C H A P T E R 156 
Opioids
PRINCIPLES OF TOXICITY
Opiate is the term for natural agents derived from the poppy plant
that have morphine-like pharmacological effects. Example opiates
include morphine and codeine. Opioid is the more inclusive term,
which refers to any synthetic, semisynthetic, or natural agent
that has morphine-like properties. Some common semisynthetic
opioids are heroin, hydrocodone, oxycodone, hydromorphone,
oxymorphone, and buprenorphine. Some common synthetic
opioids are fentanyl, methadone, and meperidine. Both opiate and
opioid are terms derived from opium, which was the Greek word
for the juice of the poppy plant (Papaver somniferum).1
Opioids are among the world’s oldest known drugs. The thera-
peutic use of opioids has been a practice since ancient times, with
the primary goals being sedation and analgesia. Opioids act on
receptors in the central nervous, cardiovascular, pulmonary, and
gastrointestinal systems and can also be used therapeutically for
their antitussive and antidiarrheal effects.
Pain is a common reason why patients present to the emer-
gency department (ED). As much as 78% of ED visits are related
to a painful condition.2 Since the Joint Commission placed
increased attention on pain management and hospitals increased
their emphasis on patient satisfaction, there has been a prolifera-
tion in the amount of opioid prescriptions written by physicians,
including emergency providers.3 This trend has not led to an
actual improvement in overall patient satisfaction but has led to
a flood of available opioids into the wider population.4 According
to the Centers for Disease Control and Prevention (CDC), there
has been a 300% increase in the sale of opioid analgesics from
1999 to 2011. In 2010 alone, enough prescription opioids were
prescribed to medicate every American adult with 5 mg of hydro-
codone every 4 hours for 1 month.5 Consequently, the United
States has seen a widespread rise in prescription opioid abuse,
overdoses, and deaths. In 2010, approximately 12 million Ameri-
cans, or 1 in 20, reported use of opioids without a prescription.
Nearly 15,000 Americans die annually due to prescription opioid
overdose, and overdoses overtook motor vehicle accidents as the
number 1 cause of accidental death in 2010.5,6
There has been a concomitant resurgence in illicit heroin use.
According to the CDC, the death rate from heroin overdose
doubled across 28 states in just 2 years, between 2010 and 2012.7
There has also been a change in demographics of heroin use.
Formerly involving primarily inner-city minority populations, the
practice has spread geographically beyond urban areas and to
white men and women in their late 20s.8 It is now believed that
prescription analgesics are the gateway to heroin use, because the
street price of heroin is often the cheaper option for opioid
dependent patients.
The wider availability of opioids has affected every population
group. This has been especially concerning for pediatric patients,
because analgesic prescriptions written for adults can end up in
the hands of children.9,10 Recreational opioid use may be associ-
ated with the teenage and young adult population, but uninten-
tional opioid overdose is also a growing concern among chronic
pain patients, geriatric patients, and obese patients; because risk
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Jenna K. Nikolaides | Trevonne M. Thompson
is increased by polypharmacy, medical comorbidities, and sleep
apnea.
Opioids come in three forms: synthetic, semisynthetic, and
natural opiates. There are prescription versions of all three forms,
which are available in many different preparations, including
tablets, liquids, patches, and even lollipops. Prescription opioids
are commonly packaged as combination preparations with acet-
aminophen, ibuprofen, and aspirin and historically existed in
combinations with atropine and camphor. Other prescription oral
preparations are formulated with opioid-receptor antagonists,
such as naloxone, which has little oral bioavailability to prevent
illicit use and tampering for intravenous abuse. There are also
prescription drugs that are not chemically classified as opioids,
but which display µ opioid receptor agonist, such as tramadol and
tapentadol.
