Volume 33 Number 8 August 2019

Relief Work
Emergency physicians are encountering ever-greater
numbers of patients with cancer, many of whom
present with debilitating pain. Although pain was once
regarded as the “fifth vital sign” — a perception that
has undoubtedly contributed to the US opioid epidemic
— clinicians are frequently accused of undertreating
chronic pain. To effectively manage cancer-related
complications, it is imperative to relieve the patient’s
suffering while staying abreast of the latest treatment
alternatives.

Torn Apart
Although aortic dissection is widely regarded as one
of the five fatal causes of nontraumatic chest pain, it
is frequently — and often tragically — misdiagnosed.
While many of these patients present with sudden,
severe, “ripping” or “tearing” chest pain, others do
not. Emergency clinicians must be prepared to interpret
both classic and rare presentations and common risk
factors associated with the disorder, for which prompt
recognition and treatment remain the best defense.

THE OFFICIAL CME PUBLICATION OF THE AMERICAN COLLEGE OF EMERGENCY PHYSICIANS

IN THIS ISSUE
Lesson 15 n Cancer-Related Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Critical ECG . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Critical Decisions in Emergency Medicine is the official
CME publication of the American College of Emergency
LLSA Literature Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
Physicians. Additional volumes are available.
Critical Image . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14
EDITOR-IN-CHIEF
Critical Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Michael S. Beeson, MD, MBA, FACEP
Lesson 16 n Aortic Dissection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 Northeastern Ohio Universities,
Rootstown, OH
Critical Cases in Orthopedics and Trauma . . . . . . . . . . . . . . . . . . . . . . . . 28
SECTION EDITORS
CME Questions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
Joshua S. Broder, MD, FACEP
Drug Box/Tox Box . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32 Duke University, Durham, NC
Andrew J. Eyre, MD, MHPEd
Contributor Disclosures. In accordance with the ACCME Standards for Commercial Support Brigham & Women’s Hospital/
and policy of the American College of Emergency Physicians, all individuals with control Harvard Medical School, Boston, MA
over CME content (including but not limited to staff, planners, reviewers, and authors) must John Kiel, DO, MPH
disclose whether or not they have any relevant financial relationship(s) to learners prior to the University of Florida College of Medicine, Jacksonville, FL
start of the activity. These individuals have indicated that they have a relationship which, in
Frank LoVecchio, DO, MPH, FACEP
the context of their involvement in the CME activity, could be perceived by some as a real or
Maricopa Medical Center/Banner Phoenix Poison
apparent conflict of interest (eg, ownership of stock, grants, honoraria, or consulting fees),
and Drug Information Center, Phoenix, AZ
but these individuals do not consider that it will influence the CME activity. Joshua S. Broder,
MD, FACEP: He owns OmniSono Inc, an ultrasound technology company, and his wife is Amal Mattu, MD, FACEP
employed by GlaxoSmithKline as a research organic chemist. All remaining individuals with University of Maryland, Baltimore, MD
control over CME content have no significant financial interests or relationships to disclose.
Lynn P. Roppolo, MD, FACEP
This educational activity consists of two lessons, a post-test, and evaluation questions; UT Southwestern Medical Center,
as designed, the activity should take approximately 5 hours to complete. The participant Dallas, TX
should, in order, review the learning objectives, read the lessons as published in the print
Christian A. Tomaszewski, MD, MS, MBA, FACEP
or online version, and complete the online post-test (a minimum score of 75% is required)
University of California Health Sciences,
and evaluation questions. Release date August 1, 2019. Expiration July 31, 2022.
San Diego, CA
Accreditation Statement. The American College of Emergency Physicians is accredited by Steven J. Warrington, MD, MEd
the Accreditation Council for Continuing Medical Education to provide continuing medical Orange Park Medical Center, Orange Park, FL
education for physicians.

The American College of Emergency Physicians designates this enduring material for a ASSOCIATE EDITORS
maximum of 5 AMA PRA Category 1 Credits™. Physicians should claim only the credit Wan-Tsu W. Chang, MD
commensurate with the extent of their participation in the activity. University of Maryland, Baltimore, MD
Each issue of Critical Decisions in Emergency Medicine is approved by ACEP for 5 ACEP Walter L. Green, MD, FACEP
Category I credits. Approved by the AOA for 5 Category 2-B credits. UT Southwestern Medical Center,
Dallas, TX
Commercial Support. There was no commercial support for this CME activity.
John C. Greenwood, MD
Target Audience. This educational activity has been developed for emergency physicians.
University of Pennsylvania, Philadelphia, PA
Danya Khoujah, MBBS
Critical Decisions in Emergency Medicine is a trademark owned and published monthly by the American
University of Maryland, Baltimore, MD
College of Emergency Physicians, PO Box 619911, Dallas, TX 75261-9911. Send address changes and
comments to Critical Decisions in Emergency Medicine, PO Box 619911, Dallas, TX 75261-9911, or to Sharon E. Mace, MD, FACEP
cdem@acep.org; call toll-free 800-798-1822, or 972-550-0911. Cleveland Clinic Lerner College of Medicine/
Copyright 2019 © by the American College of Emergency Physicians. All rights reserved. No part of
Case Western Reserve University, Cleveland, OH
this publication may be reproduced, stored, or transmitted in any form or by any means, electronic or Nathaniel Mann, MD
mechanical, including storage and retrieval systems, without permission in writing from the Publisher. Greenville Health System, Greenville, SC
Printed in the USA.
Jennifer L. Martindale, MD, MSc
The American College of Emergency Physicians (ACEP) makes every effort to ensure that contributors Mount Sinai St. Luke’s/Mount Sinai West,
to its publications are knowledgeable subject matter experts. Readers are nevertheless advised that the New York, NY
statements and opinions expressed in this publication are provided as the contributors’ recommendations
at the time of publication and should not be construed as official College policy. ACEP recognizes the David J. Pillow, Jr., MD, FACEP
complexity of emergency medicine and makes no representation that this publication serves as an UT Southwestern Medical Center, Dallas, TX
authoritative resource for the prevention, diagnosis, treatment, or intervention for any medical condition,
George Sternbach, MD, FACEP
nor should it be the basis for the definition of or standard of care that should be practiced by all health
Stanford University Medical Center, Stanford, CA
care providers at any particular time or place. Drugs are generally referred to by generic names. In some
instances, brand names are added for easier recognition. Device manufacturer information is provided Joseph F. Waeckerle, MD, FACEP
according to style conventions of the American Medical Association. ACEP received no commercial support University of Missouri-Kansas City School of Medicine,
for this publication. Kansas City, MO
To the fullest extent permitted by law, and without
limitation, ACEP expressly disclaims all liability for EDITORIAL STAFF
errors or omissions contained within this publication, Rachel Donihoo, Managing Editor
and for damages of any kind or nature, arising out of rdonihoo@acep.org
use, reference to, reliance on, or performance of such Suzannah Alexander, Publishing Assistant
information.
ISSN2325-0186(Print) ISSN2325-8365(Online)
 Relief Work
Cancer-Related Pain

LESSON 15

By Jonathan Glauser, MD, MBA, FACEP; and Sarah Money, MD

Dr. Glauser is a professor of emergency medicine at Case Western Reserve University
in Cleveland and serves on the faculty in the Department of Emergency Medicine at
MetroHealth Medical Center/Cleveland Clinic in Ohio. Dr. Money specializes in pain
medicine at the University of Michigan Hospitals/Michigan Medicine in Ann Arbor.

Reviewed by Sharon E. Mace, MD, FACEP

OBJECTIVES
On completion of this lesson, you should be able to:
1. Differentiate between acute, chronic, bone, abdominal,
and breakthrough pain.
2. Identify and treat the potential causes of muscle cramps
in cancer patients.
3. Recognize specific pain syndromes in cancer patients
that are unrelated to the malignancy.
4. Describe the therapies that can be employed to relieve
intractable pain as well as specialized nonpharmacologic
pain management techniques.
FROM THE EM MODEL
1.0 Signs, Symptoms, and Presentations
1.2 Pain
CRITICAL DECISIONS
n How can acute pain be differentiated from chronic
pain?
n How can cancer-related bone or abdominal pain be
diagnosed and managed?
n How can breakthrough pain be recognized and
managed?
n What causes muscle cramps in cancer patients, and
how can they be managed?
n What nonmalignancy-related syndromes can also
cause pain?
n What newer therapies can relieve intractable pain?
n What nonpharmacologic therapies can help control
cancer pain?

Emergency physicians are encountering ever-greater numbers of patients with cancer, many of whom present with
debilitating pain.1 Although pain was once regarded as the “fifth vital sign” — a perception that has undoubtedly contributed
to the United States opioid epidemic — clinicians are frequently accused of undertreating chronic cases. To effectively
manage cancer-related complications, it is imperative to relieve the patient’s suffering while staying abreast of the latest
treatment alternatives.

August 2019 n Volume 33 Number 8 3

 CASE PRESENTATIONS
■ CASE ONE
A 60-year-old woman presents
with paratracheal pain and
posterior neck pain. She was
recently diagnosed with laryngeal
carcinoma and underwent a
complete laryngectomy with
negative borders.
Her vital signs are blood
pressure 127/84, heart rate 82 and
regular, respiratory rate 18, and
temperature 36.8°C (98.2°F). She is
not in acute respiratory distress and
has no stridor or secretions from a
tracheostomy. Her lungs are clear
to auscultation. There is no further
treatment plan for her tumor.
More than 15 million Americans
were living with cancer in 2018,
approximately 609,000 of whom
died from the disease.2,3 By 2020, an
estimated 17 million new cases will
be diagnosed worldwide per year.4
Annually, between 1 and 3 million
emergency department visits in the
United States are related to cancer.5 In
light of these eye-opening statistics, it
is paramount to understand how this
vulnerable population uses emergency
services.6
Certain cancer emergencies, such as
spinal cord compression, superior vena
cava syndrome, and febrile neutropenia,
are well covered in emergency medicine
training curricula; however, clinicians
may be unaware that pain can indicate
decompensation, a new complication, or
cancer recurrence.
Palliative Care and Opioids
As subspecialties of emergency
medicine, hospice and palliative care
can relieve suffering, provide comfort,
and prevent pain. In response to a
growing need, Improving Palliative Care
in Emergency Medicine Collaboration
was created in 2010 as a resource
development and dissemination
initiative.7 The role of emergency
clinicians in caring for patients along
chronic illness trajectories is critical,
particularly in light of the widespread
undertreatment of cancer pain.8
4 Critical Decisions in Emergency Medicine
■ CASE TWO
A 58-year-old man who was
recently diagnosed with stage 4
pancreatic carcinoma presents
with a pain flare. He complains of
significant, sharp abdominal pain
with cramping and nausea.
His vital signs are blood
pressure 152/92, heart rate 110,
respiratory rate 18, temperature
37°C (98.6°F), and oxygen
saturation 98% on room air. On
physical examination, his lungs are
clear to auscultation; scleral icterus
is noted. His abdominal tenderness
is maximal in the midepigastrium,
and he has active bowel sounds.
Despite the fact that a great number
of palliative care patients take oral
morphine on a regular basis, long-term
opioid use is known to impair cognitive
function and compromise the immune
and endocrine systems.9 As a result,
many clinicians are loath to prescribe
them.8 These risks and others, including
addiction, may be of negligible concern
when caring for terminally ill patients,
for whom pain is perhaps the most
feared complication of their disease.10
Even so, some institutions have
tried to limit the number of opioid
prescriptions issued by the emergency
department to a few days’ supply
because of the risk of drug diversion,
noting that the street value of one
oxycodone tablet can be as much as
$40.11,12 Although cancer pain may
be best addressed by oncology and
primary care, approximately one-third of
emergency department patients receive
narcotics during their visit or are given a
prescription upon discharge.13
Horror stories of physicians
writing thousands of prescriptions for
controlled substances over a 1-year
period or facing homicide charges for
opioid prescribing have, so far, failed
to implicate emergency physicians.
In fact, according to a recent report,
opioid prescriptions written by
emergency physicians average only
15 pills; furthermore, very few of
■ CASE THREE
A 72-year-old man with a history
of basal cell carcinoma presents with
localized skin pain at his cancer site.
Although the pathology report indicates
that the lesion was completely excised
3 months earlier, the patient complains
of point tenderness at the operative site.
His vital signs are blood pressure
134/78, heart rate 72, respiratory rate
16, temperature 36.4°C (97.5°F), and
oxygen saturation 100% on room air.
The patient’s lungs are clear, and his
surgical incision is well healed. He
says that oxycodone has been effective
in relieving his symptoms, but his
prescription has run out.
these prescriptions are for long-acting
agents, patches, or extended-release
medications.14 Despite this encouraging
evidence, emergency medicine deals
with a disproportionate share of
narcotic-related problems, including
overdose and withdrawal, ensuring
its high profile in substance abuse
discussions. As such, clinicians should
consult risk-stratification tools when
prescribing opioids.
A high-risk situation may exist if
there is a history of alcohol or drug
misuse, either by the patient or the
family. It is important to recognize
that patients who request early refills
or obtain prescriptions from multiple
sources may be exhibiting drug-seeking
behaviors. Clinicians can help mitigate
this risk by using one dedicated
pharmacy and performing regular pill
counts.15
CRITICAL DECISION
How can acute pain be
differentiated from chronic pain?
Chronic pain syndromes, which
affect between 30% and 50% of patients
who are being actively treated for a
solid tumor and 70% to 90% of those
with advanced disease, are usually
related to the cancer itself.1 Acute pain
syndromes, on the other hand, are
often iatrogenic — a consequence of
diagnostic or therapeutic intervention.
However, tumors can cause acute pain
due to pathologic fractures, bowel
obstruction, direct invasion, perforated
viscus, or a hemorrhage into the tumor
(eg, hepatocellular carcinoma).
Obstruction of a ureter or bile
duct can require stenting, surgery,
or percutaneous decompression, so
clinicians should avoid assuming that
acute pain is simply a symptom of
progressive cancer. Nociceptive pain can
be caused by ongoing tissue damage,
whereas neuropathic pain can result
from nervous system dysfunction.
As many as 33% of cancer patients
report pain after curative treatment,
and 64% of those with metastatic
or terminal disease suffer from pain.
The World Health Organization
(WHO) has established a three-step
analgesic “ladder” that can be used to
manage cancer pain (Figure 1). For
mild discomfort, acetaminophen or a
nonsteroidal anti-inflammatory drug
(NSAID) is indicated.16
For mild to moderate pain, weak
opioids (eg, codeine, tramadol, or
dihydrocodeine) are recommended, in
combination with nonopioid analgesics.
The rationale for adding an opioid to a
nonopioid is to introduce a drug with
a different mechanism of action — a
FIGURE 1. WHO Analgesic Ladder
FREED
CANC M FROM
Opio
id for
to s e
process that can improve pain control
while reducing the need for opioids.17
With weak opioids, however, a “ceiling
effect” can occur, in which increasing
dosages past a certain threshold
intensifies side effects without improving
the effectiveness of the analgesia.
For moderate to severe pain, the
most commonly used opioid analgesics
include morphine, methadone,
oxycodone, hydromorphone, fentanyl,
alfentanil, buprenorphine, and
oxymorphone. Oral morphine is often
the opioid of first choice for moderate
to severe cancer pain, and one-third of
the dose can be given parenterally as an
equivalent dose.18 These agents can also
be combined with nonopioid analgesics.
CRITICAL DECISION
How can cancer-related bone or
abdominal pain be diagnosed
and managed?
Chronic pain in cancer patients is
most often caused by bone metastases.
Lung, breast, and prostate tumors are
the most common primary tumors that
lead to bone metastatic pain; thyroid
and kidney tumors are less frequent
causes. Myeloma is the most common
hematologic malignancy associated with
O
ER PA
IN
m odera
lytic bone lesions. Neoplastic spinal cord
compression must also be considered to
prevent irreversible neurologic deficits.
Stretching of the hepatic capsule
by metastases or a primary hepatoma
can cause chronic pain, as can tumor
infiltration of the pancreas or chronic
intestinal obstruction from a neoplasm
or adhesions. Adhesions, ascites,
omental spread of the tumor, and
seeding of the peritoneum from the
tumor can all cause pain as well.
Scintigraphy, CT, and MRI are more
diagnostically sensitive than plain films,
which require an approximate 40%
change in bone density before bone
metastases can be identified.19 Bisphosph­
onates such as etidronate, clodronate,
pamidronate, and alendronate have
antiresorptive effects that can reduce
bone cancer pain and tumor-induced
bone destruction (Figure 2).3,17,19
CRITICAL DECISION
How can breakthrough pain be
recognized and managed?
Breakthrough cancer pain (BTCP)
is defined as a transient exacerbation
that is either spontaneous or related to
a trigger. This transitory flare occurs
against a background of relatively well-
controlled, baseline pain, assuming that
the patient’s symptoms are moderately
stable and adequately controlled.18,20
BTCP is somewhat ill-defined and lacks
objective tests or diagnostic criteria.
It is important to note that patients
may be unable to separately quantify

