Control of pain and anxiety
Systemic analgesic protocols are outlined and related to the types of procedure for which they are suitable. Considerations of dosing schedules and preoperative and postoperative regimens are discussed. Local anaesthetic drugs in common use are described together with their mechanisms of action. Drug dosages, including maximum safe doses are covered, as are the types of complication that can arise from the use of local anaesthetics. The use of vasoconstrictors with a local anaesthetic is also explained.
The role of conscious sedation is outlined with both the indications and contraindications. Nitrous oxide and the benzodiazepines are described. Various sedation techniques are outlined together with the methods for monitoring patients during and after sedation.
The assessment of patients for general anaesthetic is covered together with the possible investigations to establish suitability and the medical conditions that can complicate general anaesthesia. Preoperative preparation of patients for general anaesthesia is described.
Nociception: Nociception has been defined as the process of detection and signalling the presence of a noxious stimulus. Detection involves the activation of specialised sensory transducers, nociceptors, attached to Aδ and C fibres.
Pain: The International Association for the Study of Pain (IASP) has endorsed a definition of pain as an ‘unpleasant sensory and emotional experience associated with actual or potential damage, or described in terms of such damage’. Pain involves a motivational-affective component as well as a sensory-discriminative dimension and can occur without nociception.
Not all noxious stimuli that activate nociceptors are necessarily experienced as pain. While the sensations we call pain, pricking, burning, aching or stinging may have an urgent and primitive quality, they can be modulated. For example, in situations of crisis or emergency, or even when an individual’s attention is simply elsewhere, noxious inputs may trigger much less pain sensation than would otherwise be expected. It is observed that fear for survival in a war situation may suppress the pain of an inflicted injury until the individual is away from the immediate danger of the front line. Equally, anxiety about undergoing elective surgery may intensify the postoperative pain experience.
The variability of human pain suggests that there are neural mechanisms that modulate transmission in pain pathways and modify the individual’s emotional experience of pain. The transmission of pain is therefore, no longer viewed as a static process using exclusive pathways from peripheral tissues through the spinal cord to the brain, but rather as messages arising from the interplay between neuronal systems, both excitatory and inhibitory, at many levels of the central nervous system (CNS).
Acute pain has been described as pain of recent onset and probable limited duration. It usually has a causal relationship to injury or disease. Patients’ report of pain stops long before healing has been completed. Pain following injury or surgery would be typical of this type of pain.
Chronic pain is frequently defined as pain lasting for long periods of time; however, it is not the duration of pain that distinguishes it from acute pain but rather the inability of the body to restore its physiological functions to normal homeostatic levels. Chronic pain commonly persists beyond the time of healing of an injury and its intensity usually bears no relation to the extent of tissue damage, indeed there may be no clearly identifiable cause.
Clinical pain may be inflammatory or neuropathic in origin; the former refers to pain associated with peripheral tissue damage, such as that produced during surgery, and the latter refers to pain resulting from nervous system dysfunction, such as is seen in postherpetic neuralgia or trigeminal neuralgia (Chapter 14).
Both inflammatory and neuropathic pains are characterised by changes in sensitivity, notably a reduction in the intensity of the stimuli necessary to initiate pain, so that stimuli that would never normally produce pain begin to do so; this is called allodynia. There is also an exaggerated responsiveness to noxious stimuli, termed hyperalgesia.
Several publications including reports by the Royal College of Surgeons and College of Anaesthetists have shown that relief of pain following surgery in the UK has been suboptimal and this issue has been recognised globally. Reasons include inadequate recognition or evaluation of pain and prescription of inappropriate drugs and inadequate doses.
