Volume 31 Number 11 November 2017

Out of Step
The foot is one of the most common sites for both
acute and chronic injuries in athletes and active patients.
The anatomical complexity and functional demands
of this all-important extremity can make these insults
particularly difficult to diagnose and treat. While
misdiagnoses can result in significant morbidity, careful
attention to physical and imaging findings and prompt
orthopedic referral can ensure a successful clinical
course.

Full Stop
With substance abuse on the rise, emergency physicians
must be better prepared than ever to recognize and
manage the signs and symptoms of withdrawal. While
such sequelae frequently are precipitated by drugs
of abuse, discontinuation of commonly prescribed
Lumbar puncture (LP) is used in the diagnostic
medications should not go overlooked. Timely
evaluation of central nervous system (CNS) processes,
identification and treatment is the best defense against
most commonly in cases of suspected infection and
the potentially deadly complications of withdrawal
subarachnoid hemorrhage. Less commonly, the
from any offending substance.
procedure is used for therapeutic purposes (eg, in cases
of idiopathic intracranial hypertension).

THE OFFICIAL CME PUBLICATION OF THE AMERICAN COLLEGE OF EMERGENCY PHYSICIANS

IN THIS ISSUE
Lesson 21 n Sports-Related Foot Injuries . . . . . . . . . . . . . . . . . . . . . . . . 3
LLSA Literature Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Critical Decisions in Emergency Medicine is the official
Critical Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 CME publication of the American College of Emergency
Physicians. Additional volumes are available to keep
Critical ECG . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 emergency medicine professionals up to date on
Lesson 22 n Withdrawal from Atypical Agents . . . . . . . . . . . . . . . . . . . 15 relevant clinical issues.

Critical Image . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21
EDITOR-IN-CHIEF
CME Questions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 Michael S. Beeson, MD, MBA, FACEP
Drug Box/Tox Box . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 Northeastern Ohio Universities,
Rootstown, OH

SECTION EDITORS
Contributor Disclosures. In accordance with the ACCME Standards for Commercial
Andrew J. Eyre, MD
Support and policy of the American College of Emergency Physicians, all individuals with
Brigham & Women’s Hospital/Harvard Medical School,
control over CME content (including but not limited to staff, planners, reviewers, and
Boston, MA
authors) must disclose whether or not they have any relevant financial relationship(s) to
learners prior to the start of the activity. These individuals have indicated that they have Joshua S. Broder, MD, FACEP
a relationship which, in the context of their involvement in the CME activity, could be Duke University, Durham, NC
perceived by some as a real or apparent conflict of interest (eg, ownership of stock, grants, Frank LoVecchio, DO, MPH, FACEP
honoraria, or consulting fees), but these individuals do not consider that it will influence the Maricopa Medical Center/Banner Phoenix Poison
CME activity. Sharon E. Mace, MD, FACEP; Baxter Healthcare, consulting fees, fees for non- and Drug Information Center, Phoenix, AZ
CME services, and contracted research; Gebauer Company, contracted research; Halozyme,
consulting fees. Joshua S. Broder, MD, FACEP; GlaxoSmithKline; his wife is employed by Amal Mattu, MD, FACEP
GlaxoSmithKline as a research organic chemist. All remaining individuals with control over University of Maryland, Baltimore, MD
CME content have no significant financial interests or relationships to disclose. Lynn P. Roppolo, MD, FACEP
Method of Participation. This educational activity consists of two lessons, a post-test, University of Texas Southwestern Medical Center,
and evaluation questions; as designed, the activity it should take approximately 5 hours to Dallas, TX
complete. The participant should, in order, review the learning objectives, read the lessons
Christian A. Tomaszewski, MD, MS, MBA, FACEP
as published in the print or online version, and complete the online post-test (a minimum
University of California Health Sciences,
score of 75% is required) and evaluation questions. Release date November 1, 2017.
San Diego, CA
Expiration October 31, 2020.
Steven J. Warrington, MD, MEd
Accreditation Statement. The American College of Emergency Physicians is accredited by
Kaweah Delta Medical Center, Visalia, CA
the Accreditation Council for Continuing Medical Education to provide continuing medical
education for physicians.
ASSOCIATE EDITORS
The American College of Emergency Physicians designates this enduring material for a
Walter L. Green, MD, FACEP
maximum of 5 AMA PRA Category 1 Credits™. Physicians should claim only the credit
University of Texas Southwestern Medical Center,
commensurate with the extent of their participation in the activity.
Dallas, TX
Each issue of Critical Decisions in Emergency Medicine is approved by ACEP for 5 ACEP
John C. Greenwood, MD
Category I credits. Approved by the AOA for 5 Category 2-B credits.
University of Pennsylvania, Philadelphia, PA
Commercial Support. There was no commercial support for this CME activity.
Target Audience. This educational activity has been developed for emergency physicians. Sharon E. Mace, MD, FACEP
Cleveland Clinic Lerner College of Medicine/Case
Western Reserve University, Cleveland, OH
Critical Decisions in Emergency Medicine is a trademark owned and published monthly by the American
College of Emergency Physicians, PO Box 619911, Dallas, TX 75261-9911. Send address changes and Jennifer L. Martindale, MD, MSc
comments to Critical Decisions in Emergency Medicine, PO Box 619911, Dallas, TX 75261-9911, or to Mount Sinai St. Luke’s/Mount Sinai West
cdem@acep.org; call toll-free 800-798-1822, or 972-550-0911. New York, NY
Copyright 2017 © by the American College of Emergency Physicians. All rights reserved. No part of this
George Sternbach, MD, FACEP
publication may be reproduced, stored, or transmitted in any form or by any means, electronic or mechanical,
including storage and retrieval systems, without permission in writing from the Publisher. Printed in the USA. Stanford University Medical Center, Stanford, CA
The American College of Emergency Physicians (ACEP) makes every effort to ensure that contributors to its
publications are knowledgeable subject matter experts. Readers are nevertheless advised that the statements RESIDENT EDITOR
and opinions expressed in this publication are provided as the contributors’ recommendations at the time Nathaniel Mann, MD
of publication and should not be construed as official College policy. ACEP recognizes the complexity of Massachusetts General Hospital, Boston, MA
emergency medicine and makes no representation that this publication serves as an authoritative resource
for the prevention, diagnosis, treatment, or intervention for any medical condition, nor should it be the basis
for the definition of, or standard of care that should be practiced by all health care providers at any particular
EDITORIAL STAFF
time or place. Drugs are generally referred to by generic names. In some instances, brand names are added Rachel Donihoo, Managing Editor
for easier recognition. Device manufacturer information is provided according to style conventions of the rdonihoo@acep.org
American Medical Association. ACEP received no commercial support for this publication.
Jessica Hamilton, Educational Products Assistant
To the fullest extent permitted by law, and without
Lexi Schwartz, Subscriptions Coordinator
limitation, ACEP expressly disclaims all liability for
errors or omissions contained within this publication, Marta Foster, Director, Educational Products
and for damages of any kind or nature, arising out of
use, reference to, reliance on, or performance of such ISSN2325-0186(Print) ISSN2325-8365(Online)
information.
 Out of Step
Sports-Related
Foot Injuries

LESSON 21

By Jeffrey P. Feden, MD, FACEP and John Kiel, DO, MPH

Dr. Feden is a clinical associate professor in the Department of Emergency
Medicine, Division of Sports Medicine at Alpert Medical School of Brown
University in Providence, RI. Dr. Kiel is a fellow in the Department of Orthopaedic
Surgery and Sports Medicine at the University of Kentucky College of Medicine
in Lexington.

Reviewed by Andrew Eyre, MD

OBJECTIVES
On completion of this lesson, you should be able to:
1. Recognize the most common osseus and soft-tissue
injuries of the foot affecting athletes and other active
individuals.
2. Explain the importance of a systematic approach to
the evaluation of athletic foot conditions, including
appropriate selection and interpretation of diagnostic
imaging.
3. Detail the significance of certain occult fractures involving
the midfoot and hindfoot.
4. Describe management principles for athletic foot injuries,
including indications for prompt specialty consultation or
referral.
FROM THE EM MODEL
18.0 Traumatic Disorder
18.1.8 Extremity Bony Trauma
CRITICAL DECISIONS
n How should the physical examination be
approached in patients with foot pain?
n Which patients require radiographs, and when is
advanced imaging warranted?
n What presentations are associated with
radiographically occult fractures?
n Which fractures require an emergent orthopedic
consultation or urgent outpatient referral?
n How should fractures of the proximal fifth
metatarsal be managed?
n Which patients can benefit from a routine out-
patient orthopedic or sports medicine evaluation?

The foot is one of the most common sites for both acute and chronic injuries among athletes and active
individuals. The anatomical complexity and functional demands of this all-important extremity can make these insults
particularly difficult to diagnose and manage. However, careful attention to the patient’s history, mechanism of injury,
physical examination, and imaging findings can guide the emergency clinician toward an accurate diagnosis and
appropriate course of treatment.

