Sedation of Phobic Dental Patients

Sedation of Phobic Dental Patients
With an Emphasis on the Use of Oral Triazolam
Part Two

Fred Quarnstrom, D.D.S. F.A.G.D., F.A.S.D.A., F.I.C.D.
Diplomate, American Dental Society of Anesthesiology

First Published: December 1996

Respiration

In all cases of dental sedation patients should remain awake. If the patient tends to fall asleep, they should be awakened. It is very difficult if not impossible to tell a patient who has just dozed off from one who is under general anesthesia. General anesthesia, if a person is well trained, has been described as great amounts of boredom occasionally dispersed with moments of stark terror. I cannot recommend too strongly that unless you are well equipped, well trained, certified (in some states) and have extra insurance coverage to cover deep sedation/general anesthesia, you do not want patients to be unconscious and it is not possible to tell physiologic sleep from general anesthesia without trying to wake the person up. If the patient awakes, keep them awake. If they do not awaken, you have a case of general anesthesia and all the risks associated with anesthesia. Your biggest problem and concern will be to assure that adequate respiration continues and that cardiovascular parameters remain constant.

If patients do not easily awaken in response to one's voice, one should evaluate their level of sedation to determine whether they may, in fact, be under general anesthesia or have some medical problem. With some drugs, our concern must be that we have depressed the respiration to the point that an adequate exchange of gas is not taking place. It is not the scope of this discussion to describe the treatment of respiratory depression or arrest. However, the presence of an open airway should be established, evaluation of the level of respiration assessed and vital signs should be taken. It should be noted that several studies have shown that watching the chest and/or reservoir bag move is not adequate to assure an adequate minute volume. Skin color has been relied on in the past as a way of assuring adequate tissue profusion. However, the arterial oxygen level can be dangerously low before we see the blue tinge of cyanosis. Anyway, cyanosis is no longer considered to be an adequate monitor of arterial oxygen levels. In this case a pulse oximeter and/or capnograph is invaluable in assessing the adequacy of ventilation.

To properly appreciate the importance of monitoring respiration as well as the advantages of the benzodiazepine drugs, it would be wise to review a topic we all learned in dental school but in all likelihood have not had reason to refer to in our practices. It is with that thought in mind that I offer the following section. This is not intended to be a complete discussion. It should be used as the minimal level of knowledge one can possess and still have some appreciation of what we are doing with the drugs we use.

Physiological basis of ventilation

Ventilation is the movement or circulation of air through the respiratory tract and is the principal component of respiration influenced by depressant drugs. We can control our ventilation by conscious effort, however, our bodies have an exquisite system of sensors, reflexes, and feedback loops to control ventilation involuntarily. The involuntary control originates in the chemosensitive area of the respiratory center located in the ventral portion of the medulla. Metabolic processes of our body produce carbon dioxide (CO2) which is carried dissolved in our blood. When CO₂combines with the water in our plasma, it forms carbonic acid which disassociates into hydrogen ions and bicarbonate ions. The negative logarithm of our hydrogen ion concentration determines the pH of our blood. It is this pH which stimulates the chemosensitive region of the respiratory center.

Carotid and Aortic Bodies

The carotid and aortic bodies are closely associated with major arteries of the neck. These harbor other chemosensitive formations sensitive to the low arterial oxygen levels of the blood. Their greatest influence occurs at tension below 60 torr. Because normal levels are well above this value 95-99 torr, these serve as a back-up to the central CO₂ sensitive chemoreceptors. Exceptions occur when the central chemo-sensitive area is depressed by sedative drugs or is tolerant to elevated CO₂ tensions that accompany chronic obstructive pulmonary disease (COPD). Ascending impulses from this area travel via the IX and X cranial nerves to the respiratory center.

Respiratory Center

Once the respiratory center is stimulated, impulses travel a short distance to the more dorsally located inspiratory area. This area produces descending neural impulses that lead to the inspiratory musculature causing a contraction of these muscles and inflation of the lung. Once the lung is inflated, stretch receptors ascend to depress the inspiratory area, allowing the inspiratory musculature to relax. This in turn allows the lungs to deflate.