Illicit opioids also exist in all three forms. Table 156.1 details
some of the known street names for opioids sold illicitly.11,12 Street
names are often unreliable, however, because they are subject to
dealers who may want to market or rebrand their product. Heroin
(diacetylmorphine), a semisynthetic opioid, is the most wide-
spread street preparation, but recent years have seen a rise in
synthetics, such as fentanyl and fentanyl analogues, often mixed
with or mislabeled as heroin.13 Illicit opioid preparations can also
be contaminated by the byproducts from the manufacturing
process, adulterated with additives to change the preparation’s
pharmacological effects, and diluted with inert substances to
increase bulk. The most common added substances are sugars,
caffeine, over-the-counter medications, other drugs of abuse,
heavy metals, and infectious agents.14,15
Toxicity can occur as a consequence of intentional overdose,
intentional recreational abuse, or as an adverse effect of therapeu-
tic use. Although different opioids have receptor preferences in
therapeutic doses, this specificity is lost at higher doses.
Opioids are well absorbed via gastrointestinal, intravenous,
intramuscular, mucocutaneous, and subcutaneous routes of
administration. Depending on the lipid solubility of the specific
opioid, they can also be absorbed through nasal, buccal, pulmo-
nary, or transdermal routes. In general, toxicity is less pronounced
but more prolonged when ingested than with parenteral admin-
istration. In therapeutic doses, an ingested opioid is absorbed in
the small intestine within 1 to 2 hours. In toxic doses, delayed
gastric emptying prolongs the absorption and clinical effects of
the opioid.
Most opioids have a large volume of distribution. Different
opioids and their metabolites cross into the blood-brain barrier
due to variations in lipid solubility. All opioids undergo hepatic
metabolism and renal elimination. Thus changes in hepatic or
renal function will alter drug clearance, which could prolong
clinical and toxic effects of the specific opioid.
CLINICAL FEATURES
The hallmarks of the opioid toxidrome are central nervous system
(CNS) depression, respiratory depression, and miosis. Miosis is
caused by stimulation of µ receptors in the Edinger-Westphal
1943
1944 PART IV  Environment and Toxicology  |  SECTION Two  Toxicology

TABLE 156.1  TABLE 156.2 

Street Names for Illicitly Obtained Opioids Special Clinical Properties of Certain Opioids
OPIOID STREET NAMES EFFECT OPIOID
Heroin Dope, Smack, H, Horse, Junk, Skag, Skunk, QRS widening, sodium channel Propoxyphene
Brown Sugar, White Horse, China White blockade
Heroin + acetaminophen Cheese QT widening, potassium channel Methadone
and diphenhydramine blockade
Codeine ± acetaminophen Captain Cody, Cody, Lean, Schoolboy, Seizures Propoxyphene, meperidine
T-threes, cough syrup
Serotonin syndrome Meperidine, methadone, tramadol,
Codeine + promethazine + Purple Drank, Sizzurp fentanyl
soft drinks and hard candy Hearing loss, ototoxicity Methadone, hydrocodone, heroin
Codeine + glutethimide Doors & Fours, Loads, Pancakes and Syrup Spongiform leukoencephalopathy Heroin via “chasing the dragon” or
Fentanyl China White, China Girl, Apache, Dance Parkinsonism inhalation of heroin vapor
Fever, Friend, Goodfella, Jackpot, Murder
8, Tango and Cash, TNT
Hydrocodone ± Vike, Watson-387
acetaminophen
opioids have been used. Look for the presence of fentanyl patches
Hydromorphone D, Dillies, Footballs, Juice, Smack over the entire body, including in the oropharynx and other bodily
Meperidine Demmies, Pain Killer orifices. If marks or scars from “skin popping,” a process where
opioids are injected subcutaneously, are seen, this could be a sign
Methadone Dollies, Amidone, Fizzies of illicit opioid use.
Methadone + MDMA Chocolate Chip Cookies Certain opioids have unique clinical findings due to their
Morphine M, Morph, Miss Emma, Monkey, White chemical structure or to their route of exposure (Table 156.2).