November 2017 n Volume 31 Number 11 3

 CASE PRESENTATIONS
■ CASE ONE
A 30-year-old military recruit
presents to the emergency
department for evaluation of a
foot injury sustained while he was
wrestling with his brother in the
backyard of their home earlier
today. He slipped and “twisted”
his right foot, and now reports
swelling and pain with an inability
to bear weight. The examination
The foot is comprised of 28 bones
(Figure 2), divided anatomically
between the forefoot (metatarsals
and phalanges), midfoot (cuneiforms,
cuboid, and navicular), and hindfoot
(talus and calcaneus). The Chopart
joint separates the hindfoot from
the midfoot, and the Lisfranc joint
distinguishes the midfoot from the
forefoot. The extrinsic muscles of the
extremity include the tibialis anterior,
extensor digitorum longus, extensor
hallucis longus, tibialis posterior, flexor
digitorum longus, flexor hallucis longus,
gastrocnemius, and soleus.
Innervation of the foot includes the
tibial, superficial and deep fibular (ie,
peroneal), saphenous, and sural nerves.
Each of these structures contributes to
sensory innervation; motor function
comes from the deep fibular nerve
and the tibial nerve and its branches.
Vascular supply to the dorsum of the
foot is provided by the anterior tibial
and dorsalis pedis arteries, whereas the
posterior tibial and peroneal arteries
supply the plantar aspect. The plantar
fascia is the major ligamentous structure
that supports the arch of the foot.
Functionally, the foot is capable of
motion in three planes: dorsiflexion/
plantarflexion, inversion/eversion,
and adduction/abduction. Supination
refers to plantarflexion, inversion,
and adduction. In contrast, pronation
describes dorsiflexion, eversion, and
abduction.
Comprehensive evaluation of a foot
injury includes a detailed history and
a systematic approach to the physical
4 Critical Decisions in Emergency Medicine
demonstrates diffuse tenderness and
swelling involving the dorsal midfoot
and forefoot. There is no ecchymosis,
and neurovascular findings are
normal. Plain radiographs of the right
foot (Figure 1) are interpreted by the
radiologist as showing soft-tissue
swelling without fracture.
■ CASE TWO
A 21-year-old woman presents
with acute left foot pain related to
examination. The patient history, an
essential starting point for evaluating
any complaint of foot pain, should focus
on several key factors: mechanism of
injury; duration, location, and character
of pain; associated swelling, bruising,
or neurological symptoms; aggravating
or provocative movements or activities;
previous injury or surgery; and ability
to bear weight.
CRITICAL DECISION
How should the physical
examination be approached in
patients with foot pain?
The musculoskeletal examination of
any patient presenting with foot pain
should include inspection, palpation,
and assessments of range of motion,
muscle strength, and neurovascular
function. The injured or painful foot
should be evaluated in comparison to
the contralateral extremity, with special
attention paid to soft-tissue swelling,
deformity, and skin discoloration. Any
wounds or lacerations should be noted,
especially in association with underlying
fractures, a finding that represents an
open fracture.
Palpation of both injured and
uninjured areas is important, and
landmarks such as the base of the fifth
metatarsal and the medial aspect of
the midfoot should be primary areas of
focus. Palpation should always include
the joints above and below the injury
site. Both active and passive ranges of
motion should be tested, as should the
strength of major muscle groups (eg,
an injury sustained during college
basketball practice yesterday. She
stepped on a teammate’s foot and
rolled her ankle, resulting in acute
lateral foot pain. Her examination is
notable for mild soft-tissue swelling
with normal skin and localized
tenderness. Plain radiographs
demonstrate a nondisplaced fracture
at the base of the fifth metatarsal.
plantarflexion, dorsiflexion, inversion,
and eversion), and sensation of all
surfaces of the foot.
A comparison to the uninjured
extremity can yield valuable
information and subtle abnormalities
that otherwise may not be appreciated.
A vascular examination consisting of
palpation of the dorsalis pedis and
posterior tibial pulses, as well as an
assessment of capillary refill, must be
performed and documented routinely.
CRITICAL DECISION
Which patients require
radiographs, and when is
advanced imaging warranted?
Aside from a history and physical
examination, plain radiographs are
a mainstay in the initial evaluation
of foot injuries and should include
anteroposterior (AP), lateral, and
oblique views. Although the criteria for
selecting patients for x-rays has been a
subject of discussion for decades, one
clinical decision rule was validated
in the early 1990s for the use of
radiography in acute ankle injuries.1
Intended to reduce unnecessary
imaging in the emergency department,
the Ottawa Ankle Rules continue to
guide imaging decisions as a means of
reducing costs without missing clinically
significant fractures.
This protocol supports imaging in
adult patients presenting with pain in
the midfoot and bony tenderness at the
navicular, cuboid, or base of the fifth
metatarsal. While these rules are well-
established and have a high sensitivity
(99%), it is important to understand that
they were intended for use in patients
with foot pain related to ankle injury
(eg, indirect injury) and should not
necessarily be applied to those with
direct foot trauma. 2
In addition to the standard three-
view x-ray series, the emergency
physician should be familiar with specific
radiographic techniques and views for
certain conditions. Weightbearing AP
and comparison views can be helpful initial diagnostic imaging modality
FIGURE 1. An AP X-Ray of the Right Foot (Case One)
in the evaluation of midfoot injuries to
assess for subtle alignment abnormalities
(eg, diastasis of the first intermetatarsal
space). However, true weightbearing
views often are difficult to achieve in
the acutely injured patient secondary
to pain. The Canale and Harris views
provide additional vantage points for the
assessment of talar neck and calcaneal
fractures, respectively.
Advanced Imaging
While plain radiographs remain the
of choice, they
generally are
unreliable for
soft-tissue and
subtle osseus
injuries, especially
those occurring in
the anatomically
complex midfoot
region. Computed
tomography
(CT) is ideal for
characterizing the
bony anatomy
and revealing
subtle fractures.
While magnetic
resonance
imaging (MRI)
also can detect
osseus injury,
this modality is
particularly useful
and sensitive
for diagnosing
soft-tissue
abnormalities.
Due to the limited
availability and
access to MRI in
the emergency
department,
CT often is the
second-line
imaging test for
identifying occult
fractures when
a high index of
clinical suspicion
exists based on
the mechanism
of injury or
worrisome
examination findings. Rapid
identification of these injuries is
essential for guiding acute decision-
making and orthopedic management.
CRITICAL DECISION
What presentations are
associated with radiographically
occult fractures?
Lisfranc Injuries
The Lisfranc “joint” describes a
complex tarsometatarsal articulation
involving ligamentous attachments
between the cuneiforms, cuboid,
and metatarsal bases. Specifically,
the relationship between the medial
cuneiform and base of the second
metatarsal (bridged by the Lisfranc
ligament) is critical to midfoot stability
and may be disrupted by high- or
low-energy mechanisms. Lisfranc
injuries range from ligamentous sprain
to fracture-dislocation. Sports-related
injuries tend to be low energy and
are more likely to be radiographically
occult. The mechanism in these cases
usually involves rotational force to
the forefoot or an axial load to a
plantarflexed foot under which the
tarsometatarsal articulation fails.
The identification of a Lisfranc
fracture (Figure 3) hinges on initial
clinical suspicion with a supporting
mechanism of injury associated
with midfoot pain (especially with
weightbearing) and an examination
that demonstrates midfoot tenderness
and soft-tissue swelling. The plantar
ecchymosis sign also has been described
in association with Lisfranc injuries
and refers to ecchymosis on the plantar
aspect of the midfoot region. 3
Malalignment at the second
tarsometatarsal articulation is the
radiographic hallmark of such fractures.
This abnormality may be visualized
on radiographs as a step-off along the
medial borders of the second metatarsal
and the middle cuneiform, and/or
diastasis of more than 2 mm between
the base of the second metatarsal and
the medial cuneiform (eg, the first
intermetatarsal space).4 On the oblique
view, the lateral borders of the third
metatarsal and lateral cuneiform should
November 2017 n Volume 31 Number 11 5
 FIGURE 2. Bones of the Foot (Plantar View)
align normally, as should the medial
borders of the fourth metatarsal and
cuboid. If clinical suspicion remains
despite unremarkable plain radiographs,
weightbearing films may be attempted.
Otherwise, advanced imaging should be
considered. 5
MRI is superior for the detection
of ligamentous injuries. However, CT
often is preferred over MRI in the
emergency department because of its
accessibility, excellent resolution for
identification of subtle fractures, and
its ability to detect bony malalignment,
which may herald a Lisfranc injury.
Cuneiform fractures and/or fractures
at the metatarsal bases may represent
avulsion of the Lisfranc ligament and
should be considered a Lisfranc injury
until proven otherwise.
The treatment of such cases
ranges from conservative to operative
management, depending on the severity
of each case. Suspected ligamentous
injuries without diastasis warrant
prompt orthopedic referral. Orthopedic
consultation is mandatory for any
midfoot injury with an associated
fracture or malalignment, as these
6 Critical Decisions in Emergency Medicine
findings indicate a higher-grade injury
or instability that often requires surgical
management. A missed or delayed
diagnosis can result in chronic pain and
disability.
Tarsal Navicular Fracture
Tarsal navicular injuries result from
acute trauma or chronic repetitive stress.
Patient presentations vary significantly
based on the mechanism of injury.
Avulsion and body fractures typically
are identified with plain radiographs.
Advanced imaging in these cases is
reserved for detailing fracture lines
and identifying concomitant soft-tissue
injuries, and rarely is indicated in the
emergency department setting.
Minor avulsion injuries from
low-energy trauma can be treated by
confining the extremity to a walking
boot for 4 to 6 weeks. Patients with
bony or avulsion fractures with concern
for significant associated ligamentous
injury should be prevented from bearing
weight, placed in a splint, and referred
for an orthopedic evaluation. MRI is
the imaging modality of choice for a
suspected stress fracture and can be
obtained in the outpatient setting.
Individuals with navicular pain,
negative radiographs, and suspicion
for stress injury similarly should be
managed with non-weightbearing
instructions and orthopedic referral.
Hindfoot Fracture
Fractures of the talus usually result
from high-energy trauma and may
affect the body, head, neck, lateral
process, or posterior process of the
talus. A radiographic evaluation
should include three views of the ankle
and three views of the foot. CT can
be obtained for diagnostic purposes
when a high index of suspicion exists
and x-rays are negative. Nondisplaced
talar body fractures may be treated
conservatively, while displaced
fractures often are treated operatively.
Displaced talar neck fractures require
an orthopedic consultation in the
emergency department. Some talar
fractures are associated with subtalar
dislocation and can be complicated by
avascular necrosis.
A fracture of the lateral process of the
talus is well-described in snowboarders.6
This high-impact injury is related
to inversion and dorsiflexion of the
ankle with an axial load, and often is
misdiagnosed as an ankle sprain given
the similar presentation of anterolateral
ankle pain with swelling. In certain
cases, CT may be necessary to establish
the diagnosis. Nondisplaced fractures
can be treated with non-weightbearing
immobilization, while displaced fractures
often require operative management. All
injuries should be referred for prompt
orthopedic follow up.
FIGURE 3. Lisfranc Fracture of the Second Metatarsal
Calcaneal fractures frequently are
related to high-energy axial loading
mechanisms, including falls from
height and motor vehicle crashes, and
