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| By Scott R. Snyder, BS, NREMT-P, Sean M. Kivlehan, MD, MPH,
NREMT-P, & Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT
Understanding
Overdose
Opioids are a secret and leading cause of death
Bob and Jerry, both EMTs, are dispatched to a reported
unconscious person at a rural residential address about
two miles from their station. They hear the ALS fly car,
staffed by their paramedic friend Linda, also sent to the
call and realize she is about 10 miles away, across town,
and will have a longer response time.
They arrive on scene to find Mrs. Smith waiting for them
at the front door.“Please hurry,” she says.“It’s my husband—
he’s on the couch, and I don’t know what’s wrong with him.”
Mr. Smith, a 52-year-old white male, presents supine and
unconscious with obviously slow, shallow and snoring
breathing and peripheral cyanosis. Bob and Jerry immediately move him to the floor, where Bob moves to the airway
while Jerry checks for a pulse.
“His radial pulse is about 80 and weak,” Jerry reports
as Bob suctions a bit of vomit from Mr. Smith’s airway.“I’m
going to start BVM ventilations,” Bob responds. “Could you
hook the bag up to some oxygen?” Bob measures and inserts
an oropharyngeal airway.“No gag reflex,” he observes and
begins ventilating Mr. Smith 12 times a minute with the BVM
while Jerry sets the oxygen flow rate at 15 lpm.
Jerry gets a history of recent events and a past
medical history from Mrs. Smith. She says she left about
five hours ago to visit a friend. Her husband decided to
stay home because he’d hurt his back the day before
while doing yard work, was in pain and wanted to rest.
Their son, who lives on the next block, came by to visit
him as she left. She returned home to find Mr. Smith on
the couch, unconscious.
Mr. Smith is very healthy without any significant
medical history and does not presently take any medications. He has no known drug allergies.
A quick physical exam reveals no obvious trauma
or any other reason for Mr. Smith’s presentation. His
pupils are 5 mms, equal and reactive to light. There is
no JVD or peripheral edema, and his lung sounds are
equal bilaterally with slight rales. There is no response
to painful stimuli.
“Any ideas?” Bob asks Jerry.
“Maybe stroke or hypoglycemia?” Jerry replies.
CONTINUING EDUCATION
Thi CE activity
TThis
Th
iis approved by
EEMS World, an
organization accredited
by the Continuing Education
Coordinating Board for
Emergency Medical Services
(CECBEMS), for 1 CEUs.
OBJECTIVES
• Review the growing
problem of opioid overdose
• Discuss clinical
presentation of opioid
overdose
• Review prehospital
management of opioid
overdose patients
EMSWORLD.com | JUNE 2013
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CE ARTICLE
Overview
Death from poisoning kills many
people in the United States every year,
and unintentional poisoning is one of
the leading causes of death by injury.
In 2010, 42,837 persons died as the
result of poisoning.1 Of these deaths,
about 77% (33,041) were unintentional, 15.5% (6,599) were the result
of suicide attempts, and 7.5% (3,197)
were of undetermined intent. To put it into
perspective, unintentional poisoning was
second only to motor vehicle crashes
(MVC) (33,687) as the most frequent
cause of death from unintentional injury
for all ages in 2010. Among persons
25–64, unintentional poisoning was
responsible for more deaths than MVCs.1
EMS education puts a focus on
trauma and injuries, but arguably less of a
focus on poisoning. With poisoning being
such a major contributor to unintentional
deaths in the U.S., it is important that
EMTs and paramedics are familiar with
the most common causes of unintentional poisoning and their treatment. This
month’s CE article focuses on the most
common cause of unintentional death by
poisoning, prescription painkiller drugs.
Data collected from 1999–2010 show
the incidence of death from prescription
painkillers has grown linearly with the
sales of these medications.
Table 1: Common Opioid
Prescription Painkillers
GENERIC NAME
BRAND NAME
Buprenorphine
Buprenex,
Suboxone,
Subutex
Butorphanol
Stadol
Codeine
Fioricet with
codeine, Tylenol
with codeine
Dihydrocodeine
Panlor, Paracodin
Fentanyl
Duragesic patch
Hydrocodone
Lorcet, Lortab,
Norco, Vicodin,
Vicoprofen
Hydromorphone
Dilaudid,
Hydromorph
Contin, Palladone
Meperidine
Demerol
Methadone
Amidone,
Dolophine,
Methadose
Morphine sulfate
Avinza, Kadian,
MS-Contin,
Oramorph,
Roxanol
Nalbuphine
Nubain
Oxycodone
Endocet,
OxyContin,
Percocet,
Percodan,
Roxicodone,
Tylox
Oxymorphone
Numorphan,
Opana
Pentazocine
Talwin
Propoxyphene
Darvon, Darvocet
Tramadol
Ultracet, Ultram
The Basics
A poison is any substance that is
harmful to your body if ingested, inhaled,
absorbed or injected. A poisoning occurs
when exposure to a substance adversely
affects the function of body systems. If a
large enough quantity is administered, any
substance has the potential to be a poison,
including seemingly harmless and even
essential substances such as vitamins.
