Despite efforts at prevention, complications and adverse drug reactions (ADRs) will arise during and after the administration of drugs for the management of pain or anxiety. In the office that has prepared for these situations, there is a greater likelihood of a successful outcome than in the unprepared or ill-prepared office. Many states, provinces, and specialty groups require that the dental office team be capable of correctly identifying and managing specific ADRs associated with parenteral sedation and general anesthesia.^1,2 These emergencies are reviewed in this chapter.

Pallasch³ has proposed the following classification of ADRs:

According to Pallasch’s system, there are three major methods by which drugs may produce adverse reactions:

Most ADRs are not life threatening. There are, however, potential responses that are life threatening, requiring immediate and effective management if the patient is to fully recover. These include the overdose reaction and the allergic response. A third, the idiosyncratic reaction, is also reviewed.

Overdose reaction (also known as “toxic reaction”) refers to those signs and symptoms manifested as a result of an absolute or relative overadministration of a drug producing elevated blood or plasma levels of that drug in specific organs (termed target organs) of the body. For central nervous system (CNS)–depressant drugs, an overdose occurs when the blood level of the drug becomes overly high in the cerebral circulation.⁴ Clinical manifestations of an overdose are related directly to the normal pharmacologic actions of the agent. For example, in therapeutic doses, barbiturates produce a mild depression of the CNS, which results in sedation or hypnosis (desirable effects). Barbiturate overdosage produces a more profound depression of the CNS, with respiratory or cardiovascular depression and a possible loss of consciousness.

Allergy is a hypersensitive state acquired through exposure to a particular allergen, reexposure to which brings about a heightened capacity to react.⁵ Clinically, there are a variety of manifestations through which allergy expresses itself. These include drug fever, angioedema, urticaria, dermatitis, depression of blood-forming organs, photosensitivity, and anaphylaxis. Certain drugs are more likely than others to elicit allergic reactions, and allergic reaction is theoretically possible with any substance.

In contrast to overdose, in which clinical manifestations are related directly to the pharmacology of the causative agent, the clinical response observed in an allergic reaction is mediated by an exaggerated response of the immune system. The degree of this response determines the severity of the allergic reaction. Allergic responses to a barbiturate, a local anesthetic, an antibiotic, a bee sting, peanuts, and shellfish are produced by the same mechanism and may appear clinically similar. Management of all allergic reactions is basically the same, whereas overdose reactions to the first three agents listed are quite dissimilar clinically and require different management.

Idiosyncrasy or idiosyncratic reactions are those ADRs that cannot be explained by any known pharmacologic or biochemical mechanism. Another definition is that an idiosyncratic reaction is any ADR that is neither an overdose nor an allergic reaction. An example of an idiosyncratic reaction is CNS stimulation (excitation or agitation) produced after the administration of a known CNS depressant such as a barbiturate.

Idiosyncratic reactions span an extremely wide range of clinical expression. For example, depression after administration of a stimulant, stimulation after administration of a depressant, and hyperpyrexia after administration of a muscle relaxant are all idiosyncratic reactions. It is usually impossible to predict in whom such reactions will develop or, indeed, the nature of the resulting idiosyncratic reaction.

Because of the unpredictability of the nature and occurrence of idiosyncratic reactions, their management is of necessity symptomatic. Of primary importance in the management of idiosyncrasy is basic life support (P → A → B → C): maintaining the airway and ensuring adequate ventilation and circulation, followed by “D” (definitive care). If seizures develop, management is based on airway maintenance and prevention of injury during the seizure.

It is thought today that virtually all instances of idiosyncrasy have an underlying genetic mechanism.⁶ These genetic aberrations remain undetected until the individual receives a specific drug, such as succinylcholine, which then produces its bizarre (nonpharmacologic) clinical expression.

Two major forms of ADR, overdose and allergy, are reviewed in this chapter; in addition, other emergency situations are discussed. Successful demonstration of the ability to manage these situations is frequently a requirement of the permitting process for parenteral sedation and general anesthesia. These complications are listed in Box 34-1.