3
ver te background pain (ie, pain experienced
) non e pain
opioid
) adju for more than half of waking hours
PAIN va nt
PERS or more than 12 hours per day).21
OR IN IS T I N
O pi
oid CR E A G The skilled use of opioid analgesics
fo r m SI N G

2
ild t is therefore critical in relieving BTCP
) no o m o d
n er (Table 1).
) a d o p i o i d a te p a i
ju va n In addition to the WHO analgesic
nt
PAI ladder, which addresses the severity
N
OR PERSI of pain, the European Association
INC S
R E A TING

Non
SI N
G
1 for Palliative Care offers similar
recommendations.16 Low-potency
) a d o pioi d medications (step II drugs) include
ju va
nt tramadol, hydrocodone, and codeine,
PA and standard higher-potency agents
IN (step III drugs) include morphine.
No significant distinction is made
between morphine, oxycodone, and
hydromorphone for the management of

August 2019 n Volume 33 Number 8 5


TABLE 1. High-Potency Drugs
for BTCP
Time to onset (oral agents):
approximately 30 minutes; duration
approximately 4 hours
Morphine
Hydromorphone
Oxycodone
Methadone (use with caution)
TABLE 2. Relative Analgesic
Ratios22
Morphine to oral oxycodone 1:1.5
Oxycodone to hydromorphone 1:4
Morphine to hydromorphone 1:5
Morphine to transdermal 75:1
buprenorphine
Morphine to transdermal fentanyl 100:1
TABLE 3. Alternative Drugs
for BTCP
Fentanyl pectin nasal spray
Fentanyl sublingual tablets
Fentanyl buccal tablets
Morphine sulfate (immediate release)
Oral transmucosal fentanyl citrate
Transdermal buprenorphine
moderate to severe cancer pain, with one
study citing a threshold of greater than
120 mg/day of morphine equivalents to
achieve relief (Table 2).1,16,22
Although methadone is an
alternative to oral morphine, it has
a long, unpredictable half-life and is
seldom available in the emergency
setting. Methadone’s half-life is
approximately 24 hours, which enables
dosing in 6- to 8-hour intervals;
however, its half-life varies between
individuals and can range from
half a day to almost a week.15 Since
methadone prolongs the QTc interval,
its use with other drugs must be
monitored. While many medications
are effective when administered
subcutaneously via butterfly catheter,
methadone can produce painful
subcutaneous nodules.
A number of other agents have been
proposed for the management of BTCP
(Table 3), including intranasal fentanyl
spray, fentanyl pectin nasal spray,
6 Critical Decisions in Emergency Medicine
fentanyl sublingual tablets, fentanyl
buccal soluble film, fentanyl buccal
tablets, oral transmucosal fentanyl citrate,
and morphine sulfate immediate release.
Transmucosal fentanyl medications
appeared to decrease pain intensity
most effectively within 1 hour or less,
and intranasal fentanyl spray has been
shown to decrease pain intensity most
effectively within 15 minutes.23 Rapid-
onset formulations (eg, transmucosal
fentanyl) appear to provide faster relief
than traditional formulations.15
Transdermal buprenorphine can
be useful for patients who are unable
to swallow. Buprenorphine is safe
for patients with renal failure, as it
is metabolized by the liver. Adding
an NSAID to opioid treatments may
also be helpful. The side effects of
these medications, especially as they
relate to cardiovascular, renal, and
gastrointestinal risks, should be weighed
against their benefits.15
CRITICAL DECISION
What causes muscle cramps in
cancer patients, and how can
they be managed?
Muscle cramps can occur in
otherwise healthy patients, without
evident cause. Metabolic culprits are
often related to diuretic use, uremia,
cirrhosis, or hemodialysis. Muscle
cramps can also be related to anterior
horn disease.24
Cancer patients are often subjected
to surgery and radiation therapy,
which can damage peripheral nerves
or nerve roots. The ensuing cramps
may respond to treatment with
phenytoin or carbamazepine. Some
chemotherapeutic agents, including
vincristine, vinblastine, and cisplatin,
are neurotoxic. Cisplatin, in particular,
can induce hypomagnesemia as well
as peripheral neuropathy. Metastatic
disease can compress or infiltrate nerve
roots. Most of the endocrine agents
used in breast cancer can also cause
cramps.24
Nerve root compression or
denervation is best detected via
electromyography.25 The appropriate
diagnostic workup depends on the
clinical presentation but can include
the measurement of electrolytes (eg,
magnesium and calcium) and muscle
enzymes (eg, creatine phosphokinase
and aldolase), and assessment of thyroid
function. Quinine (300 mg) taken at
bedtime may help control nocturnal
cramps.26
CRITICAL DECISION
What nonmalignancy-related
syndromes can also cause pain?
Some chemotherapeutic agents
can lead to neurotoxicity. Vincristine,
in particular, can cause orofacial pain
in the distribution of the trigeminal
and glossopharyngeal nerves, inducing
pain in the throat, teeth, mandible,
and ears. Pain can be moderate to
severe, with onset within hours of
vincristine administration. Fortunately,
the symptoms tend to be self-limited;
however, mastication and swallowing
can be so painful that the patient is
unable to eat or swallow.27
Trigeminal neuralgia can result
from meningiomas, lymphomas,
metastatic tumors, cholesteatomas,
and squamous cell carcinomas,
along with other cancers. Treatments
include alcohol blocks, percutaneous
rhizotomy, radiofrequency ablation,
and carbamazepine.28 Glossopharyngeal
neuralgia from tumor involvement of the
ninth cranial nerve can cause stabbing
pain in the throat or neck that radiates
to the ear. In fact, any tumor that
compresses a nerve root can induce a
neuropathy.
Laxatives can mitigate constipation,
a common and often refractory
side effect of treatment with opioid
analgesics. Although oral naloxone has
low bioavailability, it can bind to opioid
receptors in the gastrointestinal tract.29
Chemotherapy-associated mucositis
can affect the entire gastrointestinal
mucosa. Oral mucositis and ulceration
of the oropharyngeal mucosa can
occur within days of the initiation of
chemotherapy, commonly with agents
such as methotrexate, doxorubicin, and
fluorouracil.
Clinical practice guidelines have
been proposed for the treatment of
oral mucositis — a common toxic
effect of radio- and chemotherapy —
including patient-controlled analgesia
(PCA) with morphine, transdermal
fentanyl, 2% morphine mouthwash,
and 0.5% doxepin mouthwash.30 Pelvic
and abdominal radiation can cause
uncomfortable side effects, including
radiation proctitis, which can precipitate
painful tenesmus, diarrhea, and bleeding.
Radiation therapy for breast cancer can
precipitate brachial plexopathy, which
can manifest as pain, weakness, and
paresthesias in the shoulder, arm, and
hand. Fortunately, this is usually a self-
limited syndrome.31
FIGURE 2. PET/CT Showing Severe Bone Destruction Indicative of Metastatic Tumors
CRITICAL DECISION
What newer therapies can relieve
intractable pain?
Lidocaine infusions have been
employed with some success to control
pain that is refractory to increasing doses
of morphine (up to 50 mg/hour), as have
adjuvant analgesics such as gabapentin,
baclofen, amitriptyline, clonidine, and
clonazepam. In one report, a 100-mg dose
of intravenous lidocaine (approximately
1.5 mg/kg) produced a rapid decrease in
pain, when given in a concentration of
8 mg/mL over 20 to 30 minutes, followed
by an infusion at 100 mg/hour or 0.5 to
2.0 mg/kg per hour.32
Neuropathic pain caused by diabetic
neuropathy, peripheral nerve injuries,
malignant nerve infiltration, or post-
herpetic neuralgia can also be relieved
by lidocaine or its oral analogue,
mexiletine; however, a history of
heart failure or liver disease should be
obtained first. Home lidocaine infusions
can be administered successfully in the
PCA setting, as long as there is 24-hour
supervision by a competent adult and the
© ZHENG ET AL.
August 2019 n Volume 33 Number 8 7

TABLE 4. Alternative Therapies
for Cancer Pain
Intrathecal drug therapy
Kyphoplasty/vertebroplasty
Percutaneous cervical cordotomy
Neuromodulation
Ultrasound-guided nerve blocks/celiac
plexus block
Palliative radiotherapy
Intrathecal neurolysis
Acupuncture
Transcutaneous electric nerve stimulation
availability of benzodiazepines, which
can be administered in the event of a
seizure.33
By contrast, subdissociative doses
of ketamine have not been validated as
an adjuvant to opioids for cancer pain
relief. N-methyl-D-aspartate (NMDA)–
receptor activation in the spinal cord can
result in central sensitization. Ketamine
and dextromethorphan have been used
as NMDA antagonists and have a role
in opioid-induced hyperalgesia. There is
only weak evidence, however, for their
efficacy in cancer pain.34 Evidence of
ketamine’s benefits comes mainly from
case series or uncontrolled studies that
evaluated doses between 100 mg and
500 mg over a 5-day period.17 Adverse
events include hallucinations, vivid
dreams, and a sense of disconnection.29
Neuropathic pain may be diminished by
the addition of pregabalin, gabapentin,
or amitriptyline.1,18
Cannabinoids have also been
examined as possible adjuvant
analgesics. Cannabinoid receptor
type 1 (CB1) receptors are prevalent
n The mainstay treatment of cancer pain is opioid-based pharmacotherapy.
n The goal is to achieve adequate pain control while minimizing the risks
associated with analgesic agents, including constipation, misuse, addiction,
and diversion.
n Opioid switching is an important technique for improving a patient’s poor
response to a particular opioid.
n The safest opioids for patients with advanced chronic kidney disease may be
fentanyl and transdermal buprenorphine.
8 Critical Decisions in Emergency Medicine
in the central nervous system, while
cannabinoid receptor type 2 (CB2)
receptors are common in the peripheral
tissues. Delta-9-tetrahydrocannabinol
may induce pain relief and psychoactive
effects. Annabidiol has analgesic and
anti-inflammatory effects. To date,
cannabinoids have shown limited merit
in the treatment of cancer pain, in part
because they have historically been
classified as Schedule I drugs by the
US Drug Enforcement Administration.
Consequently, few practitioners
are permitted to legally prescribe
them, although laws are continually
changing.29,35
The epidural or intrathecal
administration of morphine, hydro­
morphone, ziconotide (a presynaptic
calcium-channel blocker), baclofen,
clonidine, or bupivacaine via
percutaneous catheters, tunneled
catheters, or implantable programmable
pumps has been employed. Indications
for these agents generally include
uncontrolled pain despite high doses of
opioids, unacceptable side effects from
analgesics, widespread bony metastases,
and cancer involving a nerve plexus.34
Adjuvant drugs for neuropathic
pain include tricyclic antidepressants
(TCAs), such as amitriptyline and
imipramine, and antiepileptics, such as
gabapentin and pregabalin.22 TCAs have
antimuscarinic side effects, including
dry mouth, constipation, and urinary
retention, and can cause sedation or
confusion as well as cardiac conduction
blocks. These medications should be
avoided in patients who are already at
risk for urinary retention.17
Other anticonvulsants for
neuropathic pain that have been
employed as adjuvant therapies
to narcotics include valproate,
carbamazepine, lamotrigine,
phenytoin, and topiramate. Notable
toxicities include aplastic anemia and
agranulocytosis with carbamazepine, and
somnolence and suicidal ideation with
gabapentin and pregabalin.17 Duloxetine,
a serotonin and noradrenaline reuptake
inhibitor, has also been shown to reduce
chemotherapy-induced peripheral
neuropathic pain in some patients.34
CRITICAL DECISION
What nonpharmacologic
therapies can help control
cancer pain?
Physicians should be aware of
medical and surgical options for the
relief of cancer pain, although they
fall outside the purview of emergency
medicine (Table 4). These proposed
interventions include transcutaneous
electric nerve stimulation, acupuncture,
and biofeedback techniques.8
An estimated 8% of patients with
cancer pain require nerve blocks.
Destructive techniques aim to induce
an irreversible conduction block, as
with 50% to 100% alcohol and 3%
to 12% phenol. Peripheral and central
sensory pathways can be ablated using
a radiofrequency-alternating current
of 50 to 500 kHz.36 Nerve blocks
can be performed paravertebrally or
via ultrasonographic guidance at the
brachial and lumbar plexus.9 Intercostal
blocks can help alleviate pain in the
chest wall.
Although visceral innervation
occurs via the autonomic nervous
system, abdominal and pelvic visceral
pain can be relieved via thoracic,
splanchnic, celiac plexus, or hypogastric
plexus blocks. Celiac plexus blocks, in
particular, can reduce pancreatic cancer
pain by 80% to 90%.36 The celiac
ganglia is located anterior to the body
on the L1 vertebra and may require
ultrasonographic or CT guidance, as
blocks have occasionally been associated
with paraplegia.34
Neural tissues can be divided with
 CASE RESOLUTIONS
■ CASE ONE
Because the 60-year-old
woman with laryngeal carcinoma
was not in acute distress, the
emergency physician consulted
with the otolaryngologist who
performed the patient’s initial
surgery. He relayed that she
received perioperative opioids but
is now in remission.
The emergency physician
prescribed her an opioid taper and
arranged follow-up care in the
pain clinic at the cancer institute.
The patient received a stellate
ganglion block 1 week later,
which provided significant relief.
■ CASE TWO
The 58-year-old man with stage 4
pancreatic carcinoma was not in
respiratory distress. He received fentanyl
and hydromorphone in the emergency
department and was admitted to an
inpatient floor for further pain control.
He was started on methadone, a
long-acting opioid that could be taken
on schedule with short-acting opioid
medications for breakthrough pain.
The clinician also discussed
intrathecal drug delivery systems,
which could be provided if high doses
of opioids failed. During his stay, the
patient received a celiac plexus block,
which produced a good effect.
■ CASE THREE
The dermatologist who performed
the surgery on the 72-year-old man with
basal cell carcinoma was unavailable
for consultation, but the patient’s chart
indicated that the surgical procedure was
uneventful and that a full recovery was
anticipated.
Acute pain management included a
topical local anesthetic and an intramuscular
dose of ketorolac. Mobilization of the
soft tissues with physical therapy was
recommended, and he was prescribed an oral
anti-inflammatory agent. The emergency
physician informed the patient that systemic
opioid pain medicine is not recommended for
localized pain.