may occur in association with pelvic
and spine fractures. Plain radiographs
should be interpreted with attention
to two particular measurements. The
Bohler angle is measured on the lateral
radiograph and represents the angle
formed by two lines drawn tangent to
the anterior and posterior aspects of
the superior calcaneus. A normal angle
FIGURE 4. Jones Fracture of the Fifth Metatarsal
ranges from 20 to 40 degrees; fracture
of the calcaneus should be suspected
when the angle measures less than 20
degrees.
The “critical angle,” also known as
the angle of Gissane, is formed by the
downward and upward slopes of the
superior calcaneal surface, normally
measuring 130 to 145 degrees. An
angle greater than 145 degrees implies
fracture. The Bohler angle has been
shown to be more useful in identifying
calcaneal fractures in the acute setting,
November 2017 n Volume 31 Number 11 7
 but deliberate measurements rarely are
necessary for diagnosis.7 As with other
tarsal fractures, CT imaging in the
emergency department is recommended
for detailing fracture patterns and
pinpointing radiographically occult
injuries. Calcaneal stress fractures may
be seen in runners and other athletes,
and suspected cases can be detected by
MRI when plain films are normal.
The course of treatment for calcaneal
fractures can be determined by the
degree of displacement and articular
involvement. Small extra-articular
fractures without Achilles tendon
involvement, small anterior process
fractures, and suspected calcaneal
stress fractures may be treated with
non-weightbearing immobilization,
and referral for prompt outpatient
evaluation. Most other fractures,
including intra-articular and displaced
fractures, must be considered for
operative management and warrant
orthopedic consultation.
CRITICAL DECISION
Which fractures require
an emergent orthopedic
consultation or urgent outpatient
referral?
Due to the potential need for
operative management and the risk of
complications, Lisfranc injuries and
other tarsal fractures with displacement
or intra-articular involvement
warrant orthopedic consultation in
the emergency department. Urgent
outpatient follow up often is sufficient
for nondisplaced or avulsion fractures.
It should be noted that compartment
n Failing to appreciate the limitations of plain radiographs for the detection
of certain injury patterns. This oversight can result in missed or delayed
diagnoses of clinically significant fractures.
n Improperly classifying a proximal fifth metatarsal fracture, leading to
misguided injury management.
n Neglecting to provide anticipatory guidance and appropriate referrals, an
oversight that can compromise recovery and return to play. Most athletic foot
injuries benefit from specialized care.
8 Critical Decisions in Emergency Medicine
syndrome can occur in association with
fractures (eg, Lisfranc and calcaneal
fractures) and other significant soft-
tissue injuries to the foot. Although
challenging to diagnose, any clinically
suspected or confirmed case of
compart­ment syndrome requires
emergent orthopedic consultation
and management. Similarly, open
fractures and injuries with associated
neurovascular compromise generally
demand immediate orthopedic
consultation in the emergency
department.
Metatarsal fractures most commonly
are the result of direct trauma or
rotational injury. Most of these
injuries are amenable to nonoperative
management, and can be identified
consistently with plain radiographs.
Nondisplaced fractures can be treated
with a hard-sole shoe and gradually
increased weightbearing as tolerated.
Fractures with greater than 3 mm of
displacement or more than 10 degrees
of angulation should be considered for
closed reduction and non-weightbearing
immobilization with orthopedic
follow-up care.
Because of the increased weight­
bearing load on the first metatarsal,
treatment of these injuries may require
greater vigilance. Phalangeal fractures,
with the exception of unstable or
displaced fractures of the great toe,
generally are benign and heal well with
minimal intervention. Most can be
treated with buddy taping, hard-sole
shoes, and weightbearing as tolerated.
CRITICAL DECISION
How should fractures of the
proximal fifth metatarsal be
managed?
Sports-related fractures of the
proximal fifth metatarsal are common
forefoot injuries that often result from
sudden force involving inversion or
adduction. The patient’s examination
invariably demonstrates tenderness at
the base of the fifth metatarsal with or
without swelling/ecchymosis. Standard
foot radiographs are indicated based
on the Ottawa rules; advanced imaging
in the emergency department is not
warranted. Fractures are classified and
treated according to the anatomical
“zone” in which they occur.
Zone 1
Tuberosity avulsion fractures, also
known as “pseudo-Jones” fractures,
occur most proximally in zone 1.
These injuries are characterized by
a transverse or oblique fracture line
that may be extra-articular or extend
to the tarsometatarsal articulation.
Because of reliable healing rates with
minimal intervention, treatment is
conservative with a hard-sole shoe or
boot immobilization with progressive
weightbearing. Surgery rarely is required
for displaced fractures with significant
articular involvement or symptomatic
nonunion.
Zone 2
The Jones fracture (Figure 4)
represents a zone 2 injury at the
metaphyseal-diaphyseal junction
resulting from forceful adduction to
a plantarflexed foot. Radiographs
demonstrate a transverse fracture
approximately 1.5 to 3 cm distal to the
tip of the metatarsal that extends to the
medial cortex and intermetatarsal space.
In contrast to zone 1 injuries, these
fractures occur in a vascular watershed
zone, which hinders healing and makes
delayed union or nonunion more likely.
Such injuries should be managed more
aggressively with a posterior short
leg splint, strict non-weightbearing
precautions, and a prompt orthopedic
referral. While these injuries may be
treated nonoperatively, competitive
athletes are pursuing early surgical
management with increasing frequency
to hasten healing time and expedite
return to play.8
Zone 3
Zone 3 injuries typically are defined
as stress fractures that occur in the
proximal diaphyseal region. Unlike
acute zone 1 and 2 fractures, these
insults may be preceded by an insidious
onset of pain related to activity that
is characteristic of bony stress injury.
Similar to zone 2 fractures, they are
prone to nonunion and initially should
be treated with immobilization and
firm weightbearing restrictions. These
fractures often warrant early surgical
intervention in competitive athletes;
prompt orthopedic referral is advised.
CRITICAL DECISION
Which patients can benefit from
a routine outpatient orthopedic
or sports medicine evaluation?
In addition to the many types of
fractures already described, athletes
are prone to other osseus and soft-
tissue injuries of the foot that will limit
their ability to compete. Although
these injuries rarely warrant emergent
attention, appropriate counseling
and outpatient referral will allow
for additional diagnostic imaging if
necessary and careful guidance back to
athletic participation.
Stress Fractures
Active patients with stress injuries
are more likely to present with insidious
pain related to repetitive microtrauma
rather than a single, sudden force.
They occur on a spectrum from stress
reaction to stress fracture, depending
on the degree and duration of insult.
Such patients often describe pain that is
worsened by activity and improved with
rest.
Stress fractures, which represent
1% to 7% of all athletic injuries, most
commonly affect the lower extremities.9
They are classified as high- or low-risk
based upon the capacity to heal without
complications. High-risk fractures occur
in the talus, tarsal navicular, and fifth
metatarsal. Conservative management
with non-weightbearing immobilization
n An understanding of foot anatomy and a systematic approach to the physical
examination is critical for establishing a working diagnosis for foot pain.
n Lisfranc injuries can be radiographically occult; an understanding of these injury
patterns coupled with a high index of suspicion can prevent misdiagnosis and
poor outcomes.
n Advanced imaging in the emergency department may be necessary to
diagnose radiographically occult but clinically significant injuries that require
urgent orthopedic evaluation and treatment.
n A bony stress injury should be considered in any athlete with progressive,
activity-related pain and negative radiographs. Such patients should be
counseled on activity restrictions and referred for an orthopedic or sports
medicine evaluation, as advanced imaging may be warranted to achieve a
definitive diagnosis.
is important, and surgical management also depends on the severity of injury
is sometimes necessary to achieve union and may be aided by reinforced
or expedite a return to competitive footwear.
athletics.
Low-risk stress fractures, including
Plantar Fasciitis
those of the calcaneus, cuneiforms, Heel pain, a complaint frequently
and cuboid, tend to heal well with encountered in both acute and
simple activity modification and a brief outpatient settings, usually manifests
period of immobilization. Except in subacute or chronic symptoms. While
more advanced cases, plain radiographs the differential diagnosis might include
will be normal. MRI is considered to calcaneal stress injury and entrapment
be the imaging modality of choice for neuropathies such as tarsal tunnel
stress reactions, while CT can be useful syndrome, plantar fasciitis is the leading
for characterizing injuries that have cause of plantar heel pain, reaching a
progressed to fracture. peak incidence between ages 40 and
Generally speaking, advanced 60 years.10 The disorder results from
imaging is not pursued in the repetitive microtrauma and strain to the
emergency department. However, plantar fascia at its origin on the medial
early identification of high-risk stress calcaneal tubercle.
fractures is crucial to good outcomes, The classic patient history includes
and suspected cases should be referred sharp “first-step pain” upon waking,
for outpatient evaluation by an accompanied by focal tenderness at
orthopedic surgeon or sports medicine the medial calcaneal tubercle. While
specialist. x-rays may demonstrate a heel spur,
this finding carries little diagnostic
Turf Toe significance. The initial treatment of
Injury to the first metatarso­ plantar fasciitis consists of conservative
phalangeal joint is common in athletes. measures such as rest, physical therapy,
A sprain of this joint is referred to as nonsteroidal anti-inflammatory drugs
“turf toe” due to the increased incidence (NSAIDs), and prefabricated or custom
seen in sports played on artificial orthotics. Recalcitrant cases may benefit
surfaces. These injuries result from from night splinting or novel treatment
hyperextension of the joint and are modalities such as extracorporeal shock
graded in severity. Low-grade sprains wave therapy. Surgical management
typically heal in a matter of weeks, with plantar fasciotomy occasionally
while high-grade injuries may warrant is necessary. Corticosteroid injections
immobilization and outpatient advanced should be used with caution due to a
imaging. Return to competitive athletics number of potential complications.
November 2017 n Volume 31 Number 11 9
 CASE RESOLUTIONS
■ CASE ONE
Despite the radiographic inter­
pretation, clinical suspicion for a
Lisfranc injury remained high. A
careful review of the military recruit’s
x-rays suggested subtle widening
between the lateral border of the medial
cuneiform and medial edge of the base
of the second metatarsal. CT imaging
revealed small avulsion fractures of
the second and third metatarsal bases,
which were consistent with a Lisfranc
fracture. The patient was evaluated by
an orthopedic surgeon and discharged
home in a posterior splint with strict
instructions to avoid bearing weight on
the injured foot. He underwent open
reduction and internal fixation 2 weeks
later.
■ CASE TWO
The young basketball player was
diagnosed with a zone 1 proximal fifth
metatarsal fracture, also known as a
tuberosity avulsion fracture or pseudo-
Jones fracture. She was immobilized
in a walking boot with instructions
to bear weight as tolerated. She
was seen by the team physician for
follow up visits at 1 and 6 weeks.
In the interim, she transitioned out
of the boot and progressed through
a rehabilitation program with the
team’s athletic trainer. She was pain-
free and demonstrated both clinical
and radiographic healing at 6 weeks,
and was cleared to return to play.