Analgesics should be prescribed according to their effectiveness and appropriate to the pain intensity reported by the patient or the anticipated postoperative pain intensity and taking into account potential adverse effects and the general health of the patient (Table 4.1). There are many clinical trials comparing analgesic effectiveness and the most effective drugs have a low NNT, where the NNT is the number of patients who need to receive the active drug to achieve at least 50% relief of pain compared to placebo over a 4–6 hour treatment period.
|Typical pain level||Type of procedure||Protocol|
|Mild pain||Forceps extraction||Paracetamol 1 g every 6 hours regularly (maximum 4 g/24 h)|
|Moderate pain||Surgical removal of tooth||Ibuprofen 400 mg every 6 hours regularly (maximum of 2.4 g/24 h) and paracetamol 1 g every 6 hours as necessary (maximum of 4 g/24 h)|
|Severe pain||Surgical removal of tooth involving bone removal||Ibuprofen 400 mg every 6 hours regularly (maximum of 2.4 g/24 h) and paracetamol 1 g/codeine 60 mg combination every 6 hours regularly (maximum of 4 g paracetamol/24 h)
When NSAIDs contraindicated: paracetamol 1 g/codeine 60 mg combination every 6 hours regularly (maximum of 4 g paracetamol/24 h)
|Severe pain for inpatients||More difficult surgical removal of teeth or major surgery||Morphine by intravenous titration or intermittent intramuscular injection|
Acetaminophen (paracetamol) possesses antipyretic activity and is an effective analgesic. It is considered safe because it does not have the side-effects such as gastrointestinal ulceration and haemorrhage, cardiorenal adverse effects or impair platelet aggregation. However, paracetamol is associated with liver toxicity, especially in patients who already have compromised liver function, cirrhosis or hepatitis. Patients should always be warned that many combination analgesics may contain paracetamol and they should only take the analgesics recommended or prescribed. Paracetamol may be administered intravenously, intraoperatively followed by oral administration after discharge home.
Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclo-oxygenase (COX) enzyme which is crucial for the production of prostaglandins that mediate pain via COX-2 but also via COX-1, for gastrointestinal mucosal protection, platelet function and protection of the inadequately purfused kidney. Consequently, NSAIDs are effective analgesics but are also responsible for the loss of gastric protection and consequent ulceration and bleeding that can occur and other effects. They are contraindicated in:
A proton pump inhibitor such as lansoprazole or omeprazole may be prescribed to take alongside the NSAID to offer some gastrointestinal protection. COX-2-selective inhibitors such as celecoxib have been specifically developed to be effective analgesics without the adverse effects of the non-selective NSAIDs. These are useful although not completely selective.
Some patients have a sensitivity to aspirin such that they develop cutaneous reactions. Asthmatic patients are at risk of experiencing bronchospasm when exposed to aspirin and other NSAIDs. These reactions are described as aspirin sensitivity rather than allergy as they are not mediated via an immune reaction. It is difficult to predict sensitivity and there is no test available. If a patient reports asthma, chronic rhinitis or urticaria and NSAIDs have previously been a trigger of acute bronchospasm, then they should be avoided and paracetamol and codeine used.
Opioids offer effective management of severe acute pain but are associated with nausea and vomiting and respiratory depression. The strong opioids such as morphine are therefore used in hospital but are not suitable for use in outpatients. Weak opioids such as codeine are used in all settings. Morphine may be administered intramuscularly, intravenously or orally and is also used in electronic or disposable devices to allow the patient to self-administer, that is, patient-controlled analgesia (PCA). Dihydrocodeine has been shown to be poorly effective for dental pain. Codeine, 60 mg, in combination with 1 g paracetamol is much more effective (with an NNT of 2.2) than either 60 mg codeine (NNT of 16.5) or 1 g paracetamol (NNT of 3.8) alone.
Analgesic drugs should be given at regular times according to their half-life and at high enough doses to ensure therapeutic plasma levels. Adequate doses of analgesics should not be withheld because of misconceptions and fears on the part of the prescriber. It is wrong to believe that pain is the inevitable consequence of surgery or that the use of opioids for acute pain in hospital will lead to addiction.
