8 Conscious sedation

Many patients regard all dental treatment, and especially surgical procedures, as potentially painful and stressful. Reactions range from ‘normal’ apprehension, through various degrees of anxiety to irrational fear or even phobia. The adverse physiological effects of these psychological responses can increase the risk of treatment and should be controlled. This is particularly important for patients suffering from medical conditions which are made worse by fear.

Conscious sedation is considered by both the United Kingdom (UK) General Dental Council and the UK Department of Health to be an integral element of the control of pain and anxiety^{1  –3}. In other words, conscious sedation is an important aspect of the modern practice of dentistry.

The UK Department of Health defines conscious sedation as ‘A technique in which the use of a drug or drugs produces a state of depression of the central nervous system enabling treatment to be carried out, but during which verbal contact is maintained throughout the period of sedation. The drugs and techniques used to provide conscious sedation should carry a margin of safety wide enough to render loss of consciousness unlikely. The level of consciousness must be such that the patient remains conscious, retains protective reflexes, and is able to understand and respond to verbal commands’².

In the UK, the most commonly used dental conscious sedation techniques (titrated intravenous midazolam or titrated inhaled nitrous oxide/oxygen) have an excellent safety record. For many patients, conscious sedation combined with effective local anaesthesia is a very acceptable alternative to general anaesthesia. Explaining the benefits and risks of local anaesthesia, sedation, and general anaesthesia is an important part of the consent process. Despite the safety, efficacy, and cost-benefits of using conscious sedation techniques there are still indications for general anaesthesia for some dental/surgical procedures and certain patient groups.

This chapter provides an introduction to conscious sedation techniques for dental or oral surgery procedures, patient assessment and treatment planning, essential pharmacology, sedation equipment, clinical sedation (‘standard’ and ‘alternative’⁴), sedation for medically compromised patients, and the avoidance/management of sedation-related complications. However, before administering any form of conscious sedation the dental team must have received appropriate training in accordance with contemporary professional guidance^{2  –8}.

A satisfactory first visit is crucial to the success of subsequent treatment under conscious sedation. There is a great deal of information to be acquired from the patient. At the same time, it should never be forgotten, that the patient is also assessing the dental team. The first meeting should ideally be out of the dental surgery environment and in the nature of an informal ‘chat’. The following areas need to be explored:

It is often helpful to get the patient to complete a questionnaire asking the nature of their fears. This breaks the ice, and other questions may be included which will steer the conversation in the right direction. Remember that for some patients even discussing dentistry can be frightening (Table 8.1).

A detailed medical history must be obtained. From the sedation point of view, special note should be made of respiratory and cardiovascular problems, and liver and kidney disease. Prescribed medication may alert the operator to undisclosed medical conditions and also raise the question of drug interactions. Some medicines potentiate the effect of sedation drugs. It may sometimes be necessary to discuss the patient's medical history with their general medical practitioner or hospital consultant. Baseline recordings of arterial blood pressure, heart rate, and arterial oxygen saturation should be obtained and the results recorded in the clinical notes.

Prescribing sedation can be beneficial in many cases (Table 8.2). The sedation technique may need to be modified to accommodate specific patient risk factors (Table 8.3). Caution should be exercised in the presence of some coexisting medical conditions and expert opinion sought in order to establish the most appropriate environment for conscious sedation (Table 8.4).

Having collected this information it is now possible to assess the operative and/or sedation risk according to the scale of physical fitness devised by the American Society of Anesthesiologists (ASA, see Chapter 2).

Patients classified as ASA 1 or 2 are generally considered suitable for treatment in a primary dental care setting. Those falling into categories 3 and 4 should be referred to a specialist centre such as a teaching hospital or specialist sedation clinic. Some patients oscillate between ASA 3 and 4 according to the severity of their disease and other factors such as the season of the year or a change in medication. Examples of this type of fluctuating condition include: poorly controlled asthma; diabetes mellitus; and epilepsy. It may be preferable to refer such patients or, better still, wait until their condition becomes more stable before providing treatment under sedation. If a patient suffers from two relevant illnesses, or appears to be ASA 2 but with the use of multiple drugs, it is probably sensible to consider the patient to be ASA 3. The ASA scale is a useful ‘shorthand’ method of recording a patient's medical status but it requires common sense and careful application in order to avoid creating either unnecessary concern or confidence.

When assessing the medical status of an elderly patient, it must be remembered that some physiological functions decline naturally with age and even the apparently healthy patient with no declared medical problems cannot be treated exactly like a young fit adult. Elderly patients with one controlled illness (e.g. angina) may be suitable for treatment in a primary care setting but the presence of two known conditions (bearing in mind that other disease processes may be present but undiagnosed) should indicate referral.

The patient's experiences at the dentist over the years are important; questioning may yield valuable information⁹ which will assist during treatment planning (Table 8.5). It must be remembered that non-anxious patients may also be better managed under sedation if the proposed dental procedure is potentially threatening and/or prolonged.

The patient's domestic circumstances are very important. An escort will be required for most sedation appointments. In addition, having responsibility for children or elderly relatives may make it difficult for the patient to attend or to be able to recover safely at home.

