34: Management of Emergencies

chapter 34 Management of Emergencies

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.


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.

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.

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.


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 following8a:

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 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.)

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 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.

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:

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).

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

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.


The previous discussions dealt with overdose reactions of varying levels of severity that occur after the administration of a single drug. Although single-drug overdose can and does occur, especially after IM, IN, or submucosal administration (because of the inability to titrate to effect), many overdose reactions reported involve the administration of multiple drugs. In many of these cases, drugs such as an antianxiety drug are combined with an opioid to provide a level of sedation and some analgesia. A local anesthetic is then added to manage operative pain. Drugs in all three of these categories are CNS depressants. Added to this, in many cases, will be nitrous oxide (N2O) and oxygen (O2), adding yet another degree of CNS depression.

Whenever more than one CNS-depressant drug is administered to a patient, the dosages of all drugs must be reduced from their usual dosage to prevent exaggerated, undesirable clinical responses. As demonstrated in Table 34-2, in most of the cases reported by Goodson and Moore, this step was not taken, with disastrous results often occurring.8

Another factor must be considered, one that most health professionals do not, as a rule, give much thought when using sedative techniques: Local anesthetics themselves are CNS depressants and can produce additive actions when administered in conjunction with drugs commonly used for sedation. The maximal dosage of local anesthetic to be administered to any patient, but especially to a child or lighter-weight adult, should be based on the patient’s body weight in kilograms (or pounds). When no other CNS depressants are being administered, this maximal dose could be reached without adverse effects if the patient is an American Society of Anesthesiologists (ASA) 1 and falls within the normal responding range on the bell-shaped curve. Table 34-3 presents the maximal recommended doses of the most commonly used local anesthetics. When a local anesthetic is administered with other CNS depressants, the local anesthetic dosage should be minimized.

A primary goal of moderate sedation is to produce a cooperative patient who still possesses their protective reflexes (e.g., swallowing, coughing, maintenance of the airway). If possible, this goal should be achieved using the simplest technique available, as well as the fewest drugs possible. Polypharmacy, the combination of several drugs, is necessary in many patients to achieve the desired level of sedation and/or analgesia. The use of drug combinations, however, increases the opportunity for ADRs while making it less obvious which drug might be responsible for any problems that arise, thereby making management of the situation more complicated.

Within the individual techniques of sedation, it is suggested that single-drug regimens are preferable to combinations of drugs. Rational drug combinations are available for use in certain situations in which they are specifically indicated. With IV drug administration, the problem of severe ADRs should not occur if the technique of titration is strictly adhered to at all times. Titration is not possible with the IM, IN, and oral routes of administration. The dentist must modify individual drug dosages before their administration. Serious ADRs are more likely to occur when the technique used was one in which titration was not possible.

Consideration must also be given to the use of multiple techniques of sedation, as opposed to multiple drugs by one technique of administration. It is not uncommon for patient who is a significant management problem to receive an oral antianxiety drug before arrival at the office. This is followed by either IM, IN, or IV sedation, and inhalation sedation and local anesthesia during the course of treatment. Whenever oral sedation with CNS depressants is used, the dosages of all subsequent CNS depressants should be evaluated carefully before their administration. This is critical when nontitratable routes of drug administration are used. With inhalation and IV sedation, careful titration of CNS-depressant drugs to the patient who has previously received oral premedication will usually produce the desired level of clinical sedation with minimal risk of adverse response by the patient.

How, then, may overdose reactions best be prevented? Goodson and Moore made the following recommendations concerning the use of sedative techniques involving the administration of opioids8:

The Dentists Insurance Company (TDIC), in a retrospective study of deaths and morbidity in dental practices over a 3-year period, concluded that in most of those incidents related to administration of drugs, there were three common factors.14

These three factors greatly increased the risk of serious ADRs, with a negative outcome the usual result.

An overdose reaction to the administration of CNS-depressant drugs may not always be a preventable complication; however, with care taken on the part of the dentist, the incidence of these events should be extremely low, with a successful outcome the result virtually every time. With techniques such as IV and inhalation sedation, in which titration is possible, overdosage should be rare. With oral, IM, and IN drug administration, in which little control is maintained over the drug’s ultimate effect because of the inability to titrate, the dentist must expend greater care in the preoperative evaluation of the patient, in the determination of the appropriate drug dosage, and in monitoring during the procedure so that excessive CNS or respiratory depression may be identified and treated immediately. When the oral, IN, or IM routes are used, the onset of adverse reactions may be delayed. An adverse reaction may not develop until after the rubber dam is in place and the dental procedure has been started. Therefore monitoring of the patient throughout the procedure becomes extremely important to the patient’s safety. My preferences, as of April 2009, in monitoring during parenteral minimal or moderate sedation are as follows:


Allergy is a hypersensitive state acquired through exposure to a particular allergen, reexposure to which produces a heightened capacity to react. Allergic reactions cover a broad range of clinical manifestations, from mild, delayed-onset reactions occurring as long as 48 hours after exposure to immediate and life-threatening reactions developing within seconds of exposure. Although all allergic phenomena are important and require thorough evaluation by the dentist, only one form, the type I, or immediate, reaction is discussed here, for it may present the dentist with a life-threatening emergency situation. A classification of allergy types is presented in Table 34-4.

Allergic reactions are mediated through immunologic mechanisms that are similar regardless of the specific antigen responsible for precipitating the response. Therefore an allergic reaction to the venom of a stinging insect may be identical to that seen after aspirin or penicillin administration in a previously sensitized individual. Allergic reactions must be differentiated from the overdose, or toxic, reaction previously discussed, in which the observed signs and symptoms are a direct extension of the normal pharmacologic properties of the drug administered. Overdose reactions are much more commonly encountered than are allergic drug reactions. Of all ADRs, 85% result from the pharmacologic actions of drugs; 15% are immunologic reactions.15 To the layperson, however, any adverse drug response is frequently labeled “allergic.”

Allergy is a frightening word to those health professionals responsible for primary care of patients. Although none of the drugs commonly used for the management of pain and anxiety has a significantly high rate of allergenicity, allergic phenomena may still arise. The only drugs mentioned in this book that, to my knowledge, have never been shown to have produced allergy are N2O and O2. Although the concept of prevention has been stressed repeatedly throughout this text, in no other situation is this concept of greater importance than with allergy. Although allergy is not the most common ADR, it is frequently involved with the most serious of these reactions.

Of the many antianxiety drugs used, the barbiturates probably possessed the greatest potential for sensitization of patients. Although not nearly as common as allergy to penicillin or aspirin, barbiturate allergy usually manifests itself in the form of skin lesions, such as hives and urticaria, or less frequently in the form of blood dyscrasias, such as agranulocytosis or thrombocytopenia. Allergy to barbiturates occurs much more frequently in persons with a history of asthma, urticaria, and angioedema.16 A documented history of allergy to any barbiturate represents an absolute contraindication to their administration.

Amongst the opioids, meperidine can release histamine locally. When meperidine is administered intravenously, this localized histamine release develops along the path of the vein through which the drug travels. This reaction is not an allergy and requires no therapeutic management. The reaction resolves after the drug leaves the area of its administration. Use of meperidine is relatively contraindicated in asthmatic patients because of potential bronchospasm induced by histamine release when the drug enters the pulmonary circulation.

Following IV administration, atropine—an anticholinergic—may produce flushing of a patient’s face, neck, and upper chest. Known as atropine flush, this is not an allergic reaction and requires no therapeutic intervention because spontaneous resolution occurs within a brief time. Atropine flush is most often seen with overdose of atropine. However, in certain sensitive individuals (those who are hyperresponders on the bell-shaped curve), the usual therapeutic dose may provoke this response.

Prevention of Allergic Reactions

Whenever any drug or combination of drugs is being considered for administration, the dentist must question the patient about any prior exposure to that drug or members of the same drug family. In addition, the patient’s medical history questionnaire must be evaluated. All questionnaires include questions concerning current drug use and prior ADRs. These two steps will, in most cases, enable the dentist to assess the possibility of an adverse drug response. Should a positive history be elicited, questioning is undertaken to determine the nature of the previous reactions. Although the questioning may vary, basic questions asked include the following:

Knowledge of the signs and symptoms of the “reaction” and its management can go far in aiding the dentist in diagnosing the alleged “allergy.”

The need for hospitalization or assistance from a second health professional usually indicates that a more serious ADR occurred. If possible, it would be prudent to speak directly to the doctor involved with the patient at that time.

Following a thorough dialogue history and review of the medical history questionnaire, it is usually possible to form a general opinion about the true nature of the reaction. If the dentist is convinced that an allergy did occur, other drugs that are structurally dissimilar to the offending drug should be selected for administration. In most cases, however, it will become obvious that the “allergy” was in fact a side effect of the drug (e.g., nausea from codeine) or that the response was psychogenic (i.e., induced by anxiety). If doubt remains as to the precise nature of the reaction, the patient should be managed, at that time, with drugs unrelated to the one(s) in question, followed by consultation with an allergist (or other appropriate individual) so that more definitive testing might be undertaken.