Tendinopathy index of suspicion for an occult, but

Acute tendon ruptures involving
the foot are uncommon. More likely,
athletes with tendon disorders will
present with subacute or chronic
pain related to tendinopathy.
“Tendinopathy” encompasses a variety
of painful conditions affecting tendons
secondary to overuse and associated
with degenerative, rather than
inflammatory, histopathologic changes.
Tendinopathies affecting the
foot include peroneal tendinopathy
(lateral ankle/foot pain), posterior
tibial tendinopathy (medial ankle/
foot pain), and insertional Achilles
tendinopathy (posterior heel pain).
While numerous treatment options have
been described in the literature, initial
treatment generally consists of activity
modification, NSAIDs, and physical
therapy with a focus on eccentric
strengthening exercises.
Summary
Foot injuries in athletes and
active individuals can range from
radiographically occult fractures to
chronic tendon conditions. A careful
history and systematic approach to the
physical examination should enable
the emergency physician to formulate
a good working diagnosis and select
appropriate imaging. Acute traumatic
injuries can be evaluated initially
with plain radiographs based upon
established clinical decision rules.
Advanced imaging should be considered
when radiographs are normal but a high
clinically significant, fracture remains.
Injuries involving the midfoot,
hindfoot, and proximal fifth metatarsal
warrant special attention, as they pose
a greater risk of morbidity and may
require operative management. Activity
modification and rehabilitation is the
mainstay of treatment for chronic foot
injuries. Prompt orthopedic or sports
medicine follow up is advisable for most
conditions that do not otherwise require
a more urgent orthopedic consultation
in the emergency department.
REFERENCES
1. Stiell IG, Greenberg GH, McKnight RD, et al. A
study to develop clinical decision rules for the use of
radiography in acute ankle injuries. Ann Emerg Med.
1992;21(4):384-390.
2. Bachmann LM, Kolb E, Koller MT, et al. Accuracy of
Ottawa ankle rules to exclude fractures of the ankle and
mid-foot: systematic review. BMJ. 2003;326(7386):417.
3. Ross G, Cronin R, Hauzenblas J, Juliano P. Plantar
ecchymosis sign: a clinical aid to diagnosis of occult
Lisfranc tarsometatarsal injuries. J Ortho Trauma.
1996;10(2):119-122.
4. Siddiqui NA, Galizia MS, Almusa E, Omar IM.
Evaluation of the tarsometatarsal joint using
conventional radiography, CT, and MR imaging.
Radiographics. 2014;34(2):514-531.
5. Bancroft LW, Kransdorf MJ, Adler R, et al. ACR
appropriateness criteria acute trauma to the foot.
J Am Coll Radiol. 2015;12(6):575-581.
6. von Knoch F, Reckord U, von Knoch M, Sommer
C. Fracture of the lateral process of the talus in
snowboarders. J Bone Joint Surg Br. 2007;89(6):772-
777.
7. Knight JR, Gross EA, Bradley GH, et al. Boehler’s angle
and the critical angle of Gissane are of limited use in
diagnosing calcaneus fractures in the ED. Am J Emerg
Med. 2006;24(4):423-427.
8. Kerkhoffs GM, Versteegh VE, Sierevelt IN, et al.
Treatment of proximal metatarsal V fractures in athletes
and non-athletes. Br J Sports Med. 2012;46(9):644-648.
9. Mayer SW, Joyner PW, Almekinders LC, Parekh SG.
Stress fractures of the foot and ankle in athletes. Sports
Health. 2014;6(6):481-491.
10. Lareau CR, Sawyer GA, Wang JH, DiGiovanni
CW. Plantar and medial heel pain: diagnosis and
management. J Am Acad Orthop Surg. 2014;22(6):
372-380.

10 Critical Decisions in Emergency Medicine

The LLSA Literature Review
Angioedema is defined as swelling of
subcutaneous or submucosal tissues
secondary to enhanced vascular
permeability, a process that allows
movement of fluid from the vascular
space into the interstitial space.
The differing pathophysiology between
the two broad types of angioedema,
bradykinin-mediated and histamine-
mediated, will help guide treatment.
Histamine-mediated angioedema can
manifest with or without the associated
features of anaphylaxis, including
urticaria or respiratory, circulatory, or
gastrointestinal symptoms. The mainstay
of treatment for this class of angioedema
includes epinephrine, histamine blockers,
and corticosteroids.
Nonhistaminergic angioedema is
caused by bradykinin accumulation. This
may result from decreased metabolism
in the case of ACE inhibitor (ACEI) use,
low functional C1-inhibitor protein levels
in hereditary angioedema (HAE) type
1, abnormal C1-inhibitor function in
HAE type 2, or acquired C1-inhibitor
(C1-INH) deficiency due to consumption
from an underlying lymphoproliferative
disorder or antibody production.
If a clear etiology is unknown,
treatment with epinephrine followed by
H1/H2 antagonists and corticosteroids
is appropriate. While these agents are
not effective for bradykinin-mediated
Critical Decisions in Emergency Medicine’s series of LLSA reviews features articles articles from ABEM’s 2017 Lifelong Learning and
Self-Assessment Reading List. Available online at acep.org/llsa and on the ABEM website.
Angioedema in
the Emergency
Department
By Zheng Ben Ma, MD, and Andrew Eyre, MD
The Brigham and Women’s/Massachusetts General Hospital Harvard Affiliated
Emergency Medicine Residency, Boston, MA
Moellman JJ, Bernstein, JA, Lindsell, C, et al. A consensus parameter for the evaluation and management of
angioedema in the emergency department. Acad Emerg Med. 2014;21(4):469-484.
angioedema, they are not contraindicated
and are potentially lifesaving. The only
acute treatment readily available for ACEI
angioedema is fresh frozen plasma (FFP),
which contains variable amounts of C1-
INH. However, FFP infusions may worsen
symptoms in hereditary cases.
Several novel therapies have been
FDA-approved for the management of
HAE attacks. These include icatibant (a
bradykinin 2-receptor antagonist that
blocks the vascular effects of bradykinin),
ecallantide (a kallikrein inhibitor, which
limits bradykinin formation), and C1-INH
concentrate. These theoretically are effective
for the treatment of HAE attacks and ACE
inhibitor-induced angioedema. However,
data is limited for non-HAE patients.
The first step in treating angioedema
is to manage the airway and address any
respiratory or circulatory abnormalities,
without initially focusing on the
underlying cause or classification of the
disease. The physical evaluation should
be focused on assessing the vital signs,
airway, skin, and abdomen. Edema of
the lips, tongue, soft palate, or posterior
pharynx should warrant closer attention.
Stridor or a hoarse voice warrants direct
visualization of the base of the tongue and
larynx by nasopharyngoscopy or video
laryngoscopy. An examination of the
airway structures should help determine
if intubation is indicated.
While no laboratory test is immediate­
ly available to help guide initial treatment,
C4 and tryptase levels drawn during
an angioedema attack are useful in
distinguishing bradykinin or histamine-
mediated etiologies during follow up.
Complement C4 levels are persistently
low in HAE cases, while tryptase may
be elevated in anaphylaxis or other mast
cell-mediated disorders manifesting as
angioedema.
KEY POINTS
n Angioedema is a physical
sign triggered by differing
pathophysiological mechanisms.
n When a clear cause is
unknown, try intramuscular
epinephrine, antihistamines, and
corticosteroids.
n Regardless of the etiology, initial
management should be focused
on correcting airway, breathing,
and circulatory abnormalities.
n Although novel therapies for
bradykinin-mediated hereditary
angioedema are emerging, data
on efficacy is limited.
n Ancillary testing, including C4 and
tryptase levels drawn during the
angioedema attack, are helpful
only during follow up to help
clarify triggering mechanisms.
November 2017 n Volume 31 Number 11 11
 The
Critical
Procedure
By Nafiha Islam, MD
Dr. Islam is a research fellow in the
Department of Emergency Medicine at
Orange Park Medical Center in Orange Park,
Florida.

Reviewed by Steven J. Warrington, MD, MEd

Ultrasound-Guided Percutaneous
Suprapubic Catheter Placement
Percutaneous suprapubic urinary bladder catheterization (suprapubic cystostomy)
sometimes is necessary for urinary drainage when placement of a transurethral
catheter is contraindicated or unsuccessful. In the emergency setting, a suprapubic
catheter (SPC) may be required for patients with urethral obstruction and/or trauma.

Contraindications Risks and Benefits Acute SPC placement can alleviate

(absolute/relative)
n No urine in bladder
n Overlying infection
n Coagulopathy
n Existing or history of pelvic cancer/
radiation, lower abdominal/pelvic
surgery, suprapubic mesh (potential
adhesions or displaced organs)
Percutaneous suprapubic
catheterization is a well-established
procedure that can be done safely and
accurately by trained physicians at the
bedside. Risks including cutaneous
or bladder bleeding, bowel/bladder
perforation, vaginal/uterine injury,
procedure failure, and potential
infection.
an obstructed bladder before it
perforates, provide a method of
sampling urine, and help overcome
urethral injuries or other obstructive
processes. The long-term benefits of
suprapubic over urinary catheters
include increased patient satisfaction
and a lower risk of urethral trauma,
stricture formation, and urinary tract

12 Critical Decisions in Emergency Medicine

infection. The reasons for improved
patient satisfaction may include the
procedure’s ability facilitate normal
voiding and the lack of urinary
incontinence secondary to sphincter
dysfunction.
Alternatives
Urethral catheter placement should
be used as a first-line treatment, when
not contraindicated. If the urethral
route is not an option, consideration
of the patient’s situation and discussion
with consultants may provide
alternative placement locations.
For example, suprapubic catheter
placement in the operating room
may be preferred for a patient with
a traumatic injury that requires a
laparotomy.
If a urine sample is indicated and
cannot be obtained by traditional
means, suprapubic aspiration may be
an alternative.
Reducing Side Effects
Ultrasound use is becoming more
common and can be used to:
1. Verify that there is enough urine
in the bladder to perform the
procedure;
2. Detect overlying loops of bowel or
other gynecological structures; and
3. Allow for direct visualization
during the procedure.
Special Considerations
The procedural steps will vary
depending on the SPC kit each
institution has at its disposal. Some
kits utilize direct puncture with a
stainless trocar or obturator device,
while others employ a trocar system
with guidewire (using the Seldinger
method). If indicated, cystoscopy also
can be used for SPC placement.
Alternatively, a central venous
catheterization kit can be used if an
SPC kit is unavailable.

TECHNIQUE
1. Obtain informed consent
and explain the procedure in
detail.
2. Gather needed equipment
(eg, syringes, needles, scalpel
blade, SPC kit). Identify what
equipment is included in your
kit.
3. Position the patient supine
with his/her legs spread
apart.
4. Palpate the bladder and
verify full distention using
ultrasound.
5. Clean the lower abdominal
area. Trim the hair in the
suprapubic region if needed.
6. Apply an antiseptic solution from the pubis to the umbilicus needle obturator into the catheter and lock it into
(repeat step twice, and allow area to dry). the port. Connect a 60-mL syringe to the port,
7. Apply sterile drapes and palpate the insertion site. and (under ultrasound guidance) advance the
8. Inject lidocaine subdermally (10-mL syringe, 25-gauge needle) at catheter-obturator unit until urine is aspirated.
the insertion site. Unlock the needle obturator from the catheter,
9. Use ultrasound guidance (with sterile set-up) to advance the advance the catheter 5 cm over the obturator, and
needle (alternating anesthesia and aspiration) into the bladder then completely remove the obturator needle.
until urine enters the syringe. 11. Follow the SPC kit instructions; if the catheter has
10. If using the Seldinger/guidewire technique: Feed the a balloon tip, inflate the balloon as directed.
guidewire into the bladder, remove the needle from guidewire, 12. Attach the extension tube to catheter, and
make a 4-mm incision at the insertion site, and thread the dilator connect to urinometer or a leg bag.
and/or catheter unit into the bladder. 13. Undrape the patient, apply drain dressing around
If using a catheter/needle/obturator technique: Make a the catheter, and secure the suprapubic tube in
4-mm incision at the insertion site (No. 11 blade), insert the place with tape.