Whilst some patients will allow a full intraoral examination, the operator may have to be content with a visual examination at this stage. Many phobic patients fear the dental probe and so this should only be used when absolutely necessary, and then with extreme caution. For a very few patients, intraoral radiographs may also be threatening or cause gagging, and so will have to be carried out under sedation.

Selection of the most appropriate method of pain and anxiety control requires careful consideration of a number of interlinking factors including the proposed dental treatment, the patient's health and degree of anxiety, the operator's training and experience, and the environment in which the treatment is to be carried out. No matter how fashionable, it is impossible to design a ‘care pathway’ or ‘protocol’ which incorporates all the relevant factors. The correct and most successful approach involves a commitment by the whole team (surgeon/sedationist/nursing staff) to careful consideration of a range of options for each individual. A ‘one size fits all’ approach to pain and anxiety management is rarely successful.

Once a preliminary dental treatment plan has been formulated the treatment options (Table 8.6) may then be considered and discussed with the patient. Advantages and disadvantages of techniques are included in Tables 8.7 and 8.8.

The simplest technique which will enable treatment to be carried out is generally considered to be the most appropriate. However, it is entirely inappropriate to subject patients to a rigid cascade of management options by only being prepared to consider more complex or ‘alternative’ forms of sedation when all ‘simpler’ techniques have failed. This is unnecessarily distressing for patients (and the dental team) and may serve to increase anxiety.

Written consent is required for both the dental procedure and the administration of conscious sedation. Consent for dentistry under conscious sedation should, under all but emergency circumstances, be obtained at the assessment appointment rather then when he/she attends for treatment. If extractions or advanced procedures are required, these must be agreed on a tooth-by-tooth basis; however, this is not usually practical for routine restorative dentistry.

Finally, patients must be given written and verbal pre- and postoperative instructions (Table 8.9) and be given the opportunity to ask questions. Some, but not all sedationists, prefer that patients are starved in preparation for treatment under conscious sedation.

Benzodiazepines act throughout the central nervous system. Specific benzodiazepine receptors are located on neuronal membranes within the brain and spinal cord. All benzodiazepines have a common core shape, which enables them to attach to these receptors. The effect of attaching benzodiazepines to cell membrane receptors is to alter an existing physiological ‘filter’.

The normal passage of information through sensory neurons to the brain is damped or filtered by the GABA (gamma-amino-butyric acid) system. GABA is an inhibitory chemical, which is released from sensory nerve endings as electrical nerve stimuli pass from neuron to neuron over synapses. Once released, GABA attaches itself to receptors on the cell membrane of the postsynaptic neuron. The postsynaptic membrane becomes more permeable to chloride ions, which has the effect of stabilizing the neuron and increasing the threshold for firing. During this period, no further electrical stimuli can be transmitted across the synapse. In this way, the number of sensory messages, which travel the whole distance from their origin to the areas of the brain where they are perceived, are reduced or filtered.

Benzodiazepine receptors are located close to GABA receptors. The effect of having a benzodiazepine in place on a receptor is to prolong the time it takes for repolarization after a neuron has been depolarized by an electrical impulse. This further reduces the number of stimuli reaching the higher centres and produces pharmacological sedation, anxiolysis, amnesia, muscle relaxation, and anticonvulsant effects.

All benzodiazepines, which are central nervous system depressants, have a similar shape with a ring structure on the same position of the diazepine part of each molecule. By contrast, flumazenil, the benzodiazepine antagonist, does not have this ring structure and has a neutral effect on the workings of the GABA system. Flumazenil is an effective antagonist, as it has a greater affinity for the benzodiazepine receptor than the active drugs and therefore displaces them. Flumazenil has a shorter half-life than midazolam. When it was first introduced there was a suggestion that administering flumazenil to a sedated patient would result in a short period of reversal followed by re-sedation some 50–60 minutes later. This is not true. The displaced midazolam continues to be redistributed and metabolized independently of the presence of flumazenil. The cessation of action of flumazenil (approximately 50 minutes) coincides with the point at which patients would normally be expected to be fit for discharge after a single dose of midazolam.

The anterograde amnesia produced by midazolam is a desirable effect in terms of reducing the patient's memory of stressful or prolonged treatment. The most profound amnesia occurs immediately after induction but some disturbance to short-term memory may persist for several hours or even until the following day. It is therefore essential to warn both patients and their escorts. It is advisable not to guarantee complete amnesia as this effect varies between patients and in the same patient on different occasions. The effect of anterograde amnesia is often misinterpreted by patients with the result that they believe that they have been unconscious. This may lead to difficulties if the patient returns for further treatment under sedation when they may insist that they are undersedated or more awake than before.

The muscle relaxant effect of benzodiazepines contributes to the difficulty in standing, walking, and maintaining balance experienced by many patients following treatment.

Allergy to the benzodiazepines is fortunately very rare. However, as the common core structure of these drugs is almost identical, a patient who exhibits an allergic reaction to any benzodiazepine must not be managed with flumazenil, which would only worsen the situation.

Metabolism of benzodiazepines takes place in the liver. It has no metabolites which are active once the parent drug has been removed. This is a major advantage of midazolam and is the principal reason for its being considered the drug of choice for outpatient conscious sedation. The water-soluble metabolites of the benzodiazepines are excreted via the kidneys.