OVERDOSE

Whenever CNS-depressant drugs are administered, the possibility may exist that an exaggerated level of CNS depression might develop. This might be noted clinically as a slightly oversedated patient, or it might result in an unconscious, apneic patient.

The group of drugs most likely to produce an overdose is the barbiturates. Barbiturates represented the first major breakthrough in the pharmacologic management of anxiety, and because of this, adverse reactions, such as allergy, addiction, and overdose, were tolerated. In the 1960s, with the introduction of the benzodiazepines (drugs that do not possess the same potential for abuse and overdose), barbiturate use declined. Description of their use in dentistry has been dropped from this edition. Previous editions of SEDATION, a Guide to Patient Management contain complete description of their use.⁷

Although the barbiturates present the greatest potential for adverse reaction, the opioid analgesics are involved with the greatest number of clinically significant episodes of overdose and respiratory depression. This is simply because opioids are more widely used than the barbiturates. As discussed elsewhere (see Chapters 7, 10, and 35), the use of opioids is popular in pediatric sedation. Opioids are often administered intravenously in conjunction with antianxiety drugs to aid in sedation and pain control in the adult patient. Goodson and Moore reported on 14 pediatric dentistry cases in which the administration of opioids (and other drugs) led to seven deaths and three instances of brain damage.⁸ Several opioids were implicated in these reactions: alphaprodine (7), meperidine (6), and pentazocine (1).

Benzodiazepines are significantly less likely to produce overdose than barbiturates and opioids, a major reason they are the most commonly administered drugs for the management of fear and anxiety.

Predisposing Factors and Prevention

The clinical efficacy of a drug depends, in large part, on its absorption into the cardiovascular system and on subsequent blood levels of the drug in various organs of the body. Only the inhalation and intravenous (IV) routes of drug administration permit titration. With oral, intranasal (IN), and intramuscular (IM) administration, absorption is more erratic, as demonstrated by the wide range of variability in clinical effectiveness. The normal distribution curve becomes important when drugs are administered via those nontitratable routes. “Average” drug doses are based on this curve; therefore diazepam 5 mg orally, provides a desired effect (anxiolysis [minimal sedation]) in the majority of patients receiving it. For some patients (about 15% of the population), however, the 5-mg dose is ineffective; these patients require a larger dose to attain the same clinical effect. These patients, termed hyporesponders, are not at risk for potential overdose when given an average dose because a lack of adequate sedation is the clinical result.

The potential danger in the use of drugs lies with patients for whom an average 5-mg dose of diazepam is too great. These are persons who are quite sensitive (not allergic) to this drug and require smaller than usual doses to obtain clinically effective sedation, the so-called hyperresponders. It is normally not possible to predict the 15% of the population that will react in this manner. A history of a prior ADR may provide a clue to this occurrence. The medical history questionnaire should be examined carefully in relation to all prior drug reactions. When a history of drug sensitivity is obtained, great care should be exercised if barbiturates and opioid analgesics are to be used. Lower-than-average doses should be administered or different drug categories substituted. Nonbarbiturate sedative-hypnotic drugs, such as the benzodiazepines and the opioid agonist/antagonists, may be used in place of these drugs.

Although the clinical nature of the overdose cannot always be predicted, there is another way in which these drugs can produce this reaction—a way that is preventable. It relates entirely to the goal being sought by the dentist when these drugs are administered. Some clinicians administer CNS-depressants, such as barbiturates and opioids, seeking to achieve deep levels of sedation in more fearful patients. When these drugs are used in this manner via the oral, IN, or IM routes of drug administration, potential for overdose increases. Most dentists who administer barbiturates in their practices encounter patients who become uncooperative (less inhibited) after receiving these drugs. The planned procedure cannot be completed because of the difficulty in managing a patient who is slightly overdosed on barbiturates. Larger doses of the barbiturate given to a fearful patient in an attempt to produce deeper levels of sedation may produce greater degrees of CNS depression, with possible loss of consciousness and significant respiratory depression.

Administering any CNS depressant seeking to obtain deeper levels of sedation via routes of administration in which titration is not possible is foolhardy and an invitation to overdose. It can be neither recommended nor condoned. Only those techniques permitting titration should be used when deeper levels of sedation are sought, and then only when the dentist and entire sedation team are thoroughly familiar with both the technique and the drugs to be administered and are able to manage all possible complications associated with the procedure.