November 2017 n Volume 31 Number 11 13

 A 55-year-old man with syncopal episodes.

The Critical ECG

Polymorphic ventricular tachycardia (VT), probable torsade de By Amal Mattu, MD, FACEP
Dr. Mattu is a professor, vice chair, and
pointes, rate 250. The rhythm is a wide complex tachycardia with varying director of the Emergency Cardiology
Fellowship in the Department of
QRS morphologies. The two main diagnostic considerations in this
Emergency Medicine at the University
setting are polymorphic ventricular tachycardia and atrial fibrillation with of Maryland School of Medicine in
Baltimore.
Wolff-Parkinson-White syndrome. The latter, however, tends to be much
more irregular; in this case, the rhythm is fairly regular. Torsade de pointes
is a specific type of polymorphic VT that is associated with prolonged QT during sinus rhythm. The condition also is
marked by a characteristic rhythmic appearance of the QRS complexes, which gradually vary from larger to smaller
and back again in amplitude, and they also gradually change in axis. A formal diagnosis of torsade de pointes would
require an ECG in sinus rhythm demonstrating a prolonged QT interval. This patient did, in fact, demonstrate this
finding on his baseline ECG. He had recently increased his dosage of methadone, a medication known to prolong
the QT interval.

From Mattu A, Brady W, ECGs for the Emergency Physician 2. London: BMJ Publishing; 2008:11,23. Reprinted with permission.

14 Critical Decisions in Emergency Medicine

 Full Stop
Withdrawal from
Atypical Agents

LESSON 22

By Aimee Mishler, PharmD, BCPS and Frank Lovecchio, DO,

FACEP, ABMT
Dr. Mishler is an emergency medicine pharmacist at Maricopa Medical Center
in Phoenix, Arizona. Dr. Lovecchio is the vice chair for research at the University
of Arizona College of Medicine and co-medical director of the Banner Poison
Drug and Information Center at Maricopa Medical Center.
Reviewed by Christian Tomaszewski, MD, MS, MBA, FACEP

OBJECTIVES
On completion of this lesson, you should be able to:
CRITICAL DECISIONS
1. Identify common withdrawal symptoms.
n What presentations should raise clinical
2. Describe withdrawal syndromes caused by common
nonprescription substances. suspicion for withdrawal, and what factors
3. List common prescription medications with high
increase a patient’s risk of complications?
withdrawal potential. n How should intrathecal baclofen withdrawal
4. Explain the signs of withdrawal from baclofen, be managed?
venlafaxine, and clonidine, and describe the best course
of treatment. n What is the best way to approach venlafaxine
withdrawal?
FROM THE EM MODEL
n How should clonidine withdrawal be managed
14.0 Psychobehavioral Disorders
14.1 Substance Use Disorders emergently?
14.1.5 Withdrawal Syndromes

With substance abuse on the rise, emergency physicians must be better prepared than ever to recognize
and manage the signs and symptoms of withdrawal. While such sequelae frequently are precipitated by drugs
of abuse, the discontinuation of commonly prescribed medications should not go overlooked. Timely identification
and treatment is the best defense against the potentially deadly complications of withdrawal from any offending
substance.1 Of particular concern are baclofen, venlafaxine, and clonidine, which can be especially problematic if
stopped abruptly.