Poisonings can be classified as intentional or unintentional. An intentional
poisoning occurs when a person administers a substance with an intent to cause
harm to themselves or another. An unintentional poisoning occurs when a person
taking or administering a substance lacks
intent to cause harm but still provides or
consumes a dangerous quantity.
A painkiller is any medication that
provides analgesia, or relief from pain.
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The analgesics most frequently involved
in unintentional death by poisoning
belong to the family of drugs known as
opioids. An opioid is a chemical that
binds to opioid receptors in the central
and peripheral nervous systems as
well as the gastrointestinal tract. When
they bind with opioid receptors in the
brain (central nervous system), opioids
produce decreased perception of and
reaction to pain, as well as increased
pain tolerance. Opioids are used to treat
acute pain (such as postoperative pain
or pain from injury), as well as chronic
pain associated with conditions such as
back/spinal injury, arthritis and cancer.
For examples of commonly prescribed
opioid medications, see Table 1.
Standard oral preparations of opioids
are readily absorbed by the gastrointestinal tract, achieving peak blood levels
about 30–60 minutes after ingestion.
Sustained-release formulas take longer
to achieve peak blood levels. Most
ingested opioids undergo first-pass
metabolism by the liver, meaning they
will be metabolized in the liver prior to
entering the systemic circulation. As a
result, the bioavailability of ingested
opioids is reduced as much as 80%
after ingestion, and at equal doses most
opioids will be much more potent when
administered intravenously (parenterally)
than by ingestion or transdermal patches.
The Growing Problem
In 2009, 91% of unintentional
poisoning deaths were caused by
prescription medications. Opioid pain
medications and benzodiazepines were
most commonly involved. Prescription
painkiller overdoses were responsible
for more than 15,500 deaths in 2009,
more than the total for cocaine and
heroin combined.2 This number is almost
four times greater than the 4,000 people
killed by prescription painkiller medications in 1999. While all prescription painkillers have contributed to the increase
in overdose deaths over the last decade,
methadone has played a central role.
More than 30% of prescription painkiller
deaths involve it, even though only 2% of
painkiller prescriptions are for it.2 More
than 12 million Americans reported using
prescription painkillers for nonmedical
reasons in 2012.3
Where do these drugs come from?
While about 17.3% of those who misuse
prescription painkillers do so with their
own medications prescribed to them,
more than three-fourths of prescription
painkillers involved in overdoses come
from prescriptions diverted to persons
without them.3 Diversion is a term used
by the Drug Enforcement Administration
to describe prescription medications
that are used for other than their original purposes. The majority of misused
prescription painkillers (55%) are
CE ARTICLE
obtained for free from friends or relatives.
Fewer persons actually buy (11.4%) or
steal (4.8%) prescription painkillers from
friends or relatives or get them from drug
dealers or strangers (4.4%).
The CDC has identified groups
susceptible to death from unintentional
overdose of prescription painkillers:4
• Men are twice as likely to die of
prescription painkiller overdoses as women.
• Middle-aged adults have the
highest overdose rates.
• Persons living in rural counties
are nearly twice as likely to overdose as
those living in urban areas.
• Whites, Native Americans and Alaska
natives are more likely to overdose.
• About 1 in 10 Native American or
Alaska natives 12 or older used prescription painkillers for nonmedical reasons in
the past year, compared to 1 in 20 whites
and 1 in 30 African-Americans.
Clinical Presentation
The diagnosis of opioid intoxication
and overdose can be reached based on
a history and physical examination. It is a
clinical diagnosis, and toxicology screens
are not always necessary. EMS providers
should concentrate on obtaining clear
histories and identifying specific components of opioid toxidromes.
A toxidrome is a group of signs and
symptoms characteristic of an exposure to a specific substance or class
of substances. The classic toxidrome
associated opioid toxicity is CNS depression, respiratory depression and miosis
(constricted pupils). Additional signs
and symptoms include GI symptoms like
nausea and vomiting, decreased motility,
ileus; cardiac symptoms including bradycardia and hypotension; and respiratory
symptoms including acute lung injury and
pulmonary edema, plus respiratory arrest.