Sustained pain causes the pain system to become sensitised and this has the effect of amplifying the pain experience significantly. Prevention of pain rather than treating pain is therefore, important and theoretically could reduce the analgesic requirements after surgery. However, the evidence for the clinical advantage of giving an analgesic before pain as opposed to giving the same analgesic after pain is still unconvincing. Despite the debate about pre-emption, it is important to give systemic analgesics before the local anaesthetic (LA) has worn off and to give LA during general anaesthesia (GA) to prevent pain in the early postoperative phase, even though this may not reduce the later analgesic requirements.
Usually intravenous (i.v.) morphine is used via an infusion pump, with a lock to limit dose for safety. Patients given this control over their own pain relief usually use smaller doses than would have been prescribed.
The oral route is preferable but tablets, capsules or oral suspension should be chosen as appropriate for age and the nature of the treatment. Alternative routes such as intramuscular, i.v. and rectal may be appropriate in hospital.
It is well established that pain and depression are related, although the reasons for the association remain unclear. This has led to the unfortunate situation in the past when the dentist or other clinician, who could not find an obvious cause of the patient’s pain, believed that the reported pain was imaginary. It is now understood that if a patient reports pain then that pain is real. It is also now understood that any emotional disturbance in a patient with pain is more likely to be a consequence than a cause of the pain and it is dangerous to ascribe pain routinely to psychological causation. Traditional concepts focused either on medical or psychological explanations for pain, but the boundaries between these are being eroded as psychogenic cause is found to have a biochemical ‘physical’ basis.
The correct selection of pain control technique for patients requiring dental treatment is important for safe and successful practice. As with other aspects of clinical dentistry, this clinical decision making is based on knowledge and experience. Generally patients for treatment under local anaesthesia will be managed by the dentist in a primary care setting, whereas those requiring a GA will be referred to hospital. However, there may be a few patients requiring local anaesthesia whose medical history dictates that they are treated in hospital. Patients requiring conscious sedation techniques are treated in both the primary care and hospital setting.
By common usage, the localised loss of pain sensation is referred to as ‘local anaesthesia’, rather than local analgesia, which would be more accurate. The word ‘anaesthesia’ implies loss of all sensation including touch, pressure, temperature and pain.
Lidocaine (lignocaine) was produced in 1943 and superseded procaine because of its pharmacological advantages. It is the gold standard historic reference LA in dentistry. It has topical anaesthetic properties and is available as a gel or spray.
Articaine has been available and commonly used in Europe and especially in Germany where first synthesised in 1969, but more recently introduced to the UK and USA. It is classified as an amide although it has both an amide and an ester link.
Procaine is the least potent. Prilocaine is three times more potent than procaine and lidocaine is four times more potent than procaine. The potency of articaine is one and a half times that of lidocaine.
Agents with high lipid solubility act more quickly. Procaine takes longer than prilocaine and lidocaine, which take about the same time (within 2 minutes for infiltration injections and 3–5 minutes for inferior alveolar nerve blocks).
Duration of action depends on the diffusion capacity of the anaesthetic agent and the rate of its elimination. Bupivacaine is an extremely soluble LA with a long duration of action (6–8 hours); it is useful for postoperative pain relief. Levobupivacaine is an isomer of bupivacaine; it has similar analgesic properties to bupivacaine but is less cardiotoxic.
Fig. 4.1 Diagram of pterygomandibular space illustrating the need to inject an adequate dose of local anaesthetic for a reliable block of inferior alveolar and lingual nerve conduction.
(A) The area covered by 1 ml of local anaesthetic, which is not sufficient to block conduction. (B) A full cartridge of local anaesthetic is necessary to block the inferior alveolar and lingual nerve conduction.
Toxic: Overdose with LA may lead to light-headedness, sedation, circumoral paraesthesia and twitching. More serious overdose can result in convulsions, loss of consciousness, respiratory depression and cardiovascular collapse. Accidental i.v. injection may lead to excessively high plasma concentration. Prilocaine has low toxicity, similar to lidocaine, but if used in high doses may cause methaemoglobinaemia.