November 2017 n Volume 31 Number 11 15

 CASE PRESENTATIONS
■ CASE ONE
A tremulous, delirious 32-year-
old man arrives via ambulance. His
wife explains that he has been acting
“funny” for several days, but his
confusion has worsened today and he
has become increasingly combative
and restless. She called 911 when he
appeared to be talking to people who
were not in the room.
On arrival, his vital signs are
heart rate 134, blood pressure 93/62,
respiratory rate 34, and temperature
40.6°C (105.1°F). The emergency
clinician begins to rule out infectious
etiologies, including sepsis and
meningitis. A review of the patient’s
medical records reveals a spinal cord
injury sustained in a car accident
6 years ago, for which he has been
receiving intrathecal baclofen for the
last 3 years. His wife explains that
the pump was refilled 8 months ago.
CRITICAL DECISION
What presentations should raise
clinical suspicion for withdrawal,
and what factors increase a
patient’s risk of complications?
Initial withdrawal symptoms from
various classes of substances, both drugs
of abuse and common prescription
medications, often overlap. This can
make it difficult to differentiate between
substances, making early identification
of the offending substance all the more
important to offset the potentially life-
threatening sequelae of withdrawal.1,2
Not only can many withdrawal
syndromes present similarly in the acute
phase, symptoms of drug cessation must
be distinguished from a re-emergence
of the disease the medication has
been prescribed to treat. If multiple
medications or interacting agents were
initiated or discontinued at the same time,
or the patient has not been compliant, it
may be particularly difficult to accurately
identify the withdrawal syndrome.3
The World Health Organization
defines withdrawal as a group of
symptoms of variable clustering and
16 Critical Decisions in Emergency Medicine
An additional workup reveals a normal
ECG, significantly elevated creatine
kinase (CK), and evidence of an acute
kidney injury.
■ CASE TWO
A 29-year-old woman presents with
1 day of headache, fatigue, dizziness,
restlessness and a sudden increase in
depression. She describes the headache
pain as severe and constant, and says
that it sometimes feels like someone is
“tasing” her head. Her vital signs are
blood pressure 162/98, heart rate 101,
respiratory rate 18, and temperature
37.6°C (99.7°F).
She has a longstanding history
of depression and has been taking
venlafaxine for the last 4 years (150
mg/day). She reveals that she recently
decided to stop taking her medication
because she had been feeling so
much better and thought it was no
severity occurring upon absolute or
relative cessation of a substance after
repeated and usually prolonged and/or
high-dose use.4 Withdrawal from some
common substances results in somatic
symptoms, whereas others manifest
psychological problems (Table 1). Patient
complaints often are generalized and
may even overlap with complications of
unrelated diseases.3
Depending on the offending substance,
symptoms can appear at cessation and
last for hours or even days. For example,
benzodiazepines commonly are divided
into three groups based upon their half-
life duration: short-acting (<12 hours),
intermediate-acting (12-24 hours), and
long-acting (>24 hours). Withdrawal
begins earlier following the cessation of
short-acting drugs; conversely, it begins
later with long-acting agents.
The timeframe in which symptoms
present depends both on patient-
specific factors (eg, history of use, other
substances ingested, hepatic and renal
functions, etc.) and substance-specific
factors (eg, half-life, type of metabolism,
purity, route of administration, etc.)
and may have significant interpersonal
longer needed. Her last dose was
approximately 48 hours ago.
■ CASE THREE
A 9-year-old boy is brought into
the emergency department by his
mother, who states the child has had
insomnia and has been complaining of
a headache and chest pain for 2 days.
He weighs 29 kg and has no past
medical history, other than attention
deficit hyperactive disorder. His vital
signs are blood pressure 136/92, heart
rate 120, respiratory rate 20, and
temperature 37.1°C (98.8°F).
His mother explains that the boy’s
psychiatrist changed his medication
1 week ago. He was taking clonidine
(0.2 mg 2x/day); however, a decision
was made to stop the drug by decreas­
ing the dose slowly over several days
(tapered 0.1 mg every 3 days). Now on
day 8, he is taking 0.1 mg twice daily.
variations (Table 2).
The true frequency of drug-related
emergencies is difficult to determine and
apt to be higher than represented in the
literature; withdrawal, in particular,
often goes unreported. By some
estimates, nearly 30% of emergency
department visits are precipitated by drug
overdose or abuse, noncompliance, and
adverse reactions.6 The most common
offending substances are drugs of abuse,
anticonvulsants, and antibiotics. The
causes of drug-related complications are
classified into the following categories:6
• Untreated indication
• Inappropriate drug selection
• Incorrect dose
• Omission/noncompliance
• Adverse drug reaction
• Drug interaction
• Drugs without an indication
Overdose or withdrawal from drugs
of abuse is oft discussed, taught in
training, and described in the literature.
However, it is important to be aware
that many prescription medications
can cause serious complications if
discontinued abruptly or tapered too
aggressively (Table 3).
 When a patient presents with common
withdrawal symptoms after recently
stopping a high-risk drug, withdrawal
from that medication should be taken
into consideration. Not only can abrupt
discontinuation from many medications
lead to withdrawal syndromes, cessation
allows the disease being treated to
reemerge, which may further complicate
the clinical picture.
CRITICAL DECISION
How should intrathecal baclofen
withdrawal be managed in the
emergency department?
Baclofen is a common medication
used to treat spasticity due to spinal cord
injury, cerebral palsy, multiple sclerosis,
and numerous other disorders. It works
by binding to the GABA B receptors,
resulting in GABA B agonism.7 Due to its
lipophobic properties, oral baclofen does
not easily cross the blood-brain barrier, a
disadvantage that can necessitate higher
doses with greater side effects, including
spasticity. Many of these complications
can be avoided by administering
intrathecal (rather than oral) baclofen.7
The baclofen pump, a battery-
operated device typically implanted into
the abdomen, houses the medication
reservoir. The pump also includes
a catheter access port that allows
drug administration by bypassing the
reservoir. This feature is particularly
important when troubleshooting
potential problems. The catheter is used
to deliver medication to a specific site
within the thoracolumbar region for
optimal effect, and also is equipped
with alarms that signal if the battery is
low or the reservoir level is insufficient.8
Currently, the only manufacturer
of the baclofen pump is Medtronic;
TABLE 1. Common Symptoms
of Withdrawal (overlap exists)1-3
Somatic Psychological
Diaphoresis Agitation
Tremor Insomnia
Malaise Anxiety
Tachycardia Dysphoria
Nausea
Vomiting
Diarrhea
the company should be contacted for
pump interrogation if a malfunction is
suspected.
There are two strategies for drug
delivery through the baclofen pump:
scheduled bolus dosing or continuous
infusion. On average, patients will require
doses between 50 and 100 mcg/day; some
may require up to 900 mcg/day with
frequent titrations until the optimal dose
is discovered.9,10 Since the medication is
delivered directly into the cerebral spinal
fluid (CSF), patients receiving intrathecal
baclofen are extremely sensitive to minor
dose adjustments; numerous reports of
both overdose and withdrawal have been
described.7 The pump should be refilled
every 6 to 12 weeks, depending on the
dose, and replaced every 3 to 5 years.11
Signs and Symptoms
If intrathecal baclofen must be
halted, it should be withdrawn over
several weeks to avoid potentially
life-threating complications. Abrupt
discontinuation precipitates the return
of baseline spasticity as well as pruritus,
anxiety, and disorientation.9 More
severe symptoms such as hyperthermia,
tachycardia, rhabdomyolysis, myoclonus,
seizure, disseminated intravascular
coagulopathy, cardiac arrest, and coma
also have been reported.7,9 In addition,
withdrawal poses a risk of neurological
complications such as hallucinations,
delirium, delusions, and paranoia.7
Baclofen appears to inhibit monoamine
neurotransmitter systems via its GABA-
like activity. During withdrawal, a release
of norepinephrine and dopamine can
spark autonomic arousal, delusions, and
hallucinations.10 Complications have been
reported within 12 hours, but more often
within 48 to 96 hours after intrathecal
baclofen interruption.10,11 The differential
diagnosis of baclofen withdrawal should
include autonomic dysreflexia, malignant
hyperthermia, serotonin syndrome,
neuroleptic malignant syndrome, sepsis,
and meningitis.7,10,12
In 2002, the Food and Drug
Administration (FDA) issued a warning
against baclofen withdrawal syndrome
after 27 cases were reported (6 of which
were fatal).9,12,13 Most patients who
experience symptoms do so when they are
close to their refill schedule.7 However,
there are a number of other reasons
for baclofen withdrawal, including
preventable errors during medication
refill and pump programming, as well
as pump malfunctions such as catheter
migration, catheter kinks, battery failure,
and empty reservoirs.7,9
Treatment
The management of intrathecal
baclofen withdrawal should include
early pump interrogation to identify
malfunctions or an empty reservoir.
While waiting for interrogation, an
abdominal x-ray (anteroposterior
and lateral views) can be helpful to
identify the catheter location and rule
out migration. A catheterogram or
surgical exploration of the pump may be
necessary.7
Pharmacological treatment options
include benzodiazepines or propofol.
Oral baclofen often is ineffective,
even at doses up to 160 mg, due to
downregulation of the GABA B receptors
in chronic users and the inability
to achieve therapeutic levels in the
cerebrospinal fluid.7,9,13 Much like
baclofen, benzodiazepines and propofol
bind to the GABA receptor; however,
these agents bind specifically to the
GABA A receptor, which is not affected
by prolonged baclofen use. While the
amount of benzodiazepine or propofol
necessary to control symptoms varies
from patient to patient, the goal of
treatment with either of these agents is
symptomatic control of spasticity and the
avoidance of seizures while maintaining
airway, breathing, and circulation
(ABCs).7,13 Patients may require higher
than average doses.
Dantrolene and cypropheptadine
have been used successfully to treat
intrathecal baclofen withdrawal;
however, evidence to support the use
of these drugs is lacking.9,13 Temporary
lumbar intrathecal catheter placement
also has been used successfully to
restore drug delivery via infusion at
pre-withdrawal doses.7 The ultimate
treatment in such cases is the restoration
of pump integrity and intrathecal
administration of the drug. It also is
important to administer intravenous
fluid hydration and consider the patient’s
levels of creatinine kinase, urine
November 2017 n Volume 31 Number 11 17
 myoglobin, serum creatinine, and blood
urea nitrogen.10 Ultimately, the pump
necessitates emergent interrogation in
any patient withdrawing from baclofen.
CRITICAL DECISION
What is the best way to approach
venlafaxine withdrawal?
Venlafaxine is an antidepressant used
for the treatment of depression, generalized
anxiety and panic disorders, obsessive
compulsive disorder, post-traumatic stress
disorder, and other illnesses. The drug
inhibits norepinephrine and serotonin
uptake (SNRI) at normal doses (150-
300 mg), with a higher selectivity for
serotonin over norepinephrine at doses
between 75 and 150 mg daily.14,15 While
withdrawal symptoms vary depending on
each patient’s current dose, an increase
in dopamine levels also is seen at doses
between 150 and 300 mg.14
Signs and Symptoms
The most common symptoms
associated with venlafaxine withdrawal
are fatigue, irritability, dizziness,
headache, gastrointestinal disturbance,
and anxiety.14-16 More severe sequelae
include paresthesia, ataxia, sleep
disturbances, vertigo, arthralgia,
tachycardia, fever, and shock-like
sensations, which have been reported
with both SNRI and selective serotonin
reuptake inhibitor (SSRI) withdrawal.14-16
These sensations have been described
as simple paresthesias such as burning
or tingling to more severe electric shock
waves that course through the body. They
include the head, neck, chest, abdomen
and extremities, and may be worsened by
movement.14
It is unknown how long venlafaxine
must be taken before withdrawal
symptoms can emerge, and what — if any
n Many substances share the initial symptoms of withdrawal; early identification of
the offending substance is imperative to avoid severe complications.
n Oral baclofen is unlikely to be efficacious for intrathecal baclofen withdrawal.
n Antidepressants and antipsychotics need to be discontinued slowly over several
weeks to avoid complications.
18 Critical Decisions in Emergency Medicine
TABLE 2. Onset of Withdrawal from Common Substances1-3
Substance Typical Onset Time
Ethanol Minor symptoms: 24 hrs
Severe symptoms: 72 hrs
BenzodiazepinesA Typical peak: 5-9 days
Methadone Peak 72-96 hrs
Heroin Minor symptoms: 6-12 hrs
Peak: 36-72 hrs
Stimulants Crash phase: 30 min
Withdrawal phase:
2-4 days
Nicotine Start within 2-4 hrs
A
Highly variable due to differing half-lives between agents within the class
— comorbidities can affect their severity.
In clinical trials, participants experienced
symptoms after 8 weeks of use; however,
complications have been confirmed
within as few as 4 weeks of cessation.14,17
While symptoms usually begin 1 to 3
days after the last dose, mild complaints
have been reported within hours after a
single missed pill.15-17
In chronic users, serotonin receptors
are downregulated; during cessation of
venlafaxine, withdrawal of serotonin