The respiratory depression associated with opioid intoxication is characterized by breathing that is both slow (bradypnea) and shallow (hypopnea). Opioids
decrease respiratory drive by suppressing
the sensitivity of the respiratory centers
in the medulla oblongata. This depression occurs in a dose-dependent manner,
with more severe depression occurring
with higher doses of opioids. Inadequate
ventilation can lead to development of
hypoxia (and cyanosis) and hypercarbia, and profound hypoxia can lead
to seizures. Acute lung injury and pulmonary edema can occur with therapeutic
opioid use but are more common after
overdose.5 The exact mechanisms are
unclear, but theories include capillary
leakage secondary to hypoxia6 or excessive negative pressure created when a
comatose patient with an obstructed
airway from a closed or collapsed glottis
attempts to breathe.7
While miosis is considered a classic
finding associated with opioid overdose,
there are factors that can prevent it from
occurring. Not all opioids will produce
miosis, and it is not typically seen with
meperidine (Demerol), pentazocine
(Talwin) or propoxyphene (Darvon,
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Activated Charcoal
Activated charcoal (AC) can
effectively bind with a wide
spectrum of drugs and poisons,
and animal and human studies
have shown it can prevent systemic
absorption of drugs and poisons
when administered within 1–2 hours
of ingestion, perhaps longer after
ingestion of sustained-release
medications. However, the use
of AC is not without controversy.
Randomized, controlled studies
have failed to show improved
outcomes in patients treated with
AC, and its use is not without risks,
such as aspiration.13 If considering
the use of AC, prehospital providers
must determine if the ingested
medication or poison will bind
with AC and if the benefits of
administration outweigh the risks.
Utilizing medical control or a poison
control center (800/222-1222) can
aid in this decision.
Darvocet) overdose. In addition, the
coingestion of another drug can alter
the clinical presentation of the patient
with an opioid overdose. About half of
prescription painkiller deaths involve at
least one other drug (benzodiazepines,
cocaine, heroin), and alcohol is a component in many overdose deaths.8 Mydriasis
(dilated pupils) can occur secondary to
coingestants or signal cerebral hypoxia
secondary to respiratory depression.9 If
miosis is absent but other symptoms of
the opioid toxidrome are present along
with physical evidence on scene, it is
safe to treat with opioid overdose as your
working diagnosis.
The hypotension associated with
opioid ingestion and overdose is typically orthostatic in nature and presents
secondary to histamine release. Nausea
and vomiting can occur secondary to
delayed gastric emptying, indirect stimulation of the vomit center in the medulla
and vestibular stimulation. Decreased
gastrointestinal motility is a common
finding with both therapeutic use and
overdose of opioids. Ileus, a severe
decrease in motility leading to bowel
obstruction, can occur in severe cases.
For reasons that are unclear, hypoglycemia often occurs with opiate overdose.
It is thought that coingestants such as
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alcohol may play a role.6
Obtain an accurate and thorough
patient history from bystanders, family
members, friends or the patient, if they
are alert, oriented and reliable. Pertinent
aspects of the history include:
• Does the patient have a history
of opioid abuse, either via prescription
medications or illicit drugs? Is there a
history of substance abuse? Is there a
history of suicide attempt?
• Does the patient have access to
opioid painkillers? Does the patient have
chronic pain/recent surgery/cancer that
could predispose them to accidental
overdose? Are they prescribed painkiller
medication, or does anyone in the home
have a prescription? Does a friend or
family member outside the home have
a prescription?
• Are prescription medication bottles
present on scene? What are the medications? Do the bottles actually contain the
medications listed on them? To whom are
they prescribed? Are there pills missing?
• Does the patient have any pills on
their person or in personal items such as
their purse or backpack? Has an attempt
been made to identify unknown pills or
tablets? (Remember to bring all pill
bottles to the ED.)
• What was the time of ingestion?
How much was ingested? Were other
medications or alcohol also ingested?
• Has the patient vomited? Were
there pills in the vomit?
Treatment
Respiratory depression is the primary
morbidity and cause of almost all the
mortality associated with opioid toxicity
and overdose.9 Therefore, opening
the airway, keeping the airway open,
correcting inadequate ventilation and
reversing hypoxia is the most important
treatment for the patient with opiate
toxicity or overdose. Open the airway
with a manual maneuver such as the
head-tilt chin-lift. A modified jaw thrust
or other manual maneuver that maintains inline cervical spine stabilization
can be used for patients who require it;
however, except in cases where overdose
is complicated by major trauma, spine
stabilization is rarely indicated. Inspect
the airway for vomit and secretions and
suction as needed. Snoring is indicative of the tongue acting as an airway
obstruction and can be anticipated in the
comatose patient who is lying supine. In
such a case, an oropharyngeal or nasopharyngeal airway opens the airway
adequately.