The inhalation and IV routes are the only routes that permit titration. A factor to be remembered regarding inhalation and IV sedation is that absorption of the drugs into the systemic circulation occurs rapidly, so drug responses (both therapeutic as well as adverse) develop suddenly. Titration remains the greatest safety feature these techniques possess and should always be used when possible. Table 34-1 summarizes the recommendations made throughout this book for the various routes of drug administration.

Table 34-1 Summary of Routes of Drug Administration Control Over Technique

Clinical Manifestations

Sedative-Hypnotics, Including Barbiturates

Barbiturates produce depression of a number of physiologic properties, including nerve tissue; respiration; and skeletal, smooth, and cardiac muscle. The mechanism of action (sedation and hypnosis) is depression at the level of the hypothalamus and the ascending reticular activating system (RAS), which produces a decrease in the transmission of impulses to the cerebral cortex. Further increases in barbiturate blood level produce depression at other levels of the CNS, such as profound cortical depression, depression of motor function, and finally depression of the medulla. This is represented diagrammatically as follows:

Minimal-to-moderate sedation (calming) → Moderate-to-deep sedation (hypnosis, sleep) → General anesthesia (unconsciousness with progressive respiratory and cardiovascular depression) → Respiratory arrest

Minimal Sedation, Moderate Sedation, and Deep Sedation

At low (therapeutic) blood levels the patient appears calm and cooperative (minimal-to-moderate sedation). As the CNS-depressant drug level in the cerebral circulation increases, the patient falls into a rousable sleep (moderate-to-deep sedation). The dentist will notice the patient’s inability to keep his or her mouth open despite reminders to do so.

In addition, when barbiturates are administered, patients at this level of barbiturate-induced CNS depression tend to overreact to stimulation, especially noxious stimulation. An unsedated adult patient may grimace in response to a painful stimulus; an adult moderately to deeply sedated with barbiturates commonly demonstrates an exaggerated response, perhaps yelling or jumping. This reflects a loss of self-control over emotion that is associated with the CNS-depressant action of the barbiturate. This reaction to noxious stimuli is extremely uncommon when benzodiazepines are administered for sedation.

With continued elevation of the barbiturate blood level, hypnosis (sleep) ensues, with a minor degree of respiratory depression (decreased depth and increased rate of ventilation). At this level of CNS depression, there is usually no adverse action on the cardiovascular system, only a slight decrease in blood pressure and heart rate, similar to that occurring in normal sleep. Dental treatment cannot be continued at this level of CNS depression because the patient is unable to cooperate with the dentist by keeping his or her mouth open and may require assistance in maintaining airway patency (head-tilt). The patient still responds to noxious stimulation but in a sluggish manner. This patient requires rescue from deep sedation until such times as they return to moderate sedation levels.

General Anesthesia

With further elevation of the barbiturate blood level, the degree of CNS depression broadens so that the patient is now unconscious (incapable of response to sensory stimulation, loss of protective reflexes with attendant inability to maintain an airway). Spontaneous respiratory efforts may still be present; however, with even further increase in barbiturate blood levels, medullary depression occurs, which is clinically evident as respiratory and cardiovascular depression. Respiratory depression is noted as shallow breathing movements at a slow or rapid rate. Ventilatory excursions of the chest are not an indication that air is entering or leaving the lungs but only that the patient is trying to bring air into the lungs. Cardiovascular depression is evident as a continued decrease in blood pressure (caused by medullary depression and direct depression of the myocardium and vascular smooth muscle) and an increased heart rate. The patient develops a shocklike appearance and has a weak and rapid pulse and cold, moist skin.

Respiratory Arrest

As the barbiturate blood level continues to increase, or if the patient is not managed adequately in the previous stage, respiratory arrest will occur. Respiratory arrest is readily managed with controlled ventilation. If ventilation is not adequately provided, cardiac arrest will ensue.