reuptake reduces the available level of
presynaptic serotonin.14 (In other words,
less serotonin binds to fewer receptors,
leading to withdrawal symptoms.)
Sensory-related complications appear
to be linked to the role of serotonin
in coordinating sensory and motor
functions. Serotonergic neurons help
coordinate motor output by inhibiting
sensory functioning. Therefore, sensory
inhibition is withdrawn when venlafaxine
is discontinued, allowing paresthesias and
shock-like sensations to manifest.14
Treatment
Withdrawal from venlafaxine has
been successfully treated with SSRIs,
supporting the theory that serotonin plays
a key role in withdrawal. Patients have
Typical Duration
1-2 weeks
10+ days (variable based on kinetics)
14+ days
7-10 days
Severe depression lasts ≈48 hrs
Minor depressive symptoms may
last several weeks
Up to 4 weeks
been successfully treated with sertraline
(50 mg/day) after venlafaxine cessation
(150 mg), with a complete remission
of symptoms by day 2. Other reports
suggest a successful taper over several
weeks (≤6 weeks) with the concomitant
administration of fluoxetine to prevent
severe symptoms.17
Although the reinitiation of
venlafaxine will combat withdrawal
symptoms, the reason for the initial
discontinuation should be considered.
Additional doses may not be the best
remedy for withdrawal in patients who
stopped taking the medication due to
intolerance. If the drug is restarted
emergently but ultimately must be
discontinued, a prolonged taper over
several weeks with close monitoring is
recommended. There are no guidelines
regarding a definitive taper schedule;
discontinuation should be handled on a
case-by-case basis, extending titration
frequency or returning to previous doses
as needed based on the patient’s response.
Ultimately, the restoration of serotonin
and/or norepinephrine levels should be
the first-line treatment for venlafaxine
withdrawal, and may be achieved by
initiating an SSRI or restarting the
medication. However, a longer treatment
course of venlafaxine (4 years vs 1 year)
coupled with chronic alcohol use may
negate the therapeutic effects of SSRIs.
CRITICAL DECISION
How should clonidine withdrawal
be managed emergently?
Clonidine is a centrally acting alpha2
agonist that frequently is used to manage
hypertension, opioid withdrawal,
Tourette syndrome, and attention deficit
hyperactive disorder. The drug’s central
alpha activity stimulates vasomotor
receptors that inhibit sympathetic outflow
to both peripheral vasculature and the
heart, leading to a reduction in peripheral
vascular resistance and heart rate (thus
decreasing blood pressure and heart
rate).18 Clonidine is available as a tablet,
transdermal patch, and IV solution used
via epidural for intractable pain. The
effects of the drug can be seen within 30
to 60 minutes, and typically last for 6 to
10 hours when given orally. Although the
transdermal patch delivers medication at a
constant rate over 7 days, it can take 2 to
3 days to reach peak effect.18
Signs and Symptoms
Symptoms of withdrawal from
clonidine include reversal of the drug’s
antihypertensive effects, increased
sympathetic activity (eg, sweating,
TABLE 3. Prescription Drugs with High Withdrawal Potential
Class of Medication
Amphetamines
Anticonvulsants1
Antidepressants
• Selective serotonin reuptake inhibitor
• Serotonin-norepinephrine reuptake
inhibitor
• Tricyclic antidepressants
• Dopamine/norepinephrine reuptake
inhibitor
Antipsychotics
Barbiturates
Beta-blockers2
Benzodiazepines
Dopamine agonists
Hypnotics
Opioids
Steroids
1
Abrupt discontinuation of anticonvulsants may result in increased seizure frequency,
but also may manifest common withdrawal symptoms.
2
Abrupt discontinuation may lead to rebound hypertension, tachycardia, or ischemia.
palpitations), and central nervous system
symptoms such as anxiety, insomnia,
nausea, and vomiting.18 Myocardial
infarction, ventricular tachycardia,
and significant hypertension have been
described after clonidine cessation, even
in those not taking the medication for
blood pressure control.19-22
Most severe cases of withdrawal
have been reported after longer use
at higher doses; however, symptoms
can arise in as few as 6 days, even in
patients taking doses as low as 0.1 mg/
daily.19-21 Withdrawal has been describe
with abrupt discontinuation, as well
as in those attempting to taper off the
medication.21 Significant increases in
blood pressure and heart rate also have
been reported, but these complications
appear to level off within 2 to 4 days.20
Urinary catecholamine
Examples
Dexmethylphenidate
Dextroamphetamine/amphetamine
Methylphenidate
Carbamazepine Topiramate
Lamotrigine
Citalopram Fluoxetine
Paroxetine Sertraline
Venlafaxine Amitriptyline
Bupropion
Clozapine Haloperidol
Fluphenazine Risperdal
Olanzapine Ziprasidone
Phenobarbital
Carvedilol Metoprolol
Propranolol
Alprazolam Diazepam
Lorazepam Temazepam
Amantadine Pramipexole
Ropinirole
Eszopiclone Zaleplon
Zolpidem
Hydrocodone Methadone
Morphine Oxycodone
Tramadol
Dexamethasone
Methylprednisolone
Prednisone
levels may spike during clonidine
withdrawal, much as they do in
cases of pheochromocytoma. This
rise corresponds with an increase in
heart rate, blood pressure, and mean
arterial pressure. 20 Withdrawal from
central-acting agents such as clonidine
presents differently than beta-adrenergic
blockers and other antihypertensive
medications. While an abrupt cessation
of any antihypertensive medication can
precipitate a return of hypertension,
other agents do not affect urine
catecholamine levels and are less likely
to produce central symptoms such as
anxiety or insomnia.
Treatment
A combination of alpha and beta
blockade has been reported to successfully
combat the hypertension and tachycardic
effects of clonidine withdrawal; however,
these agents do not appear to be effective
for managing insomnia or anxiety.21
Researchers also have described symptom
reduction using a combination of
prazosin, an alpha1 blocker (10 mg 2x/
day); atenolol, a selective beta1 blocker
(50 mg/day); and chlordiazepoxide, a
benzodiazepine (10 mg 2x/day).
There are other reports of successful
treatment with the combination
propranolol, a nonselective beta blocker;
phentolamine, an alpha1 blocker; and
labetalol, a nonselective beta blocker
with alpha-blocking activity; and
various combinations of vasodilators (eg,
hydralazine or nitroprusside) and beta
blockers.19-21 Administering clonidine,
when appropriate, may be the optimal
treatment to combat the sympathetic and
central effects of withdrawal.
Patients should be monitored closely;
additional tests also should be considered,
including an ECG, head CT, and
measurements of urinary catecholamine,
troponin, and serum creatinine levels.
Although there is no definitive taper
schedule, the drug should be reduced
gradually with close monitoring. In most
cases, decreasing the dose and frequency
over a period of 7 to 10 days is prudent.
Summary
Withdrawal syndromes from both
prescription and nonprescription drugs
commonly are encountered in the
emergency department. Regardless of
November 2017 n Volume 31 Number 11 19
 CASE RESOLUTIONS
■ CASE ONE
The confused man’s wife provided
contact information for the pump
manufacturer, which was contacted for
device interrogation. Meanwhile, an
abdominal x-ray was used to confirm
proper pump placement.
The patient received an IV fluid
bolus of normal saline (2 liters) followed
by maintenance fluids and several
IV diazepam boluses (in escalating
doses, starting at 10 mg). A total of
220 mg of diazepam was administered
over 4 hours. Cardiopulmonary and
end-tidal carbon dioxide monitoring
were continued, and no significant
interventions were needed.
An empty reservoir ultimately was
identified as the culprit of the patient’s
the offending substance, the initial signs
of withdrawal often present similarly,
potentially clouding the differential
diagnosis. Many prescription drugs
require prolonged tapering before
discontinuation, and should not
be stopped abruptly. In particular,
withdrawal from baclofen, venlafaxine,
and clonidine poses a significant risk of
morbidity and must be identified early.
If intrathecal baclofen withdrawal is
suspected, interrogation and restoration
of the pump is the ultimate therapy.
Oral baclofen may be ineffective due
to its inability to effectively cross
the blood-brain barrier. Withdrawal
from venlafaxine presents much like
withdrawal from SSRIs, and symptoms
may be negated with either the
reinitiation of venlafaxine at previous
doses or the administration of an SSRI.
Clonidine withdrawal may mimic
n Assuming only drugs of abuse cause withdrawal, or failing to obtain an adequate
medication history.
n Delaying interrogation of a baclofen pump when a patient presents with signs
of withdrawal.
n Assuming a medication can be abruptly discontinued without complications.
20 Critical Decisions in Emergency Medicine
withdrawal symptoms, and a refill was
carried out. His symptoms were completely
resolved within 6 hours of restarting
intrathecal baclofen. His creatine kinase
levels trended down and his acute kidney
injury resolved over the next 48 hours.
■ CASE TWO
The young woman with a severe
headache underwent a head CT and
laboratory tests, including a basic
metabolic panel (BMP), complete blood
count (CBC), and coagulation studies; all
were within normal limits.
Psychiatry was consulted, and it was
determined that the patient’s symptoms
were the result of venlafaxine withdrawal.
She was admitted for observation and
venlafaxine (150 mg/day) was reinitiated.
Her symptoms resolved completely within
pheochromocytoma via sympathetic
outflow, which manifests hypertension,
tachycardia, and increased urinary
catecholamine levels. Treatment with
alpha and beta blockade (eg, using
labetalol) can negate the cardiovascular
effects; however, it may not be effective
against the symptoms of clonidine
withdrawal.
REFERENCES
1. Kosten TR, O’Connor PG. Management of drug and
alcohol withdrawal. NEJM. 2003;348(18):1786-1795.
2. West R, Gossop M. Overview: a comparison of
withdrawal symptoms from different drug classes.
Addiction. 1994;89(11):1483-1489.
3. Hodding GC, Jann M, Ackerman IP. Drug withdrawal
syndromes. West J Med. 1980;133(5):383-391.
4. Management of substance abuse: withdrawal state.
2016. Available at: http://www.who.int/substance_
abuse/terminology/withdrawal/en/. Accessed
November 21, 2016.
5. Streetdrugs: a drug identification guide. Long Lake,
MN: Publishers Group West, LLC; 2015: 50-53, 60-
67,74-76.
6. Patel P, Zed PJ. Drug-related visits to the
emergency department: how big is the problem?
Pharmacotherapy. 2002;22(7):915-923.
12 hours. She was educated regarding
withdrawal syndrome and cautioned to
taper off the medication slowly.
■ CASE THREE
The young boy underwent a workup
that included an ECG, BMP, CBC, and
coagulation studies, which were normal.
A head CT and abdominal ultrasound
showed no abnormalities. The patient
received intravenous sodium chloride
(0.9% bolus) and clonidine (0.1 mg), and
his blood pressure returned to normal.
He and his mother were instructed to
return to his previous clonidine dosage
(0.2 mg 2x/day), monitor his blood
pressure twice daily, and follow up with
the boy’s psychiatrist for a different
titration schedule.
7. Watve SV, Sivan M, Raza WA, Jamil FF. Management
of acute overdose or withdrawal state in intrathecal
baclofen therapy. Spinal Cord. 2012;50(2):107-111.
8. Medtronic. (2003). SynroMed® II programable
pumps. Retrieved from: http://manuals.medtronic.
com/wcm/groups/mdtcom_sg/@emanuals/@era/@
neuro/documents/documents/contrib_240049.pdf.
9. Mohammed I, Hussain A. Intrathecal baclofen
withdrawal syndrome-a life-threatening complication
of baclofen pump: a case report. BMC Clin
Pharmacol. 2004;4:1-5.
10. Leo RJ, Baer D. Delirium associated with baclofen
withdrawal: a review of common presentations
and management strategies. Psychosomatics.
2005;46(6):503-507.
11. Kao LW, Armin Y, Kirk MA, Turner MS. Intrathecal
baclofen withdrawal mimicking sepsis. J Emerg Med.
2003;24(4):423-427.
12. Coffey RJ, Edgar TS, Francisco GE, et al. Abrupt
withdrawal from intrathecal baclofen: recognition
and management of a potentially life-threatening
syndrome. Arch Phys Med Rehabil. 2002;83(6):735-
741.
13. MedWatch Safety Alert – Lioresal (baclofen injection)
2002. Available at: [http://www.fda.gov/medwatch/
safety/2002/baclofen.htm]. Accessed October 18,
2017.
14. Reeves RR, Mack JE, Beddingfield JJ. Shock-
like sensations during venlafaxine withdrawal.
Pharmacotherapy. 2003;23(5):678-681.
15. Sabljic V, Ruzic K, Rakun R. Venlafaxine withdrawal
syndrome. Psychiatr Danub. 2011;23(1):117-119.
16. Luckhaus C, Jacob C. Venlafaxine withdrawal
syndrome not prevented by maprotiline but
resolved by sertraline. Int J Neuropsychopharmacol.
2001;4(1):43-44.
17. Parker G, Blennerhasett J. Withdrawal reactions
associated with venlafaxine. Aust N Z J Psychiatry.
1998;32(2):291-294.
18. Sica DA. Centrally acting antihypertensive agents: an
update. J Clin Hyertens (Greenwich). 2007;9(5):399-
405.
19. Berge KH, Lanier WL. Myocardial infarction
accompanying acute clonidine withdrawal in a
patient without a history of ischemic coronary artery
disease. Anesth Analg. 1991;72(2):259-261.
20. Geyskes GG, Boer P, Dorhout Mees EJ. Clonidine
withdrawal mechanisms and frequency of rebound
hypertension. Br J Clin Pharmac. 1979;7(1):55-62.
21. Reid JL, Campbell BC, Hamilton CA. Withdrawal
reactions following cessation of central alpha
adrenergic receptor agonists. Hypertension. 1984;6(5
Pt 2):II71-75.
22. Nakagawa S, Yamamoto Y, Koiwaya Y. Ventricular
tachycardia induced by clonidine withdrawal. Br
Heart J. 1985;53(6):654-658.
 The Critical Image
A 46-year-old man presents with stridor. According to first responders, he By Joshua S. Broder, MD, FACEP
had attempted to open a soda bottle using his teeth when the cap become Dr. Broder is an associate professor and the
dislodged, and was either swallowed or aspirated. The patient appears to be in residency program director in the Division
of Emergency Medicine at Duke University
acute respiratory distress and is moved immediately to the resuscitation bay. Medical Center in Durham, North Carolina.