Allergic: Approximately two million dental local anaesthetic injections are administered daily around the world. Reports of allergic reactions are extremely rare. In the past, they may have been associated with the preservative (methylparaben) that was included in the cartridge or antioxidant (metabisulphite) used to stabilise the adrenaline in amide-type anaesthetics. If a patient gives a history compatible with an allergic reaction (rash, swelling or bronchospasm), rather than psychogenic reaction or the consequences of i.v. injection (tachycardia), then they should be referred for allergy testing. Hypersensitivity reactions occur mainly with the ester-type local anaesthetics such as benzocaine, cocaine and procaine. Latex-free plungers and seals are used by most manufacturers.
• The patient may experience an ‘electric shock’ type of sensation if the needle touches the inferior alveolar nerve and the injection should only start after withdrawing the needle 1 mm; otherwise direct damage resulting in long-term paraesthesia may result.
Skin: Lidocaine 2.5% and prilocaine 2.5% (EMLA) or 4% tetracaine (amethocaine) (AMETOP gel). EMLA (eutectic mixture of LA) is contraindicated in infants under 1 year and AMETOP is not recommended in infants under 1 month.
Application method: The LA is applied to the skin and covered with a dressing. The dressing and gel is removed before venepuncture 60 minutes (EMLA) or 30 minutes (AMETOP) later. Systemic absorption is low from skin but topical LAs should never be applied to wounds or mucous membranes, where absorption is rapid.
Most LAs (except cocaine) cause blood vessel dilatation and, therefore, a vasoconstrictor is added to diminish local blood flow and slow absorption of the LA. In practice, LAs still enter the systemic circulation quite rapidly but vasoconstrictors are useful to accelerate the onset, lengthen the duration and increase the depth of anaesthesia. They also reduce the local haemorrhage, which can be very helpful during surgical procedures. However, vasoconstrictors should never be used for infiltration of the ears, fingers, toes or penis as ischaemic necrosis may result. The concentration used is higher in dentistry than in medicine, particularly in the UK.
• Contraindicated in pregnancy as it is similar to oxytocin and there is a possibility of uterus contraction, although the dose is actually very small compared with the dose of oxytocin used by obstetricians to induce labour.
Prilocaine with felypressin is often recommended for use in patients with ischaemic heart disease rather than lidocaine with adrenaline (epinephrine), but there is no evidence that it is any safer. The latter is a more effective LA.
Lidocaine is an effective LA and commonly used in dentistry around the world. It is available in dental cartridges as a plain 2% solution or with adrenaline (epinephrine). An adrenaline (epinephrine) concentration of 1:100 000 is more common around the world but a higher concentration of 1:80 000 has typically been used in the UK.
Prilocaine is available as a 4% plain solution or as a 3% solution with 0.02 IU/ml felypressin. If a vasoconstrictor must be avoided, then plain 4% prilocaine is more effective than plain 2% lidocaine. Prilocaine is used in combination with lidocaine as the dermal anaesthetic eutectic mixture of local anaesthetics (EMLA).
Articaine is available as a 4% solution with either 1:100 000 or 1:200 000 adrenaline (epinephrine). Articaine is very effective when used for infiltration anaesthesia. It has neurotoxic properties and can cause prolonged anaesthesia and paraesthesia when used for regional block anaesthesia. However, articaine has a short half-life of about 20 minutes which is advantageous in relation to its toxicity.
Bupivacaine is available as 0.25%, 0.5% and 0.75% solutions in ampoules but not dental cartridges. The two lower concentrations are available plain or with 1:200 000 adrenaline (epinephrine). Bupivacaine has a slow onset of anaesthesia but then provides pulpal anaesthesia for about 2 hours and soft tissue anaesthesia for about 8 hours.