Stuff Propoxyphene is associated with sodium channel blockade prop-
erties, causing QRS widening, in addition to PR and QT interval
Oxycodone ± O.C., Oxycet, Oxycotton, Oxy, Hillbilly prolongation, which lead to its withdrawal from the market.20
acetaminophen Heroin, Percs Methadone is known to block human ether-a-go-go related gene
Oxymorphone Biscuits, Blue Heaven, Blues, Mrs. O, O (hERG) potassium channels, causing QTc prolongation.21 Pro-
Bomb, Octagons, Stop Signs poxyphene and meperidine have been associated with hypertonic-
ity, myoclonus, and seizures. Meperidine, methadone, tramadol,
Pentazocine Yellow Footballs
and fentanyl inhibit serotonin reuptake and are associated with
MDMA, N-methyl-3,4-methylenedioxyamphetamine. serotonin syndrome.22,23 Sensorineural hearing loss has been
reported with both acute and chronic use of heroin, methadone,
and hydrocodone, thought to be due to direct ototoxicity.24,25
Heroin has also been found to be associated with Parkinsonian
nuclei of the third cranial nerve. This effect may be unreliable or symptoms. A practice known as “chasing the dragon,” wherein
masked by co-ingestants, and thus respiratory depression is the heroin is heated in aluminum foil and the vapor inhaled, has been
essential feature of opioid intoxication.16 Respiratory depression found to be associated with spongiform leukoencephalopathy,
is caused by opioids’ effect on the medullary respiratory center via with symptoms of psychomotor retardation, dysarthria, ataxia,
suppressing its sensitivity to hypercapnia and overriding the and tremor.26
hypoxic drive. When combined with CNS depression, prolonged Patients who hastily ingest loosely packaged bags of illicit
hypopnea can lead to hypoxia causing further neurologic compli- drugs are known as “body stuffers.” Patients who internally conceal
cations. Long-term opioid use is known to cause dependence and dense and meticulously packaged packets of illicit drugs for the
appears to contribute to central sleep apnea, as well as structural purpose of trafficking are known as “body packers.” Heroin is a
and functional changes in the brain.17,18 common drug seen in both stuffers and packers. Both populations
Acute lung injury can be seen in opioid overdose, and pulmo- are at risk for severe and prolonged opioid toxicity if the packets
nary edema can cause a failure of oxygenation. This manifests as leak or rupture.27 However, heroin “stuffers” generally do not
desaturations on pulse oximetry, despite an adequate respiratory ingest enough to cause serious effects when compared to “packers”
rate, and rales on lung examination. The cause of acute lung who may have lethal amounts of concentrated product in their
injury in opioid overdose is not clearly elucidated but may be gastrointestinal tract.
related to a capillary leak phenomenon.
Other signs and symptoms commonly associated with opioids DIFFERENTIAL DIAGNOSES
include relative bradycardia, mild hypotension, pruritus, skin
flushing, nausea, vomiting, and bowel dysfunction. Hypotension, The diagnosis of opioid intoxication is usually based on history,
pruritus, and flushing are caused by non-allergic histamine vital signs, and physical examination with recognition of its
release; an effect more pronounced with morphine. Nausea and characteristic toxidrome: hypopnea, stupor, and miosis. All of
vomiting are frequently seen, even in therapeutic doses of opioids, these findings are not consistently present, and the clinical picture
and are responsive to antiemetics and more potent opioids. may be complicated by co-intoxicants. The essential finding in
Decreased gastrointestinal motility, delayed gastric emptying, opioid intoxication is respiratory depression.16 Other intoxica-
constipation, and ileus are all commonly seen and exist on the tions may present similarly, such as clonidine, guanfacine, valproic
spectrum of opioid-induced bowel dysfunction.19 acid, gamma-hydroxybutyrate, ethanol, sedative hypnotics, and
The skin should be examined in a patient exhibiting the atypical antipsychotics. Non-toxicologic considerations include
opioid toxidrome, because it may give diagnostic clues as to which pontine stroke or hemorrhage.

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DIAGNOSTIC TESTING
No laboratory test or drug screen should be relied upon by a clini-
cian to make the diagnosis of opioid toxicity. The presence of the
toxidrome and rapid response to naloxone are the two most
important diagnostic clues. End-tidal carbon dioxide and oxygen
saturation monitoring may be helpful for recognition of respira-
tory depression and hypoxia, but are not as necessary as observa-
tion of the patient’s respiratory rate.
A 12-lead electrocardiogram is a useful diagnostic for identify-
ing QRS widening, as seen in propoxyphene use, or for QTc
prolongation, as seen in methadone use. If the patient has audible
pulmonary rales on examination, then a chest radiograph is useful
to evaluate for acute lung injury. If the opioid preparation is
unknown, then acetaminophen and salicylate levels should be
measured, because many prescription opioids are sold as combi-
nation preparations. Hypoglycemia is the only consistent labora-
tory abnormality found in opioid toxicity. It is generally mild but
can contribute to the decreased level of consciousness seen in
opioid overdose.