Although the involuntary respiratory control is most important during sleep and drug induced sedation or unconsciousness, it is also important in our minute-to-minute functioning while awake. It should be remembered that this system can be overridden by voluntary control. This is important as it allows us to talk. One should not forget that while the patient is conscious ventilation can be controlled voluntarily. Simply stated, a conscious but sedated patient can be told to breathe, should hypoventilation occur.

CNS depressants can depress ventilation by a number of methods. The opioid drugs - those which stimulate the mu receptors - depress the sensitivity this system has for pH changes. This leads to a situation where the volume of air moved is less for any given concentration of CO2, but as the level of CO₂ rises the increase in respiration to this increase is much less than normal (the response curve is "shifted to the right" but the slope of the curve is also depressed). This can lead to high CO₂ levels. If the CO₂ exceeds concentrations of 10%, it too is a respiratory depressant. The mu antagonists have also been found to depress peripheral hypoxic drive. Benzodiazepines, in contrast to the opioids, tend to depress the slope of the CO₂ response curve but do not appear to shift it to the right. It is fairly difficult to cause serious problems to respiration with benzodiazepines, with the possible exception of midazolam.

One further drug deserves mention. Subanesthetic doses of nitrous oxide (30% to 60%), such as used for sedation in dental practice, have little if any influence on the CO₂ response but have produced a 65% reduction in the hypoxic drive. This could present serious problems if a deeply sedated patient has had CO₂ mechanism depressed by opioid drugs or is a COPD patient.

Monitoring techniques

The solution to the aforementioned problems lies in several areas:

Use drugs that minimally depress respiration;
Avoid combinations of different drugs that affect several areas at once, and
Monitor the patient to assure that adequate arterial oxygen levels are maintained and that CO₂levels do not increase.

Hypoventilation is characterized by a reduction in arterial oxygen tension and an elevation of arterial CO₂ tension. With the advent of pulse oximetry, it is now possible to easily monitor oxygen saturation of hemoglobin. Equipment also exists to monitor end-tidal CO₂ tension. Although elevated CO₂ tension is generally regarded as the earliest sign of hypoventilation, the equipment is extremely expensive. Pulse oximetry shows the oxygen saturation of hemoglobin. In addition, most machines also display pulse rate. Knowing the saturation of hemoglobin, one can approximate the arterial oxygen tension, assuming a normal pH of the blood. Although 90% saturation provides reasonable assurance of adequate arterial oxygen tension, 95% is preferred. One should not overestimate the value of this information. Although normal haemoglobin saturation reasonably assures adequate oxygenation, this does not rule out an elevated CO₂ tension. If the clinician supplements the patient with enriched oxygen concentrations (as is common when administering nitrous oxide) that may sustain hemoglobin saturation despite hypoventilation. Well oxygenated patients may hypoventilate to the point of significant hypercapnia. Therefore, when using pulse oximetry, oxygen supplementation should be reserved for those cases in which adequate arterial oxygen cannot be sustained, despite verbal commands. This should be a rare event when using light to moderate sedation for ASA I and II patients. By allowing the patient to breathe room air, the oximeter will function more effectively as an early warning of hypoventilation. Although oximetry is not equivalent to capnography, it is valuable in alerting the dentist that ventilation is depressed. The importance of monitoring a patient's respiration can not be overemphasized. If that patient is awake and responding to verbal commands, we can usually assume our patients are safe. If they are unconscious (asleep?), we must have more concern. Several studies of medical and dental anesthesia have shown inadequate ventilation to be the most common cause of death or brain damage. Cheney and Jastak, after reviewing malpractice cases, arrived at the conclusion that airway management represents the most common etiologic factor in brain damage and death in general anesthesia problems. It is the cases of the idiosyncratic reaction, overdose, or the patient on other drugs that were not reported to us that give us the most concern. It is possible for these patients to become unconscious. As practitioners we must be prepared to monitor and assist the respiration of such a patient if it should become necessary. To know if assistance is needed, we need to know the status of the oxygenation of the patient's tissues.

