CONTINUING EDUCATION IN HONOR OF NORMAN TRIEGER, DMD, MD

Adverse Drug Reactions in Dental Practice

Daniel E. Becker, DDS
Associate Director of Education, General Dental Practice Residency, Miami Valley Hospital, Dayton, Ohio

Adverse reactions may occur with any of the medications prescribed or administered
in dental practice. Most of these reactions are somewhat predictable based on the
pharmacodynamic properties of the drug. Others, such as allergic and pseudoallergic
reactions, are less common and unrelated to normal drug action. This article will
review the most common adverse reactions that are unrelated to drug allergy.

Key Words: Adverse drug reactions; Drug side effects; Dentistry.

A dverse drug reactions occur in 10–20% of hospital-

ized patients and in approximately 7% of those in
the ambulatory setting.1 By convention, adverse drug
geal musculature and thereby reduce pharyngeal paten-
cy. Even mild degrees of respiratory depression may be
intense enough to prevent patients from overcoming the
reactions are categorized as type A or type B. Type B obstruction, but patients will generally breathe if airway
reactions were addressed in a previous continuing patency is improved. It is always sound practice to
education article in this journal and consist mostly of position the patient as upright as possible, tilt the head
idiosyncrasy or drug allergy.2 Type A reactions are the upward, and protrude the mandible when necessary.
focus of this article. They are more common and are Respiratory depression proceeds in a dose-response
generally attributable to known pharmacological or toxic manner, and the intensity is further increased when the
effects of the drug. The typical pharmacopeia in dental various classes are used in combination. Minimal to
practice is relatively small, consisting primarily of moderate sedation carries little risk for clinically signif-
sedatives, local anesthetics, analgesics, and antibiotics.
icant respiratory depression, but deep sedation and
The most common adverse effects will be addressed for
general anesthesia introduce substantial risk for both
each of these classes.
respiratory depression and airway obstruction. (See
Table 1.) The individual drug classes differ in their
predilection for depressing central hypercapnic drive or
SEDATIVES, OPIOIDS, AND GENERAL
ANESTHETICS peripheral hypoxemic drive. For example, the opioids
primarily depress central hypercapnic drive whereas the
Respiratory depression is the most significant side effect potent inhalation agents depress hypoxemic drive. At
of all drug classes used for procedural sedation and higher doses there is less selectivity and both drives
general anesthesia. However, before embarking on this become depressed.
discussion, it is important to distinguish respiratory Potent inhalation anesthetics depress tidal volume
depression from anatomical airway obstruction. Most while generally increasing respiratory rate; their net
of the drug classes used for procedural sedation and influence on minute ventilation varies. In contrast, the
general anesthesia produce relaxation of glossopharyn- intravenous sedatives and opioids usually depress both
tidal volume and respiratory rate. Benzodiazepines
Received November 20, 2013; accepted for publication November produce the least intensity of respiratory depression,
27, 2013. but this increases when they are combined with other
Address correspondence to Dr Daniel E. Becker, Associate
drugs or high doses are administered. For example,
Director of Education, General Dental Practice Residency, Miami
Valley Hospital, One Wyoming St, Dayton, OH 45409; debecker@ doses intended to induce unconsciousness may produce
mvh.org. transient episodes of apnea.
Anesth Prog 61:26–34 2014 ISSN 0003-3006/14
Ó 2014 by the American Dental Society of Anesthesiology SSDI 0003-3006(14)

26
Anesth Prog 61:26–34 2014 Becker 27

Table 1. General Influences of Sedation Levels and General Anesthesia3

Minimal Sedation Moderate Sedation Deep Sedation
(Anxiolysis) (Conscious) (Periods of Unconsciousness) General Anesthesia
Airway Unaffected No intervention required Intervention may be required Intervention often required
Spontaneous ventilation Unaffected Adequate May be inadequate Frequently inadequate
Cardiovascular function Unaffected Usually maintained Usually maintained May be impaired