Opioids, such as morphine, codeine, and heroin, are reliably
detected on most qualitative antibody-based enzymatic immuno-
assay urine toxicology screens. Some semisynthetic and synthetic
opioids, such as hydrocodone, methadone, and fentanyl, however,
are often missed on typical urine drug screens unless they are
specifically measured. A urine test result can remain positive
for up to 72 hours after last use, depending on the half-life of the
drug used. A large poppy seed ingestion can lead to a positive
opioid screen, although federal workplace testing guidelines have
raised the confirmatory morphine concentration threshold to
2000 ng/mL to avoid positive screens for commonplace poppy
seed ingestions.28,29 Advanced screening methods detecting for
6-monoacetylmorphine, a specific metabolite of heroin, can be
used to confirm heroin use.30
MANAGEMENT
Stabilization and Supportive Care
The ED physician should direct efforts at stabilizing the patient’s
airway, oxygenation, and ventilation. This can be accomplished
with a combination of basic supportive measures and titrated use
of antidotal therapy. Patients with acute lung injury may require
oxygen and positive-pressure modalities, such as bi-level positive
airway pressure, continuous positive airway pressure, or mechani-
cal ventilation with positive end-expiratory pressure.
Decontamination
Because many opioids are extended-release preparations and also
delay gastric motility, activated charcoal has been used in the past,
but there are no data to support the effectiveness of this practice.
Additionally, naloxone is an effective antidote for opioid overdose,
and sedation from opioid intoxication could lead to charcoal
aspiration. Gastric lavage similarly is not recommended because
the risks outweigh the benefits. Whole bowel irrigation is not
generally useful, but it can be considered for body packers (see
Chapter 149).
Enhanced Elimination
There are no clinically effective techniques for enhanced elimina-
tion of opioids.
Antidote Therapy
Naloxone is a competitive opioid antagonist that rapidly reverses
the effects of opioid intoxication. Because of the rapid clinical
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C H APTER 156  Opioids 1945
response, it can also aid in the diagnosis of opioid overdose.
Naloxone is ineffective orally because its bioavailability is minimal
due to first-pass metabolism. It is effective via intravenous, sub-
cutaneous, intramuscular, inhalational, and endotracheal routes.
It is indicated when an opioid intoxicated patient has significant
CNS or respiratory depression.
In the ED, naloxone is usually administered intravenously
with empirical dosing. The dose ranges from 0.04 mg to 15 mg,
depending on the amount and formulation of the opioid taken,
the patient’s weight, and whether the patient is opioid dependent.
In general, it is best to start with low doses and to increase doses
as needed to alleviate respiratory depression. The exception to this
is the arrest or near-arrest situation where opioids are the sus-
pected cause. In this scenario, recommended starting doses are
0.4–2.0 mg. In chronic opioid users, the minimal effective nalox-
one dose should be used so as not to precipitate acute withdrawal.
In this population, when respiratory status is adequate, we recom-
mend starting with doses of 0.04 mg of naloxone, followed by
titration of subsequent doses. Acute opioid withdrawal is unpleas-
ant for the patient. Opioid withdrawal is not, in isolation, life-
threatening, and naloxone has an excellent safety profile. The
clinician should not be reluctant to dose naloxone as needed, even
if opioid withdrawal symptoms develop.
Naloxone’s onset of action, when administered intravenously,
is less than 2 minutes, and the duration of action is anywhere
between 20 minutes and 2 hours, which is shorter than the dura-
tion of action of most opioids. Reversal of respiratory depression
usually occurs at low doses, but dosing is repeated until the desired
effect is achieved. If respiratory depression is not reversed after
the administration of high doses of naloxone (10 to 15 mg), then
it is unlikely that opioid intoxication is the cause of the symptoms.