surgery or a radiofrequency lesion via bisphosphonates zoledronic acid and antidopaminergic medication, such as
percutaneous cordotomy to interrupt pamidronate can also reduce pain. haloperidol or metoclopramide. Opioid-
decussating fibers of the spinothalamic Dexamethasone has been shown to related constipation can be resolved with
tract, usually at the cervical level, C1 and decrease multifocal bone pain and laxatives such as senna, poorly absorbed
C2 vertebrae contralateral to the pain. pain caused by metastatic spinal cord sugars such as sorbitol or lactulose, or
Cordotomy can only reliably be used to compression.15 methylnaltrexone.17,23 Increased fiber
abolish pain and temperature sensation Vertebroplasty — the process of intake and hydration can also be helpful.
below the level of the C4 dermatome. injecting acrylic bone cement into the Moreover, hypercalcemia should be
Neuromodulation, the technique vertebral body under fluoroscopic addressed, if present.
of altering nerve activity by applying guidance — may successfully treat axial Summary
electric current, often entails peripheral back pain due to malignant vertebral In the coming years, emergency
stimulation, motor cortex or deep brain body disease or an osteoporotic wedge physicians are likely to encounter
stimulation, or more commonly, spinal fracture. Kyphoplasty attempts to greater numbers of cancer patients. As
cord stimulation with wires or paddles restore vertebral body height via the such, they must remain cognizant of
adjacent to the dorsal columns.34 repeated inflation of a balloon injected the unique issues associated with the
Palliative radiotherapy may provide into the vertebral body prior to injection management of this high-risk population
pain relief caused by bony metastases. of the cement.36 while staying abreast of the newest
Strontium-89 and radium-223 have Although opioid-related emesis can treatments for cancer-related pain.
been used successfully to treat pain be distressing, it can be managed by Well-prepared clinicians can use
from metastatic prostate cancer.37 The switching analgesics or administering an opioids to relieve suffering while
minimizing the risks of adverse
outcomes, including constipation,
misuse, addiction, and diversion.
When managing cancer-related pain,
it is equally important to be aware of
alternative interventions, including
adjuvant medications, cannabinoids,
n Overlooking non–cancer-related causes of pain.
palliative radiotherapy, and nerve blocks,
n Ignoring the potential benefits of radiotherapy, hormonal therapy, or steroids
which may provide some relief to those
as well as pure analgesic treatments for skeletal pain.
with intractable symptoms.
n Failing to detect and stabilize pathologic fractures.
n Ignoring the potential benefits of bisphosphonate therapy or radionuclide REFERENCES
1. Mercadante S. Cancer pain. Curr Opin Support
therapy for bone pain. Palliat Care. 2013 Jun;7(2):139-143.
n Withholding a potent opioid, such as morphine, hydromorphone, fentanyl, or 2. Cancer Facts & Figures 2018. American Cancer
Society website. https://www.cancer.org/research/
oxycodone. cancer-facts-statistics/all-cancer-facts-figures/
cancer-facts-figures-2018.html. Accessed July 16, 2019.

August 2019 n Volume 33 Number 8 9

 3. Jimenez-Andrade JM, Mantyh WG, Bloom AP, 28. Cheng TM, Cascino TL, Onofrio BM.
Ferng AS, Geffre CP, Mantyh PW. Bone cancer pain. Comprehensive study of diagnosis and treatment
Ann N Y Acad Sci. 2010 Jun;1198:173-181. of trigeminal neuralgia secondary to tumors.
4. Frankish H. 15 million new cancer cases per year by Neurology. 1993 Nov;43(11):2298-2302.
2020, says WHO. Lancet. 2003 Apr;361(9365):1278. 29. Gaertner J, Schiessl C. Cancer pain management:
5. Merriman KW, Todd KH, Wattana MK. Emergency what’s new? Curr Pain Headache Rep. 2013 Apr;
department visits among cancer patients in Harris 17(4):328.
County, Texas. Oral abstract presented at: MEMC 30. Lalla RV, Bowen J, Barasch A, et al. MASCC/ISOO
VIIth Mediterranean Emergency Medicine Congress; clinical practice guidelines for the management
September 8-11, 2013; Marseille, France. of mucositis secondary to cancer therapy. Cancer.
6. Brown J, Grudzen C, Kyriacou DN, et al. The 2014 May 15;120(10):1453-1461.
emergency care of patients with cancer: setting 31. Salner AL, Botnick LE, Herzog AG, et al. Reversible
the research agenda. Ann Emerg Med. 2016 Dec; brachial plexopathy following primary radiation
68(6):706-711. therapy for breast cancer. Cancer Treat Rep. 1981
7. Lamba S, DeSandre PL, Todd KH, et al. Integration Sep-Oct;65(9-10):797-802.
of palliative care into emergency medicine: the 32. Wallace MS, Dyck JB, Rossi SS, Yaksh TL. Computer-
Improving Palliative Care in Emergency Medicine controlled lidocaine infusion for the evaluation of
(IPAL-EM) collaboration. J Emerg Med. 2014 Feb; neuropathic pain after peripheral nerve injury.
46(2):264-270. Pain. 1996 Jul;66(1):69-77.
8. Deandrea S, Montanari M, Moja L, Apolone G. 33. Ferrini R, Paice JA. How to initiate and monitor
Prevalence of undertreatment in cancer pain. A infusional lidocaine for severe and/or neuropathic
review of published literature. Ann Oncol. 2008 pain. J Support Oncol. 2004 Jan-Feb;2(1):90-94.
Dec;19(12):1985-1991. 34. Bell RF, Eccleston C, Kalso EA. Ketamine as an
9. Wilson J, Stack C, Hester J. Recent advances in adjuvant to opioids for cancer pain. Cochrane
cancer pain management. F1000Prime Rep. 2014 Database Syst Rev. 2012 Nov 14;11:CD003351.
Feb 3;6:10. 35. O’Neil ME, Nugent SM, Morasco BJ, et al.
10. Lemay K, Wilson KG, Buenger U, et al. Fear of pain Benefits and harms of plant-based cannabis for
in patients with advanced cancer or in patients posttraumatic stress disorder: a systematic review.
with chronic noncancer pain. Clin J Pain. 2011 Feb; Ann Intern Med. 2017 Sep 5;167(5):332-340.
27(2):116-124. 36. Scott-Warren J, Bhaskar A. Cancer pain
11. Neven DE, Sabel JC, Howell DN, Carlisle RJ. The management: part II: interventional techniques.
development of the Washington State emergency BJA Educ. 2015 Apr;15(2):68-72.
department opioid prescribing guidelines. J Med 37. Nilsson S, Franzén L, Parker C, et al. Two-year
Toxicol. 2012 Dec;8(4):353-359. survival follow-up of the randomized, double-blind,
12. Opioid prescribing guidelines. Ohio Department of placebo-controlled phase II study of radium-223
Mental Health and Addiction Services website. chloride in patients with castration-resistant
https://mha.ohio.gov/Researchers-and-Media/ prostate cancer and bone metastases. Clin
Combating-Opiate-Abuse/Opioid-Prescribing- Genitourin Cancer. 2013 Mar;11(1):20-26.
Guidelines. Accessed August 23, 2017.
13. Mazer-Amirshahi M, Mullins PM, Rasooly I, van den
Anker J, Pines JM. Rising opioid prescribing in adult
U.S. emergency department visits: 2001-2010. Acad
Emerg Med. 2014 Mar;21(3):236-243.
14. Hoppe JA, Nelson LS, Perrone J, et al. Opioid
prescribing in a cross section of US emergency
departments. Ann Emerg Med. 2015 Sep;66(3):
253-259.e1.
15. Portenoy RK. Treatment of cancer pain. Lancet. 2011
Jun 25;377(9784):2236-2247.
16. World Health Organization. Cancer Pain Relief: With
a Guide to Opioid Availability. 2nd ed. Geneva,
Switzerland: World Health Organization; 1996.
17. Vardy J, Agar M. Nonopioid drugs in the treatment of
cancer pain. J Clin Oncol. 2014 Jun 1;32(16):1677-1690.
18. Ripamonti CI, Santini D, Maranzano E, Berti M, Roila F;
ESMO Guidelines Working Group. Management
of cancer pain: ESMO clinical practice guidelines.
Ann Oncol. 2012 Oct;23(suppl 7):vii139-vii154.
19. Mercadante S. Malignant bone pain: pathophysiology
and treatment. Pain. 1997 Jan;69(1-2):1-18.
20. Davies AN, Dickman A, Reid C, Stevens AM,
Zeppetella G; Science Committee of the
Association for Palliative Medicine of Great Britain
and Ireland. The management of cancer-related
breakthrough pain: recommendations of a task
group of the Science Committee of the Association
for Palliative Medicine of Great Britain and Ireland.
Eur J Pain. 2009 Apr;13(4):331-338.
21. Webber K, Davies AN, Cowie MR. Accuracy of a
diagnostic algorithm to diagnose breakthrough
cancer pain as compared with clinical assessment.
J Pain Symptom Manage. 2015 Oct;50(4):495-500.
22. Caraceni AC, Hanks G, Kaasa S, et al. Use of
opioid analgesics in the treatment of cancer pain:
evidence-based recommendations from the EAPC.
Lancet Oncol. 2012 Feb;13(2):e58-e68.
23. Zeppetella G, Davies A, Eijgelshoven I, Jansen JP.
A network meta-analysis of the efficacy of opioid
analgesics for the management of breakthrough
cancer pain episodes. J Pain Symptom Manage.
2014 Apr;47(4):772-785.e5.
24. Siegel T. Muscle cramps in the cancer patient:
causes and treatment. J Pain Symptom Manage.
1991 Feb;6(2):84-91.
25. Baruah JK. Nocturnal cramp in chronic lumbosacral
radiculopathies [abstract]. Ann Neurol. 1985;
18(1):161.
26. Henry J. Quinine for night cramps. Br Med J (Clin
Res Ed). 1985 Jul 6;291(6487):3.
27. McCarthy GM, Skillings JR. Jaw and other orofacial
pain in patients receiving vincristine for the
treatment of cancer. Oral Surg Oral Med Oral Pathol.
1992 Sep;74(3):299-304.

10 Critical Decisions in Emergency Medicine

 A 57-year-old woman with intermittent chest pain that has become persistent in the last 3 hours.

The Critical ECG

Sinus rhythm with first-degree atrioventricular (AV) block, rate 83, acute By Amal Mattu, MD, FACEP
anterior-lateral myocardial infarction (MI), possible inferior MI of undetermined Dr. Mattu is a professor, vice chair, and
director of the Emergency Cardiology
age. The PR interval is 210 msec, diagnostic of a first-degree AV block. Q waves Fellowship in the Department of
Emergency Medicine at the University
with ST-segment elevations (STEs) are present in anterior leads V2 to V4, and STEs
of Maryland School of Medicine in
are also present in lateral leads I and aVL, consistent with an acute MI of the Baltimore.
anterior and lateral walls.

From Mattu A, Brady W. ECGs for the Emergency Physician 2. London: BMJ Publishing; 2008. Reprinted with permission.

August 2019 n Volume 33 Number 8 11

 The LLSA Literature Review

Pediatric Nontraumatic
Hip Pathology
By Alexander Salazar, MD, LT; and Daphne Morrison Ponce, MD, LCDR
Naval Medical Center, Portsmouth, Virginia
Reviewed by Andrew Eyre, MD, MHPEd
Neville DNW, Zuckerbraun N. Pediatric nontraumatic hip pathology. Clin Ped Emerg Med. 2016 Mar;17(1):13-28.