All benzodiazepines produce respiratory depression. This is usually mild in healthy patients if the drug is administered intravenously by slow titration. It can, however, be a significant problem in unwell or elderly people. Even in a fit healthy individual, a fast injection or a large quantity of midazolam has the potential to depress respiration to the point of apnoea.

Benzodiazepine-induced respiratory depression affects all patients who are sedated with these drugs by any route of administration. For this reason, respiration must be monitored clinically by observation of the rate and depth of breathing and, since it is not always easy to detect small changes in respiratory function, a pulse oximeter is mandatory. Capnography is considered desirable by some authorities but it is not currently a practical proposition.

Benzodiazepines have few significant cardiovascular effects in healthy people. There is a decrease in mean arterial pressure, cardiac output, stroke volume, and systemic vascular resistance. This may present as a small fall in arterial blood pressure immediately following induction of sedation. However, this is normally compensated by the baroreceptor reflex and is of negligible clinical significance except in people with compromising cardiovascular disease.

Propofol (Diprivan 1%) is a synthetic phenol anaesthetic induction agent which has rapid onset, short duration (2–4 minutes) and fast recovery. In lower doses it is a safe and effective sedative agent. However, in order to maintain sedation at a constant level, it is necessary to administer propofol by continuous infusion. The elimination half-life is about 60 minutes in fit patients.

Propofol is sometimes painful on injection particularly when a small vein is used. However, injecting into a large vein and/or adding 1 ml of 1% plain lidocaine (approximately 0.1 mg/kg) to each 20 ml (200 mg) of propofol helps to reduce the pain. Pain on injection is of greater significance for conscious sedation than the induction of anaesthesia.

Propofol's pharmacokinetic properties make it very useful for short procedures when sedation is required for only a few minutes, for example, the extraction of a single tooth. Recovery occurs rapidly after the drug is discontinued. The short redistribution half-life prevents the accumulation of drug in the body and, as a consequence, propofol is also an appropriate agent for much longer cases, for example, maxillofacial or implant surgery. There is no antagonist agent for propofol.

As with midazolam, propofol tends to depress respiration. The frequency of hypersensitivity reaction is similar to that of other anaesthetic induction agents. Propofol is not currently recommended for use in patients with any history of epilepsy.

For some patients, midazolam on its own does not provide an adequate degree of sedation. In these cases a combination of agents may make treatment possible, thereby avoiding the need for general anaesthesia. The most frequently used combination of agents is an opioid and midazolam. Individual opioids, like benzodiazepines, act through central nervous system receptors and have either agonist or antagonistic actions. These drugs produce a number of therapeutic effects including analgesia, sedation, and euphoria. Their undesirable effects include cardiorespiratory depression and nausea and vomiting. The most important of these in relation to conscious sedation is respiratory depression. Great care must always be taken when a combination of an opioid and a benzodiazepine is used for sedation.

In dental sedation the most frequently used opioid is fentanyl (and its derivatives). When an opioid/midazolam combination is administered it is imperative that the opioid is given before midazolam is titrated. The incidence of vomiting is about 30% using this technique. It is sometimes necessary to administer an antiemetic. If any opioid is used for sedation, naloxone (Narcan) must be available. Naloxone is an opioid antagonist and reverses respiratory depression, analgesia, and sedation.

Nitrous oxide is an anaesthetic gas. It has a blood/gas solubility coefficient of 0.47 and a MAC (minimum alveolar concentration) of 105%. The blood/gas solubility coefficient determines the rate at which the gas concentration in the lungs equilibrates with that being administered which, in turn, relates to the speed of induction and of recovery. Nitrous oxide is poorly soluble in blood and so induction and recovery are rapid.

MAC value relates to the potency of the gas and determines the concentration needed to induce sedation. Nitrous oxide is not very potent, which means that it is a very safe gas for conscious sedation. In sufficient concentrations (in excess of 100%), the drug will induce light surgical anaesthesia, but only at the expense of adequate oxygenation. In lesser concentrations, it has excellent analgesic and sedative properties. There are very few cardiovascular or respiratory effects and no direct depression of myocardial function or reduction in ventilation. The drug has a central analgesic and anaesthetic effect (the exact mechanism is not clear) and is excreted unchanged via the lungs very rapidly after discontinuing its administration.

Sevoflurane is a fluorinated derivative of methyl isopropyl ether which was first synthesized in the early 1970s¹⁰. It has a MAC of 2% and a blood gas solubility coefficient of 0.6. These physical characteristics make sevoflurane a potent anaesthetic agent with rapid uptake and speedy recovery. It is pleasant to inhale, non-irritant and non-pungent.

The properties that make sevoflurane a useful anaesthetic agent also make it a promising sedation agent. However, a specially calibrated vaporizer is required in order to titrate low concentrations of sevoflurane (up to 1%) in oxygen (or nitrous oxide and oxygen). Sevoflurane is partly metabolized (5%) and so some care is required in people with severe liver or kidney disease.

At present sevoflurane is not widely used for dental sedation because of the practical problems associated with incorporating a vaporizer into any of the currently available dental inhalational sedation machines.