In addition to respiratory influences, these drug classes Unlike diphenhydramine or hydroxyzine, prometha-
may also lower arterial blood pressure and heart rate. zine (Phenergan) also acts as a dopamine receptor
Cardiovascular influences are rarely significant at doses antagonist, an action shared by other antiemetic drugs
intended for minimal to deep sedation, but with doses such as prochlorperazine (Compazine) and droperidol
and combinations intended for general anesthesia the (Inapsine). Although dopamine receptor blockade within
risk for hypotension may become more substantial. A the chemoreceptor trigger zone provides an added
summary of respiratory and cardiovascular influences of antiemetic mechanism, this identical action within the
the most commonly used drugs is provided in Table 2. basal ganglia introduces the risk for extrapyramidal
Benzodiazepines and propofol produce anterograde syndromes. This is a collective term for several
amnesia when administered at sedative dosages.5 This is conditions including acute dystonia, akathisia, and
an inability to recall events that occur while conscious but Parkinsonism. Acute dystonias generally present as
under the influence of a medication. The term is not spasms of the tongue, facial, and neck muscles, whereas
applicable during general anesthesia because the patient akathisia presents as a subjective feeling of restlessness
is unconscious. Although anterograde amnesia is an and a compelling need to move about. These behaviors
attractive effect during unpleasant procedures, it may may be mistaken for agitation, and their distinction is
also be problematic should a need arise to alter a dental critical to avoid an inclination to further sedate the
treatment plan. These issues must be taken into account patient. Although extrapyramidal symptoms are bizarre,
prior to the procedure and the vested escort educated and generally frighten the patient and practitioner alike,
regarding the patient’s lack of judgment during recovery they are never life threatening. The added anticholiner-
at home. gic action of diphenhydramine is useful for countering
acute episodes should they occur.7
A final note on promethazine is worth mention. Like
ANTIHISTAMINES AND ANTIEMETICS
other phenothiazine as well as butyrophenone deriva-
tives, it has antagonist actions on vascular alpha
The antihistamines and related antiemetics are com-
receptors, which increases risk for postural hypotension,
monly used in regimens for procedural sedation but also
especially in the elderly.
are indicated for minor allergic reactions and nausea or
vomiting. When used alone they have little influence on
respiration, but they may potentiate respiratory depres- Table 2. Relative Respiratory and Cardiovascular Influences of
Selected Drugs4
sion produced by opioids and other sedatives. All of
these agents have anticholinergic action, but peripheral Heart Mean Arterial
side effects are rarely if ever encountered, although Ventilation Rate Pressure
mouth dryness might be a nuisance to some patients. Intravenous agents
Central cholinergic blockade can be another matter, Diazepam ++ ,** +
however. Cognition and memory are functions of Midazolam ++ ** ++
cholinergic neurotransmission, and degeneration of Methohexital +++ ** ++
Propofol +++ , ++
cholinergic neurons is the key component of Alzheimer’s Etomidate + , +
dementia. Drugs having central anticholinergic actions Ketamine ,+ ** **
should probably be avoided in elderly patients, particu- Fentanyl +++ ++ ,+
larly those having evidence of dementia.6 Moreover, Meperidine +++ * +
high doses of anticholinergic drugs can result in a Inhalation agents
‘‘central anticholinergic syndrome’’ that includes delirium Nitrous oxide , , ,
and combativeness. During lengthy treatment under Desflurane ++ ,* ++
Sevoflurane + , +
sedation it is important to not exceed conventionally
suggested doses for these agents. * Reflex increase due to decline in mean arterial pressure.
28 Adverse Drug Reactions in Dental Practice Anesth Prog 61:26–34 2014