Pediatric nontraumatic hip complaints can be caused by a spectrum of disorders that range from benign
and self-resolving to life-threatening. Any child who presents with hip or knee pain accompanied by an
altered gait or refusal to bear weight should be evaluated for these diagnoses (see table opposite).
). Proper diagnostic testing and disposition decisions can be guided by a careful physical examination, a
complete medical history, and focused imaging and laboratory evaluations.
DISCLOSURES
KEY POINTS The views expressed in this article are those of
the authors and do not necessarily reflect the
n Children with nontraumatic hip pathologies frequently present with pain in the official policy or position of the Dept. of the Navy,
hip, thigh, or knee; an altered gait; or refusal to bear weight. Dept. of Defense, or the US Government. We are
n In patients with a hip-joint pathology (eg, effusion, hemarthrosis, or fracture), the military service members.
hip rests in flexion, abduction, and external rotation. This work was prepared as part of our official
n An ultrasound of the hip can identify an effusion but cannot distinguish between duties. Title 17 U.S.C. 105 provides that
sterile and septic joint effusions. “Copyright protection under this title is not
n When ordering hip radiographs, it is important to obtain both comparison and available for any work of the US Government.”
Title 17 U.S.C. 101 defines a US Government
pelvic views (specifically, anteroposterior [AP] and frog-leg views). work as a work prepared by a military service
n MRI is sensitive and specific; however, timing, costs, sedation considerations, member or employee of the US Government as
and availability can limit the modality’s applicability. part of that person’s official duties.

Critical Decisions in Emergency Medicine’s series of LLSA reviews features articles from ABEM’s 2019 Lifelong Learning and
Self-Assessment Reading List. Available online at acep.org/moc/llsa and on the ABEM website.

12 Critical Decisions in Emergency Medicine

Disorder Description Epidemiology History/Examination Diagnosis Clinical Course Management
Self-limited • Most common cause • Acute-onset pain with • Clinical diagnosis is • Disease is self-limited • Arrange follow-up
inflammation of nontraumatic hip limp or unwillingness based on the history and typically resolves in with a primary care
and effusion complaints to bear weight and examination. 3–10 days. physician.
TRANSIENT
SYNOVITIS

of hip joint • Mean age 4.7 yrs, with
of unknown age range of 3–8 yrs;
etiology male predominance
• Usually unilateral
• History of preceding
illness
Idiopathic • Children aged 2–12 yrs
LEGG-CALVÉ-PERTHES
• Usually well appearing • Improvement with
NSAIDs is reassuring.
• Hip x-rays are rarely
necessary. Ultrasound
can reveal effusions.
• Subacute symptoms • Radiographs can
• Ibuprofen can reduce • Prescribe
the length of symptoms. scheduled NSAIDs.
• Disease may recur, • Counsel parents
typically in the first year. on anticipatory
guidance and
reasons to return.
• Disease is self-limited to • An orthopedic

avascular • 4 times more common with painless or painful confirm the diagnosis; 1–2 yrs. referral for
necrosis of the in boys; bilateral in limp however, x-rays may • Irreversible deformity ongoing
capital femoral 10%–15% of cases • Limp often noticed be normal early in the occurs when the outpatient
DISEASE

epiphysis • Incidence:
0.2–19.2 per 100,000
• Obesity and
hypercoagulability
(common predis­
posing factors)
Displacement • Estimated incidence:
SLIPPED CAPITAL FEMORAL
incidentally to minor disease course. femoral head fragment management is
trauma • Proceed to MRI testing dislodges or soon after. required.
• Limited hip abduction based on clinical
and internal rotation suspicion, or refer to an
orthopedist for further
evaluation.
• Subacute presentation • On AP films, the • Prognosis is excellent • Request an

of the femoral 10 per 100,000 • History of recent, Klein line — from the if the intervention is immediate
head from the children minor trauma that superior aspect of the made before severe orthopedic
femoral neck • More common in boys does not explain femoral neck — should displacement or consultation.
through the • Mean age 12 yrs symptoms intersect the epiphysis osteonecrosis occurs. • Treatment involves
EPIPHYSIS

epiphyseal • Obesity (risk factor) • Knee pain (15%–50%) of the femoral head (low stabilizing the
plate • ≤24% with bilateral • Altered gait (common) sensitivity). epiphysis and
disease • Alternatively, the preventing
disorder can be progression.
diagnosed if the • Maintain non–
epiphyseal width lateral weight-bearing
to the Klein line is >2 mm status.
(79% sensitivity).
Inflammation • Most commonly • Classically high fever, • Gold-standard • Obtain cultures • An emergent
(SEPTIC ARTHRITIS AND OSTEOMYELITIS)

of joint space spread hemato­ toxic appearance treatment requires prior to giving orthopedic
from infection; genously from distant • Hot, painful, swollen isolating the pathogen antibiotics. Consult consultation
OSTEOARTICULAR INFECTIONS

osteomyelitis source joint of short duration from the site of with orthopedics if and surgical
may be an • In children <2 yrs, (<1 wk) infection or isolating the perioperative antibiotics intervention are
isolated close proximity of • Severe or complete pathogen from blood. are considered. necessary.
problem or blood vessels to the resistance to passive • Obtain blood and joint • Consider coverage for • Provide empiric
coexist with proximal femoral range of motion cultures, CBC, and Kingella kingae, the broad-spectrum
septic arthritis physis allows infection • Inability to bear weight inflammatory markers. most common cause of antibiotics to cover
to spread into or use the affected • The Kocher criteria osteoarticular infections staphylococci and
the epiphysis and joint (common) accompanied by in children <4 yrs. patient-specific
contiguous hip joint; c-reactive protein • Initiate IV antibiotics, risks.
cited as a reason testing is ≤98% followed by oral
septic arthritis is found sensitive. antibiotics.
most commonly in • While MRI is both • Downtrending
youngest populations sensitive and specific, c-reactive protein levels
it is costly and often indicate a response to
difficult to obtain. treatment.
Monoarticular • Rare cause of acute, • Mean incubation is 3.4 • Synovial studies cannot Varies by stage of Lyme • <8 yrs = amoxicillin
hip arthropathy nontraumatic hip pain; months (2 wks–2 yrs). differentiate Lyme from disease • >8 yrs = doxy­
LYME ARTHRITIS

however, testing may • Dissemination (>33%) septic arthritis. cycline

be warranted if in an
endemic region and a
septic hip is suspected
• Most common in
children aged 5–15 yrs
Osteosarcoma • Peak incidence in
and Ewing adolescence
sarcoma:
most common
MALIGNANCY
• Brief, intermittent • The disease is • Course duration
attacks of swelling and difficult to diagnose based on the
pain in ≥1 large joint without other clinical stage of disease
• Hip pain seldom manifestations.
severe or debilitating • Patients in endemic
areas should undergo
serum serologic testing.
• Tumor-related pain, • Laboratory studies are Varies by severity • Provide an
with or without a mass, often normal. immediate
painless mass, or • Plain radiography (the oncology referral.
pathologic fracture first-line diagnostic

primary bone • Most common test) will reveal both

cancers symptoms: pain (with malignant and benign
Leukemia: or without activity), patterns.
can cause leg palpable mass
pain and a • Constitutional
limp due to symptoms uncommon
bone-marrow
expansion

August 2019 n Volume 33 Number 8 13

 The Critical Image
A 76-year-old man with colon cancer and end-stage renal disease By Joshua S. Broder, MD, FACEP
presents with substernal, pleuritic chest pain for 2 days. He reports a Dr. Broder is an associate professor and the
residency program director in the Division
nonproductive cough without a fever. He underwent dialysis earlier today of Emergency Medicine at Duke University
and was recently hospitalized for hernia-related complications, which were Medical Center in Durham, North Carolina.
managed nonoperatively.

The patient’s vital signs are blood pressure 116/84, heart rate 125, respiratory rate 22, temperature 37.6°C (99.7°F), and
oxygen saturation 98% on room air. He is alert and in no acute distress. His lungs are clear, and his heart rate is tachycardic
and irregularly irregular. He has no abdominal tenderness, and his legs show bilateral pitting edema to the knees.

The patient’s ECG is shown below. The emergency physician reviews the patient’s chest x-ray and compares it to a
radiograph from his recent admission before taking additional diagnostic and therapeutic steps.

KEY POINTS frankly hypotensive — a factor that could have prevented

the clinical identification of tamponade physiology — but
n Pericardial effusion and tamponade were suspected
his systolic blood pressure during this visit was nearly
based on the patient’s physical examination findings,
50 mm Hg lower than the baseline measured during his
ECG (which demonstrates new atrial fibrillation and
recent hospital admission.
subtle electrical alternans), and chest x-rays. The
n Rate controlling the patient’s atrial fibrillation could result
diagnoses were then confirmed using point-of-care
in sudden deterioration, as his ventricular filling and
ultrasonography.
stroke volume were impaired by the pericardial effusion.
n It can be extremely valuable to compare current x-rays Maintaining cardiac output (stroke volume multiplied by
with previous ones. This juxtaposition can highlight heart rate) is thus dependent on the increased heart rate.
acute changes like the cardiac silhouette enlargement
seen in this case.
CASE RESOLUTION
n The recognition of impending pericardial tamponade
The patient underwent an emergency pericardial window
is particularly important, as management errors can and spontaneously converted to normal sinus rhythm.
occur without a proper diagnosis. This patient was not

14 Critical Decisions in Emergency Medicine

 A B

A. Upright anterior-posterior (AP) chest x-ray. This image B. AP radiograph from the patient’s recent admission. This
shows a cardiac silhouette that occupies more than half the image shows a narrow cardiac silhouette. Given the rapid
diameter of the chest. change, a pericardial effusion was suspected.

ß C–D. Point-of-care
C Pericardial D Pericardial ultrasound, subxiphoid view.
effusion effusion The images reveal a large
Right pericardial effusion with septa.
The right ventricle shows near
atrium
collapse during diastole, a
finding that is consistent with
pericardial tamponade.
Right
ventricle

â E-G. CT angiograms of the

chest. Following an intravenous
fluid bolus, CT angiography
was used to evaluate for
a concomitant pulmonary
Left embolism or aortic dissection,
Left
ventricle given the patient’s chest pain,
atrium
cancer history, and recent
hospitalization.

E Aortic arch F Main pulmonary arteries G Pericardial

without dissection without embolus effusion

Ascending
aorta Descending
without aorta without
dissection dissection

August 2019 n Volume 33 Number 8 15

 The Critical Procedure
Delivering an Infant With Shoulder Dystocia
By Steven J. Warrington, MD, MEd
Dr. Warrington is the director of the Emergency Medicine Residency Program and academic chair
of the Department of Emergency Medicine at Orange Park Medical Center in Orange Park, Florida.

When forced to occur in the emergency department or without the aid of an obstetrician, an unexpected
delivery can be complicated by a variety of life- and limb-threatening problems, including shoulder
dystocia and breech positioning. While attempts should be made to have appropriate specialists on
hand to oversee the process, emergency physicians can overcome potential obstacles by understanding
how to perform basic childbirth maneuvers. Here, we focus on two techniques for delivering an infant
with shoulder dystocia, the McRoberts maneuver and application of suprapubic pressure.

Benefits and Risks Both shoulder dystocia and Alternatives

When combined, the McRoberts
maneuver and the application of
suprapubic pressure have been shown to
enable the delivery of more than 50% of
neonates with shoulder dystocia, without
the need for further interventions. Because
these procedures improve the likelihood
of timely vaginal delivery, they also reduce
the risk of hypoxia and poor outcomes.
various delivery methods can inflict
trauma on the newborn, including
fractures and nerve injuries.
Additionally, delays in delivery can
lead to both short- and long-term
sequelae. Complications such as
postpartum hemorrhage and trauma
to surrounding tissues can also pose
risks to the mother.
Multiple methods and maneuvers,
including cesarean delivery, can
reduce the risks of shoulder dystocia.
Nonsurgical methods include
intentionally fracturing the newborn’s
clavicle, manually rotating the fetus,
and repositioning the mother onto her
hands and knees.

16 Critical Decisions in Emergency Medicine

Reducing Side Effects
The best way to achieve good
outcomes is to perform the outlined
maneuvers correctly. It is particularly
important to avoid common mistakes,
such as mistakenly applying pressure to
the fundus. When exerting suprapubic
pressure, careful attention should be
paid to which direction the fetus is
facing. Pressure should be applied at an
angle to bring the fetus’s shoulder closer
to the anterior chest and sternum, with
a goal of decreasing the widest portion
of the shoulder girdle. For instance, if
the fetus is facing the mother’s right
side, pressure should be applied from
the mother’s left suprapubic region
downward and inward so that the
neonate’s shoulder (which may be
hung on the pubis) is compressed
toward its sternum and anterior chest.
Special Considerations
Unfortunately, shoulder dystocia
can be difficult to recognize.
Precautionary maneuvers should be
considered if the delivery regresses
or the infant’s head seems to push
forward and pull backward against
the perineum (ie, “turtle sign”).
At least two assistants are required to
perform the McRoberts maneuver, one
stationed at each of the mother’s legs. It
can also be helpful to enlist the support of
an obstetrician, neonatologist, neonatal
response team, or anesthesiologist. Because
some cases require operative management,
it can be beneficial to notify the surgical
team of the impending delivery.
Every successful delivery should be
followed by ongoing monitoring to
address potential complications, including
maternal soft-tissue injuries and postpartum
hemorrhage, and to assess the need for
neonatal resuscitation.

TECHNIQUE

1. Recognize the presence of shoulder

dystocia.
2. Call for assistance (a minimum of
two assistants).
3. Instruct each assistant to hold one
of the mother’s legs, just proximal
to the knee. The legs should be
hyperflexed by pulling them back
toward the abdomen and chest.
With a goal of straightening the
sacrum, the assistant may need to
increase or decrease the pressure
used to push or pull the leg.
4. Identify the direction that the fetus
is facing.
5. Instruct an assistant to apply
suprapubic pressure with the fist
or ball of the hand, just above the
bony pubis. McROBERTS MANEUVER
6. Confirm that suprapubic pressure is The technique consists of sharply flexing the thighs up onto the
being applied to the right location. abdomen while an assistant simultaneously provides suprapubic
pressure (vertical arrow).
To verify positioning, the clinician
can reach from the perineal region Note: If these techniques fail, consider other approaches, including rotational
above to palpate the bony pubis. maneuvers, intentional fracture of the clavicle, or repositioning of the mother.

