References
Complications of conscious sedation: causes and management
From Volume 44, Issue 11, December 2017 | Pages 1034-1040
Article
In 2009, the Adult Dental Health Survey stated that 12% of adults who had ever attended a dentist reported having extreme dental anxiety based on the Modified Dental Anxiety Scale.1 As dental practitioners, patients often comment on their anxiety or past experiences which they deem as being unpleasant. An alternative option to treating patients with severe dental anxiety under local anaesthesia alone may be through delivery of conscious sedation.
Conscious sedation is defined 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 with the patient is maintained throughout the period of sedation. The drugs and techniques used to provide conscious sedation for dental treatment should carry a margin of safety wide enough to render loss of consciousness unlikely.
The level of sedation must be such that the patient remains conscious, retains protective reflexes, and is able to respond to verbal commands.’2
Pharmacology
In conscious sedation, the drugs most often used are Nitrous Oxide and Oxygen for inhalational sedation and Midazolam for intravenous sedation. The properties of these two most commonly used drugs are summarized below.3
Inhalational sedation (IHS)
Nitrous Oxide is the most frequently used drug for inhalational sedation. With each breath of Nitrous Oxide, the partial pressure of the gas in the alveoli is raised. As the partial pressure increases, the Nitrous Oxide crosses the alveolar membrane into the bloodstream and is carried to the brain. Nitrous Oxide functions by passing down a pressure gradient from areas of high to low partial pressures. The low solubility of Nitrous Oxide enables rapid onset of sedation to occur. Another benefit of poor solubility is that, when Nitrous Oxide is no longer delivered, recovery is swift, since the Nitrous Oxide dissolved in the blood is eliminated rapidly via the lungs.
Nitrous Oxide also has a high Minimum Alveolar Concentration (MAC) which therefore indicates that it has a low potency, making it an ideal drug for conscious sedation. Nitrous Oxide also has a minimal effect on the cardiorespiratory system.3
There are three planes of inhalational sedation (Table 1).3 Planes I and II are usually deemed adequate for dental sedation.
Plane | Effect | Concentration of Nitrous Oxide (%) |
---|---|---|
I | Moderate sedation and analgesia | 5–25 |
II | Dissociation sedation and analgesia | 20–55 |
III | Complete analgesia | 50–70 |
Intravenous sedation
Midazolam is a benzodiazepine agonist and has an elimination half life of 1.5–2 hours. To understand the mechanism of Midazolam, it is essential to be aware of the role of Gamma-Aminobutyric Acid (GABA) which is an inhibitory neurotransmitter. GABA is released from presynaptic sensory nerve endings as a nerve stimulus passes from neurone to neurone across synapses. GABA then attaches to receptors which are located on the cell membrane of the postsynaptic neurone. This increases the permeability of the postsynaptic neurone to chloride ions, which stabilizes the neurone and prevents the passage of sensory stimuli. Benzodiazepine receptors are also located on the cell membranes close to the GABA receptors. This prolongs the time taken for repolarization; therefore the number of stimuli reaching the higher centres is reduced, thus initiating sedation, anxiolysis, anticonvulsant effect and amnesia.4 Midazolam also causes muscle relaxation by mimicking the inhibitory action of glycine.
Benzodiazepines can cause a side-effect of respiratory depression, mainly due to a reduced sensitivity of the central carbon dioxide chemoreceptors, which therefore lessens the ability of the respiratory centre to increase the respiratory drive in the presence of hypercarbia. Benzodiazepines also cause minor cardiovascular effects such as lowering the blood pressure by approximately 25%. There is also a compensatory increase in heart rate and therefore cardiac output is maintained.
Complications
Dental sedation is rarely associated with serious complications but minor adverse effects can be frequent. Clinicians should be aware that anxiety-related complications can also occur in patients undergoing sedation. For instance, medical emergencies may be triggered by anxiety, such as in patients with epilepsy or asthma.
Clinicians who provide conscious sedation should be able to recognize and manage sedation-related complications. With regards to inhalational sedation, there are few potential complications which may occur. These include equipment failure, inadequate sedation, poor patient experience and, rarely, nausea or vomiting. Inhalational sedation can be unpredictable in an adult, therefore this paper focuses primarily on potential complications of intravenous sedation.