Other nonbarbiturate sedative-hypnotic drugs (i.e., benzodiazepines) also possess a potential to produce overdose, although this is quite a bit less likely to occur as with the barbiturates. The potential for overdose varies greatly from drug to drug, and to varying degrees all sedative-hypnotic drugs have this potential.

Opioid Agonists

Meperidine, morphine, fentanyl, alfentanil, and sufentanil are frequently used parenteral opioids. Meperidine and fentanyl are the most popular.

Meperidine, like most opioid agonists, exerts its chief pharmacologic actions on the CNS. Therapeutic doses of meperidine produce analgesia, sedation, euphoria, and a degree of respiratory depression. Of principal concern, of course, is the respiratory depressant action of the opioid agonists. They are direct depressants of the medullary respiratory center. In humans respiratory depression from opioid agonists is evident even at doses that do not disturb the level of consciousness. Respiratory depression produced by opioids is dose dependent: The larger the dose, the greater the level of respiratory depression. The opioid agonist/antagonists nalbuphine and butorphanol offer the combination of analgesia and sedation with minimal respiratory depression.

Death from opioid overdose almost always results from respiratory arrest. All phases of respiration are depressed: rate, minute volume, and tidal volume. The respiratory rate may fall below 10 breaths per minute. Rates of 5 to 6 breaths per minute are not uncommon. The cause of this decreased respiratory rate is a reduction in responsiveness of the medullary respiratory centers to increases in carbon dioxide tension (Pco₂) and also a depression of the pontine and medullary centers that are responsible for respiratory rhythm.

The cardiovascular effects of meperidine are not clinically significant when the drug is administered within its usual therapeutic dose range. Following IV administration of meperidine, however, there is normally an increase in the heart rate produced by the atropine-like vagolytic properties of meperidine. Even at overdose levels the blood pressure remains quite stable until late in the course of the reaction, when it falls, primarily as a result of hypoxia. The administration of O₂ at this time will produce an increase in blood pressure despite continued medullary depression. Overly high blood levels of opioid agonists can lead to loss of consciousness.

Overdose reactions to both the sedative-hypnotics and opioid agonists are produced by a progressive depression of the CNS that is manifested by alterations in the level of consciousness and as respiratory depression that ultimately results in respiratory arrest. The loss of consciousness produced by barbiturates or opioid agonists is not always the result of unintentional overdose—these drugs are commonly administered as the primary agents in general anesthesia (see Chapter 31). However, when moderate sedation is the goal, unintended loss of consciousness and respiratory depression/arrest must be considered as complications of drug administration.

The duration and the degree of this clinical reaction vary according to the route of administration, the dose administered, and the patient’s individual sensitivity to the drug. In most situations oral and rectal administration result in reduced CNS depression but with a longer duration; IM, IN, and submucosal administration result in a more profound level of depression of relatively long duration, whereas IV administration produces the most profound level of depression, but of shorter duration than that seen with the other techniques. The onset of respiratory depression after IV administration may be quite rapid, whereas that following oral or rectal administration is considerably slower. Onset is intermediate in IM, IN, and subcutaneous administration.

Management

Sedative-Hypnotic Drugs

Management of sedative-hypnotic drug overdose is predicated on correcting the clinical manifestations of CNS depression. Stated another way, according to the “new” definitions of sedation from the American Society of Anesthesiologists⁹ and the American Dental Association,¹⁰ the dentist administering sedation must be capable of “rescuing” the patient who inadvertently descends into a level of CNS-depression beyond that which is intended.

Of primary importance is recognition and management of respiratory depression through the administration of basic life support (BLS). Benzodiazepines can be reversed through administration of the specific reversal agent, flumazenil. Unfortunately, there is no effective antagonist that reverses the CNS-depressant properties of the barbiturates.

Diagnostic clues to the presence of an overdose of a sedative-hypnotic drug include the following^8a:

• Recent administration of a sedative-hypnotic drug

• Lack of response, or extremely lethargic response, to sensory stimulation. (Decreased level of consciousness: sleepy → unconscious)

• Respiratory depression (rapid rate, shallow depth)

• Loss of motor coordination (ataxia)

• Slurred speech

Step 1: Terminate Treatment. The rate at which clinical signs and symptoms of overdose develop will vary with route of administration. Onset following IV administration will occur within minutes, within 10 to 30 minutes following IM administration, and within 45 minutes to an hour following oral administration.