LOCAL ANESTHETICS and avoid their use for nerve blocks, opting instead for
agents formulated in lower concentrations.10,11
Local anesthetics are remarkably safe when used in As local anesthetics are absorbed from the injection
proper doses and concentrations, but they are certainly site, their concentration in the bloodstream rises and the
capable of producing both local and systemic toxicity. peripheral and central nervous systems are depressed in a
Ischemic necrosis of tissues may follow injections of local dose-dependent manner.8 (See Figure 1.) Low serum
anesthetics. This can be due to the irritating nature of a concentrations are used clinically for suppressing cardiac
solution, pressure from large volumes, or constriction of arrhythmias and status seizures, but as their concentration
the vasculature by vasopressors. This concern is greatest rises, local anesthetics produce drowsiness. At higher
when injecting into attached mucosa such as the hard concentrations, convulsive seizures occur and are the
palate. There is also mounting concern regarding direct initial life-threatening consequence of local anesthetic
neurotoxicity related to formulations containing high overdose. This is presumably due to selective depression
concentrations, such as 4% articaine and prilocaine. of cortical inhibitory tracts allowing unopposed activity of
Local anesthetics can produce direct toxicity to nerve excitatory pathways.8,13 This selectivity is lost as serum
trunks, leading to persistent paresthesias. Although the concentrations rise even further and all pathways are
dental community has been slow to reach consensus inhibited, resulting in coma, respiratory arrest, and
regarding this issue, it should be appreciated that medical eventually cardiovascular collapse. Evidence of lidocaine
anesthesia literature is emphatic in claiming that greater toxicity may commence at serum concentrations .5 lg/
concentration of local anesthetic solutions increases risk mL, but convulsive seizures generally require concentra-
for direct neurotoxicity to nerve trunks: tions .10 lg/mL. If maximum recommended doses
published in conventional references are adhered to,
‘‘All the clinically used local anesthetics can produce excessive serum concentrations are unlikely to occur.
direct toxicity to nerves if they achieve sufficiently high It is essential that local anesthetics be respected as
intraneural concentrations. Clinicians should be aware central nervous system depressants, and they potentiate
that the concentrations of formulated local anesthetic any respiratory depression associated with sedatives and
solutions are neurotoxic per se and that their dilution, opioids. Furthermore, serum concentrations required to
in situ or in tissue, is essential for safe use.’’8 produce seizures are lower if hypercarbia (elevated carbon
Local anesthetic concentrations of 2% or 3% carry dioxide) is present. This is the case when respiratory
little risk, but 4% articaine and prilocaine formulations depression is produced by concurrent administration of
most certainly introduce added risk. Haas and Lennon sedatives and opioids. Goodson and Moore have docu-
first reported an increased incidence of paresthesias in mented catastrophic consequences of this drug interaction
Canada following the introduction of articaine in the mid- in pediatric patients receiving procedural sedation, along
1980s.9 When 4% articaine was first submitted for with excessive dosages of local anesthetics.14
approval to the Food and Drug Administration in the
United States, it was identified as having a higher risk for
paresthesia than 2% lidocaine.
More recently, Garisto et al10 reviewed claims of
paresthesia in the United States during the period of
November 1997 through August 2008 and found 248
cases of paresthesia following dental procedures. Most
cases (~95%) involved mandibular nerve blocks, and in
89% of these the lingual nerve was affected. Compared
to other local anesthetics, paresthesia was found to be
7.3 times more likely with 4% articaine and 3.6 times
more likely with 4% prilocaine. Similar findings from
reports of paresthesia in Denmark were published by
Hillerup et al11 and even more convincing is their
demonstration of greater neural toxicity for 4% com-
pared to 2% articaine in sciatic nerve preparations.12 As
with all drugs, each practitioner needs to perform a risk-
benefit analysis before using a medication. Only if the
benefit of using a 4% concentration outweighs the risk
for a patient should it be considered for use. It might be Figure 1. Approximate serum concentrations and systemic
wise to limit the use of 4% concentrations for infiltration influences of lidocaine.
Anesth Prog 61:26–34 2014 Becker 29