Midazolam is the benzodiazepine of choice for intravenous dental sedation¹¹. It has a variety of presentations (e.g. 10 mg/5 ml; 10 mg/2 ml; 5 mg/5 ml). The more dilute presentations are easier to administer in small increments whilst observing the patient's response. The National Patient Safety Agency has recently recommended that the 5 mg/5 ml concentration is the most appropriate for sedationists¹². Whatever concentration is used, a titration technique must always be used in order to reduce the risk of oversedation. It is impossible to determine the correct dosage of midazolam by any form of calculation based on the patient's physical characteristics, for example, age, body weight, body mass index (BMI), or body surface area. Overdosage and/or excessively rapid bolus injections often cause profound respiratory depression or even respiratory arrest. Midazolam produces a period of sedation (acute detachment from the individual's surroundings) for 20–30 minutes followed by a state of relaxation for a further hour or so.

Anxiolysis differs from sedation. Anxiolysis (literally ‘dissolving anxiety’) may be described as ‘dissociating the patient from the perceived threat’. An ideal sedation drug would be anxiolytic rather than merely sedative, as this would leave the patient fully aware, but completely unconcerned about the dental treatment. Unfortunately, no such drug exists. It is important to consider the degree of anxiolysis and not just the depth of sedation when assessing the quality of sedation.

Midazolam produces anterograde amnesia (a reduction in recall following administration of the drug) so most patients have little or no recall of the operative procedure. This effect must, of course, be fully explained to both the patient and their escort before discharge.

Allergy to any benzodiazepine represents an absolute contraindication to intravenous sedation with midazolam. However, benzodiazepine allergy is very rare. A degree of caution is needed when using midazolam during pregnancy and breastfeeding, severe psychiatric disease, alcohol or drug abuse, impaired hepatic function, phobia of needles and injections, poor venous access, and when there are doubts about the ability to provide a suitable escort home.

Since the vast majority of adult patients (under 65 years of age) require more than 5 mg midazolam to produce effective sedation, the most commonly used size is 10 ml (two ampoules of 5 mg/5 ml). All patients undergoing intravenous sedation must have a flexible plastic cannula placed in a vein, so as to ensure reliable, continuous venous access throughout the procedure¹³. The most convenient cannula sizes are 20G and 22G.

It is important to ensure that the patient is fully prepared for the procedure and that the dental team is fully prepared for the patient. All the necessary equipment and drugs must be readily available. Nothing is more disconcerting to an anxious patient than having to wait whilst missing items are located or faulty equipment replaced. Having induced sedation, it is then important that the dentist is ready to proceed without delay.

The appearance of the clinical environment is also important in putting the patient at ease. Many dental surgeries are frankly alarming. It is important to avoid having cardiopulmonary resuscitation posters and anatomical diagrams displayed within the patient's line of vision and to keep threatening equipment covered. Someone must offer friendly support from the moment the patient enters the surgery. Having one person do this is better than relying on the whole team, as everyone may assume that it is someone else's responsibility.

Before any clinical procedure is started, it is important to check the patient's identity, medical history, and blood pressure. Written consent must have been obtained for both the procedure and the sedation. It is also imperative to confirm that the patient has a responsible adult escort, who is able and willing to look after the patient for the rest of the day. A patient, who is unable to provide a suitable escort, must not be sedated unless arrangements have been made for an overnight stay. If there are any doubts, it is better not to proceed with the use of sedation. A final check should be made to ensure that the patient has emptied their bladder.

The following description of the administration of intravenous midazolam (10 mg/10 ml) is appropriate for most fit and healthy adult patients between the ages of 16 and 65. However, even within this age group, variation in the response to sedation is common.

The dental chair should be adjusted to the supine position. Electromechanical monitoring must be established before the patient is sedated, in order to establish baseline readings. Pulse oximetry is mandatory¹⁴. Continuous blood pressure monitoring and an electrocardiogram (ECG) may be advisable for seriously unfit patients. If supplemental oxygen is indicated, this is the time to apply the nasal cannulae and turn on the oxygen (a flow of 2 litres per minute is sufficient).

A suitable vein must first be cannulated after appropriate skin preparation. The use of topical anaesthetic agents such as Ametop or Emla reduces the discomfort of venepuncture, but these creams must be applied some time before venepuncture in order to achieve good analgesia.

The prepared drug in a 10-ml syringe is attached to the port of the cannula and injected slowly, according to the regimen described below. The patient should be warned of a cold sensation at the needle site and perhaps also as the drug travels up the arm. Provided the sedationist is sure that the needle is correctly sited, the patient should be reassured that this sensation will pass within a short period of time. The injection must be stopped immediately if pain is felt radiating distally as this could indicate arterial injection.

A recommended titration regimen for intravenous midazolam sedation in healthy patients 16–65 years of age is to administer 2 mg (2 ml) injected over 30 seconds, pause for 90 seconds, and administer further increments of 1 mg (1 ml) every 30 seconds until sedation is judged to be adequate. Talk to the patient and watch for any adverse responses, in particular respiratory depression.

The correct dose has been given when there is a slurring of speech, and/or a slowed response to commands and the patient exhibits a relaxed demeanour. With midazolam, ptosis is an unreliable sign and so this should not be used to judge the adequacy of sedation. Some sedationists estimate the depth of sedation by asking the patient to close their eyes and then trying to touch the tip of their nose with an index finger. Inability to demonstrate the appropriate level of coordination is reputed to indicate that the patient is adequately sedated.