Patients with inadequate breathing
require ventilations with a bag-valve
mask and 100% oxygen. The goal is to
correct the bradypnea and hypopnea
associated with opioid toxicity. A ventilation rate of 10–12 per minute with
enough tidal volume to result in normal
chest rise and fall should be adequate.
Use a pulse oximeter to monitor the
SpO2, which will reflect the effectiveness of ventilation and correction of the
hypoxia. If available, monitoring end-tidal
carbon dioxide can help gauge the effectiveness of ventilation and correction of
hypercarbia. For patients with acute lung
injury and pulmonary edema, continuous
positive airway pressure is an effective
adjunct that improves lung ventilation,
pushes pulmonary edema back into
the bloodstream and helps keep alveoli
inflated in diseased states.
If airway control and ventilation are
successful with BLS measures, endotracheal intubation can be withheld until
after administration of naloxone, as the
patient’s altered level of consciousness and respiratory depression can be
expected to resolve. Reserve endotracheal intubation for those with uncontrollable airways or who remain in prolonged
comatose conditions.
Naloxone is the antidote of choice
for opiate intoxication and overdose. It is
a pure opioid antagonist that competes
for and blocks opiate receptors, reversing
the effects of circulating opioids in the
blood. Because naloxone has a greater
affinity for opioid receptors than the
opioid drugs themselves, it is effective
in reversing the effects opioids have on
the body. Naloxone can be administered
via the oral, intravenous, intramuscular,
subcutaneous, endotracheal and intranasal routes. While the IV administration of naloxone has been the domain
of paramedics for many years, the ease
and efficacy of intransal (IN) administra-
CE ARTICLE
and nasal gastric tubes can improve
patient outcomes by placing a gastric
tube and administering activated charcoal
via the NG/OG tube when patients cannot
be trusted to swallow. Involving medical
control in a decision this important—and
with a procedure that has such significant
side effects—is always a good idea.
really hurt and I wanted some relief.”
He is transferred to the ambulance and
transported to the ED without incident,
though he requires an additional 1.2 mg
of IV naloxone en route.
Scenario Conclusion
2. Centers for Disease Control and Prevention. Vital Signs:
Prescription Painkiller Overdoses in the U.S., www.cdc.gov/
vitalsigns/painkilleroverdoses/.
The paramedic, Linda, arrives on
scene and takes a report from Bob and
Jerry. She immediately asks Mrs. Smith,
“Are there any pain medications in the
house—maybe an old prescription for
him or one for you?”
“No,” Mrs. Smith replies,“but my son
takes pain medications. He’s had many
back surgeries and is out of work on
disability. Should I call him?”
“Please do,” Linda replies. She then
administers 2.0 mg of naloxone IN
and prepares to place Mr. Smith on the
cardiac monitor while Jerry sets up her
equipment for an IV attempt.
“He’s waking up, and his breathing
is picking up,” Bob says, pulling the BVM
off Mr. Smith’s face but continuing to give
oxygen via blow-by.
“Well, that answers that question!”
Linda says with a smile.
“If this is an opioid overdose, why
are his pupils not pinpoint?” Bob asks.
“I know some opioid overdoses won’t
result in pinpoint pupils, but I’m not sure
which ones,” Linda replies.
“My son is coming right over,” Mrs.
Smith says as she comes back from the
kitchen. “He says he gave my husband
some of his Demerol because he was in
so much pain.”
Linda initiates IV access with an
18-gauge catheter in Mr. Smith’s left arm.
Mr. Smith is now conscious and alert to
pain. His son arrives, visibly upset, and
tells the EMS crew and his mother how
he gave his father five 100-mg tablets of
Demerol to use for his back pain. “I told
him to be careful with it and not take more
than one every six hours,” the son laments.
“I didn’t mean for this to happen!”
Mr. Smith’s level of consciousness
and mental status eventually improve to
where he can describe taking all 500
mg of the Demerol “because my back
REFERENCES
1. Centers for Disease Control and Prevention. Web-based
Injury Statistics Query and Reporting System (WISQARS),
www.cdc.gov/injury/wisqars/index.html.
3. Substance Abuse and Mental Health Services
Administration. Results from the 2010 National Survey on
Drug Use and Health: Summary of National Findings, www.
samhsa.gov/data/nsduh/2k10nsduh/2k10results.htm.