Although all local anesthetics carry similar risk for have been thoroughly reviewed in previous continuing
central nervous system toxicity, it should be noted that education articles in this journal.16,17 Epinephrine is the
bupivacaine exhibits greater potential for direct cardiac vasoconstrictor used most commonly, and produces the
toxicity than other agents.8,13 The explanation is not systemic cardiovascular effects illustrated in Figure 2.
fully established but is thought to be related to the fact Even small doses of epinephrine produce these cardio-
that bupivacaine has greater affinity for the inactive and vascular effects; this is unequivocal. At issue is the actual
resting sodium channel configurations and dissociates magnitude and whether or not these influences pose a
from these channels more slowly. This delays recovery significant risk to a particular patient. The most often
from action potentials, rendering cardiac tissues suscep- cited guidelines suggest that a 2-cartridge limit be
tible to arrhythmias. This concern is relevant for certain imposed for patients with cardiovascular disease, but
medical procedures during which bupivacaine is admin- this is naı̈ve. Ultimately, the decision requires the dentist
istered in very high doses. It has never been found to to exercise sound clinical judgment based on a thorough
occur with doses up to the maximum recommended in analysis of each patient under consideration.
dental anesthesia. Generally, the hemodynamic influences of epineph-
When considering the toxicity of any drug class, one rine are witnessed within 5 minutes of injection and have
should be mindful of metabolites, as well as the parent completely subsided in 10–15 minutes. If for any reason
drug. A metabolite of prilocaine, 0-toluidine, can oxidize the medical status of a patient is in question, a sensible
the iron in hemoglobin from ferrous (Fe2þ) to ferric protocol is to record baseline heart rate and blood
(Fe3þ). Hemes so altered do not bind oxygen, and normal pressure preoperatively and again following every 20–
hemes on the same hemoglobin molecule do not readily 40 lg administered (~1–2 cartridges containing a
release their oxygen. This form of hemoglobin is called 1 : 100,000 epinephrine concentration). Virtually any
methemoglobin, and when .1% of total hemoglobin is ambulatory patient can tolerate the cardiovascular
so altered, the condition is called methemoglobinemia. influences of this amount. If the patient’s vital signs
Patients appear cyanotic and become symptomatic remain stable for 5 minutes following injection, addition-
when the proportion of methemoglobin exceeds 15%. al doses may be administered and followed by a similar
Hemoglobin saturation by pulse oximetry will decline pattern of reassessing vital signs. One should also
despite clinical evidence of adequate oxygenation and consider using lower concentrations of epinephrine.
ventilation. At methemoglobin levels of up to 35%, Despite the popularity of epinephrine 1 : 100,000,
oxygen saturation via pulse oximetry decreases by an concentrations greater than 1 : 200,000 (5 lg/mL)
amount proportional to the concentration of methemo- offer little if any advantage. Greater concentrations do
globin until the latter reaches approximately 35%. At not provide better onset or duration for inferior alveolar
higher methemoglobin levels, the oxygen saturation nerve block.19,20 Nor do higher concentrations reduce
levels out at about 85%.15 The condition becomes life local anesthetic serum concentrations.21
threatening when methemoglobin levels exceed 50–
60%, and it is managed using intravenous methylene
blue, which reduces the hemes to their normal state.
Methemoglobinemia attributed to prilocaine is unlikely to
follow the administration of recommended doses.
Rarely, one may encounter a patient with hereditary
methemoglobinemia, which contraindicates the use of
prilocaine.