Complications can occur at any stage, hence they have been divided into three sections: Pre-sedation, Peri-sedation and Post-sedation (Table 2).
Pre-sedation | Cannulation-related | Failure |
Extravasation | ||
Haematoma intra-arterial | ||
Poor case selection | ||
Peri-sedation | Drug-related | Over-sedation |
Under-sedation | ||
Respiratory depression | ||
Cardiovascular depression | ||
Paradoxical effects | ||
Disinhibition | ||
Hiccups | ||
Sexual fantasies | ||
Allergies | ||
Treatment-related | Procedural time | |
Post-sedation | Hypotension |
Pre-sedation
Cannulation-related
Failure
Cannulation may be challenging in patients with anxiety, obesity, a history of difficult venepuncture, previous intravenous drug use and even in cold weather. Other reasons for cannulation failure could be due to patients having collagen disorders, increased difficulty in elderly patients or in patients who have had frequent intravenous access due to their medical history, such as patients with haematological conditions. Failure may occur if a suitable vein cannot be identified or there is difficulty in inserting the cannula into the lumen of a vein. The vein may be completely missed, the needle may be pushed completely through the vein, or flashback may not occur if the wall of the vein is entered instead of the lumen.
Most suitable veins can be found in the dorsum of the hand or the antecubital fossa (Figure 1). An alternative site is colloquially known as the Houseman's as it is regarded as the ‘go-to’ vein for Senior House Officers; the cephalic vein. The following steps for cannulation are listed below and are illustrated in Figure 2:
Tips for cannulation
Extravasation (tissuing)
This occurs when the cannula enters the extravascular tissues instead of the venous circulation. This occurs if the needle fails to penetrate the lumen or completely crosses the vein, resulting in the cannula being positioned in the subcutaneous tissues. This can be readily identified by localized swelling after flushing 0.9% saline through the cannula (Figure 3). If this occurs, the cannula should be removed and a new cannula will need to be sited.
Haematoma
Although this is a complication which is usually only identified post-sedation, it is caused pre-sedation. Haematoma can occur when blood leaks out of the cannula site if the cannula has come out through the other side of the vessel wall. In order to prevent this, correct insertion of the cannula is vital as well as application of pressure over the site on removal of the cannula.
Intra-arterial insertion
This is a rare incident, historically occurring when a ‘butterfly’ or simple needle was used. Anatomical knowledge and site selection is fundamental for prevention. If this occurs, the cannula must be removed, pressure should be applied to the site and the arm should be raised. Referral to a hospital is required for further management.
Poor case selection
Reasons for this may be due to poor venous access or case complexity which exceeds the sedation window. Furthermore, the potential for poor compliance should also be assessed at initial consultation. For instance, a patient with needle phobia should be asked if this is due to intra-oral or extra-oral needle phobia before a decision is made to undertake intravenous sedation.
Peri-sedation
Drug-related
Respiratory depression
This is the most frequent and significant complication of intravenous sedation with Midazolam.
As aforementioned, benzodiazepines cause respiratory depression and most patients have a reduced rate and depth of breathing. This effect occurs mainly within the first 10 minutes of sedation but may occur at any stage. Other causes of respiratory depression are over-sedation, positioning of the patient, especially with extraction of lower molars which may cause depression of the mandible, allergy to the benzodiazepine agent and inhalation of foreign objects. It is important to check airway patency and to ensure that the neck is in a neutral position to prevent airway obstruction.
Obstructive sleep apnoea is another cause for respiratory depression in sedation. Patients with obstructive sleep apnoea must be assessed owing to the risk of further airway obstruction, as well as increased sensitivity to sedation. This highlights the importance of continuous pulse oximetry and adequate monitoring to identify any degree of respiratory depression.
Hypoventilation can also cause hypoxia and carbon dioxide retention. If this happens, the patient's neck should be extended and the patient should be asked to take deep breaths. Usually this alone is sufficient to manage respiratory depression. If, in the rare instance where the latter is unsuccessful, the airway should be opened using a head tilt chin lift or jaw thrust and a ventilating bag with oxygen should be used to provide intermittent positive pressure ventilation. If this measure fails to resolve the problem, slow intravenous Flumazenil 500 mcg should be administered together with continued ventilation and encouragement for the patient to breathe.