The Reservoir Bag

In the 1960's, watching the reservoir bag was used on several popular TV programs as a means of determining when it was time to discontinue surgery and give condolences to the next of kin. At least one manufacturer suggested that the presence of a reservoir bag on our nitrous oxide machines could have a negative psychologic effect on some patients. Why do we need one unless it is to monitor the passage of the patient to the great beyond? On the other hand, there have been several studies that show one should not depend on movement of the bag as an accurate indication of the adequacy of respiratory exchange. Fortunately, the lay person's medical knowledge has improved over the years and everyone can now recognize a "flat line" as the determining factor.

Pulse Oximeter

The advent of an affordable pulse oximeter has made our life much easier and the patient's life more secure. By passing two different frequencies of light through various tissues, and reading the absorption of the two frequencies and evaluating these differences, this device can determine the percentage of oxygen saturation of the arterial blood with great accuracy. In addition to O2 saturation, most equipment also shows pulse rate and some shows a pletysmograph of the pulse wave. The use of such monitoring has made general anesthesia much safer and consequently has decreased the frequency of tragic outcomes. Although not strictly necessary for sedation, the security the equipment provides would be sorely missed if I no longer had a such a device to monitor my sedation patients.

However, there is at least one possible caveat to their use: If a patient is given supplemental oxygen, their hemoglobin saturation will approach 100%. In patients with severe respiratory complications, oxygen saturation could be normal even though exchange rates were inadequate to cleanse the blood of CO₂. This could lead to high CO₂ levels and resulting low pH of the blood. As was pointed out, however, the patient will be damaged more by a lack of O2 than by high CO₂ levels. This potential problem can be circumvented by limiting sedation to patients with no significant respiratory problems.

Capnography

Equipment now exists that constantly senses a patient's expired gas. It then gives a reading of the concentration of CO₂ in these gasses. This information can be invaluable when monitoring patients with respiratory problems or those undergoing general anesthesia but it is not necessary for the sedated patient. Typically, this equipment indicates end tidal carbon dioxide (ETCO₂) concentrations. ETCO₂ is the last portion of an expired breath. The concentration of CO₂ in the expired gas at the very end of an expiration closely approximates the concentration of CO₂ in the alveoli and that of the venous blood. Many machines also show graphically the shape of the breath. This can be of interest as it quickly shows a patient who may be taking very long shallow breaths or rapid shallow breaths that could lead to respiratory insufficiency. The shape of the breath also can be an aid in diagnosing some respiratory pathology, including chronic obstructive lung disease and asthma. These machines have alarms that respond to apnea as well as high and low ETCO₂ levels, alerting the practitioner when preset parameters are broached. It is interesting to take a normal, healthy, nonsedated patient and monitor them with the pulse oximeter and capnograpy. Have this patient hold their breath for a minute and watch the reading. The capnograph immediately shows apnea, and the alarm sounds when the apnea has exceeded the preset limit, usually about 20 seconds. At one minute, the pulse oximeter usually starts to show a drop in oxygen saturation, although typically it will still be reading in excess of 95% saturation. Once the patient starts breathing, the ETCO₂ will read high until the build up of CO₂ has been removed; the oxygen saturation will continue to fall for 30 seconds to a minute. In our trials, however, we were never able to set off the low O₂ saturation alarms. The capnograph is a much more sensitive indicator of respiratory depression/cessation.

If our patient is on supplemental oxygen before they hold their breath, the pulse oximeter will normally be reading 99 to 100% saturation and will remain at that level until the person starts breathing again, even though their CO₂ levels will have climbed significantly. It is possible to counter the warnings of a pulse oximeter by having a patient on supplemental oxygen.

Cardiovascular Concerns

For our sedation patients, pulse rate and blood pressure should be monitored. In my study and in practice I have a constant pulse rate displayed by the pulse oximeter. In addition, I feel a preoperative blood pressure should be recorded and updated at least every 15 minutes, provided the patient remains awake. Should the patient become unconscious, I would assume they are under general anesthesia or have had some medical problem and I would monitor blood pressure at least every 5 minutes until I have a conscious patient.