Patients over the age of 65 years often require much smaller doses of midazolam. A suggested administration regimen for these patients is 1mg injected over 30 seconds followed by a wait of at least 4 minutes, then additional 0.5-mg increments given every 2 minutes until sedation is adequate. Patients in this age group often need no more than 2 mg in order to provide more than an hour of sedation.

Local analgesia should be administered shortly after this state is attained. Approximately 30–40 minutes of sedation time is usually available and this should be more than adequate for most procedures. It is acceptable to top-up the sedation from time to time, if the procedure is prolonged, but this is rarely necessary during the first 20 minutes. Additional increments of midazolam should be small, 1 or 2 mg is usually adequate (less in the elderly).

At the end of the procedure, the patient should remain under the direct supervision of the sedationist or suitably trained recovery staff. No patient may be discharged until sufficiently recovered so as to be able to stand and walk without assistance. Although most patients will not be fit for discharge until at least 1 hour following the administration of the last increment of midazolam, there is no fixed time limit and recovery staff should be discouraged applying rigid criteria.

The patient should be discharged into the care of the escort, who must also be given written and verbal instructions. The patient should rest quietly at home for the remainder of the day and refrain from drinking alcohol, driving and operating machinery for a minimum of 8 hours. It is important to make the escort aware that the patient should be observed for the first few hours, not simply put to bed out of sight. It is unreasonable and unnecessary to demand that patients travel home by private rather than public transport.

In addition to any electromechanical devices (e.g. pulse oximeter), the sedationist and nurse must be constantly aware of the patient's respiratory rate and depth, the presence of airway obstruction, depth of sedation, and skin colour¹⁰. Periodic estimation of systemic arterial blood pressure and continuous ECG monitoring may be advisable for some unfit patients.

Respiratory rate is quite variable (12–20 breaths per minute in adults), but this is nearly always reduced during sedation and so must be monitored closely. The depth of breathing is also reduced. Apnoea may occur with an overdosage of (or idiosyncratic response to) midazolam. Such side effects are potentially life threatening if recognition and management is not swift. Some degree of respiratory depression is probably present in all sedated patients, but serious problems are most likely to occur immediately following induction.

Pulse oximetry measures the patient's arterial oxygen saturation and pulse rate from a probe, which is attached to the finger or ear lobe. The pulse oximeter detects changes in the patient's oxygen supply, oxygen uptake by the lungs, and the delivery of oxygen to the tissues via the circulation but does not monitor the adequacy of ventilation. Regardless, this it is a useful monitor of both respiratory and cardiovascular function. However, correct functioning can be affected by metallic nail varnish or excessive light falling on the probe. Oxygen saturations below 90% should be investigated and the cause corrected. Asking the patient to take several deep breaths resolves the majority of cases of midazolam-induced respiratory depression. If this fails, intermittent positive pressure ventilation (IPPV) should be instituted and the administration of flumazenil considered.

Bradycardia or tachycardia during sedation should be investigated. The former may be due to hypoxia or vagal stimulation, whilst the latter is often the result of painful stimuli. Most pulse monitors have audible alarms, which can be set to give audible and visible warning if the heart rate falls or rises beyond clinically acceptable levels. For ASA 1 and 2 patients, bradycardia and tachycardia alarm limits are normally 50 beats/min and 150 beats/min respectively.

Flumazenil (Anexate) antagonizes the action of midazolam, reversing the sedative, cardiovascular, and respiratory depressant effects (but not the amnesia). Although flumazenil is usually recommended for use only in emergency situations (e.g. benzodiazepine overdose), elective reversal may be necessary for some patients. In this case, it is imperative that the usual postoperative instructions for intravenous sedation are given and followed. Although flumazenil has a shorter half-life than midazolam, clinically significant re-sedation does not occur when midazolam is used for short clinical procedures.

Oral and intranasal sedation are useful where the patient is needle phobic and will not accept venepuncture. The sedation produced may be adequate for the dental procedure to be carried out or it may then be necessary to administer intravenous sedation in the normal way.

The most commonly used drug is midazolam. In adults, the standard oral dose is 20 mg and the standard intranasal dose is 10 mg. Note that neither of these routes involves titration and so both are potentially less safe than intravenous sedation. Midazolam is has a bitter taste and so must be added to a strong-flavoured fruit juice for oral administration. Intranasal midazolam is much more rapidly absorbed than oral midazolam but may cause short-lasting nasal irritation, sneezing, and, occasionally, mild epistaxis. Intranasal midazolam is most effective when a high concentration formulation (40 mg/ml) is employed. This is not commercially available but is obtainable from some hospital pharmacies with a manufacturing facility. Figure 8.1 shows the intranasal administration of midazolam using a 1-ml syringe fitted with a mucosal atomization device (MAD).

The operative and postoperative management of patients, who have received oral or intranasal midazolam, is very similar to that for intravenous midazolam. The depth of sedation is similar but rather less predictable, monitoring with a pulse oximeter is mandatory, and the discharge and escort criteria are identical. It is recommended that patients who receive intranasal or oral sedation should have a cannula inserted as soon as adequate sedation has been achieved⁴.