VASOCONSTRICTORS: EPINEPHRINE AND

LEVONORDEFRIN

Vasoconstrictors are combined with local anesthetics to Figure 2. Cardiovascular influences of epinephrine. The graph
provide hemostasis in the operative field and to delay is adapted from Hersh et al.18 Average of cardiovascular
anesthetic absorption. This influence is mediated by changes were recorded following injection of 7 cartridges (11.9
activation of alpha-1 receptors on submucosal vascula- mL) of articaine containing either 1 : 100,000 or 1 : 200,000
ture, but, following systemic absorption, cardiovascular concentrations of epinephrine (~120 and 60 lg respectively).
Although actual changes were mild, consider that all volunteers
influences can result from their activation of additional were healthy young adults taking no medications. Even so, 2
adrenergic receptors as well. The doses and cardiovas- volunteers experienced palpitations. Also note confirmation of
cular influences of both epinephrine and levonordefrin the dose-dependent responses for 60 versus 120 lg.
30 Adverse Drug Reactions in Dental Practice Anesth Prog 61:26–34 2014

ANALGESICS Despite this recommendation, it is still acceptable to

prescribe 4 g daily for healthy adults when managing
Nonsteroidal Anti-Inflammatory Drugs brief periods of postoperative pain (3–5 days). In
healthy adults, hepatotoxicity may occur after ingestion
The most frequent adverse effects of nonsteroidal anti- of a single dose of 7.5–10 g (150 mg/kg in children),
inflammatory drugs (NSAIDs) relate to their gastrointes- and 20–25 g or more is potentially fatal.27 These
tinal (GI) toxicity: mucosal erosion and ulceration. amounts can be considerably lower in patients with
Parenteral administration does not preclude this risk hepatic compromise.
because inhibition of normally protective prostaglandins Hepatic injury from acetaminophen is due mainly to a
occurs regardless of the route of administration. It is single toxic metabolite, N-acetyl-p-benzoquinone imine,
important to distinguish dyspepsia (upset stomach) from which is formed by oxidation of the drug. With
GI toxicity, which reflects actual mucosal damage. The therapeutic doses in healthy subjects, oxidation is a
incidence of dyspepsia attributed to NSAIDs does not minor metabolic pathway, and glutathione conjugates
correlate with mucosal injury. For example, buffered and inactivates the toxic metabolite.27 (See Figure 3.)
aspirin is less likely to produce gastric upset but carries
similar risk for mucosal damage as regular aspirin.22
Patients receiving antithrombotic therapy with either
antiplatelet or anticoagulant drugs are at risk for more
significant bleeding from NSAID-induced mucosal injury.
NSAIDs increase the risk for GI bleeding twofold to
threefold in patients medicated with clopidogrel (Plavix)
and fourfold to fivefold in those taking warfarin.23
Concerns regarding NSAID-induced mucosal injury are
particularly important for older patients.
Actual antiplatelet influences for most NSAIDs are
generally overstated. Although nonaspirin NSAIDs all
prolong bleeding times to some degree, this does not
correlate with significant clinical bleeding following
minor surgical procedures.24 However, they are gener-
ally withheld prior to major thoracic, abdominal, or
orthopedic procedures.
Prostaglandins play an essential role in renal perfu-
sion, and their inhibition is believed to account for
reported cases of nephrotoxicity following chronic
NSAID use. In the healthy patient, nephrotoxicity
attributed to NSAIDs requires high doses for extended
periods, eg, a year or more.25 However, a patient with
compromised renal function relies more heavily on
prostaglandins for adequate function, and acute renal
failure can occur within 24 hours of NSAID administra- Figure 3. Acetaminophen toxicity. The major portion of
tion. NSAIDs must never be prescribed for patients acetaminophen is metabolized to nontoxic metabolites excret-
having compromised or questionable renal function. ed in urine. Only 5–15% is oxidized by cytochrome P450 (CYP
450) enzymes to a potentially toxic metabolite, N-acetyl-p-
benzoquinone imine (NAPQI). The normally small amounts of
this metabolite are readily converted to harmless mercapturic
Acetaminophen acid conjugates by glutathione. When high doses of acetamin-
ophen are consumed, glutathione can be depleted, allowing
NAPQI to accumulate and produce hepatic necrosis. Also,
Acetaminophen has virtually no adverse effects when normal biotransformation is diminished with compromised liver
administered at conventional doses in healthy pa- function, including that associated with malnutrition and
tients.26 Hepatotoxicity is the principal adverse effect alcohol abuse. Toxicity can be further accentuated by ethanol
associated with excessive dosages. Formerly the max- consumption, which induces CYP 450 activity, leading to
greater portions of acetaminophen converted to NAPQI.
imum recommended dose was 4 g daily, but recently Emergency management of acetaminophen overdose consists
the Food and Drug Administration has reduced the daily of administering high doses of acetylcysteine, which replenish-
maximum to 3 g in an effort to curtail excessive use. es glutathione.
Anesth Prog 61:26–34 2014 Becker 31