The advantages of oral triazolam sedation

Oral sedation with triazolam is simple to administer and, because of the nature of the drug, it is convenient and safe to use. Triazolam is readily available from any pharmacy and does not require any extra equipment to administer. Reports of adverse drug reactions are rare and tend to be relatively mild. A major plus for all oral sedatives is that it is not necessary to administer an injection or start an intravenous line. (The last thing most phobic patients need is a needle puncture before they are sedated.) Patients readily accept oral sedation, although recently some have declined triazolam because of the adverse press it has generated when used as a sleeping pill. Finally, oral sedation is relatively inexpensive for our patients.

Historically, we have used barbiturates and narcotics, both of which have significant effects on respiration and circulation. Diazepam has been used with good effects, but it is slow being absorbed and has a very long half-life. On the other hand, triazolam is a drug that has been around for some time but has been used primarily to aid sleep. In this context, it has received bad press because of side effects that have shown up in patients that use it over an extended period of time. It is the most commonly prescribed sleeping pill used in the US; 7.2 million prescriptions are written annually. It should be emphasized that triazolam is not approved by the FDA as a sedative for dental purposes.

Triazolam has the advantage of being absorbed rapidly, achieving peak blood levels in 1.3 hours; its half-life is 2-3 hours, much shorter than diazepam. In addition, it may be up to eight (8) times more effective as a hypnotic than diazepam. Yet, triazolam has very little effect on the circulatory or respiratory system. Several studies have shown no changes in blood pressure, pulse, or percentage of oxygen saturation and only a slight change in respiratory rate. It is metabolized in the liver by the P450 mixed function oxidase system on the smooth endoplasmic reticulum. It is excreted 90% in the urine, 9% in the faeces. Its metabolites are not sedative as is the case with diazepam. It does react adversely when taken with a popular antacid, Cimetidine (Tagamet), which inhibits the P450 system of the liver.

Pharmacology

Structure-activity relationship

The unique properties of triazolam are attributed to its chemical configuration. The nitrogen atom prevents it from being water soluble. Medazolam has a carbon in this position and thus is water soluble and suitable for IV administration. One chlorine atom is responsible for potency; without this chlorine it is one fifth as potent. Larger alkyl substitutions also decrease potency. The second chlorine is necessary for benzodiazepine action. Bromo and nitro substitution are only weakly anxiolytic. The nitro version is anticonvulsant as illustrated by clonazepam. The triazolo ring and attached methyl group are responsible for the rapid oxidation by the liver enzymes, resulting in a short elimination half life and conversion to metabolites that are rapidly excreted. The methyl group also makes more potent.

Absorption

Triazolam reaches a rapid peak within 1.3 hours, faster in the elderly and in young women. This occurs more rapidly in daytime than at night, due to longer predose fasting period and is as much as 2 times quicker after a 12 hour fast. Eighty-five percent (85%) is absorbed into the blood stream, 15% passes through in the faeces. It is absorbed 28% faster if given sublingually where some of it is absorbed, but most of it is swallowed.

Distribution

The distribution of triazolam shows no difference in obese and normal patients. It is 89% bound to plasma, 49% to serum proteins, crosses readily into the central nervous system because of high lipid solubility, and crosses the placental barrier and milk of rats.

Metabolism and Elimination

Triazolam is oxidized in the first pass in the liver by the cytochrome P450-mediated oxidatative system. There have been 6 metabolites identified. Alpha hydroxytriazolam and 4-hydroxytriazolam make up 69% and 11% of the metabolites, respectively. Alpha hydroxytriazolam is 50-100% of the pharmacological activity of triazolam. It is present in the plasma in only very low levels and that which is present is the conjugate form and not active. Triazolam has no active metabolites. Its half- life averages 1.2 to 3.3 hours, but slower at night. Half-life is longer in the elderly because of lower liver oxidizing capacity. There is no change with kidney dialysis but it is slower with cirrhosis. Ninety-one percent (91%) is eliminated in urine and 9% in faeces within 72 hours.