Although midazolam does not have a product licence for oral or intranasal administration, both routes are commonly used in dentistry and medicine. However, practitioners should not use these routes without appropriate training and clinical experience. Experience of cannulation and intravenous sedation are essential⁴.

The following techniques must only be used by appropriately trained and experienced practitioners in an appropriate environment.

Patients, who are not adequately sedated using intravenous midazolam alone, may sometimes be successfully managed by administering a small bolus of an opioid drug prior to titrating the midazolam. Whilst it is usually preferable to use a single drug-sedation technique, using a combination technique may avoid the need for general anaesthesia.

The opioid selected should ideally have a shorter duration of action than midazolam so as to avoid prolonged recovery. For dentistry, fentanyl (Sublimaze) is now the most commonly used drug. It is administered as a slow 50-mcg fentanyl bolus. After 1 minute, appropriate titrated increments of midazolam are administered. It should be noted that the total dose of midazolam will be probably be considerably less that that required without the opioid.

All opioid drugs have the potential to cause dangerous respiratory depression necessitating prompt and effective management from the dental team. Nausea and vomiting are common and unpleasant side effects.

In subanaesthetic doses and when administered in an appropriate manner, propofol is a reliable and safe drug for intravenous sedation with a considerably shorter distribution half-life than midazolam. By comparison with midazolam, recovery is rapid and patients report feeling ‘clear-headed’ more quickly. Amnesia is often less profound. Propofol confers a greater degree of anxiolysis than sedation and patients appear less sleepy than with midazolam. When administered by continuous infusion, propofol is more controllable than titrated midazolam and the depth of sedation may be varied during the procedure. It is particularly useful both for very short cases and for long procedures. There are few contraindications to propofol but it should be avoided if there is known or suspected allergy to any of its components or for patients with epilepsy. There is still concern about the use of propofol for sedation in very young children.

Propofol infusion techniques are not suitable for use by an operator-sedationist. The technique may only be used by a second practitioner who has received specific training. For a fit adult of normal build, 30 mg of propofol (1%) is given by slow manual injection (this bolus is not weight-related) and an infusion started at an initial rate of 300 mg (30 ml) per hour. Sedation usually occurs within 1–2 minutes. The infusion rate may need to be adjusted during long procedures.

Particular care is needed with procedures lasting longer than 30 minutes in order to avoid too deep a level of sedation. Careful clinical monitoring and pulse oximetry is mandatory. Although respiratory depression may occur, it appears to be less marked than is the case with midazolam. As with all dental sedation techniques, the use of effective local analgesia is essential. The procedure for recovery is similar to that for midazolam. The criteria for discharge and instructions for after-care suggested for midazolam should be observed.

Both midazolam and propofol have been used successfully in patient-controlled sedation (PCS) systems. An infusion pump with a demand system allows the patient to control the depth of sedation. Overdosage is prevented by a time-based lockout. In addition to making the patient feel more in control, PCS may optimize the level of sedation and thus reduce the incidence of both under- and oversedation.

TCI using propofol for dental sedation is currently under investigation and development and offers some promise. However, if these systems are to be effective the algorithms chosen to determine the infusion rate must be based on data from patients who suffer real dental anxiety/phobia.

The use of nitrous oxide and oxygen in subanaesthetic concentrations was popularized as a method of sedation during the late 1940s. Machines which are designed to deliver a variable concentration of nitrous oxide in oxygen suitable are readily available.

Nitrous oxide has excellent anxiolytic, sedative, and analgesic properties, with little or no depression of myocardial function or ventilation. Induction and recovery are rapid and it has a wide margin of safety. Inhalational sedation may also be used to facilitate cannulation in some needle-phobic patients. The variation between individual patients is such that, whilst one person may be adequately sedated with 20% nitrous oxide, another individual may require in excess of 50%. A titration technique of administration is employed in order to avoid the risk of oversedation.

Because of the relatively poor solubility of nitrous oxide in blood and body tissues, there is rapid outflow of nitrous oxide across the alveolar membrane, when the incoming gas flow is stopped. This may dilute the percentage of alveolar oxygen available for uptake by up to 50%. This phenomenon is called diffusion hypoxia and is prevented by giving 100% oxygen for at least 2 minutes at the end of the procedure.

There are very few contraindications to inhalational dental sedation but they include nasal obstruction (e.g. cold, polyps, deviated septum), cyanosis at rest, poor cooperation, first trimester (12 weeks) of pregnancy, and fear of masks.

Modern inhalational sedation (relative analgesia, RA) machines are similar to traditional Boyle's anaesthetic machines, but modified so as to make them safe for use by a dental seditionist (Figure 8.2).

Most portable inhalational sedation machines are designed to operate with two nitrous oxide and two oxygen cylinders for safety. A pin index system ensures that the nitrous oxide and oxygen gas cylinders cannot be accidentally interchanged. The popular MDM (Matrx Medical, Inc., Orchard Park, New York, USA) RA machine head has flow meters for nitrous oxide and oxygen, a control valve for regulating the total gas flow, and a mixture dial for adjusting the percentage of oxygen and nitrous oxide. All modern inhalational sedation machines are incapable of delivering a gas mixture containing less than 30% oxygen and also have a failsafe mechanism which shuts off the nitrous oxide if oxygen ceases to flow.