Over-sedation
The Rapid Response Report (2008) highlighted the risk of over-sedation in adult conscious intravenous sedation and resulted in the discontinuation of high strength Midazolam 5 mg/ml (2 ml and 10 ml ampoules) or 2 mg/ml (5 ml ampoule), which has since been replaced with low strength Midazolam (1 mg/ml in 2 ml or 5 ml ampoules).5 However, if over-sedation does occur to a small degree, this may result in a patient becoming uncooperative and may be caused by the sedationist not being able to identify signs of sedation properly, not titrating the drug appropriately, or the patient may have a delayed reaction to the sedative. Signs and symptoms of over-sedation may include snoring, not opening the mouth, not obeying verbal commands, drowsiness, poor concentration and co-ordination, dizziness and mental confusion. Over-sedation may increase the risk of deterioration and loss of consciousness such that there may be a loss of the airway.
Mild over-sedation in inhalational sedation can cause the patient to become alarmed and attempt to remove the nasal mask. This may result in loss of co-operation for inhalational sedation in future. For both inhalational and intravenous sedation, the drug should be titrated and subtle signs of sedation should be recognized. Consideration should also be given for past doses of sedation at previous visits for patients. Elderly patients may also require an alteration in the titration dosage to minimize the risk of over-sedation.
Under-sedation
This may affect treatment success and may even lead to treatment being abandoned as a result of poor compliance. Under-sedation will also increase a patient's dental phobia and may result in refusal of sedation in future. Monitoring of patients' anxiety and response to treatment during sedation will help assess this. As with over-sedation, prevention is essential through titration to optimize sedation prior to commencement of treatment. Management of under-sedation must not include delayed ‘topping up’ of the dose of Midazolam as this is ineffective after the initial sedation titration has been carried out. However, despite under-sedation being not ideal, treatment may be attempted if patient co-operation permits or more likely may have to be stopped.
Cardiovascular depression
Both Nitrous Oxide and Midazolam have minimal cardiovascular effects. Midazolam decreases sympathetic activity and can cause hypotension within safe limits. Furthermore, the heart rate may reduce during sedation due to anxiolysis, but usually the heart rate will remain above the normal resting heart rate due to baroreceptor reflexes compensating for a fall in blood pressure. Occasionally, there can also be an increase in heart rate due to inadequate administration of local anaesthesia and the patient feels pain. Alternatively, bradycardia may also arise due to over-sedation. Another cardiovascular effect to be aware of is the possibility of postural hypotension occurring due to supine positioning of the patient during treatment. A sufficient period for monitoring recovery is essential.
Paradoxical effects
This occurs when a patient's anxiety is increased rather than reduced and is more common in children and adolescents. In such an instance, one may think additional Midazolam may be beneficial but this often exacerbates the problem. In this case, treatment should be abandoned and the patient should be allowed to recover. Alternative sedation modalities, such as oral Midazolam, may be better suited.3 Propofol may also be advantageous over oral Midazolam as there are fewer incidences of paradoxical effects.
Failure of local anaesthesia can also cause a paradoxical effect as a patient's anxiety levels may indicate sedation is inappropriate for the level of anxiety. If the paradoxical reaction is due to a poor assessment of the patient's anxiety levels or the patient becomes distressed at cannulation, oral Midazolam may be more appropriate. Appropriate pre-assessment of the patient is required to ensure that the most effective anxiety management technique is chosen.
Disinhibition
This is defined as an unexpected altered mental state or acute excitement, which may manifest in a number of ways including aggression, hostility, agitation, talkativeness, impulsivity, excitation, disorientation or hallucinations after sedation. There may also be dysphoria or depression. It is difficult to predict in which types of patient this is more likely to occur, but associated factors are thought to be extremes of age (the very young or elderly), history of psychosis or other psychiatric disturbances, history of violent behaviour, alcoholics, drug use and high pre-operative anxiety.6,7 Management of this complication is mainly by the dental team addressing this with the patient and determining whether treatment can be completed. In some cases, treatment may have to be abandoned.