If naloxone does reverse the symptoms but the patient later
develops recurrent respiratory depression, then repeated naloxone
doses, a continuous naloxone infusion, or endotracheal intuba-
tion should be considered. When starting a naloxone infusion,
one-half to two-thirds of the bolus dose that effectively reversed
intoxication is given hourly, although individual patient responses
may vary depending on dose, tolerance, and dependency. This is
usually enough to maintain respiratory effort without producing
withdrawal.
In situations where intravenous access is not easily obtained,
naloxone can also be given via intramuscular, intranasal, or nebu-
lized routes. Intranasal naloxone has proved a viable, alternative
to intravenous administration, especially for prehospital provid-
ers. Both 0.4  mg/mL and 1  mg/mL solutions of naloxone, delivered
into each nare using an atomizer device, have been used.31 Nebu-
lized naloxone—2 mg of naloxone is mixed with 3 mL of saline—
has also been shown to be a safe, effective, and gradual way to
reverse opioid intoxication in both the ED and prehospital set-
tings.32,33 Care must be taken in selecting the optimal patient for
nebulized naloxone. A patient with profound respiratory depres-
sion, such as a respiratory rate of less than six breaths per minute
or cyanosis, will not receive enough naloxone to obtain the desired
clinical effect.
Nalmefene and naltrexone are opioid antagonists with longer
half-lives and duration than naloxone. Nalmefene’s duration of
action is 4 to 10 hours, and naltrexone’s duration of action is 24
to 72 hours. These are generally not used in the ED because of
concern for inducing a prolonged withdrawal state. Naloxone
titration remains the treatment of choice for opioid reversal in the
acutely intoxicated patient.
DISPOSITION
Patients who present with heroin toxicity can be successfully
treated in the ED. Opioid-toxic patients who use longer acting
opioids may require an observation admission. Body stuffers
who remain asymptomatic after 6 hours of observation may be
1946 PART IV  Environment and Toxicology  |  SECTION Two  Toxicology
discharged. Asymptomatic body packers, however, require admis-
sion until the packets have been passed or retrieved. If an overdose
is severe, involves multiple drugs, requires multiple doses of nal-
oxone, naloxone infusion, or endotracheal intubation, then
intensive care unit (ICU) admission is appropriate.
The observation period following the administration of nalox-
one is dependent on the opioid implicated in the poisoning.
Overdoses of long-acting opioids or sustained-released opioid
preparations will require longer observation periods. In cases
of heroin-only overdose, an observation period of up to 4 hours
is generally sufficient. If there are no signs of recurrent toxicity
after an appropriate observation period, the patient may be
discharged, have a psychiatric evaluation, or be referred for sub-
stance abuse counseling and treatment depending on the clinical
situation.
In recent years, as the opioid overdose epidemic has grown,
there have been increased efforts to expand access to naloxone as
a public health measure intended to save lives.34 In many states,
police officers have been added to the ranks of those trained to
administer naloxone. There are also community- and hospital-
based initiatives to educate users and bystanders on out-of-hospital
naloxone use and then distribute or prescribe naloxone directly to
patients or bystanders. Both intranasal and intramuscular auto-
injector delivery methods have been used.35 These programs are
showing that providing opioid overdose education and out-of-
hospital naloxone to drug users and to bystanders can help reduce
opioid overdose mortality.36
Another emerging public health effort is the use of prescrip-
tion drug monitoring programs, which are currently available in
49 states in the United States. To decrease the opioid burden in
the community, the emergency provider can use these programs
KEY CONCEPTS
• The opioid toxidrome includes three prominent findings—CNS
depression, miosis, and most importantly, respiratory depression—
but presentations may be variable.
• A negative urine screen is unreliable, and absence of detection
should not deter a diagnosis of opioid intoxication when clinical
findings support it.
• Airway protection, oxygenation, ventilation, and early administration
of naloxone are the cornerstones for management of patients with
opioid toxicity.
• The duration of action of many opioids, especially after overdose, is
significantly longer than that of naloxone. Patients responsive to
The references for this chapter can be found online by accessing the accompanying Expert Consult website.
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to access a patient’s prescription opioid history prior to prescrib-
ing a new opioid upon discharge.37 Currently, there is a policy
under consideration to expand this database to the federal level
to better monitor patients who cross state borders for multiple
opioid prescriptions.