August 2019 n Volume 33 Number 8 17

 It’s a jungle out there!
Let CDEM be your guide.
Don’t miss Critical Decisions’ new podcast,
hosted by emergency medicine experts
Danya Khoujah, MD and Wendy Chang, MD.

Get entertained and informed by real-life cases and new clinical

approaches to managing everything from animal bites and broken
bones to drug withdrawal and stab wounds.

A
PO LL SUBSCRIBE AND DOWNLOAD TODAY
-
D NE AT ACEP.ORG/PODCASTS.
CA W
ST Decisions in Emergency Medicine
18 Critical
!
 Torn Apart
Aortic Dissection

LESSON 16

By Matthew C. Kostura, MD
Dr. Kostura is a clinical assistant professor of emergency medicine at the Cleveland
Clinic Lerner College of Medicine in Ohio.

Reviewed by Sharon E. Mace, MD, FACEP

OBJECTIVES
On completion of this lesson, you should be able to: CRITICAL DECISIONS
1. Distinguish the various dissection classification systems. n Which patients warrant an aortic dissection
2. Describe the most common complaints and risk factors workup?
for patients with an aortic dissection.
n Can a D-dimer test be used to rule out an aortic
3. Discuss the most sensitive imaging modalities for
evaluating aortic dissections and the pitfalls of each. dissection?
4. Determine a treatment plan for patients with an aortic n Which imaging modalities can reliably confirm an
dissection.
aortic dissection?
5. Identify which cases require emergent surgical
management. n How should hypotension be managed in patients
with an aortic dissection?
FROM THE EM MODEL
n Which aortic dissections require an immediate
3.0 Cardiovascular Disorders
3.3 Disorders of Circulation surgical consultation?
3.3.1 Arterial

Although aortic dissection is widely regarded as one of the five fatal causes of nontraumatic chest pain, it is
frequently — and often tragically — misdiagnosed. While many of these patients present with sudden, severe,
“ripping” or “tearing” chest pain, others do not. Emergency clinicians must be prepared to interpret both classic and
rare presentations and common risk factors associated with the disorder, for which prompt recognition and treatment
remain the best defense.

August 2019 n Volume 33 Number 8 19

 CASE PRESENTATIONS
■ CASE ONE
An 84-year-old woman with
a history of atrial fibrillation,
hypertension, and coronary artery
disease presents with chest pain. She
describes the pain, which woke her
from sleep, as constant, severe, tearing,
midsternal, and radiating to the right
chest and upper back between the
shoulder blades. She was admitted to
the hospital 1 week ago with chest
pain; her symptoms, which were
attributed to pericarditis, improved
with the administration of steroids and
colchicine. She says that today’s chest
pain “feels different.” She underwent
a mitral valve replacement several
years ago but denies a history of prior
cardiac stents or coronary artery
bypass grafting.
The patient is taking warfarin. Her
initial vital signs are blood pressure
125/75, heart rate 85, respiratory rate
20, temperature 37°C (98.6°F), and
oxygen saturation 98% on room air.
She is in moderate pain and is mildly
diaphoretic. A cardiac examination
reveals a regular rate and rhythm,
no murmurs, and equal bilateral
radial pulses. Her lungs are clear to
auscultation bilaterally; she is mildly
Acute aortic dissection is a rare
(6,000-10,000 US cases per year) but
particularly deadly diagnosis; mortality
can be as high as 2% for every hour that
the pathology goes untreated.1-4 Further
complicating the dilemma, treatments
for other chest pain “killers,” such as
ST-segment elevation myocardial infarction
(STEMI) and pulmonary embolism, often
involve antiplatelet and anticoagulation
therapies — treatments that can cause life-
threatening complications in patients with
aortic dissection.
CRITICAL DECISION
Which patients warrant an
aortic dissection workup?
To determine which cases should
be evaluated for an aortic dissection,
it is important to understand the
pathophysiology of the disease. The
aortic wall is comprised of three layers:
20 Critical Decisions in Emergency Medicine
tachypneic but is in no respiratory
distress. An ECG shows a normal
sinus rhythm with nonspecific T-wave
changes; the results are similar to
those documented during her previous
hospital admission.
■ CASE TWO
A 35-year-old man presents with
burning chest pain in his lower
substernal chest and epigastrium that
radiates to his mid to lower back. He
rates his pain, which began a few hours
ago, as a 9/10. He denies prior medical
problems but smokes a pack of cigarettes
every day, occasionally drinks alcohol,
and sometimes uses cocaine, with the
last reported use 3 days ago. He denies
intravenous (IV) drug use.
His initial vital signs are blood
pressure 220/149, heart rate 104,
respiratory rate 16, temperature 37°C
(98.6°F), and oxygen saturation 100%
on room air. His physical examination
is notable for mild tachycardia but no
murmurs. His lung sounds are clear to
auscultation bilaterally. His abdominal
examination reveals mild epigastric
tenderness but no rebound or guarding.
He also has a diminished pulse in
the right foot, compared to his other
(from innermost to outermost) the
intima, media, and adventitia. Dissection
begins with a tear in the intima, which
causes the layers within the plane of
the media to separate. These layers can
then dissect again through the intima
and back into the vessel lumen at a
more distal location, creating a true
lumen (where blood flows freely) and
a false lumen (within the media layer).
Alternatively, the distal dissection may
dissect through the adventitia, leading to
aortic rupture and exsanguination.
The two systems commonly used to
classify aortic dissections — Stanford
and DeBakey — are generally based on
the location of the initial intimal tear:
Stanford Classification
• Type A — all dissections involving
the ascending aorta, regardless of
origin (Figure 1)
extremities. His ECG reveals sinus
tachycardia and nonspecific T-wave
abnormalities.
■ CASE THREE
A 52-year-old woman presents
with severe chest and left leg pain,
which started suddenly at rest. She
has a history of hypertension, takes
multiple prescription medications, and
is a former smoker, but she has no
history of coronary artery disease. Her
initial vital signs are blood pressure
70/40, heart rate 79, respiratory rate
22, temperature 36.4°C (97.5°F), and
oxygen saturation 100% on room air.
She is light-headed and feels worse
when sitting up, but she denies fainting.
On cardiovascular examination,
faint heart sounds are noted, with a
possible diastolic murmur. Her left,
lower extremity is cooler than the
right, and it is difficult to palpate a
pulse in the left foot. On pulmonary
examination, the patient is tachypneic,
with some crackles at the bases, up
to the mid-lung fields. A stat ECG is
concerning for ST-segment elevations
in leads V1 and V2 , with diffuse ST-
segment depressions in the inferior and
lateral leads.
• Type B — all dissections that do
not involve the ascending aorta
(Figure 2)
DeBakey Classification
• Type I — tear starts in the ascending
aorta and propagates distally
to involve the aortic arch and
descending aorta
• Type II — tear starts in and is
confined to the aortic arch
• Type III — tear originates in the
descending aorta (past the origin
of the left subclavian artery) and
propagates distally
Risk Factors and Presentations
Although patients with both type A
and type B dissections commonly present
with chest pain, it is not a universal
complaint; other symptoms and clinical
examination findings associated with
dissections must also be weighed. Much pulse deficit, this finding may portend common in those with type A dissections.
of the data used in retrospective studies a positive likelihood ratio of 5.7 for an Patients can present with syncope or
on dissection are derived from the aortic dissection.2 Patients with type B shock, but again, these symptoms are less
International Registry of Acute Aortic dissections more commonly present with common with type B dissections.
Dissection, which collects information back pain and hypertension. Pulse deficits Depending on where the dissection
from more than 40 hospital systems may also be present, but they are more flap extends, other organ systems can
worldwide (Tables 1 and 2).
In those with classic presentations,
FIGURE 1. Type A Aortic Dissection
the chest pain is sharp, tearing or
stabbing, and severe; the pain comes
on suddenly and often radiates to the
back. Approximately 84% of patients
Dissection
with an aortic dissection experience an in ascending
abrupt onset of pain, and 90% describe aorta
the intensity of symptoms as severe.2 Dissection in
Abrupt onset is one of the most specific descending
aorta
characteristics of an aortic dissection,
compared to other acute causes of chest
pain.5 However, not every patient presents
classically, and some (≈6.4%) may even
present without pain.6 Moreover, an
estimated 16% to 38% of patients without
chest pain are initially misdiagnosed.6
Other common symptoms of type A
aortic dissections include back pain, The dissection flap begins in the aortic root and extends through the entire aorta.19,20
shock, and syncope. If the dissection is
proximal enough, it may dissect into the
pericardium and cause subsequent cardiac FIGURE 2. Type B Aortic Dissection
tamponade, a pathology that is associated
with double the mortality rate.5 Proximal
extension of an aortic dissection can even
affect blood flow to the coronary arteries,
causing STEMI. Decreased blood flow to
the coronary arteries can be caused by a
number of processes, including complete
coronary obstruction by the false lumen,
the dissection plane extending through
the coronary arteries, and hypotension
and poor coronary artery perfusion.
Dissection flap
Severe aortic regurgitation, which
can also restrict blood flow, can
elevate troponin levels and lead to the
misdiagnoses of acute coronary syndrome
(ACS) and non–ST-segment elevation Left subclavian artery
myocardial infarction (NSTEMI).
Not only does this complication cause
diagnostic delays, it can also result in
improper or even fatal treatment with
anticoagulation.
When managing these cases, it is
imperative to listen for new murmurs,
which are discovered in nearly 50% of
patients. These findings are often the
result of aortic valve insufficiency, the
most commonly recognized cardiac
complication of type A dissections.2,3 The dissection flap begins just beyond the left subclavian artery.19,20
Although only 30% of patients have a