The mixed gases emerge at the common gas outlet to which the breathing system is connected. The reservoir bag is useful for adjusting the total gas flow to an individual patient's minute volume and also for monitoring respiration during treatment.

Although designs vary, all modern inhalational sedation breathing systems comprise an inspiratory limb, a nasal mask, and an expiratory limb. Nasal masks are available in a variety of styles and sizes. Older style breathing systems must be cold sterilized, but some of the newer materials are suitable for autoclaving. Modern nasal masks have both fresh gas and scavenging connectors.

Having checked that the inhalational sedation machine is working and that extra gas cylinders are available (or that piped gases are flowing), the patient is laid supine in the chair and the procedure explained.

The machine is then adjusted to administer 100% oxygen at a flow rate of 6 l/min and the correct size nasal mask selected. Patients often prefer to place the mask over their own nose. It is important to maintain a steady flow of conversation and encouragement. The oxygen flow rate (minute volume) may be checked by observing the movement of the reservoir bag. If there is under- or overinflating, the gas flow must be increased or decreased respectively. Ten per cent nitrous oxide is then added (90% oxygen) and the patient informed that he/she may feel light-headed, have changes in visual/auditory sensation, tingling of hands and feet, suffusing warmth, and a feeling of remoteness from the immediate environment. This concentration is maintained for one full minute, during which plentiful verbal reassurance is given. The concentration of nitrous oxide is increased by 10% for a further full minute (to a total of 20% nitrous oxide) and then in increments of 5% until the patient appears and feels sufficiently relaxed.

Nitrous oxide concentrations of between 20% and 50% commonly allow for a state of detached sedation and analgesia without any loss of consciousness or danger of obtunded laryngeal reflexes. At these levels, patients are aware of operative procedures and are cooperative without being fearful. If, after a period of relaxation, the patient becomes restless or apprehensive, it is probable that the concentration of nitrous oxide is too high.

Having carried out the dental procedure, the nitrous oxide is turned off and 100% oxygen administered for 2 minutes (to prevent diffusion hypoxia). Recovery is usually complete within 15–30 minutes.

The sedationist and the dental nurse must be aware of the patient's respiration (rate and depth), the presence of airway obstruction, depth of sedation, and skin colour. Electromechanical devices (e.g. pulse oximeter, sphygmomanometer, ECG) are not indicated unless the patient has serious medical problems.

Long-term exposure to nitrous oxide may result in an increased incidence of liver, renal, and neurological disease, and there is evidence of bone marrow toxicity and interference with vitamin B12 synthesis, which may lead to signs and symptoms similar to those of pernicious anaemia. For this reason, the UK Health and Safety Executive specify a maximum level of 100ppm of nitrous oxide time-weighted over 8 hours²⁸. In order to achieve this level and so keep nitrous oxide pollution to a minimum, scavenging must be employed. Systems for use with active scavenging differ from those for use with passive removal of waste gases. Active scavenging is achieved by connecting the expiratory limb of the breathing system to a low power suction device, whilst passive scavenging often involves simply placing the open end of the expiratory tube as far away as possible, preferably outside the operating environment.

In the UK, inhalational sedation using a titrated dose of nitrous oxide in oxygen is the only completely tried and tested conscious sedation technique currently recommended for children under 12 years of age.

Intravenous sedation with midazolam has often been said to be reliably unpredictable in patients under 16 years of age and predictably unreliable below the age of 12. Some young patients sedate satisfactorily whilst others become disinhibited, more anxious, or even frankly aggressive. Despite a number of recent studies it has not been possible to identify any factors which may be used to predict the likelihood of success. Until more research has been carried out, therefore, intravenous midazolam should only be considered for children when other options have been considered. In any case, these techniques must only be used by experienced sedationists or anaesthetists working in an appropriate environment⁴. The use of flumazenil to manage a young patient with disinhibition following intravenous midazolam is not recommended as the data currently available suggests that the situation is often made worse rather than improved. Propofol is widely used for adult sedation but there are still reservations about its use for sedation in very young children.

Orally administered benzodiazepines such as temazepam and midazolam, appear to produce more reliable sedation for this age group. However, the time taken for the drug to act is much less predictable than with intravenous sedation owing to differences in the rate of gastric absorption, first-pass metabolism, and protein binding. Most patients become sedated somewhere between 10 and 30 minutes following oral administration. Midazolam appears to be the more predictable drug in this respect with a typical time of onset of about 12 minutes. Its widespread use in the UK in dental and medical disciplines has shown this to be a safe, appropriate, and effective technique. Orally administered antihistamines have been used for paediatric sedation in medicine for many years but their use in dentistry has been mostly limited to special care patients.

Benzodiazepines may also be administered intranasally and although this technique offers a number of advantages for certain groups, particularly very young patients, needle phobics, and those with disabilities, the route requires specific training and experience.

Whichever technique is used for paediatric sedation it is a requirement that the practitioner and the team are experienced in the use of the drug and its route of administration. It is important to remember that oral and intranasal sedation produces a similar level of sedation to that achieved by intravenous midazolam and so the pre- and postoperative instructions to the patient, monitoring, and arrangements for discharge must be identical to that for intravenous sedation. Oral sedation should not be regarded as a safer or easier option than intravenous sedation. In many ways it is potentially less safe owing to the poor predictability of onset, depth of sedation, and recovery.