WITHDRAWAL
Withdrawal occurs in tolerant patients when opioids are stopped
or an antagonist is administered. In withdrawal, the patient goes
into a hyperadrenergic state. The symptoms include yawning,
piloerection, CNS excitation, tachypnea, mydriasis, tachycardia,
hypertension, nausea, vomiting, diarrhea, abdominal cramps, and
myalgias. CNS excitation takes the form of restlessness, agitation,
dysphoria, and insomnia. Cognition and mental status are usually
unaffected. In general, opioid withdrawal is uncomfortable but
not life-threatening. As with opioid toxicity, no diagnostic test
exists for opioid withdrawal. It is diagnosed based on the patient’s
symptoms and signs.
Treatment for the withdrawing patient in the ED is supportive
and symptom-based: intravenous fluids, electrolyte replacement,
and antiemetics. Clonidine, an alpha2-agonist, can be used to
suppress sympathetic hyperactivity and shorten the duration of
withdrawal. For long-term maintenance therapy, addiction clinics
can provide or prescribe methadone, a long-acting opioid, as a
replacement for heroin to both prevent withdrawal and treat
addiction. Buprenorphine and buprenorphine-naloxone com-
bined as a single product have recently been added to the outpa-
tient treatment armamentarium for opioid abuse.38 Opioid
withdrawal alone typically does not require inpatient treatment.
Some patients with severe symptoms may require admission.
naloxone should be observed for recurrence of respiratory depression,
because they may require further doses of naloxone.
• Community naloxone programs and prescription drug monitoring
programs are two new ways in which the medical profession is trying
to curb the epidemic of opioid-related deaths.
• Opioid withdrawal syndrome does not include altered cognition.
Patients with known or suspected opioid withdrawal who also have
altered cognition should be evaluated for another cause of the
altered cognition.

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CHAPTER 156: QUESTIONS & ANSWERS
156.1. Most opioids cause mild hypotension related to
histamine release and bradycardia. Which of the
following opioids can also cause sodium channel
blockade and QRS widening?
A. Hydromorphone
B. Meperidine
C. Morphine
D. Oxycodone
E. Propoxyphene
Answer: E. Propoxyphene and its metabolite norpropoxyphene
can cause QRS widening. None of the other listed opioids has
significant effects on the cardiac conduction system.
156.2. Which of the following laboratory abnormalities is most
commonly seen in opioid overdose?
A. Hypocalcemia
B. Hypochloremia
C. Hypoglycemia
D. Hypokalemia
E. Hyponatremia
Answer: C. Hypoglycemia is the only consistent laboratory abnor-
mality found in opioid overdose. It is generally mild but can
contribute to the decreased level of consciousness seen in opioid
overdose.
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Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2020. Elsevier Inc. Todos los derechos reservados.
C H APTER 156  Opioids 1946.e1
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156.3. A 32-year-old man presents with confusion, nausea,
vomiting, diarrhea, and abdominal pain. His friends
report that he is withdrawing from heroin. Vital signs
reveal mild hypertension, tachycardia, and tachypnea.
Physical examination is significant for confusion,
mydriasis, diaphoresis, lacrimation, piloerection, and
mild diffuse abdominal tenderness. Which of the
following signs and symptoms makes you concerned that
this may not be a simple opioid withdrawal case?
A. Confusion
B. Diarrhea
C. Mydriasis
D. Piloerection
E. Tachycardia
Answer: A. Opioid withdrawal almost always causes restlessness,
agitation, and anxiety. Cognition and mental status are not
affected in simple opioid withdrawal and, if present, should
prompt the clinician to search for other causes instead of or in
addition to withdrawal.
156.4. A 20-year-old woman is brought to the emergency
department (ED) after being found with decreased
mental status at a club. Vital signs indicate mild
hypotension and bradycardia. She is drowsy but
1946.e2 PART IV  Environment and Toxicology  |  SECTION Two  Toxicology
arousable, and she has an otherwise normal physical
examination. Upon receiving naloxone 2 mg IV, her
mental status immediately improves and soon thereafter
she vomits. She now reports nausea but has no other
complaints. She states she took some “pain pills” to get
high but does not know what they were. What
diagnostics tests should be performed?