Hiccups
Some patients experience hiccups after intravenous Midazolam. This is self-limiting but may remain for several hours or overnight. The mechanism for this is not fully known but is thought to be caused by over-sedation, rapid delivery or a combination of both factors. The patient should be reassured that there is no risk associated with hiccupping. Usual management of normal hiccups can also be effective, such as giving the patient a drink.
Sexual fantasies
This is a known adverse effect reported in the literature in patients who have received intravenous sedation with Midazolam.8 During sedation, there must always be at least a second person present who not only monitors the patient but also serves as a chaperone. This should also be the case when a patient is being recovered.
Allergies
Benzodiazepine allergy is rare and there have been few reported cases of anaphylaxis.9 Clinicians should be aware of signs of a type I hypersensitivity reaction, as well as signs of potential anaphylactic reaction. A thorough medical history should be taken to assess for allergies. In the rare event of an anaphylactic reaction, the anaphylaxis algorithm should be followed, including administration of intramuscular adrenaline which may be life-saving.10 It is imperative that the patient is not given Flumazenil in allergic reactions due to the rebound effect of the Midazolam.
Treatment–related
Procedural time
This may occur if the treatment duration exceeds the sedation window and a patient recovers before treatment has been completed. This sedation window can vary from patient to patient, therefore appropriate treatment planning is required to ensure that the appropriate sedation technique is selected related to treatment time. This should be identified at the assessment visit by accounting for factors such as procedural complexity and operator experience. For example, if there are multiple anticipated surgical extractions, multi-visit treatment should be arranged or general anaesthesia may be more suitable.
Post-sedation
Hypotension
This is defined as a systolic blood pressure of less than 90 mmHg and can occur due to a decrease in the systemic arterial blood pressure following intravenous sedation. This is more common in elderly patients.11 Continual non-invasive blood pressure monitoring should be undertaken as per recent guidelines.12 Careful titration of the sedative should be carried out in patients with a low pre-operative blood pressure. These patients should also be slowly moved from a supine to seated position owing to the risk of postural hypotension as discussed previously. Although postoperative hypotension is self-limiting and does not require treatment as such, encouraging oral fluids postoperatively can, to some extent, help increase blood pressure.
Delayed recovery
Recovery following Nitrous Oxide sedation is usually rapid and occurs within several minutes. However, intravenous Midazolam recovery can be more variable due to redistribution of the drug from the receptor sites. Management of this involves careful monitoring and patience. Flumazenil should not routinely be given in cases of delayed discharge with no significant respiratory depression.
Measures to check recovery include patients being stable on their feet, able to walk unaided and Romberg's sign (no swaying or falling when patients have their eyes closed and are standing with their feet close together).
Nausea/vomiting
This is most often associated with general anaesthesia rather than sedation.13 Should this occur, it is more likely to be anxiety-related rather than directly caused by Midazolam or Nitrous Oxide. However, if patients report a history of this post-sedation, an anti-emetic drug, such as Metoclopramide, may be beneficial during sedation induction. It is important to ensure that the anti-emetic does not cause sedation itself.
The Intercollegiate Advisory Committee for Sedation in Dentistry (IACSD) Guidelines state that there is conflicting information regarding whether patients should be fasted or not prior to conscious sedation.12 The guidelines also state that, with minimal and moderate sedation, airway reflexes are preserved. However, if over-sedation takes place, these reflexes may be lost and there is a risk of potential aspiration. There is also a warning that clinicians who sedate patients who are not fasted should be able to justify their reasoning behind this.
Conclusions
Conscious sedation can be an effective means for managing anxiety in dental patients. Fortunately, complications of sedation are rare; providing dental team members have received satisfactory sedation training and adequate monitoring of the patient is undertaken during sedation. Patient selection and assessment is also imperative to reduce complications.
Sedation practitioners should be aware of the recent guidelines published by the IASCD.12 This document summarizes key aspects of delivery of sedation, including patient assessment, perioperative monitoring, complications and assessment of patient recovery. Overall, complications may occur at several stages of sedation, but it is prevention that is vital.