Inhalational sedation using sevoflurane in oxygen, or a mixture of nitrous oxide and oxygen, is currently receiving research attention and it appears to be useful for younger patients¹⁰. At present, sevoflurane sedation must be administered only by practitioners trained in anaesthesia.

Serious complications associated with carefully administered conscious sedation are rare. Minor problems are more common. Fortunately most minor problems are easily managed by a well-prepared dental team. Careful case selection, based on a detailed medical, dental, and social history, will often allow the dental team to anticipate potential difficulties and take appropriate action.

The most serious potential complication associated with intravenous sedation is respiratory depression. The effect is normally most pronounced during the first 10 or so minutes of sedation. It is also sometimes seen later if there is a lull in clinical activity. The difficulty in recognizing mild or even moderate respiratory depression underlines the necessity for continuous pulse oximetry in addition to careful clinical monitoring. However, patients who are receiving supplementary oxygen therapy can record apparently acceptable oxygen saturations despite significant hypoventilation secondary to sedation. Vigilance is paramount.

Prompt action is necessary. Ask the patient to take several deep breaths. In the majority of cases, this will resolve the problem. If this fails summon help, open the airway (head tilt/chin lift or jaw thrust), and perform IPPV ventilation using a ventilating bag, preferably with an oxygen supply attached.

Administer flumazenil (500 mcg by slow intravenous injection) if there is no return to adequate spontaneous ventilation. Continue to ventilate and encourage breathing.

Obstruction of the airway may occur during any form of sedation. Excessive downward pressure from the dental practitioner without adequate support of the mandible during the extraction of molar teeth is a common cause. Accumulation of water and dental debris in the oropharynx can also be a problem. This is easily managed by the use of properly positioned high-volume suction.

Extravascular injection of midazolam is usually uncomfortable. If this occurs the cannula must be repositioned. Intra-arterial injection is rare and causes pain distal to the injection site. If this is suspected, the injection should be stopped and the cannula re-sited. Whilst painful, intra-arterial midazolam is unlikely to cause long-term sequelae. However, some sedative/analgesic agents can provoke severe spasm and may necessitate giving an antispasmodic such as papaverine.

A small amount of oversedation with intravenous midazolam is not usually a serious problem. The most common effect is poor patient cooperation with the patient refusing to open his/her mouth and so treatment is delayed. Gross oversedation using midazolam may cause profound respiratory depression or even apnoea requiring prompt and effective management (discussed previously).

Mild oversedation with nitrous oxide is often more troublesome as the patient may feel panicky and reject further treatment. Oversedation of young children is particularly undesirable. Intentional undersedation, in the belief that it is safer, is pointless and may lead to increased dental phobia. Failing to provide an adequate depth of sedation is a common failure of the inexperienced sedationist.

Many patients show signs of mild disinhibition when sedated with midazolam, for example, giggling, crying, talkativeness, or panic attacks which may seriously interfere with dental treatment. Firm management by the dental team may restore calm but further bouts may occur. Aggressive and abusive behaviour is probably another manifestation of disinhibition.

Intravenous midazolam sometimes results in a paradoxical effect. The patient becomes more rather than less anxious and treatment may not be possible. This is particularly common in children and adolescents. The administration of more midazolam often makes matters worse and the effects of flumazenil are unpredictable. The best approach is to abandon treatment and allow the patient to rest quietly.

Recovery from intravenous midazolam is variable due to variability in redistribution of the drug from the receptor sites (short-term recovery) followed by metabolism and excretion (long-term recovery). Some groups of patients, particularly those taking or using central nervous system depressant drugs have notoriously unpredictable recovery times. For the majority of these patients, management simply involves patience and careful monitoring. Flumazenil may be helpful but should not normally be used when the patient has psychiatric or medical conditions which involves treatment with potent central nervous system depressants or stimulants, in particular benzodiazepines.

All intravenous sedation drugs tend to cause a decrease in the systemic arterial blood pressure. Unlike respiratory depression, the fall in blood pressure is usually self-limiting and, as such, requires no active treatment. A patient with a naturally low arterial blood pressure should be moved slowly from the supine position to the sitting position to reduce the possibility of postural hypotension.

A small number of patients experience hiccups following intravenous sedation with midazolam. Most cases appear to be associated with either excessive midazolam or rapid injection (or both).

Much has been written about the occurrence of sexual fantasies in patients receiving intravenous sedation using midazolam. The extent of the problem is unknown. The best advice which can be offered is to ensure that no sedated or recovering patient is ever left alone with only one member of the dental team.

Conscious sedation techniques are not always successful. Early recognition of impending failure is important in order to avoid starting a dental procedure which it may not be possible to complete. An open and honest discussion with the patient and their escort will reduce the disappointment of a failed sedation appointment. Alternative sedation techniques or general anaesthesia should be considered.

Conscious sedation, combined with regional anaesthesia, can offer a safer alternative to general anaesthesia for some oral and maxillofacial surgical procedures. Careful patient selection and evaluation is the key to a successful and satisfactory outcome. As the process is potentially dangerous in unskilled hands, sedation should only be conducted by those fully trained and totally familiar with the techniques involved.