Step 2: P-Position the Patient. The conscious patient may be placed in any position which is comfortable for them; however, in the patient who is either semiconscious or unconscious, the supine position with his or her legs elevated slightly is much preferred (Figure 34-1). The goal in this scenario, regardless of the level of consciousness, is to maintain adequate cerebral blood flow.

Step 3: A-Airway, B-Breathing, C-Circulation; (Basic Life Support), as indicated. A patent airway must be ensured and the adequacy of breathing assessed. Head-tilt or head tilt–chin lift may be necessary for airway patency at this time (Figure 34-2). The presence or adequacy of the patient’s spontaneous ventilatory efforts is next assessed by the rescuer, who places his or her ear 1 inch from the patient’s mouth and nose, listening and feeling for exhaled air while looking at the patient’s chest to determine whether spontaneous respiratory efforts are present. Maintenance of a patent airway is the most important step in the management of this patient. Step 4b, (see later discussion), providing adequate oxygenation, is contingent on successfully maintaining a patent airway.

Step 4: D-Definitive Care

Step 4a: Summon medical assistance, if needed. In a situation in which the patient loses consciousness following barbiturate administration, it might be prudent to consider summoning medical assistance. The requirement for medical assistance varies depending on the dentist’s training in airway management and anesthesiology. If the patient remains conscious but is overly sedated, seeking medical assistance is more of a judgment call by the dentist. When in doubt, it is always wiser to seek assistance sooner rather than later. Inadvertant loss of consciousness is highly unlikely to be noted when benzodiazepines are administered as the sole sedative agent.

Step 4b: Administer oxygen. This patient may exhibit different types of breathing. He or she may be conscious but overly sedated, responding, but slowly, to painful stimuli. In this situation the patient will probably be able to maintain his or her own airway and be breathing spontaneously and somewhat effectively (as noted on the pulse oximeter). The rescuer need only monitor the patient, assist with airway maintenance (e.g., head tilt–chin lift) and, if desired, administer oxygen through a demand valve or nasal cannula.

Figure 34-1 The unconscious patient should be placed in the supine position with the legs elevated slightly.

(From Malamed SF: Medical emergencies in the dental office, ed 6, St Louis, 2007, Mosby.)

Figure 34-2 The head tilt–chin lift technique and “look-listen-feel.”

The patient might be more deeply sedated and barely responsive to stimulation, with a partially or totally obstructed airway. In this situation assisted ventilation is essential in addition to airway maintenance. With patency of the airway ensured, the patient should receive oxygen via full-face mask or nasal hood. If spontaneous breathing is present but shallow, assisted positive-pressure ventilation is indicated. This is accomplished by activating the positive-pressure mask just as the patient begins each respiratory movement (just as the chest begins to expand). The positive-pressure mask is activated by depressing the button on top of the mask until the patient’s chest rises and then releasing the button. With the self-inflating bag-valve-mask device, the bellows bag is squeezed at the start of each inhalation. With both devices, an airtight seal of the mask and head-tilt must be maintained at all times. If respiratory arrest occurs (no visible respiratory efforts), controlled artificial ventilation (rescue breathing) must be initiated. The recommended rate for the adult is one breath every 5 seconds (12 per minute) and one breath every 3 seconds for the child aged 1 to 8 years (20 per minute) and the same rate for the infant younger than 1 year old (20 per minute).¹¹ Expansion of the patient’s chest is the only sure sign of successful ventilation. Overinflation should be avoided as this leads to abdominal distention, resulting in inadequate ventilation and an increased risk of regurgitation.

Step 4c: Monitor vital signs. The patient’s vital signs should be monitored throughout the episode. Blood pressure, heart rate and rhythm, pulse oximetry and respiratory rate are monitored and recorded every 5 minutes. A member of the emergency team is assigned to this task. If the blood level of the sedative-hypnotic drug increases significantly, blood pressure may decrease while the heart rate increases. In the absence of blood pressure and pulse (e.g., cardiac arrest), chest compressions must be initiated immediately.