Drug interactions

Cimethedine reduces the first pass liver clearance by decreased metabolism and reduction in hapatic blood flow due to decrease in cytochrome P450-mediated oxidatative system. The same effect occurs with erythromycin, isoniazid, an antitubercular agent and possibly some oral contraceptives.

Effects

Central Nervous System

All the benzodiazepines have clinically useful anti-anxiety, sedative-hypnotic, anticonvulsant and skeletal muscle relaxant properties. They all depress CNS to some degree, tending to be more anti-anxiety oriented as compared with barbiturates and other sedative-hypnotics. They depress the limbic system and areas of the brain associated with emotion and behavior, particularly the hippocampus and the amygdaloid nucleus. The major effects are attributed to an interaction with the Gamma Amino Butyric Acid (GABA) receptor complex; it alters the chloride ion channels to increase the frequency of their opening. It potentiates GABA. It is now known that there are several GABA receptor sites. Thus, in the future we may have drugs more specific to anti-anxiety with fewer side effects. Benzodiazepines also interact with the glycine receptors, alter opiate peptide concentrations and 5-HT decreases, a precursor of Seratonin.

Cardiovascular system

In normal therapeutic doses, the benzodiazepines cause few alterations in cardiac output or blood pressure when administered intravenously to healthy persons. Slightly greater than normal doses cause slight decreases in blood pressure, cardiac output, and stroke volume in normal subjects and patients with cardiac disease, but these changes are not usually clinically significant. Triazolam did not affect cardovascular dynamics in doses 4 to 8 times normal.

Respiratory system

Benzodiazepines are respiratory depressants. However, given alone to a healthy patient they have little effect. They potentiate other CNS depressants. Medazolam is one that can cause respiratory depression and apnea. Triazolam did not depress respiratory response to CO2 in doses 4 to 8 times normal.

Reproduction

In rats, slightly reduced fertility occurred but the drug did not affect their postnatal development.

Recovery

One method of measuring recovery is to have the patient stand with their eyes closed. Patients were normal after 3.5 hours with a 0.25 mg dose, after 5 hours with a 1. mg. dose, and after 7 hours with a 2. mg. dose. A visual coordination study (following a randomly moving dot with their finger) had patients back to normal after ingesting 0.25 mg in 5 hours and 0.5 mg in 11.5 hours. One study using 0.5 mg had an incident of side effects of 8% sleepiness and 4% headache, dizziness, neuritis, dry mouth.

Mechanisms of action

Benzodiazepines have two current hypotheses of receptor interaction - either a multi-receptor or a single receptor with multiple conformations. Gamma-aminobutyric acid (GABA), an amino acid transmitter in the brain, has no known function besides serving as a neurotransmitter and occurs almost exclusively in the brain. GABA reduces the firing of neurons and is an inhibitory neurotransmitter. It is the transmitter at 25 to 40 percent of all synapses in the brain, thus, quantitatively, it may be the brain's predominant transmitter.

Benzodiazepines

Diazepam relieves anxiety, but produces some drowsiness, which is tolerated after several weeks of use. Unfortunately, benzodiazepines are somewhat addicting, with withdrawal symptoms if dosage is stopped. The biggest advantage of the benzodiazepines is the fact that overdoses are rarely lethal. The dose necessary to create problems is many times the therapeutic dose. In this sense, they are among the safest drugs known.

How Benzodiazepines Act

It was established in the 1960's that benzodiazepines and many other sedatives act by affecting the synapse. Cross tolerances were shown with the barbiturates, meprobamate and alcohol. Benzodiazepines act at a different but closely related recognition site. Alcohol, barbiturates and meprobamate all act at the same site. These drugs, as opposed to the benzodiazepine drugs, all put animals to sleep with only modestly higher doses than are required for sedation. This is true in a number of other behavioral tests.