August 2019 n Volume 33 Number 8 21

 are major risk factors. These patients
TABLE 1. Presentation of Type A
often present at a much younger age
Dissections2,3,15
(<40 years) than the “typical” dissection
Incidence of
patient. An anatomical abnormality,
Symptom Symptom
such as an aortic aneurysm, coarctation
Chest pain 81%-83%
of the aorta, or a bicuspid aortic valve, is
New aortic murmur 45%
Normal blood 45% also a risk factor for a dissection.
pressure Early repair of a thoracic aneurysm
Back pain 43% can help increase long-term survival, but
Hypertension 28%-32% then again, recent instrumentation of the
Pulse deficit 26%-31% aorta or aortic valve is also a risk factor
Shock 13% for an aortic dissection. Moreover, a
Syncope 12%-19%
family history of an aortic pathology is
Altered mental 12%
also a risk factor, as are cocaine abuse,
status
pregnancy, and inflammatory vasculitis.
Lower-extremity 10%
As such, patients should be screened for
ischemia
potentially undiagnosed conditions.
Cerebrovascular 8%
accident An aortic dissection detection risk
Cardiac tamponade 5% score (ADD-RS) has been developed
Congestive heart 5% based on the American Heart Association
failure (AHA) and American College of
Cardiology 2010 guidelines (Table 3).
TABLE 2. Presentation of Type B Although ADD-RS can help clinicians
Dissections6,15,20 remember the biggest risk factors for
dissection, no such tool is capable of
Incidence of
Symptom Symptom ruling out the pathology alone.
Back pain 70%
Chest pain 67%-71% CRITICAL DECISION
Hypertension 66%-71%
Can a D-dimer test be used to
Normal blood 27%
pressure rule out an aortic dissection?
Pulse deficit 19%-21% While multiple studies have
Syncope 3%-5% investigated whether a D-dimer test can
Shock 3%
rule out an aortic dissection, results have
be affected by the reduced blood flow. been mixed. Ideally, if a population in
Mesenteric ischemia, for example, can which D-dimer results reliably ruled out
cause abdominal pain in patients with disease were found, physicians could
a type B dissection and, if present, avoid subjecting patients to unnecessary
can significantly increase mortality. radiation exposure and costly workups.
Acute kidney injuries, paraplegia due The reported sensitivity of a D-dimer
to occlusion of the spinal artery, and test to rule out dissection, however,
even lower limb ischemia are potential ranges from 52% to 100%, and
but rare complications. Some experts specificity ranges from 33% to 89%,
recommend including aortic dissection making its reliability controversial.7 The
in the differential diagnosis for every 2015 American College of Emergency
patient with chest pain accompanied by Physicians (ACEP) clinical policy
a symptom involving any other organ. on nontraumatic aortic dissection
In addition to the clinical features of discourages the use of a D-dimer
aortic dissection, physicians must also alone for ruling out aortic dissections.
Furthermore, ACEP discourages the use
consider the risk factors. The “classic”
patient profile is a man in his 60s or 70s of existing clinical decision rules for
with a history of hypertension. In fact, identifying patients at low risk for the
dissections occur at a 2:1 ratio for men pathology (level-C recommendation).8
to women, although women are more According to a 2015 meta-analysis
likely to present atypically.2 Underlying published in the Annals of Emergency
connective tissue disorders, such as Medicine, a D-dimer cutoff under
Marfan and Ehlers-Danlos syndromes, 500 ng/mL may rule out aortic dissections
22 Critical Decisions in Emergency Medicine
with a sensitivity of 98%. The accuracy
of the test appeared to be even higher in
patients who had been categorized as low
risk by clinical scoring systems.1 However,
the accuracy of the data has been
questioned, as the study may have been
subjected to bias. Another meta-analysis
published in 2016 found that D-dimer
values less than 500 ng/mL could rule out
acute aortic syndromes with a sensitivity
between 95% and 97%.9 Further studies
have ruled out acute aortic dissections
by combining a low-risk ADD-RS with a
negative D-dimer test (<500 ng/mL) with
a diagnostic sensitivity between 93.5%
and 98.7%.5,10 While promising, the
evidence is mostly retrospective and is
not definitive.
The 2018 ADvISED trial used a low-
risk ADD-RS and a negative D-dimer
test to rule out aortic dissections and
other acute aortic syndromes, including
penetrating aortic ulcers, intramural
hematomas, and aortic ruptures. The
overall incidence of acute aortic
syndromes in this population was 13%.
Using a negative D-dimer value less than
500 ng/mL and an ADD-RS of 0 or 1
failed to detect an acute aortic syndrome
in 1 in 300 patients (98.8% sensitivity).11
Unfortunately, the study had several
limitations. The clinicians were aware of
the ADD-RS and D-dimer results, which
may have affected their decision to
pursue definitive imaging; additionally,
fewer than half of the diagnoses were
confirmed by imaging, surgery, or an
TABLE 3. ADD-RS2
High-Risk Conditions
Marfan syndrome
Connective tissue disease
Family history of aortic disease
Known aortic valve disease
Recent aortic manipulation
Known thoracic aortic aneurysm
High-Risk Chest, Back, or
Abdominal Pain Features
Abrupt onset, severe in intensity
Ripping, tearing, stabbing, or sharp in
quality
High-Risk Examination Features
Pulse deficit
Systolic blood pressure differential
Neurological deficit
Murmur of aortic insufficiency
Hypotension or shock
autopsy. While the research is promising,
further validation is needed to determine
if this strategy meets appropriate safety
and efficacy criteria.
CRITICAL DECISION
Which imaging modalities
can reliably confirm an aortic
dissection?
CT angiography (CTA) of the
aorta, magnetic resonance angiography
(MRA) of the chest and abdomen, and
transesophageal echocardiography (TEE)
can all detect an acute aortic dissection
with sensitivities and specificities at or
above 98%.
CTA of the aorta (chest and
abdomen) may be the most reliable
test in the acute setting due to its rapid
availability and high sensitivity, but this
decision must be weighed against the
risks of radiation and contrast exposure.
Multidetector helical CT scanners
have an even greater sensitivity and
specificity when compared to older
scanners that produce thicker slices.
Generally, a noncontrast scan coupled
with a contrast scan can help detect subtle
intramural hematomas. ECG gating can
also reduce the risk of cardiac motion
artifacts, which can trigger pulsations
that mimic dissection, especially near
the aortic root. These artifacts can be
problematic when evaluating young
patients with tachycardia, even with a
multidetector CT scan.
While 3D reconstruction has not
been shown to increase diagnostic
accuracy, it can be a valuable tool when
planning surgical and endovascular
approaches to treatment.2
MRA of the chest and abdomen
can also be used to detect aortic
dissection, but time constraints and
the inability to perform the test on
patients with metallic devices limit its
use in the emergency department. It
may be an option, however, as part of
an inpatient workup, if the patient has
contraindications to iodine contrast
and cannot undergo a CTA of the
aorta. MRA with and without contrast
is preferred by the American College
of Radiology; however, a noncontrast
MRA is acceptable if gadolinium is
contraindicated. ECG gating can help
improve the test’s accuracy in the
thoracic aorta near the aortic root.
TEE, another imaging modality
with a high sensitivity and specificity
for diagnosing aortic dissections,
can be useful for evaluating patients
with significant contraindications to
IV contrast. TEE can also identify
other complications, such as aortic
regurgitation or pericardial effusion
with a tamponade physiology.2 While
pericardial effusion can also be seen
on CT, TEE is a real-time, portable,
dynamic test that can be performed
while the patient is in the operating
room undergoing repair (Figure 3).
Unfortunately, the modality is not
readily available at most institutions,
and it requires sedation or possible
endotracheal intubation.
While bedside ultrasound is now a
common part of the acute workup for
patients with chest pain, transthoracic
echocardiography (TTE) has a sensitivity
of only 77% to 80% and a specificity
between 74% and 96% for detecting
proximal aortic dissections.2 Bedside
emergency physician–performed TTE
can help if the initial results are positive,
but the sensitivity of even a radiology-
performed TTE is not high enough to
reliably rule out an aortic dissection.
In addition to identifying a dissection
flap on ultrasound, the aorta is generally
dilated at the area of the dissection. For
reference, in healthy adults, the aortic
root diameter should be 4.0 cm or less
and should gradually taper more distally
down the aorta. Additionally, the aorta
of a healthy person expands by just
under 1 mm for every decade of life,
from middle age to late adulthood.5
Nearly every emergency department
patient with chest pain undergoes a chest
x-ray. Although often emphasized in
medical school, a widened mediastinum
or abnormal aortic contour seen on chest
x-ray has a sensitivity of only 64% to
71%, which is not high enough to rule
out aortic disease.5 A completely normal
chest x-ray may have a sensitivity of 90%
for detecting aortic pathologies. While the
test can be helpful for evaluating low-risk
cases, it is not sensitive enough to rule out
disease in all patients.
Other findings that may be seen on
chest x-ray include a “double-density”
aortic appearance that comes from the
true and false lumens, obliteration of
the aortic knob, and displacement of the
trachea to the right. While none of these
findings is specific enough to confirm the
disease, any new finding should prompt
more definitive imaging.
CRITICAL DECISION
How should hypotension be
managed in patients with an
aortic dissection?
According to the 2010 AHA guide­
lines for the initial management of aortic
dissections (both type A and type B),
the overall goal is to reduce aortic wall
stress. The first step is to decrease the
heart rate to a goal of 60 beats per
minute to mitigate the shearing force.
Pharmacologic Management
The first-line medication for heart rate
reduction is a beta-blocker; the second-
line drug is a nondihydropyridine calcium-
channel blocker (eg, diltiazem) for
patients with clear contraindications to
beta blockade. For instance, caution must
be used when giving a beta-blocker to
patients with acute aortic regurgitation, in
whom the agent can block compensatory
tachycardia. As such, it is imperative to
listen for a new murmur when managing
any acute aortic dissection.
If hypertension persists even when
the patient’s heart rate is controlled,
systolic blood pressure should be
reduced (<120 mm Hg). Angiotensin-
converting enzyme (ACE) inhibitors
(eg, IV enalaprilat) or vasodilators
(eg, nitroprusside or nitroglycerin) can
help meet this goal. Vasodilators should
not be started before heart rate control
has been achieved to avoid the risk
of reflex tachycardia, which can arise
when the blood pressure is reduced first.
Unfortunately, these recommendations
are only backed by level-C evidence;
current targets are based on expert
opinion, as no specific blood pressure
or heart rate targets have demonstrated
improved morbidity or mortality.8
When considering beta-blockers for
rate control in patients with dissections,
esmolol, labetalol, and metoprolol
are among the best choices. Esmolol,
a beta-1 antagonist, has a rapid onset
(≤1 minute) and a short half-life, making
August 2019 n Volume 33 Number 8 23

FIGURE 3. Type A Aortic Dissection With Moderate Pericardial Effusion19,20
Dissection flap
Dissection flap
it ideal for titrating to effect. Because the
drug is metabolized by RBC esterases,
pharmacokinetics can change in patients
with significant anemia; otherwise,
esmolol is not dependent on renal or liver
function. In addition to slowing the heart
rate via beta-1 blockade, labetalol is an
alpha-1 and beta-2 antagonist that can
help reduce blood pressure. The drug’s
onset is 2 to 5 minutes, with a peak of 5
to 15 minutes; however, labetalol’s half-
life is longer than that of esmolol.
Once rate control has been achieved,
nitroprusside can be used for blood
pressure reduction. A potent direct
arterial and venous dilator that works
through the release of nitric oxide,
nitroprusside has a quick onset of action
and a short half-life. It is important to
note, however, that the drug’s hypotensive
effects are sometimes unpredictable,
especially in patients with underlying left
ventricular hypertrophy and preload-
dependent diastolic heart failure.
Nicardipine, a dihydropyridine
calcium-channel blocker, is another
good option for blood pressure control.
24 Critical Decisions in Emergency Medicine
Pericardial effusion
The drug has minimal inotropic effects,
preferentially causing arterial dilation
without significantly altering preload.
While its onset is rapid, nicardipine has a
much longer half-life than nitroprusside.
Of note, nicardipine is metabolized in
the liver, so it can be used for patients
with renal failure.
Clevidipine is another dihydro­
pyridine calcium-channel blocker,
similar to nicardipine but with a
short half-life (1 minute), that is also
metabolized by RBC esterases. Because
it avoids reductions in preload, reflex
tachycardia is rare with clevidipine;
thus, some physicians use it as a first-line
medication for blood pressure reduction
in cases of hypertensive crises. Finally,
enalaprilat is an IV ACE inhibitor that
can be used for blood pressure control,
but its half-life is long at 35 hours. It
can also cause a dramatic drop in blood
pressure in patients in a high-renin state.
Adequate pain control is important
when managing an acute aortic
dissection because it can help prevent
pain-related elevations in blood
pressure and heart rate. IV opioids are
often preferred, as IV nonsteroidal anti-
inflammatory drugs (eg, ketorolac) can
increase the risk of bleeding or acute
kidney injury if the dissection involves the
renal arteries. IV fentanyl may be a good
choice for hypotensive patients because it
does not create the histamine-like effects
seen with other opioids, such as morphine.
Avoiding Complications
Hypotensive patients can be
particularly challenging to manage.
Although emergency physicians aim to
maintain an adequate blood pressure to
perfuse organs and prevent end-organ
damage, many medications that support
blood pressure can cause tachycardia,
which can lead to propagation of the false
lumen. One study found more inhospital
complications in patients with aortic
dissections who presented with either
low (<80 mm Hg) or high systolic blood
pressures (>150 mm Hg).12 A systolic
blood pressure under 80 mm Hg at
presentation is independently associated
with increased mortality.12
First, clinicians must consider the
potential causes of hypotension, including
a pericardial effusion and subsequent
cardiac tamponade, severe aortic
regurgitation, acute myocardial infarction,
blood loss into the false lumen, or a
rupture of the dissection into the pleural
space or mediastinum. If any of these
complications are present, immediate
surgical repair is required. It is crucial to
involve surgical consultants early in the
management of any hypotensive patient
with a dissection. Furthermore, a bedside
TTE can be used to determine the presence
of cardiac tamponade, as an emergent
pericardiocentesis for stabilization may be
required prior to operative repair.
An estimated 3% of proximal
aortic dissections also dissect into the
coronary arteries, a complication that
can cause ACS and lead to hypotension.13
Antiplatelets and anticoagulants can cause
significant morbidity and mortality in
patients with STEMI precipitated by a
dissection, with fatality rates as high as
71%.4 Anytime a patient’s history fits, an
ECG shows STEMI, and a dissection is
suspected, an emergent workup should be
initiated first.
Additional management of hypotensive
patients with an aortic dissection includes
resuscitation with IV fluids and the
emergency release of blood for those with FIGURE 4. Extension of a Type B Dissection in the Abdomen
an acute aortic rupture. Primary beta-1
agonists (eg, epinephrine and dopamine) Renal artery
should be avoided once a vasopressor has
been started, due to the risk of increasing Celiac artery
the patient’s heart rate and propagating
the dissection. Medications with alpha-1
adrenergic activity (eg, phenylephrine and
Dissection flap
norepinephrine) may be more effective for
supporting blood pressure, although reflex
tachycardia can still occur.
Emergency clinicians should also
SMA
watch for “pseudohypotension” by
checking the patient’s blood pressure
in all four limbs and comparing the
readings. Decreased blood flow to the The left, upper panel shows the origin of the celiac artery from the compressed true
lumen. The right, upper and left, lower panels show the origin of the right renal artery
subclavian artery that branches off
from the false lumen. The right, lower panel shows the origin of the celiac artery and
the false lumen can cause a low blood superior mesenteric artery from the compressed true lumen.19,20
pressure reading in that limb only,
even when the patient is not otherwise
prior to surgery (eg, neurologic deficits, fenestration or puncturing the intimal
systemically hypotensive.
shock, or coma) should be managed flap to relieve pressure from the false
CRITICAL DECISION operatively. Surgical repair, however, lumen and restore true lumen blood
is not without risk. The incidence of flow. Endovascular therapy alone is
Which aortic dissections postoperative stroke may be 15% or being studied for the treatment of type A
require an immediate surgical more, and perioperative mortality is an dissections, but this approach has not
consultation? estimated 25%.5,14 If patients survive yet been validated.
the perioperative period, their 1-, 5-, Type B Dissections
Type A Dissections and 8-year survival rates are favorable.15
Complicated type B dissections also
All Stanford type A dissections, Advanced age is not a definitive
require surgical repair, including:
complicated Stanford type B dissections, contraindication to surgical repair. • Dissections with associated limb,
and hypotensive patients with aortic In cases of aortic valve insufficiency, spinal, or mesenteric ischemia
dissection require an immediate the native valve can often be preserved • Hemodynamic instability, including
surgical consultation for operative by repairing the aortic root; occasionally, persistent hypertension despite
repair. Inhospital mortality significantly complete valve replacements are optimal medical management
improves with surgical, rather than necessary. In patients with mesenteric • Aortic ruptures
medical, management of type A ischemia, a disorder that often arises • Rapidly increasing aortic size
dissections, with an estimated mortality when an overfilled false lumen bulges Thoracic endovascular aortic repair
reduction of at least 30%.5,8,13 Even into the true lumen (Figure 4), the (TEVAR) stents have been approved for
patients with unfavorable presentations surgical technique may require the treatment of descending thoracic
aortic dissections. The repair mechanism
involves integrating the endovascular
stent graft over the proximal intimal
tear to redirect blood flow through the
true lumen (Figure 5). The goal is to
induce thrombosis and prevent blood
n In addition to patients with chest pain, consider an aortic dissection in those flow in the false lumen that is blocked
with back pain and syncope, a new murmur, or shock.
by the stent. Over time, the thrombosis
n ACEP clinical policy discourages using a D-dimer test alone to rule out an is reabsorbed, leading to improved
aortic dissection. More prospective studies are needed to validate clinical risk-
hemodynamics.
scoring systems when used alone or in combination with a D-dimer test.
One single-center study compared
n Use quick-onset, titratable IV medications to treat hypertension and avoid
similarly matched patients with type B
tachycardia in patients with an acute aortic dissection.
dissections who either received TEVAR
n Mortality is time dependent. As such, surgical colleagues should be consulted
early — even before a definitive diagnosis is made — if clinical suspicion for a or were medically managed. The
type A or complicated type B dissection is high. patients selected for TEVAR were those
with intractable pain or refractory