In most cases of barbiturate or nonbarbiturate sedative-hypnotic (e.g., benzodiazepine) drug overdose, the patient can be managed in this manner until the cerebral blood level of the drug decreases and the patient returns to the desired level of CNS-depression (consciousness returns) or until emergency assistance arrives. Recovery occurs as a result of redistribution of the drug within compartments in the body, not biotransformation. The patient becomes more alert and responsive, breathing improves (becomes deeper), and if the blood pressure had been depressed, it returns to near baseline levels. The length of time for this process to occur depends on the drug administered (short-acting versus long-acting drug) and its route of administration.

Step 4d: Establish an intravenous line, if possible. If an IV infusion has not previously been established, it is prudent to establish one at this time, if training and availability of equipment permit. Although there are no effective antidotal drugs for barbiturate overdose, hypotension may be treated effectively through intravenously administered solutions or drugs. As blood pressure decreases, however, veins become progressively more difficult to locate and to cannulate. Gaining venous access at the earliest possible time may prove invaluable later. Venipuncture should be attempted only if the dentist is trained in this technique, the necessary equipment is available, and the patient continues to receive adequate care (BLS) from other personnel. A patent airway is more important than a patent vein.

Step 4e: Definitive management. Definitive management of sedative-hypnotic overdose produced by a barbiturate is based on maintenance of a patent airway and adequacy of ventilation until the patient recovers. Signs and symptoms of hypotension are evaluated by monitoring vital signs and determining the adequacy of tissue perfusion.*

Benzodiazepine overdosage may be reversed by IV or IM administration of flumazenil, a specific benzodiazepine antagonist. Flumazenil is administered intravenously at a dosage of 0.2 mg in 15 seconds, waiting 45 seconds to evaluate recovery. If recovery is not adequate at 1 minute, an additional dose of 0.2 mg may be administered. This is repeated every 5 minutes until recovery occurs or a dose of 1.0 mg has been delivered.¹²

Step 5: Recovery and Discharge. In the event that the overdose is profound, requiring assistance from emergency medical personnel, the patient may need stabilization and transportation to a hospital for observation and full recovery. Should this be necessary, the dentist should always accompany the patient to the hospital. Box 34-2 outlines the steps to follow to manage sedative-hypnotic overdose.

Box 34-2

Management of Sedative-Hypnotic Overdose

Recognize problem

(Recent administration of CNS-depressant drug: decreased level of consciousness; respiratory depression; loss of motor coordination; slurred speech)

↓

Discontinue dental treatment

↓

P−Position patient in supine position with feet elevated

↓

A→B→C−Assess airway and breathing, palpate carotid pulse for up to 10 seconds

↓

D−Provide definitive management as needed

Activate emergency medical service if recovery not immediate

Administer O₂

Monitor vital signs

Establish IV line if possible

Provide definitive management:

• Administer intravenous flumazenil for benzodiazepine overdose

• Continue P-A-B-C−for barbiturate overdose

Permit recovery and discharge patient

A, Airway; B, breathing; C, circulation; CNS, central nervous system; D, definitive care; IV, intravenous; P, position.

Most cases of sedative-hypnotic overdose involving benzodiazepines are considerably less severe, with diminished responsiveness and slight respiratory depression noted. Management consists of positioning, airway maintenance, and assisted ventilation until recovery. Emergency medical assistance is not usually required. Before discharge in the custody of a responsible adult, the patient must be capable of standing and walking without assistance. In no circumstance should the patient be discharged alone or if not adequately recovered.

Drugs used in management include oxygen and, if benzodiazepines are involved in the overdose, flumazenil. The need for medical assistance with altered consciousness varies with the training and experience of the dentist.

Opioid Analgesics

Oversedation and respiratory depression are the primary clinical manifestations of opioid overdose. Cardiovascular depression typically does not develop until late in the opioid overdose reaction, especially if the patient is placed in a supine position. Management of the patient who has received an absolute or relative overdose of an opioid is similar to that described for the sedative-hypnotic drugs with one major addition: A specific antagonist is available to reverse the clinical actions of opioid agonists.

