain, the more spontaneous the episodes, the greater the frequency of sleep loss, the more severe the pain, the greater the response to hot rather than cold (indeed sometimes cold may relieve), the more likely it is that the pain will be judged irreversible. Indeed, severe pulpal pain of the sort described may sometimes be associated with a relatively normal pulp (Seltzer et al., 1963; Dummer et al., 1980). In the case shown, placement of cast onlays resulted in pain characteristic of irreversible pulpitis, however, the patient was able to tolerate the pain and in time, the pain resolved. Many years on, the teeth respond normally to pulp tests and remain free of apical disease (Fig. 10.16). Patients unable to tolerate the pain would opt to have the pulps extirpated, therefore, the correct term for the diagnosis is pulpalgia rather than pulpitis.

Fig. 10.16 (a) Symptoms consistent with irreversible pulpitis were triggered following placement of cast onlays on the mandibular molars; (b) symptoms resolved spontaneously after 2–3 months, whilst the teeth continued to respond normally to pulp tests, remaining free of apical disease many years afterwards

Cracked tooth syndrome (CTS) may also result in pulpitis and the crack may need additional management by placement of an orthodontic band to prevent cuspal flexure and catastrophic fracture. The degree of pain may vary considerably, from momentary pain on encountering heat and cold to spontaneous pain or pain on biting. The pain on biting will have a sharp quality, while the pain on hot and cold may vary from sharp to a dull aching quality. A fibreoptic light may be useful in locating and determining the extent of the cracks (Fig. 10.17) but they are not always visible in the early stages of CTS.

Fig. 10.17 Use of fibreoptic light to illustrate the extent of an incomplete fracture (courtesy of Dr CC Youngson, Liverpool Dental Institute)

Treatment

If it is judged that the pain is due to reversible pulpitis, treatment involves removing the source of dentinal or pulpal irritation. In the case of sensitive dentine, patent dentinal tubules may be treated using fluoride or desensitizing agents. Dental caries and faulty restorations should be removed and replaced with a sedative dressing, typically containing zinc-oxide/eugenol (Fig. 10.18).

Fig. 10.18 Dressed molar tooth

If it is judged that the pain is due to irreversible pulpitis, the pulp should be extirpated (Fig. 10.19). The ideal emergency treatment for irreversible pulpitis is to remove the diseased pulp completely and to clean and prepare the pulp canal system. Irrigating the pulp chamber with a 2.5–5.0% solution of sodium hypochlorite ensures disinfection before canal instrumentation. If time does not allow this, removal of pulp tissue from the pulp chamber and coronal part of the root canals is often effective. The use of corticosteroid preparations in vital root canals has been advocated in situations where complete instrumentation is inconvenient or impossible because profound anaesthesia cannot be secured. In the presence of severe pulpal inflammation, the effectiveness of local anaesthesia is reduced as discussed above.

Fig. 10.19 Mandibular molar with thickening of PDL space and condensing osteitis

In cracked teeth, dentine bonded materials may prove useful in small cavities as an interim restoration before constructing a restoration giving occlusal protection (Fig. 10.20). Once a vertical crack is initiated, the treatment goal is to prevent catastrophic propagation and retain the tooth for as long as possible; some teeth can last up to 10 years with cuspal protection.

Fig. 10.20 Gold partial coverage restoration giving occlusal protection

Where a crack involves the pulp and symptoms suggest an irreversible pulpitis, all restorations should be removed from the tooth and the extent of the crack determined. If the crack has propagated to a fracture and a portion of the tooth is mobile it should be removed, examined, and the possibility of restoring the remaining tooth substance established (see Fig. 10.14a). Examination of the extracted fragment allows accurate assessment of the restorability of the tooth. Where the fracture runs into the apical periodontal attachment apparatus, as in this case, then extraction is the only option (see Fig. 10.14b,c). If the tooth is restorable, root canal treatment may commence. Should the fracture line run through the floor of the pulp chamber, then it is unlikely that the tooth will respond to treatment in the long term.

In cases where the tooth is cracked but is incomplete, the crown should be supported with a metal band (Fig. 10.21) and root canal treatment commenced. The long-term prognosis of posterior teeth with oblique fractures above the alveolar crest and involving only the roof of the pulp chamber is higher than vertical fractures involving the floor of the chamber (Fig. 10.22).