August 2019 n Volume 33 Number 8 25


FIGURE 5. Insertion of a Stent
AORTIC DISSECTION INSERTION & EXPANSION
hypertension. While the groups had
no statistically significant difference in
narcotic use or mortality, the patients with
TEVAR showed improvements in aortic
diameter.16
There is mounting evidence to
show the superiority of endovascular
repair over an open surgical approach
for the treatment of complicated type B
dissections.5 However, operative
repair is preferred for patients with an
underlying connective tissue disorder,
such as Marfan, Loeys-Dietz, or Ehlers-
Danlos syndromes. Because the proximal
portion of the tear is often just distal to
the left subclavian artery, open surgical
repair is frequently performed via a left
thoracotomy, with the patient in deep
hypothermic circulatory arrest.
Complications associated with open
surgical repair include a high rate of
inhospital mortality (≈30%), acute renal
failure, stroke, mesenteric ischemia, and
spinal cord ischemia.5,13 The mortality
associated with TEVAR is much lower
— between 6% and 8%, with similar
rates of stroke but lower rates of spinal
cord ischemia.5,13 Retrograde dissection
is another feared early complication of
TEVAR, although the overall risk is low.
Traditionally, uncomplicated type B
dissections have been medically managed
with close surveillance. Patients managed
this way have an inhospital mortality
rate as low as 10%; such cases may
ultimately require operative repair if
the dissection anatomy worsens or new
symptoms develop.17 One retrospective
study that compared outcomes in
patients who received TEVAR versus
nonoperative medical management for an
26 Critical Decisions in Emergency Medicine
dissection in an undifferentiated patient
with chest pain.
STENT GRAFT Most cases can be confirmed by
FULLY EXPANDED
a CTA of the aorta; however, when
contraindications are noted, MRA and
TEE are acceptable alternatives. While
a chest x-ray or TTE cannot reliably
rule out an aortic dissection, positive
findings may indicate the need for
further workup. Unfortunately, there is
not enough evidence to validate the use
of a D-dimer test, clinical risk scores,
or a combination of both to rule out
an aortic dissection. As such, imaging
studies remain the gold standard for
evaluating these cases.
uncomplicated type B dissection found Rate control, followed by
more adverse events in the medically blood pressure control, remains the
managed group, but no difference in the recommended initial treatment for
5-year mortality rate.18 Another study acute aortic dissections. Typically, IV
with an extended follow-up period beta-1 antagonists are the first-line
showed a long-term mortality benefit medications for rate control, followed by
in the TEVAR group. These findings nitroprusside or an IV dihydropyridine
suggest that while TEVAR does not calcium-channel blocker. It is also
improve medium-term mortality, it imperative to rule out secondary causes
may have long-term benefits (10-15 of hypotension (eg, cardiac tamponade)
years out).18 Despite these studies, more and involve surgical colleagues early.
definitive evidence is needed. If a pressor must be added, clinicians
Summary should choose medications with minimal
Aortic dissection is a rare disease inotropic effects.
with a high mortality rate; prompt All type A and complicated type B
recognition and treatment are key to dissections require emergent surgical
survival. Historical clues (eg, severe, management. TEVAR is approved for
sudden-onset chest pain) can help focus complicated type B dissections, and
the diagnosis, but it is imperative to there is mounting evidence to suggest its
remember that patients can also present advantages over open surgical repair.
atypically. High-risk features, including
REFERENCES
an existing aortic valve or connective 1. Asha SE, Miers JW. A systematic review and meta-
tissue disease, or a high-risk family analysis of D-dimer as a rule-out test for suspected
acute aortic dissection. Ann Emerg Med. 2015 Oct;
history, increase the probability of aortic 66(4):368-378.
n Assuming that a young, otherwise healthy patient could not have an aortic
dissection. This pathology can affect virtually anyone.
n Failing to remember that TTE is not sensitive enough to rule out a dissection.
However, a bedside transthoracic cardiac ultrasound can be used to evaluate
acute chest pain and rule out cardiac tamponade.
n Incorrectly ruling out an aortic dissection based on a negative D-dimer test
when assessing a patient with suspicious historical complaints, examination
features, or risk factors.
n Neglecting to consider aortic dissection in the differential diagnosis of
patients with chest pain accompanied by symptoms in other organ systems.
 CASE RESOLUTIONS
■ CASE ONE
Although the elderly woman’s
differential diagnosis was broad, her
most concerning risk factor was the
sudden-onset, tearing chest pain.
Her chest x-ray showed a widened
mediastinum, when compared to a
prior chest x-ray, and a CT of the
aorta revealed an acute type A aortic
dissection. The patient’s INR was
therapeutic at 2.7; given the acute
dissection, however, she was given
vitamin K and 4 units of fresh frozen
plasma to reverse her coagulopathy.
An esmolol drip successfully controlled
her heart rate, and her systolic blood
pressure remained near 120 mm Hg.
Cardiothoracic surgery took the
patient directly to the operating room,
where her dissection was repaired.
She did well postoperatively and was
discharged home on antihypertensive
medications, with regular surveillance to
monitor for complications.
■ CASE TWO
The 35-year-old man’s chest
x-ray was negative for an acute
cardiopulmonary pathology, and his
initial laboratory studies, including
a troponin T test, were negative.
The patient’s hypertension and pain
persisted despite multiple doses of
2. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010
ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/
SVM guidelines for the diagnosis and management
of patients with thoracic aortic disease. A report of
the American College of Cardiology Foundation/
American Heart Association Task Force on Practice
Guidelines, American Association for Thoracic
Surgery, American College of Radiology, American
Stroke Association, Society of Cardiovascular
Anesthesiologists, Society for Cardiovascular
Angiography and Interventions, Society of
Interventional Radiology, Society of Thoracic
Surgeons, and Society for Vascular Medicine.
Circulation. 2010 Apr;121(13):e266-e369.
3. Kamalakannan D, Rosman HS, Eagle KA. Acute aortic
dissection. Crit Care Clin. 2007 Oct;23(4):779-800, vi.
4. Upadhye S, Schiff K. Acute aortic dissection in the
emergency department: diagnostic challenges and
evidence-based management. Emerg Med Clin North
Am. 2012 May;30(2):307-327, viii.
5. Erbel R, Aboyans V, Boileau C, et al. 2014 ESC
guidelines on the diagnosis and treatment of aortic
diseases: document covering acute and chronic
aortic diseases of the thoracic and abdominal aorta
of the adult. The Task Force for the Diagnosis and
Treatment of Aortic Diseases of the European Society of
Cardiology (ESC). Eur Heart J. 2014 Nov 1;35(41):
2873-2926.
6. Fan KL, Leung LP. Clinical profile of patients of acute
aortic dissection presenting to the ED without chest
pain. Am J Emerg Med. 2017 Apr;35(4):599-601.
7. Mussa FF, Horton JD, Moridzadeh R, Nicholson J,
Trimarchi S, Eagle KA. Acute aortic dissection and
morphine. A CTA of the aorta confirmed
a type B dissection, beginning distally
to the aortic arch and distally to the left
subclavian artery, extending down to the
iliac arteries, and causing near-complete
occlusion of the right iliac artery. On
closer examination, the patient’s right,
lower extremity was cool and pale when
compared to his left extremity, indicating
a complicated type B aortic dissection.
Vascular surgery was emergently
consulted, a labetalol drip was started
to improve heart rate control, and
nitroprusside was added to reduce his
blood pressure prior to surgery.
Vascular surgery placed a TEVAR
stent in the descending aorta. Although
the patient’s postoperative course was
complicated by continued lower-extremity
weakness, physical therapy eventually
cleared him for discharge. He was sent
home on antihypertensive medications, and
drug counseling was arranged to address
his cocaine abuse, which likely contributed
to the dissection.
■ CASE THREE
Although the 52-year-old woman with
chest and left leg pain had an ECG that
met STEMI criteria, her cool and painful
left, lower extremity raised concern for
a dissection complicated by extremity
ischemia. In light of the patient’s chest
intramural hematoma: a systematic review. JAMA.
2016 Aug 16;316(7):754-763.
8. American College of Emergency Physicians Clinical
Policies Subcommittee (Writing Committee) on
Thoracic Aortic Dissection; Diercks DB, Promes SB,
et al. Clinical policy: critical issues in the evaluation
and management of adult patients with suspected
acute nontraumatic thoracic aortic dissection.
Ann Emerg Med. 2015 Jan;65(1):32-42:e12.
9. Watanabe H, Horita N, Shibata Y, Minegishi S, Ota
E, Kaneko T. Diagnostic test accuracy of D-dimer for
acute aortic syndrome: systematic review and meta-
analysis of 22 studies with 5000 subjects. Sci Rep.
2016 May 27;6:26893.
10. Suzuki T, Distante A, Zizza A, et al. Diagnosis of
acute aortic dissection by D-dimer: the International
Registry of Acute Aortic Dissection Substudy on
Biomarkers (IRAD-Bio) experience. Circulation. 2009
May 26;119(20):2702-2707.
11. Nazerian P, Mueller C, Soeiro AM, et al. Diagnostic
accuracy of the aortic dissection detection risk
score plus D-dimer for acute aortic syndromes: the
ADvISED Prospective Multicenter Study. Circulation.
2018 Jan 16;137(3):250-258.
12. Bossone E, Gorla R, LaBounty TM, et al. Presenting
systolic blood pressure and outcomes in patients with
acute aortic dissection. J Am Coll Cardiol. 2018 Apr
3;71(13):1432-1440.
13. Ankel FK. Aortic dissection. In: Marx JA, Hockberger
RS, Walls RM, et al, eds. Rosen’s Emergency
Medicine: Concepts and Clinical Practice, vol. 1. 8th
ed. Philadelphia, PA: Saunders; 2014:1124-1128.
14. Dumfarth J, Kofler M, Stastny L, et al. Stroke after
pain and hypotension, a limited bedside
TTE was performed, which revealed a
moderate pericardial effusion but no
cardiac tamponade. The patient had a
poor cardiac squeeze and an estimated
ejection fraction of 40%. In addition,
her aortic root was significantly wider
than normal (5.0 cm), although this
finding was not 100% diagnostic. Her
chest x-ray was notable for moderate
pulmonary edema, but she maintained
a 97% oxygen saturation on a
nonrebreather mask.
A CTA of the aorta confirmed
a type A aortic dissection, with the
proximal dissection flap extending
through the aortic valve and distal flap
involving the left common iliac artery.
The patient was resuscitated with IV
fluids, and a low-dose norepinephrine
drip was used to limit her tachycardia
and maintain her systolic blood
pressure near 80 mm Hg.
The emergency physician focused
on getting the patient to the operating
room, where the cardiothoracic surgeon
placed an aortic root graft and replaced
her aortic valve. She remained intubated
in the ICU until her pulmonary edema
cleared. She was eventually transferred
to a skilled nursing facility, where she
recovered well, and was discharged
home 2 weeks later.
emergent surgery for acute type A aortic dissection:
predictors, outcome and neurological recovery.
Eur J Cardiothorac Surg. 2018 May 1;53(5):1013-1020.
15. Pape LA, Awais M, Woznicki EM. Presentation,
diagnosis, and outcomes of acute aortic dissection:
seventeen-year trends from the International
Registry of Acute Aortic Dissection. J Vasc Surg. 2016
Feb;63(2):552-553.
16. Laquian L, Scali ST, Beaver TM, et al. Outcomes
of thoracic endovascular aortic repair for acute
type B dissection in patients with intractable pain
or refractory hypertension. J Endovasc Ther. 2018
Apr;25(2):220-229.
17. Suzuki T, Isselbacher EM, Nienaber CA, et al. Type-
selective benefits of medications in treatment of
acute aortic dissection (from the International Registry
of Acute Aortic Dissection [IRAD]). Am J Cardiol. 2012
Jan 1;109(1):122-127.
18. Arnáiz-García ME, González-Santos JM, Arnáiz-García
AM, Arnáiz J. Endovascular repair or best medical
treatment: what is the optimal management of
uncomplicated type-B acute aortic dissection?
J Thorac Dis. 2017 Oct;9(10):3458-3462.
19. Cullen EL, Lantz EJ, Johnson CM, Young PM.
Traumatic aortic injury: CT findings, mimics, and
therapeutic options. Cardiovasc Diagn Ther. 2014
Jun;4(3):238-244.
20. Suzuki T, Mehta RH, Ince H, et al. Clinical profiles and
outcomes of acute type B aortic dissection in the
current era: lessons from the International Registry
of Aortic Dissection (IRAD). Circulation. 2003 Sep 9;
108(suppl 1):II312-II317.
August 2019 n Volume 33 Number 8 27
 Critical Cases
in Orthopedics and Trauma
Airway Management in Blunt Head Trauma
By Cory Clugston, MD; Dan Eraso, MD; and John Kiel, DO, MPH
University of Florida College of Medicine – Jacksonville

A 27-year-old man with obvious craniofacial trauma arrives via helicopter after crashing his car into
a stationary trailer truck at an unknown speed. EMS reports that the patient was unresponsive at
the scene with a Glasgow Coma Scale score of 3. A King airway tube was placed en route.
On arrival, the patient’s vital signs are blood pressure 125/75, heart rate 123, and oxygen
saturation 85% on bag-valve-mask (BVM) ventilation. He has critical injuries involving the frontal
sinus, orbits, and nares, with unstable frontal bones and severe periorbital hematomas. His maxilla
and mandible appear to be intact, and he has no trauma to his trunk or extremities. Although
there is mild bleeding from his nares and oropharynx, his airway is generally visible and intact,
and his trachea is midline. A surgical marker is used to label the cricothyroid membrane.

Acute Airway FIGURE 1. Pneumothorax Visualized on Ultrasound

Management
It can be particularly
challenging to establish a
definitive airway in patients
with blunt head trauma.
Depending on the clinical
circumstances and established
protocols, EMS may place
a supraglottic airway device
(SAD) or endotracheal tube
(ETT) in the field. Ideally,
the emergency department
should be informed of the
patient’s pending arrival,
so airway equipment can
be prepared. Important tools
include a BVM and other
oxygen delivery devices,
direct and video laryng­
oscopes, ETTs (multiple
sizes), suction devices, an
elastic bougie, SADs, and a
surgical airway kit.