The maximum recommended doses are given in Table 4.2. Articaine has not been recommended by the manufacturer for use in children under 4 years of age, although dentists have been known to use it and find it effective in children between 2–3 years.
|Preparation||Maximum dose in healthy adult||Child (20 kg)|
|2% Lidocaine||4.4 mg/kg up to 300 mg (7 cartridges)||2 cartridges|
|3% Prilocaine||6.0 mg/kg up to 400 mg (6 cartridges)||1.8 cartridges|
|4% Prilocaine||6.0 mg/kg up to 400 mg (4.5 cartridges)||1.4 cartridges|
|4% Articaine||7.0 mg/kg up to 440 mg (5 cartridges)||1.5 cartridges|
Some patients are overly anxious about routine dental treatment, while others, who may be able to cope with uncomplicated treatment, may be distressed by more unpleasant procedures such as minor oral surgery with local anaesthesia alone. Management approaches vary according to the severity of the anxiety, the age of the patient, the degree of cooperation and the medical history. Psychological approaches have been widely used and range from informal and common-sense methods to formal relaxation training, hypnosis and cognitive behavioral therapy (CBT). These techniques are safe, free from side-effects and give the patient a sense of control.
An increasing number of patients are managed with conscious sedation techniques in combination with a LA but the more severely anxious and uncooperative may require treatment under a GA. As patient awareness of the risks of anaesthesia and the availability of sedation has increased, so the demand and popularity of conscious sedation for dentistry has increased. The control of pain and anxiety is fundamental to the practice of dentistry.
The aim of a sedation technique is to keep the patient conscious and cooperative but in a state of complete tranquillity. Ideally, the patient should have the sensations of warmth, confidence and a pleasant degree of dissociation from the realities of the situation. Sedation with drugs is not a replacement for, but rather an adjunct to, a caring and sympathetic attitude towards the patient. Conscious sedation may be defined as a state of depression of the central nervous system produced by a drug or drugs, enabling treatment to be carried out, and during which communication is maintained, such that a patient will respond to command throughout the period of sedation. The techniques used should carry a margin of safety wide enough to render unintended loss of consciousness unlikely.
Routes of administration: Sedative drugs may be administered by a variety of routes, for example, via the lungs, via the gastrointestinal tract (orally or rectally), intranasally, by intramuscular injection or directly into the circulation by intravenous injection. The most popular are the inhalational, oral and i.v. routes.
Risk avoidance: When using sedation techniques, it is important to avoid risks and the dentist should only proceed with methods with which he or she feels competent, in an environment that is adequately equipped and with staff that are appropriately trained. There should always be a second person present who is trained in the care of sedated patients. While UK dental schools provide undergraduate students with the necessary knowledge and skills to enable them to provide conscious sedation to patients, the British General Dental Council currently recommends additional postgraduate training. It is essential that dentists and their staff working in these fields are familiar with the appropriate regulations according to their country of practice.
All dental treatment facilities must have appropriate equipment and drugs for resuscitation at hand, the dentist and his or her team must have the skills to use them in an emergency whether providing conscious sedation techniques or treatment under local anaesthesia alone.
Psychological indications: Anxiety may be the most obvious and common reason for prescribing conscious sedation rather than LA alone but it is important to confirm this by discussion, rather than accept a request for sedation from a patient who may not be aware of its implications or of treatment alternatives. It may be necessary to justify the selection and patient preference alone is not sufficient reason. Extremely anxious and phobic patients may require GA for their dental management or consideration of other strategies such as cognitive behavioral therapy (CBT).
Dental indications: Moderately difficult or prolonged procedures such as dental implant surgery may be an indication for sedation. Some patients who are happy to undergo routine dental treatment with a LA alone, may require sedation to accept more invasive surgical procedures. Extensive dental treatment or surgery may require GA.