Opioids its effects for nonmedical reasons, generally for pleasure.

It is a complex psychiatric phenomenon, but it should not
As addressed earlier in this article, respiratory depression be considered an adverse effect of the drug per se.
is a significant side effect of opioids included in sedation Addictive behavior can be reinforced by an opioid, but it
and anesthesia regimens but is rarely a concern at the is not a pharmacodynamic property. For example, an
conventional doses prescribed for postoperative pain. opioid-dependent patient who lacks addictive behavior
Analgesic doses are more commonly associated with can be easily weaned from opioid dosages without fear of
constipation and nausea. The inhibitory effect of opioids precipitating addictive behavior. In contrast, an addicted
on GI motility is highly variable among patients, but for patient will seek the drug despite having no remaining
those susceptible, a stool softener should be suggested. evidence of dependence or medical need for the drug.
Patients having a history of nausea and vomiting with Opioids should not be withheld on the presumption that
opioids should be encouraged to remain stationary for an the patient will become addicted, but they must be
hour or so following each dose. Vestibular influences prescribed cautiously for patients who demonstrate
potentiate opioid actions within the vomiting center and addictive personality. Patients who are dependent on
chemoreceptor trigger zone of the medulla.28,29 opioids for medical reasons or exhibit addictive behavior
Fear of dependence and addiction often results in should not be prescribed or administered agonist-
underprescribing of opioids for severe acute, chronic, antagonists such as pentazocine or nalbuphine or weak
and even terminal pain. This unfortunate practice is due agonists such as tramadol or tapentadol because they
to poor understanding of these terms. Dependence may precipitate withdrawal.
occurs when the body accommodates to the influences of
a drug and, upon sudden discontinuation, the patient
experiences a withdrawal syndrome that generally ANTIBIOTICS
includes reactions opposite those produced by the
particular drug. For example, opioids produce sedation, There are surprisingly few complications associated with
lethargy, and constipation. A patient experiencing antibiotic therapy other than drug allergies addressed
opioid withdrawal becomes excited, and experiences previously2 and tetracycline staining of developing teeth.
abdominal cramping and diarrhea. If opioid doses are Otherwise, their principal complications are opportunis-
tapered gradually, a dependent patient will not experi- tic yeast infections or GI complications such as nausea,
ence withdrawal. Patients consuming opioids regularly diarrhea, and colitis.
for more than a week can develop some degree of
dependence. This may require gradual tapering of the
dosage to avoid withdrawal symptoms, which can be
Opportunistic Yeast Infection
confused as an exacerbation of their painful condition.
However, this does not mean the patient has become
Candida albicans is a fungus also referred to as yeast
addicted.29,30
because of its manner of growth. It is a normal
Following repeated administration, patients develop
component of oropharyngeal and vaginal flora. Over-
tolerance to opioids. This is to say that greater doses are
growth is ordinarily prevented by resident bacteria, but
required to produce the same intensity of effect formerly
this control may be lost when patients are immunocom-
provided by a smaller dose. Tolerances to analgesia,
promised or treated with antibiotics. It is not uncommon
sedation, and respiratory depression occur simultaneous-
for female patients to experience opportunistic vulvo-
ly, but curiously, there is no tolerance to the constipating
vaginitis following antibiotic therapy. For susceptible
effects of opioids. This is problematic for the patient with
patients, the use of probiotics should be encouraged, as
chronic or terminal pain. Although staggering doses may
they repopulate the colon and cross the perineum into
be required to control pain and will generally not
the vaginal tract. When infection occurs, the patient can
jeopardize the patient’s respiratory status, constipation
obtain an over-the-counter antifungal, or the dentist may
can become extremely severe. Similar doses, if admin-
prescribe a course of fluconazole.
istered to patients who have not developed tolerance, ie,
opioid-naive patients, can be lethal. Issues regarding
tolerance and dependence must be considered when
managing dental pain for patients who are medically Antibiotic-Associated Diarrhea
dependent as well as those who are chronic opioid
abusers. The incidence of diarrhea attributed to those antibiotics
Addiction is distinct from dependence or tolerance. It commonly used in dentistry ranges from 2 to 10%, and
is a compulsive behavior centered on seeking a drug and may be as high as 25% with amoxicillin/clavulanic acid
32 Adverse Drug Reactions in Dental Practice Anesth Prog 61:26–34 2014