Steps in the management of this situation follow. The clinical picture may vary from minor alterations in consciousness, with minimal respiratory depression, to the unconscious, apneic patient.

Diagnostic clues to the presence of an opioid overdose include the following⁸:

• Altered level of consciousness

• Respiratory depression (slow rate; normal to deep depth)

• Miosis (contraction of pupils of the eyes)

Step 1: Terminate Treatment

Step 2: P-Position the Patient. The patient is placed in the supine position with legs elevated slightly.

Step 3: A-Airway, B-Breathing, C-Circulation; (Basic Life Support), as indicated. A patent airway is ensured, and breathing is monitored. Opioids produce a decrease in the rate of breathing with little change in tidal volume. Therefore the depth of ventilation is usually increased.

In most cases of opioid overdose the patient remains conscious, although not fully alert or as responsive. Assistance in airway maintenance may be desirable (e.g., head tilt–chin lift). With more profound depression, unconsciousness and respiratory arrest may occur, necessitating reassessment of airway and breathing. Because the cardiovascular system is relatively unaffected by opioid overdose if oxygenation is maintained (airway patency and adequate ventilations are maintained), especially in the supine patient, the blood pressure and heart rate should remain close to baseline values.

Step 4: D-Definitive Care

Step 4a: Summon medical assistance, if needed. Depending on the level of consciousness, the degree of respiratory depression, the training of the dentist in emergency care and anesthesiology, and the availability of equipment and drugs, emergency medical assistance might be indicated at this time. As noted in the prior section on sedative/hypnotic overdose, the goal in managing this situation is to “rescue” the patient from this overly deep level of CNS-depression, managing them until they either return to the “desired” level or help arrives on the scene to take over management. If unconsciousness and respiratory arrest are present, emergency medical assistance should be summoned immediately if the dentist is not well trained in anesthesiology. In the hands of a dentist well trained in emergency care and anesthesiology (e.g., general anesthesia), management of this patient may continue to include the administration of antidotal drugs (see Step 4e).

Step 4b: Administer Oxygen. Oxygen is administered and rescue breathing performed if needed. The administration of oxygen is especially important in the early management of opioid overdose. Minimal cardiovascular depression is normally present and, when present, is a result of hypoxia secondary to respiratory depression. The administration of oxygen to a patient with a patent airway prevents or reverses opioid-induced cardiovascular depression, including dysrhythmias that may be evident.

Step 4c: Monitor and record vital signs. Vital signs are monitored every 5 minutes and recorded. Should pulse and blood pressure be absent, cardiopulmonary resuscitation (P → A → B → C) is initiated immediately.

Step 4d: Establish venous access, if possible. With the cardiovascular system minimally effected by opioid overdose (with the patient in the supine position), it should be possible to establish an IV infusion in most patients. The availability of IV access will expedite definitive therapy.

Step 4e: Antidotal drug administration. Definitive management is available when an opioid is the likely cause of the overdose. Even when what could normally be considered a small dose of an opioid has been given (to a hyperresponding patient), an opioid antagonist should be administered to the patient if excessive respiratory depression (or apnea) has developed. No drug will be administered to this patient before the steps of BLS (P → A → B → C) have been assessed and performed, as needed. At this time an opioid antagonist is administered. Naloxone is the drug of choice and should, if possible, be administered intravenously to take advantage of the more rapid onset of action with this route. If the IV route is unavailable, IM administration is acceptable. The onset of action is slower after IM administration, but naloxone will prove to be effective if an opioid is responsible for the respiratory depression. Regardless of the route by which naloxone is administered, the emergency team must continue to provide the necessary steps of BLS from the time of naloxone administration until its onset of action (determined by increased patient responsiveness and more adequate and rapid ventilatory efforts).