A. Acetaminophen
B. Arterial blood gas
C. Chest radiograph
D. Lactate
E. Urine drug screen
Answer: A. Because many prescription opioid medications are
combinations of an opioid and acetaminophen, ibuprofen, or
salicylate, concentrations of acetaminophen and salicylate should
also be ordered. Acetaminophen overdose might otherwise remain
undiagnosed but, if identified, can be treated with an existing
antidote, N acetylcysteine. The chest radiograph is not indicated
unless a pulmonary complication is suspected. Lactate and a urine
drug screen would not change patient management.
156.5. Which of the following medications can be used to treat
opioid withdrawal?
A. Clonidine
B. Dextromethorphan
C. Diphenhydramine
D. Nalmefene
E. Valproic acid
Answer: A. Clonidine suppresses the sympathetic hyperactivity
of opioid withdrawal. Dextromethorphan is an opioid derivative
used as a cough suppressant, but it does not treat the symp-
toms of opioid withdrawal. Diphenhydramine and valproic acid
have no role in opioid withdrawal. Nalmefene is an opioid antago-
nist similar to naloxone but with a longer duration of action.
Administration of nalmefene would worsen opioid withdrawal
symptoms.
156.6. A 14-month-old child is brought to the emergency
department (ED) 4 hours after he was found with his
grandmother’s antidiarrheal medication bottle. A pill
count identifies that only one Lomotil tablet is missing.
The child is playful, has a normal respiratory rate and
pattern, and has a soft abdomen with normal bowel
sounds. Appropriate management includes which of the
following?
A. Administration of activated charcoal
B. Administration of naloxone
C. Admission to a monitored unit
D. Discharge home
E. Gastric lavage
Answer: C. Activated charcoal and gastric lavage are means of
gastrointestinal decontamination and are not routinely recom-
mended in opioid toxicity. Opioid intoxicated patients with
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central nervous system (CNS) and respiratory depression should
be treated with naloxone, but asymptomatic patients do not
require antidote administration. Asymptomatic patients with
known or suspected Lomotil (diphenoxylate/atropine) ingestion
should be observed in a monitored setting for delayed onset of
toxicity from the metabolite of diphenoxylate.
156.7. An 18-year-old male is driven to the emergency
department (ED) by friends and carried into the triage
area. He has agonal respirations and is cyanotic.
Immediate resuscitative measures include bag-valve-mask
(BVM) ventilation, establishment of an intravenous (IV)
line, and administration of 0.4 mg of naloxone. The
patient’s respiratory status improves and although sleepy,
he is able to answer some questions. During subsequent
monitoring, the patient’s respiratory status again
declines, and he requires two additional doses of
naloxone. Additional treatment should include which of
the following?
A. Nalmefene
B. Naloxone infusion
C. Hemodialysis
D. Suboxone
E. Subutex
Answer: B. This patient likely has toxicity from a long-acting
opioid agent, and a continuous infusion of naloxone will be neces-
sary for ongoing reversal of toxicity. Nalmefene is a longer-acting
opioid antagonist but is not preferred over naloxone infusion
because naloxone allows for dose titration. Suboxone and Subutex
are agonist agents used in the treatment of withdrawal. Opioids
are not dialyzable due to large volumes of distribution.
156.8. A 26-year-old female is brought to the emergency
department (ED) from the local airport by law
enforcement. She is sleepy and mumbles incoherently in
a foreign language. Vital signs include the following:
blood pressure, 104/66; respiratory rate, 14 breaths
per minute; and temperature, 98.6° F. Which of the
following tests might identify the cause of this patient’s
symptoms?
A. Abdominal radiograph
B. Electrocardiogram (ECG)
C. Electroencephalogram (EEG)
D. Head computed tomography (CT)
E. Urine drug screen
Answer: A. An abdominal radiograph would likely reveal multiple
packets of illicit opioid in the gastrointestinal tract of this body
packer. One or more of the packets has leaked, producing the
opioid toxicity. A urine drug screen may not identify an opioid
but would not identify the internal packets. A head computed
tomography (CT) scan would not be helpful unless associated
head trauma is suspected. An EEG and ECG would not provide
specific information to identify the internal packets.