His vital signs are blood pressure 144/94, heart rate 130, respiratory rate 30,
temperature 37.3°C (99.2°F), and oxygen saturation 100% on room air. He
is stridulous and tripoding. Despite his tachypnea, he can answer questions
intermittently. No foreign bodies are visible in the oropharynx. He is tachycardic;
the remainder of his examination is unremarkable.

Soft-tissue radiographs of the neck are obtained while preparations for airway management are made.

A B

Bottle cap

Bottle cap
posterior Trachea
to airway

A. An anterior-posterior (AP) soft-tissue x-ray shows a circular B. A lateral soft-tissue x-ray confirms that the foreign
radioopaque foreign body, corresponding to a bottle cap. The body is posterior to the airway, within the esophagus.
object is seen en-face, with an “O” shape. This suggests that the
object lies in the esophagus (remembered by the British spelling
“oesophagus”).

CASE RESOLUTION
The patient was taken to the operating room and intubated to prevent
aspiration; the foreign body was then removed endoscopically.

November 2017 n Volume 31 Number 11 21

 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 entirety.

QUESTIONS Submit your answers online at acep.org/newcriticaldecisionstesting; a score of 75%

or better is required. You may receive credit for completing the CME activity any time
within three years of its publication date. Answers to this month’s questions will be
published in next month’s issue.

1
A Lisfranc injury may disrupt which articulation?
A. Calcaneonavicular 6 Which of the following mechanisms can lead to
turf toe?
B. Metatarsophalangeal A. Hyperextension at any metatarsophalangeal joint
C. Talonavicular B. Hyperextension at the first metatarsophalangeal
D. Tarsometatarsal joint
C. Hyperflexion at any metatarsophalangeal joint

2 A recreational long-distance runner presents with

subacute, progressive midfoot pain localized to
the tarsal navicular. What is the most appropriate
D. Hyperflexion at the first metatarsophalangeal
joint

7
management of a patient with a suspected bony or Which of the following radiographic findings is
avulsion fracture? consistent with a Lisfranc injury?
A. Activity modification, referral to physical therapy, A. Anteroposterior (AP) view showing a step off at
and orthopedics the medial borders of the first metatarsal and
B. Hard-sole shoe, partial weightbearing, and follow medial cuneiform
up with primary care physician B. AP view showing a step off at the medial borders
C. Immobilization, non-weightbearing precautions,
of the second metatarsal and middle cuneiform
and orthopedic follow up
C. AP view showing a step off at the medial borders
D. Immobilization, weightbearing as tolerated, and
of the third metatarsal and lateral cuneiform
orthopedic follow up
D. Oblique view showing a step off at the lateral
borders of the fourth metatarsal and cuboid

3 Which of the following conditions is most likely to

warrant orthopedic consultation in the emergency
department?
A. Avulsion fracture of the tarsal navicular
8 An 18-year-old man presents with acute foot and
ankle pain following a snowboarding injury. What
radiographic finding might be expected?
B. Displaced talar neck fracture
A. Fracture of the anterior process of the calcaneus
C. Jones fracture
D. Second metatarsal shaft fracture B. Fracture of the body of the talus
C. Fracture of the lateral process of the talus
D. Fracture of the neck of the talus
4 Which bones comprise the midfoot?
A. Cuneiforms, metatarsals, navicular, cuboid
B.
C.
Cuneiforms, navicular, cuboid
Metatarsals, navicular, cuboid
9 Which of the following radiographic
measurements are associated with a calcaneal
fracture?
D. Talus, calcaneus, navicular, cuboid
A. Decrease in Bohler angle and decrease in the

5 Which combination of motions allows for supination angle of Gissane

of the foot? B. Decrease in Bohler angle and increase in the
A. Dorsiflexion, eversion, adduction angle of Gissane
B. Dorsiflexion, inversion, abduction C. Increase in Bohler angle and decrease in the
C. Plantarflexion, inversion, abduction angle of Gissane
D. Plantarflexion, inversion, adduction D. Increase in Bohler angle and increase in the
angle of Gissane

22 Critical Decisions in Emergency Medicine


10 A Jones fracture occurs at which anatomical site of the
fifth metatarsal? 16 A 42-year-old man presents with return of
spasticity previously controlled by an intrathecal
baclofen pump. What is the best treatment
A. Distal metaphyseal-diaphyseal junction
B. Proximal diaphysis regimen for this patient?
C. Proximal metaphyseal-diaphyseal junction A. Intrathecal pump interrogation, symptom
control with baclofen tablets, and a switch from
D. Proximal tubercle
intrathecal to oral baclofen
B. Intrathecal pump interrogation, symptom control

11 Which of the following symptoms commonly are

associated with withdrawal?
A. Agitation, lacrimation, and euphoria
B. Diaphoresis, tachycardia, and agitation
C. Euphoria, hallucinations, and nausea
D. Nausea, mydriasis, and hallucinations
with dantrolene, and temporary intrathecal
baclofen infusion
C. Intrathecal pump interrogation, symptom control
with lorazepam, and restoration of intrathecal
baclofen
D. Temporary baclofen infusion

12 A patient presents with nausea, tremors, insomnia,

and agitation. He has prescriptions for oxycodone/
17 What precipitates the neuropsychiatric symptoms
acetaminophen, paroxetine, and docusate, but says
he has been out of all medications for about 2 days.
Which agent(s) might be causing his withdrawal
symptoms?
A. Docusate
B. Oxycodone/acetaminophen
C. Oxycodone/acetaminophen and paroxetine
D. Paroxetine
commonly associated with the cessation of
baclofen?
A. Direct GABAB activity during withdrawal
B. Epinephrine release during withdrawal
C. GABAB upregulation and release of glutamate
during withdrawal
D. Monoamine neurotransmitter activity and
release of norepinephrine and dopamine during
withdrawal

18 When do symptoms of venlafaxine withdrawal

13 Which of the following symptom(s) should raise typically manifest?

suspicion for venlafaxine withdrawal? A. 1 hour after a missed dose
A. Fatigue and irritability B. 1-3 days after cessation, but mild symptoms
have been reported within hours of a missed
B. Hallucinations
dose
C. Hypotension
C. 2-4 days after cessation
D. Visual disturbances D. 4-8 hours after cessation

14
Which class of prescription drugs is least likely to
cause withdrawal complications?
19 Which of the following symptoms are most likely
to result from clonidine withdrawal?
A. Antipsychotics A. Ataxia, lethargy, and seizure
B. Diuretics B. Confusion, mydriasis, and hypertension
C. Dopamine agonists C. Hypertension, palpitations, and anxiety
D. Opioids D. Tachycardia, seizure, and vertigo

15 Which symptoms should raise suspicion for baclofen
withdrawal? 20
What is the optimal treatment to combat the
sympathetic and central effects of clonidine
withdrawal?
A. Spasticity, lethargy, tachycardia
B. Spasticity, miosis, pruritus A. Atenolol
C. Spasticity, tachycardia, hyperthermia B. Clonidine
C. Phentolamine
D. Spasticity, tinnitus, seizure
D. Propranolol

ANSWER KEY FOR OCTOBER 2017, VOLUME 31, NUMBER 10

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

November 2017 n Volume 31 Number 11 23

 Drug Box
DELAFLOXACIN
By Adam J. Smith, MD and Frank Lovecchio, DO, MPH, FACEP,
Maricopa Medical Center, Phoenix, Arizona
Delafloxacin is a fluoroquinolone recently approved for the
treat­ment of bacterial skin and soft-tissue infections, including
methicillin-resistant Staphylococcus aureus.
Mechanism of Action
Inhibits DNA gyrase (topoisomerase II) and topoisomerase
IV enzymes, which are required for bacterial DNA replication,
transcription, repair, and recombination.
Indications
• Treatment of acute bacterial skin and skin structure infections
caused by susceptible isolates. It has activity against staph­
ylococci (including methicillin-resistant strains), Gram-negative
bacteria (including Pseudomonas aeruginosa and Entero­
bacteriaceae), and some anaerobes (including Clostridium
difficile); does not have activity against enterococci.
• Noninferior to the combination of vancomycin and
aztreonam.
• Reserve for patients who do not respond to or tolerate
first-line antimicrobial agents.
Dosing
Adult: (Oral) 450 mg every 12 hours for 5-14 days;
(IV) 300 mg every 12 hours for 5-14 days
Renal (eGFR 15 to 29 mL/minute/1.73 m2): 200 mg IV every
12 hours
Not recommended in patients with end-stage renal disease
requiring hemodialysis.
Precautions
Contraindicated in patients with hypersensitivity to delaflox­acin
or other fluoroquinolones. Common adverse effects include
diarrhea and nausea (8%) and headache (3%).
FDA Boxed Warning
Fluoroquinolones are associated with disabling and potentially
irreversible serious adverse reactions that may occur together,
including tendinitis and tendon rupture, peripheral neuropathy,
QTc prolongation and CNS effects. May exacerbate muscle
weakness related to myasthenia gravis; avoid use in patients with
known history of the disease.
Tox Box
TRICYCLIC ANTIDEPRESSANTS
By Clifford Masom, MD, and Christian A. Tomaszewski, MD, MS,
MBA, FACEP, University of California, San Diego
Tricyclic antidepressants (TCAs) are pharmacologically related
drugs for treating depression, neuralgic pain, migraines, enuresis,
and ADHD. Although supplanted by selective serotonin reuptake
inhibitors, TCAs still have a high mortality index; just 1-2 pills
(>15 mg/kg) can be fatal in children.
Pharmacokinetics (not dialyzable)
• Peak concentration 2-8 hours ­• High protein binding
­• Highly lipophilicity ­• High volume of distribution
­• Hepatic metabolism
Mechanism of Action
Sodium channel and alpha blockade; serotonin/norepinephrine
reuptake inhibition; antimuscarinic
Clinical Presentation (>5 mg/kg)
• Central nervous system: Agitation, lethargy, seizures
• Cardiac: QRS prolongation, ventricular dysrhythmias, hypotension
• Pulmonary: Aspiration, acute respiratory distress syndrome
• Toxidrome: May be antimuscarinic (anticholinergic)
Diagnostic Evaluation
• Monitor for ECG changes (eg, early tachycardia, prolonged QRS,
or terminal R wave in aVR/Brugada pattern).
• Measure glucose and electrolytes and/or venous blood gas
levels if acidosis is suspected. TCA levels are delayed and not
relevant.
Patient Management
• ­Decontaminate with activated charcoal if <1 hour post ingestion
and airway is protected.
­• Intubate early.
­• Provide cardiovascular support with IVF and norepinephrine.
­• Treat wide QRS (>110 msec), especially if hypotensive.
­• Sodium (Na) bicarbonate (1-2 mEq/kg IV bolus)
— May repeat every 3-5 min, avoid pH >7.5
— May substitute Na acetate in cases of Na bicarbonate shortage
­• ­Hypertonic saline 3% 1-2 mEq/kg IV (second line)
• ­Treat seizures with benzodiazepines and propofol (if refractory).
• ­ Discharge if asymptomatic with normal ECG 6 hours post
ingestion.