Receptor Sites

It was shown that all these drugs interact with the neurotransmitter GABA. When GABA binds with a receptor site on the neurons, it slows the neuron's rate of firing. The GABA receptor is an integral membrane protein. It extends through the bilayered outer membrane of the postsynaptic neuron. GABA has two receptors designated GABA-A and GABA-B. The A receptor changes the ion permeability of the chloride-ion. The B receptor changes the ion permeability of the potassium-ion. In both instances, the effect is the same. Research in the early 60's showed that inhibitory effects of GABA were potentiated by alcohol, barbiturates, meprobamate and benzodiazepines.

In 1977 two groups showed the existence of specific benzodiazepine receptors in the brain. GABA has similar sites. Benzodiazepines only bind to the GABAs. If either is present, the other's binding ability is enhanced. It is assumed that either effects the shape of the binding site of the other. Both binding sites are on one large protein molecule. Thus, the effects of diazepam are explained by the increased activity of GABA.The receptor sites are concentrated in parts of the brain that regulate emotional behavior. Within the limbic system, high concentrations are found in the Amygdala. A third receptor site has been shown to exist on the large protein. It is a sedative-convulsant site. This is the site of action of alcohol, barbiturates, and meprobamate and may be effected by drugs that cause convulsions. It was shown that all three sites interact with the other two sites. GABA inhibits synaptic transmission by widening the chloride-ion channels in the neuronal membrane. The receptor site looks much like eight long beads arranged side by side to form a tunnel. Each bead is a molecular helictical structure. Connecting the beads is a linear stretcher strung through the helictical beads which loops from bead to bead. Loops of this material form the A and B sites. It is through the resulting pores that chloride-ions enter the cell. The entrance of chloride-ions into the cell changes the charge across the neuronal membrane making it more difficult for the neuron to depolarize. It appears that the sedative-convulsant site is part of the chloride-ion channel. GABA increases the size of the chloride-ion channel; the more GABA, the bigger the channel. Benzodiazepines increase the effect of small levels of GABA. Benzodiazepine blockers (flumazenil) do not inhibit the effect of GABA. GABA blockers, however, block the effect of Benzodiazepines. Alcohol, barbiturates and meprobamate, by stimulating the sedative convulsant site, enlarge the chloride-ion channel in the presence of basal levels of GABA. Picrotoxin and other convulsants prevent the widening of the chloride-ion channel even in the presence of large amounts of GABA. It has also been suggested that GABA may influence both dopamine and serotonin levels in the central and peripheral nervous systems.

Contraindications to Triazolam

Before a practitioner uses any medication, they should be knowledgeable of its pharmacology. Likewise every practitioner, but particularly those using sedatives, should be able to initiate resuscitation, including cardiopulmonary resuscitation and artificial ventilation as well as assisting ventilation. The equipment necessary to provide these emergency treatments must, of course, be available. There are a few absolute contraindications to the use of triazolam. Patients who are known to be hypersensitive to triazolam or other benzodiazepine drugs should avoid its use. Myasthenia gravis patients should be avoided as triazolam has a muscle relaxation effect. Glaucoma patients should avoid all benzodiazepines as these drugs raise intraocular pressure by increasing the outflow resistance to aqueous humor. (However, this can often be reversed by pilocarpine.) All the benzodiazepine drugs are tiatrogenic and should not be given to pregnant women. As triazolam has been shown to pass through the lacrimal glands of mice into the milk, it should not be given to lactating mothers. As it is a CNS depressant, it should be given cautiously to anyone on other CNS depressants. Because of their depressant effect on the liver mechanisms that metabolize triazolam, it should be given cautiously in patients receiving cimetadine (Tagamet), erythromycin, izonizid and some oral contraceptives.

Relative contraindications

There are detailed studies of triazolam's use as a sedative with pediatric and geriatric populations and practitioners should be cautious when giving triazolam to these groups. There have been reports of suicide attempts by psychiatric patients. Suicidal tendencies were unmasked, creating this paradoxical behavior Concurrent drug administration should be avoided as the possibility exists of displacement of other drugs from albumin binding cites. The final relative contraindication is the fact that triazolam has not been approved by the FDA for dental sedation or the sedation of children.

Adverse effects

Adverse effects have been reported in less than 4 percent of patients. Most adverse effects have been reported with doses greater than .5 mg. or when combined with other CNS depressants.