The time elapsing between exposure of the patient to the antigen and the development of clinical signs and symptoms is of great importance. As a rule, the more rapidly signs and symptoms evolve after exposure to an allergen, the more intense the ultimate response will be. Conversely, the greater the length of time is between exposure and onset, the less intense the reaction usually is. However, cases of anaphylaxis have been reported to arise many hours after exposure. Of importance, too, is the rate at which signs and symptoms progress once they appear. If they appear and increase in severity rapidly, the reaction is more likely to become life threatening than one that progresses slowly or not at all.

Skin Reaction

Allergic skin reactions are the most common sensitization reaction to drug administration. Many types of allergic skin reaction may occur, the two most important types being localized anaphylaxis and drug eruption. Drug eruption constitutes the most common group of skin manifestations of drug allergy. Included in this category are urticaria, erythema (reddening), and angioedema (localized swelling).

Urticaria is associated with wheals (smooth, slightly elevated patches of skin) and often with intense itching (pruritus). Angioedema is a process in which localized swelling occurs in response to an allergen. Several forms of angioedema exist, but clinically they appear to be similar. The skin is usually of normal color (unless accompanied by urticaria or erythema) and temperature, and pain and itching are uncommon. The areas most commonly involved are the hands, face, feet, and genitalia. Of special concern is the potential involvement of the lips, tongue, pharynx, and larynx, leading to obstruction of the airway (laryngeal edema).

Allergic skin reactions, if the sole manifestation of allergy, are usually not considered life threatening. However, a skin reaction that develops rapidly after drug administration may be the first indication of the generalized reaction to follow.

Adhesive tape used during IV sedation is a fairly common cause of dermatologic reactions, the adhesive being the allergen. The usual response to this tape is erythema and urticaria developing around the site where the tape has been placed. In adhesive-allergic individuals, hypoallergenic tapes are recommended for use.

Generalized Anaphylaxis

Generalized anaphylaxis is the most dramatic and acutely life-threatening form of allergy and may lead to clinical death within a few minutes. It may develop after the administration of an antigen via any route but is most likely to occur after parenteral administration. The time from antigenic challenge to the onset of reaction varies greatly, but typically the reaction develops rapidly, reaching a maximum within 5 to 30 minutes. Delayed responses of 1 hour or more have been reported. It is believed that this is the result of the rate at which the antigen enters into the circulatory system.

Signs and symptoms of generalized anaphylaxis are highly variable. Four major clinical syndromes are recognized: skin reactions, smooth muscle spasm (gastrointestinal and genitourinary tracts and respiratory smooth muscle), respiratory distress, and cardiovascular collapse. In typical generalized anaphylaxis, the symptoms progressively move through these four areas; however, in cases of fatal anaphylaxis, respiratory and cardiovascular disturbances predominate and are evident early in the reaction.

In the typical generalized anaphylactic reaction, the patient may begin to complain of feeling sick with intense itching, flushing, and giant hives developing over their face and upper chest. Nausea, possibly followed by vomiting, may also occur. These early symptoms are primarily related to the skin. Other responses noted early in the reaction include conjunctivitis, vasomotor rhinitis (increased mucus secretion in the nose), and pilomotor erection (the feeling of hair standing on end).

Associated with the development of skin symptoms are various gastrointestinal and genitourinary disturbances related to spasm of smooth muscle. Severe abdominal cramps, nausea and vomiting, diarrhea, and fecal and urinary incontinence may occur.

Respiratory symptoms normally follow. However, in rapidly developing reactions, all symptoms may occur within a short time with considerable overlap. In particularly severe reactions, respiratory and cardiovascular symptoms may be the only signs present.

Respiratory symptoms begin with a feeling of substernal tightness or pain in the chest. A cough may develop in addition to wheezing and dyspnea. If the respiratory disturbances are severe, cyanosis may develop, noted initially in mucous membranes and nail beds. Laryngeal edema may also develop, producing acute airway obstruction.

Signs and symptoms of cardiovascular disturbance follow and include pallor, lightheadedness, palpitation, tachycardia, hypotension, and cardiac dysrhythmias, followed by loss of consciousness and cardiac arrest. With loss of consciousness, the anaphylactic reaction may more properly be called anaphylactic shock.

The duration of the anaphylactic reaction or any part of it may vary from minutes to a day or more. With prompt and app/>

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Jan 5, 2015 | Posted by in General Dentistry | Comments Off on 34: Management of Emergencies

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