Medical and behavioural indications: Systemic disorders such as mild angina, controlled hypertension or controlled anxiety-induced asthma, may be an indication for the use of sedation as this minimises the psychological response to stress and so will reduce the activity of the sympathetic nervous system. This may avoid, or at least reduce, the likelihood of an angina or asthma attack or of raising the systemic blood pressure. Those with cardiorespiratory compromise should receive supplemental oxygen.
In disorders such as spasticity, multiple sclerosis or parkinsonism, where a patient may be eager to cooperate but physically unable to do so, benzodiazepine sedation may be of use because of its muscle relaxant properties. Similarly, patients with controlled epilepsy may benefit from the anticonvulsant property of benzodiazepines. Anxiety-induced gagging is often very successfully managed with sedation.
Psychological and social contraindications: It is better to admit defeat and arrange for treatment under a GA than to attempt sedation of a totally uncooperative patient. Successful sedation requires a patient to have sufficient intellect, insight and cooperation. Psychologically immature individuals unmanageable with LA alone may exhibit disinhibited or childish behaviour when sedated and so a GA may be needed.
Patients who are unable to provide a responsible adult (over 16 years) to accompany them, escort them home and remain with them for the rest of the day are not suitable for treatment with intravenous sedation or GA.
Dental contraindications: Prolonged or difficult oral surgery is a contraindication to treatment under any form of sedation as this may stretch both the patient and operator beyond their limits of endurance. It must also be remembered that sedation techniques do not reduce surgical morbidity. Planned GA may be preferable.
Systemic disease: Severe forms of systemic disease such as a recent myocardial infarct or poorly controlled or severe hypertension or angina, may be obvious contraindications for sedation for GA, but even hay fever or the common cold may contraindicate inhalational sedation if there is nasal obstruction.
Respiratory disease: Chronic obstructive pulmonary diseases (COPD) such as bronchitis, emphysema or bronchiectasis are contraindications. Such patients are particularly sensitive to the respiratory depression associated with benzodiazepines and anaesthetic drugs. Also, patients whose respiration is driven by a low partial pressure of oxygen rather than their partial pressure of carbon dioxide are likely to have their hypoxic drive removed by the relatively high concentration of oxygen administered during inhalational sedation. Patients with impaired cardiac function, as well as those with chronic obstructive pulmonary disease may be subject to hypoxic drive.
Pregnancy: Women who are, or may be pregnant, should preferably not be sedated or given a GA. Nitrous oxide inactivates vitamin B12, inhibits DNA formation and may be teratogenic. Its use in elective situations is therefore, contraindicated, particularly during the first trimester when cell differentiation is occurring. Nitrous oxide may be used safely, however, during late pregnancy and indeed is frequently used for pain relief during childbirth. Animal experiments have not indicated any teratogenic risk with midazolam, but evaluation in human pregnancy has not been undertaken and it would, therefore, be unwise to use it unless considered essential. High doses of benzodiazepines in the last trimester of pregnancy have been reported to produce irregularities of the fetal heart rate, hypotonia, poor sucking and hypothermia in the neonate. Midazolam should not, therefore, be used during the last trimester. Caution must be exercised when using intravenous sedation for breastfeeding mothers. If using midazolam, it is reasonable to ask the mother not to breastfeed for 8 hours after the sedation and use synthetic or pre-expressed milk during this time.
Liver and kidney disease: Since benzodiazepines are metabolised by the liver and excreted by the kidneys, diseases affecting these organs may interfere with recovery. Alcoholics may have some degree of liver damage and should therefore, be sedated with caution.
Psychiatric disorders: Patients with severe psychiatric or personality disorders may also be unsuitable for sedation as disinhibiting effects may be observed. Patients taking CNS depressants, such as potent analgesics, tranquillisers or sleeping tablets, may be unpredictably sensitive to or tolerant of sedation. The possibility of severe respiratory or cardiovascular depression should be considered when using benzodiazepines.