4. Op cit., Centers for Disease Control and Prevention,
Vital Signs.
5. Soto J, Sacristan JA, Alsar MJ. Pulmonary oedema due
to fentanyl? Anaesthesia, 1992 Oct; 47: 913–4.
6. Bardsley CH. Chapter 160: Opioids. In: Marx J,
Hockberger R, Walls R, Rosen’s Emergency Medicine, 7th
ed. Mosby, 2010.
7. PulmCCM. Managing Opioid Overdose in the ICU
(Review, NEJM), http://pulmccm.org/2012/critical-carereview/managing-opioid-overdose-in-the-icu-review-nejm/.
8. Warner M, Chen LH, Makuc DM. Increase in fatal
poisonings involving opioid analgesics in the United
States, 1999–2006. NCHS Data Brief, 2009 Sept, www.
cdc.gov/nchs/data/databriefs/db22.pdf.
9. Doyon S. Chapter 180: Opioids. In: Tintinalli JE, et al.,
Tintinalli’s Emergency Medicine: A Comprehensive Study
Guide, 7th ed. New York: McGraw-Hill, 2011.
10. Robertson TM, Hendey GW, Stroh G, Shalit M. Intranasal
naloxone is a viable alternative to intravenous naloxone
for prehospital narcotic overdose. Prehosp Emerg Care,
2009 Oct–Dec; 13(4): 512–5.
11. Barton ED, et al. Efficacy of intranasal naloxone as a
needleless alternative for treatment of opioid overdose in
the prehospital setting. J Emerg Med, 2005 Oct; 29(3):
265–71.
12. Morbidity and Mortality Weekly Report. Communitybased opioid overdose prevention programs providing
naloxone—United States, 2010. MMWR, 2012 Feb 17;
61(6): 101–5.
13. Olson KR. Activated charcoal for acute poisoning: one
toxicologist’s journey. J Med Toxicol, 2010; 6: 190–8.
Scott R. Snyder, BS, NREMT-P, is a faculty member at
the Public Safety Training Center in the Emergency
Care Program at Santa Rosa Junior College, CA.
E-mail [email protected].
Sean M. Kivlehan, MD, MPH, NREMT-P, is an emergency medicine resident at the University of California,
San Francisco. E-mail [email protected].
Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P,
WEMT, is performance improvement coordinator
for Vitalink/Airlink in Wilmington, NC, and a lead
instructor for Wilderness Medical Associates. E-mail
[email protected].
SCOTT SNYDER, SEAN KIVLEHAN
AND KEVIN COLLOPY are featured
speakers at EMS World Expo 2013,
Sept. 8–12, Las Vegas Convention
Center, Las Vegas, NV.
For more information, visit EMSWorldExpo.com
tion has been explored with favorable
results, and it arguably is a safe and
effective treatment that can be utilized
in the EMS environment.10,11 In fact, IN
naloxone is so easy to administer that
nonmedical persons have been trained
in its use in community-based opioid
overdose prevention programs, with positive outcomes. In the February 17, 2012
issue of Morbidity and Mortality Weekly
Report, the CDC reported that more
than 53,000 laypersons from at least
15 states had been trained in administration of IN naloxone and reported
the successful reversal of over 10,000
episodes of opioid overdose.12
The dose of naloxone is 0.4–2.0 mg
for adults and children. Higher doses may
be required for synthetic opioids such
as fentanyl. Naloxone administration can
result in acute withdrawal symptoms in
patients who are physically dependent
on their drug. Patients with suspected
opioid dependency can receive a titrated
dose of naloxone starting at 0.4 mg and
administered in 0.4-mg increments until
respiratory depression is corrected.
Naloxone can also be a valuable
diagnostic tool, as in the case of a patient
with an altered level of consciousness of
unknown etiology. In many prehospital
protocols, such a patient would receive a
dose of naloxone. If the patient responds,
it can be concluded that opioids at least
contributed to the patient’s decreased
level of consciousness.
Consider administration of activated
charcoal in patients who are conscious,
alert and oriented, can protect their
airway, and have an oral opioid ingestion
that occurred within the hour.6,9 Activated
charcoal has fallen out of favor for oral
overdoses in general, but it has a proven
benefit in patients when given soon after
drug ingestion. Given orally, the common
dose in children and adults is 1.0 g/kg,
or adults may receive a limited dose of
50–100 g.6 As the risk of vomiting is high
in patients with opioid toxicity, consider
carefully the risk of decreasing mental
status and level of consciousness, loss of
the ability to protect the airway, and the
possibility of vomiting or regurgitation
and subsequent aspiration.
Paramedics who routinely place oral
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