The office should have an effective, efficient emergency protocol. This should include a person to be continuously in the room with the patient from the time of administration of the drug until they are judged able to leave the office. The patient should not be allowed to sleep at any time while in the office. Vital signs should be taken at regular intervals, every 15 minutes or more often if there is any indication of over-sedation, i.e. tendency to sleep, etc. Management of adverse reactions should be planned before the drug is used and reviewed on a periodic basis. It should be noted that most adverse effects will be prevented by complete history-taking, physical examination and appropriate adjustment of drug dosage. Recognition of an emergency situation must be followed by initiation of a stabilization routine. This essentially entails the A-airway, B-breathing, and C-circulation of basic cardiac life support. Opening and maintaining a patient's airway is of paramount importance as is monitoring vital signs. Calling Emergency Medical Services should follow if any doubt exists as to how to proceed.

Protocol in our office

It should be stressed that we do not want a patient who is asleep. If a patient sleeps they are over-sedated and should be kept awake by verbal commands. We do not worry if the patient is disappointed by their level of sedation because the amnesia that is common to this technique will allow them to forget most if not all of the appointment. It should be emphasized with children that they may still cry during the appointment. If they are controlled enough to allow dentistry to be safely done, they are adequately relaxed and crying, although distracting to the practitioner, is an indication of adequate ventilation.

Because dental sedation is a new, unreported use of triazolam, I feel we should be extremely cautious. I suggest not treating any person who has any medical problem, however slight.

At a pre-appointment interview, we review medical history to determine that there are no contraindications. At that time, I review with the patient the following points:

They are to have no alcohol or other sedatives for twenty-four hours before the appointment.
There should be no chance that they are pregnant.
They have none of the other contraindications.
They will have an adult take them home after the appointment and stay with them that evening.
As with all sedatives, they cannot drive, operate machinery or undertake any activity that could be hazardous. This includes such activities as walking unaided, climbing stairs, etc.
They should not undertake positions of responsibility, care of children, etc.
They should not make important decisions, legal or monetary, etc., for the rest of the day.
They should not have alcohol or other sedatives for twenty-four hours after the appointment

The Procedure

The patient comes to the office one hour before we wish to start their dental procedure. I determine the appropriate dose and have them take the triazolam at that time. Many authors have reported on the appropriate dosage for sleep enhancement. Suggested dosages range from 0.125 mg. to 0.5 mg. I administer a dose that is lower than I think will be adequate the first time I treat a patient. An assistant stays in the operatory with them for the next hour taking vital signs, blood pressure, pulse, and respiration every 15 minutes with instructions to alert me if there is any change. The assistant is instructed to talk with them to assure that they remain awake. I check to see if there is any sign of sedation at thirty minutes. If there is no sedation evident, I will administer one half the original dose. If even slight sedation is noted at that time, we normally will have adequate sedation for the procedure. (Many patients will be disappointed at the end of the forty minutes by the relative lack of sedation. They are assured that this is normal and they will be adequately sedated by the time we start.) I have found that about 75% of patients have amnesia from this point which lasts for 2-3 hours. All patients have had some amnesia of the appointment. The dental procedure is started at 45 minutes to 1 hour after administration of the drug. I continue to monitor vital signs and talk to the patient to be sure they are awake.

Once the appointment is complete we keep the patient in the dental chair until they are able to walk and I determine they are able to safely leave the office. Post operative instructions, the same as were given to the patient in the pre-appointment interview (see above), are reviewed with the adult who is going to take the patient home and watch over them the rest of the day. In addition, my home phone is given to this adult who is encouraged to call if they have any questions or problems. Finally, an assistant accompanies the patient out to the car supporting the patient so there is no chance of a fall.

It should be noted that the second appointment will normally be easier than the first. It has never been necessary to use a higher dose if the first dose was adequate. Also, as this is a class IV drug, it is necessary to keep careful accounting records on its use.

Next Page: Triazolam: a clinical study in a general dental office

Return to Dentistry On-Line Professional Pages