(Augmentin).31 In general, diarrhea is related to an 1. Avoid antiperistaltics. Accumulation of toxin can

imbalance in the normal intestinal flora favoring oppor- worsen the infection.
tunists. The use of probiotics to prevent or manage 2. Stop the current antibiotic and prescribe metronida-
antibiotic-associated diarrhea remains controversial. zole 500 mg TID 3 10–14 days.
Nevertheless, current evidence suggests they are indeed 3. If there is no improvement after 2–3 days (based on
effective and should be suggested for particularly frail severity), or it subsides and recurs, refer the patient to
patients or those who have experienced diarrhea with his or her family physician, who will evaluate fluid/
antibiotic regimens in the past.32 electrolyte status. For severe cases the physician may
Clinically, the challenge when managing a patient with switch metronidazole to oral vancomycin, which is
diarrhea is to distinguish so-called nuisance diarrhea from not absorbed but provides its action locally within the
that associated with Clostridium difficile disease. colon. However, oral vancomycin is shockingly
Although C difficile infection accounts for only 10– expensive and will be initiated only in extreme cases.
20% of nuisance cases, it is the principal culprit in the
vast majority of colitis cases. Mild symptoms (1 or 2 It is significant that diarrhea from C difficile infection
generally occurs within 5–10 days of commencing an
unformed stools per day) in patients who have previously
antibiotic, but it has been reported to occur as late as 6–8
experienced diarrhea with antibiotics favor nuisance
weeks following clindamycin use. However, this compli-
diarrhea and may be managed using antiperistaltics and
cation is unheard of following abbreviated use of
changing the antibiotic to a narrower spectrum if
clindamycin for prophylaxis of infective endocarditis.
possible.31,33

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34 Adverse Drug Reactions in Dental Practice Anesth Prog 61:26–34 2014

CONTINUING EDUCATION QUESTIONS

1. Anterograde amnesia may occur with which of the 3. Opioids produce which of the following side effects?
following?
(1) addiction (2) dependence (3) tolerance
(1) minimal sedation (2) moderate sedation (3) general
anesthesia A. 1 and 2
B. 1 and 3
A. 1 and 2 C. 2 and 3
B. 1 and 3 D. 1, 2, and 3
C. 2 and 3
D. 1, 2, and 3
4. Clostridium difficile colitis is most often associated
with which antibiotic?
2. Extrapyramidal side effects may occur with which of
the following?
A. Amoxicillin
B. Cephalexin
A. Diphenhydramine C. Clindamycin
B. Hydroxyzine D. Metronidazole
C. Midazolam
D. Promethazine