Following IV administration, naloxone’s actions are noted within 1 to 2 minutes (if not faster) and within 10 minutes following IM administration (in the presence of a near-baseline blood pressure). Naloxone is available in a 1-ml ampule containing 0.4 mg (adult dosage form) or 0.02 mg (pediatric dosage form). The drug is loaded into a plastic disposable syringe, and when the IV route is available, 3 ml of diluent (any IV fluid) is added to the syringe, producing a final concentration of 0.1 mg/ml of naloxone (adult) or 0.005 mg/ml (pediatric). The drug is then administered intravenously to the adult at a rate of 1 ml/min until the ventilatory rate and alertness increase. In children the IV dose is 0.01 mg/kg.¹³ If naloxone is administered intramuscularly, a dose of 0.4 mg (adult) or 0.01 mg/kg (pediatric) is administered into a suitable muscle mass, such as the middeltoid (adult) or vastus lateralis (child or adult), or sublingually (if the patient is unconscious).

A potential problem when reversing opioid overdose with naloxone is the fact that its duration of clinical activity may be shorter than that of the opioid it is being used to reverse. This is especially true in cases in which a longer-acting opioid agonist such as morphine is administered; it is less likely to occur with meperidine and even more unlikely with fentanyl and its analogs alfentanil, sufentanil, and remifentanil. When the opioid action is of greater duration than the intravenously administered naloxone, the dentist and staff will notice an initial improvement in the patient’s clinical picture as the naloxone begins to act and then see a recurrence of CNS depression approximately 10 minutes or more later (following IV administration of naloxone). Because the opioid producing the overdose continues to undergo redistribution and biotransformation during this time, in the event that such a rebound effect does occur, it would quite likely be much less intense than the initial response. In cases in which longer-acting opioids (e.g., morphine) have been administered intramuscularly or submucosally, it is recommended that the initial IV dose of naloxone be followed with an IM dose (0.4 mg [adult] or 0.01 mg/kg [pediatric]). In this way, as the clinical action of the IV naloxone dose is waning, the level of naloxone from the IM dose will be reaching a peak, minimizing the likelihood of a relapse of significant respiratory or CNS depression. The administration of naloxone in opioid overdose is important but not the most critical step in overall patient management (see later discussion).

Step 5: Permit Recovery. The patient is continuously observed and monitored after the administration of naloxone until clinical recovery becomes evident. The patient may be transported to a recovery area within the dental office but should remain under constant supervision for at least 1 hour. On the other hand, if the dentist considers it prudent, the planned dental treatment may continue. Once again, whether to continue treatment of this patient at this time is a judgment that can be made only by the dentist, and only after taking into consideration the status of the patient and the level of expertise of the dentist and staff in recognizing and managing this situation. A patient demonstrating oversedation with an opioid might be considered an emergency in the office of a less well-trained (in anesthesiology and airway management) dentist, whereas in the office of a more well-trained dentist this same situation could represent nothing more than a minor occurrence, one which is readily managed in a routine manner.

If doubt exists, dental care should be discontinued. Vital signs are recorded every 5 minutes during the recovery period. Oxygen and suction must be available, and trained personnel must be present.

Step 6: Discharge. Patient discharge might require transport to a hospital facility for observation or follow-up care. In most cases, however, hospitalization is unnecessary. Following an adequate period of recovery (minimum 1 hour under observation) in the dental or medical office, the patient can be discharged in the custody of a responsible adult companion, using the same recovery criteria established for parenteral sedation and general anesthesia.

Box 34-3 outlines the steps to follow in management of opioid overdose.

Box 34-3

Management of Opioid Overdose

Recognize problem

(Altered level of consciousness; respiratory depression; miosis)

↓

Discontinue dental treatment

↓

P−Position patient in supine position

with feet elevated

↓

A→B→C−Assess airway, breathing, and circulation

↓

D−Provide definitive management as needed

Activate emergency medical service as needed

Administer O₂

Monitor vital signs

Establish IV line, if possible

Provide definitive management:

• Administer IV or IM naloxone

• Continue P−A−B−C as needed

Permit recovery and discharge patient

A, Airway; B, breathing; C, circulation; D, definitive care; IM, intramuscular; IV, intravenous; P, position.

Drugs used in management include oxygen and naloxone.

The need for medical assistance in the presence of altered consciousness or unconsciousness will depend upon the dentist’s training and experience.