REFERENCES
1. Bakhsh A, Ritchie M. Video
laryngoscopy vs. direct
laryngoscopy. Acad Emerg Med.
2019 Feb;26(2):259-260.
2. Jung JY. Airway management of Left image demonstrates normal pleural sliding. Right image reveals an absence of lung
patients with traumatic brain injury/
C-spine injury. Korean J Anesthesiol. sliding.
COURTESY OF MARK RAMZY, DO
2015 Jun;68(3):213-219.

28 Critical Decisions in Emergency Medicine

 FIGURE 2. Landmarks for Chest Tube Insertion TABLE 1. Rapid Sequence
Intubation Checklist
q Physiological issues addressed
q Induction agent/muscle relaxant
q Post-intubation analgesia/sedation
q ±Push-dose epinephrine
q Failed plan verbalized
q Cricothyrotomy evaluation
q Denitrogenated ≥3 minutes
q Apneic oxygenation with nasal
cannula at 15 L/minute
q Oxygenated ≥95% (±CPAP)
Serratus q Look in mouth (dentures?)/assess
anterior neck range of motion
muscle q Positioning
Latissimus q Pulse oximetry visible or audible
dorsi muscle q Access — reliable and tested
Posterior
axillary line Anterior Fourth q Airway kit laid out
axillary line interspace q BVM (±PEEP valve) on oxygen
q Waveform capnograph on BVM
Midaxillary line Pectoralis q Video laryngoscope
major muscle
q Backup laryngoscope
q Oropharyngeal airway, bougie,
supraglottic airway, scalpel
q Suction x 2
KEY POINTS q External laryngeal manipulation/
n If the patient arrives with a SAD, endotracheal intubation should be prioritized. head elevation/collar briefing
However, an airway device that is providing adequate oxygenation and ventilation q Eye and face protection
can be left in place while other resuscitative measures are initiated. ADAPTED FROM EMCRIT.ORG

n It is imperative to evaluate for direct airway trauma; facial and oropharyngeal

injuries, including blood (especially expanding hematomas or arterial bleeding);
bony instability; and oropharyngeal foreign bodies. The trachea should be CASE RESOLUTION
examined for midline stability, and the location of the cricothyroid membrane The patient was aggressively
should be noted. preoxygenated to approximately
n Endotracheal intubation should be initiated following the initial airway examination. 90%. The supraglottic device was
If time permits, preoxygenation should be optimized with an airway device, BVM, removed; succinylcholine and
and nasal oxygenation (with or without an oral- or nasopharyngeal airway adjunct). etomidate were administered; and
Pretreatment with lidocaine or fentanyl may help reduce intracranial pressure a definitive airway was established,
caused by blunt head trauma. Patients with spontaneous respirations should be using a video laryngoscope,
medicated to undergo rapid sequence intubation (Table 1). bougie, and 7-0 ETT. Although
n Video laryngoscopy can increase the likelihood of first-pass success and decrease correct tube placement was
movement of the cervical spine.1,2 The cervical spine should be immobilized with in- confirmed, the patient’s oxygen
line stabilization, and the airway team should be prepared with suction. If intubation saturation remained below 85%.
fails and the patient remains hypoxic, a cricothyrotomy should be performed. Bilateral lung sliding was noted
Correct placement of the ETT should be confirmed by waveform capnography, on ultrasound. Given the patient’s
colorimetry, the presence of bilateral breath sounds, a symmetrical chest rise, hypoxia and mechanism of injury,
and chest radiography. Patients who remain hypoxic after tube placement require the clinician initiated a bilateral
further monitoring. tube thoracostomy, which was
n A hemo- or pneumothorax should be considered for those with diminished or unremarkable with minimal blood
hyper-resonant, unilateral breath sounds. These diagnoses can be confirmed by output. A cardiac ultrasound
the absence of lung sliding (Figure 1). Although chest x-rays can be helpful, they failed to identify pericardial
are less sensitive than ultrasonography for the evaluation of such cases. Unstable effusion. Given the mechanism of
patients should undergo a needle decompression at the fourth or fifth intercostal injury, mannitol was administered
space along the anterior axillary line. Following needle decompression, definitive empirically. After 20 minutes of
management of a hemo- or pneumothorax entails a tube thoracostomy (Figure 2), resuscitation, the patient became
using a water-suction device. bradycardic (indicative of the
n Ultrasonography should also be used to evaluate for pericardial effusion, a Cushing reflex) and pulseless. CPR
reversible cause of thoracic trauma. was discontinued, and he expired.

August 2019 n Volume 33 Number 8 29

 CME
Reviewed by Lynn Roppolo, MD, FACEP

Qualified, paid subscribers to Critical Decisions in Emergency Medicine may receive

CME certificates for up to 5 ACEP Category I credits, 5 AMA PRA Category 1
Credits™, and 5 AOA Category 2-B credits for completing this activity in its

QUESTIONS entirety. Submit your answers online at acep.org/cdem; a score of 75% or better
is required. You may receive credit for completing the CME activity any time within
3 years of its publication date. Answers to this month’s questions will be published
in next month’s issue.

1 Which drug is often the first-line treatment

for moderate to severe cancer pain? 7 Which statement accurately describes a characteristic
of methadone?
A. Codeine A. It has a predictable half-life
B. Hydrocodone B. It has no effect on the QTc interval
C. Morphine C. It is a long-acting opioid
D. Tramadol D. It is free of side effects when administered
subcutaneously

2 Which of the following pathologies is least

likely to cause bone pain?
8 Which drug class is most specific for the treatment of
bone pain?
A. Breast cancer
B. Kidney cancer A. Bisphosphonates (pamidronate, ibandronate, clodronate)
C. Opioid abuse B. Gabapentinoids (gabapentin, pregabalin)
D. Pancreatic cancer C. Sodium-channel drugs (mexiletine, lidocaine)
D. Tricyclic antidepressants

3 Which system is least likely to be adversely

affected by NSAIDs?
9 What electrolyte disturbance should be addressed in
cancer patients with constipation?
A. Cardiovascular
B. Dermatologic A. Hypercalcemia
C. Gastrointestinal B. Hypernatremia
D. Renal C. Hypokalemia
D. Hypomagnesemia

4 Which medication is categorized as an

NMDA antagonist?
10
Which antiepileptic medication has been employed as an
adjuvant therapy for neuropathic pain in cancer patients?
A. Buprenorphine
B. Fentanyl A. Carbamazepine
C. Ketamine B. Levetiracetam
D. Morphine C. Lorazepam
D. Magnesium

5 Which of the following drugs has the

highest potency?
11
According to the 2010 AHA guidelines, medical
management of a hypertensive, tachycardic patient with
A. Codeine
B. Hydrocodone a nontraumatic aortic dissection includes which goal(s)?
C. Morphine A. Blood pressure control alone, with a goal of <120 mm Hg
D. Tramadol B. Blood pressure control first, with a goal of <120 mm Hg,
followed by heart rate control, with a goal of <60 beats

6 Orofacial pain is a potential side effect

of which chemotherapeutic agent?
per minute
C. Heart rate control alone, with a goal of <60 beats per
A. Doxorubicin minute
B. Fluorouracil D. Heart rate control first, with a goal of <60 beats per
C. Methotrexate minute, followed by blood pressure control, with a goal
D. Vincristine of <120 mm Hg

30 Critical Decisions in Emergency Medicine

12
A 53-year-old man presents with sudden-onset,
tearing, substernal chest pain. Which underlying
anatomical abnormality increases his relative risk
for a thoracic aortic dissection?
A. Bicuspid aortic valve
B. Left ventricular hypertrophy
C. Mitral valve prolapse
D. Renal artery aneurysm
17 Which of the following pathologies does not
require emergent surgical repair?
A. DeBakey type 1 dissection
B. Type A dissection
C. Type B dissection with uncontrolled blood
pressure despite optimal medical management
D. Uncomplicated type B dissection

18 Which of the following describes an

13 A 38-year-old woman with a history of Marfan
syndrome, hypertension, and diabetes mellitus
presents with severe, sudden-onset chest pain
that began 2 hours ago. She is hypertensive,
tachycardic, and in obvious distress; a diastolic
murmur is noted. Which test is the most
appropriate for ruling out an aortic dissection?
A. Chest x-ray
B. CTA of the aorta
C. D-dimer
D. TTE
19
uncomplicated aortic dissection?
A. Type B dissection accompanied by signs of
ischemia in the right, lower extremity
B. Type B dissection accompanied by syncope
C. Type B dissection in a patient who is unable to
lift his lower extremities
D. Type B dissection in a patient whose serial
imaging studies reveal a rapidly enlarging aorta
What is the most commonly recognized cardiac
complication of type A aortic dissections?
A. Aortic valve insufficiency

14
Which of the following complaints represents a
“high-risk” concern for an aortic dissection?
B.
C.
Atrial fibrillation
Cardiac tamponade
A. Chest pressure that developed gradually over a D. Mitral valve prolapse
few hours and is worse with exertion
B. Pain localized to the scapula that is worse with
movement and exacerbated by palpation
20 A 77-year-old man presents with chest pain and
syncope. His ECG shows nonspecific T-wave
changes, and his vital signs are notable for a heart
C. Severe, tearing, sudden-onset chest pain that is
difficult to describe due to its severity rate of 70 beats per minute and blood pressure of
82/50 mm Hg. A CT scan reveals a type A aortic
D. Shortness of breath that becomes worse with
dissection, with no signs of rupture or pericardial
deep inspiration
effusion. His hemoglobin level is normal. Despite

15 Which symptom is most commonly associated
with type B aortic dissections?
fluid resuscitation with a 20-mL/kg bolus of normal
saline, he remains hypotensive and feels dizzy.
What is the next best step?
A. Back pain
B. Hypotension A. Administer a second bolus of normal saline
C. Pulse deficit (30 mL/kg), and monitor his blood pressure
D. Syncope B. Slowly titrate a norepinephrine drip with a goal
MAP of 65 mm Hg while carefully monitoring

16 Which medication is the best choice for heart rate
control when beta-blockers are contraindicated?
the patient for worsening tachycardia
C. Slowly titrate a phenylephrine drip with a goal
A. Diltiazem MAP of 65 mm Hg, and consult with surgery
B. Esmolol regarding an emergent repair
C. Nicardipine D. Start an epinephrine drip with a goal MAP of
D. Nitroprusside 65 mm Hg

ANSWER KEY FOR JULY 2019, VOLUME 33, NUMBER 7

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20
B D B D C D A A A D A C C C B A B C B C

August 2019 n Volume 33 Number 8 31

 Drug Box Tox Box
CAPSAICIN METFORMIN POISONING
By Frank LoVecchio, DO, MPH, FACEP By Christian A. Tomaszewski, MD, MS, MBA, FACEP
Maricopa Medical Center, Phoenix, Arizona University of California, San Diego
Capsaicin, a natural component of several species of chili peppers Metformin, a popular biguanide, was originally developed
belonging to the genus Capsicum, is used as an analgesic in topical from a medieval diabetic treatment, the French lilac. Although
ointments and dermal patches and to reduce the symptoms of hypoglycemia is unlikely, the drug can cause severe metformin-
peripheral neuropathy. The agent has also been suggested as associated lactic acidosis in an acute overdose or when
a treatment for cannabinoid hyperemesis syndrome, a disorder accumulated in renally impaired patients.
associated with chronic cannabis abuse and cyclic or intractable Mechanism of Action
episodes of nausea, vomiting, and abdominal pain. • Inhibits hepatic gluconeogenesis
Mechanism of Action • Enhances peripheral glucose utilization
Capsaicin, a transient receptor potential vanilloid 1 (TRPV1) agonist, • Decreases fatty acid oxidation
activates TRPV1 ligand-gated cation channels on nociceptive nerve Kinetics
fibers, resulting in depolarization, initiation of an action potential, • 2-hour peak; 3- to 6-hour half-life (normal glomerular
and pain-signal transmission to the spinal cord. Exposure to the filtration rate)
drug desensitizes the sensory axons and inhibits the initiation of • Negligible metabolism
pain transmission. • Mainly (90%) renal excretion
Adult Dosing • Toxic dose: >5 g in adults; >100 mg/kg in children
Muscle/joint pain Clinical Manifestations
Topical: Apply a thin film of cream, gel, liquid, or lotion to affected • Hypoglycemia (rare)
areas 3 to 4 times per day. • Lactic acidosis
Sinelee (brand-name) patch (0.025%, 0.03%, 0.0375%, 0.05%): Apply • Abdominal pain, nausea, vomiting
1 patch to the affected area for up to 8 hours (maximum 4 patches • Blindness, hypotension, altered mental status
daily). Do not use for >5 consecutive days. Diagnostics
Neuropathic pain • Finger-stick glucose
Qutenza (brand-name) patch: Apply patch(es) to the most painful • Acetaminophen (and salicylate) levels in an overdose
area for 60 minutes. Up to 4 patches may be applied in a single • Venous blood gas and/or basic metabolic panel
application. Repeat ≥3 months, as needed. Pretreat the area with • Serum lactate
a topical anesthetic prior to patch application. Treatment and Disposition
Cannabinoid hyperemesis syndrome (off label) • For a large, acute overdose (<1 hour), consider orally activated
Apply cream (0.075%) to a 15- × 25-cm area in the periumbilical charcoal
region; reapply every 4 hours until symptoms resolve. • Pressors, as needed
Diabetic neuropathy (off label) • Hemodialysis (or continuous venovenous hemofiltration) if:
Apply cream (0.075%) 4 times per day. — Elevated lactate (>20 mmol/L)
— Severe metabolic acidosis (pH <7.0)
Precautions — Low sodium bicarbonate (<5 mEq/L)
Potential adverse effects include localized erythema or pain (>10%), — Failure to improve with supportive care (>2-4 hours)
hypertension (2%; transient), papules (6%), local dryness (2%), • Discharge at approximately 6 hours (8 hours for extended
pruritus (2%), nausea (5%), vomiting (3%); localized pruritus (6%), release) post ingestion if:
localized edema (4%), nasopharyngitis (4%), sinusitis (3%), and — No metabolic acidosis
bronchitis (2%). — Asymptomatic
Pregnancy category B • Admit if symptomatic or acidosis worsens