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Volume 23 • Number 11
In This Issue
Lesson 21
Lesson 22
Necrotizing Soft Tissue Infections . . . . . . . . . . . . . . . . . . . . . . . . Page 2
The Drug Box . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 8
The LLSA Literature Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 9
Hyperbaric Therapies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 11
The Critical Image . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 21
CME Questions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 22
The Critical ECG . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 24
Contributors
2009
July
H. Edward Seibert, MD, FACEP, and Alexander Fernandez, MD, wrote “Necrotizing Soft
Tissue Infections.” Dr. Seibert is an assistant residency director at Thomas Jefferson University Hospital,
Department of Emergency Medicine, Philadelphia, Pennsylvania. Dr. Fernandez is chief resident at Thomas
Jefferson University Hospital, Department of Emergency Medicine.
Amal Mattu, MD, FACEP, reviewed “Necrotizing Soft Tissue Infections.” Dr. Mattu is coordinator of
the Emergency Medicine/Internal Medicine Combined Residency Training Program and director of academic
development in the Emergency Medicine Residency Training Program at the University of Maryland School
of Medicine in Baltimore.
Colin G. Kaide, MD, FACEP, UHM, Sorabh Khandelwal, MD, UHM, and S. Erica Brown, MD,
wrote “Hyperbaric Therapies.” Dr. Kaide is an associate professor of emergency medicine at Ohio
State University Medical Center, Columbus, Ohio. Dr. Khandelwal is an associate professor of emergency
medicine and director of hyperbaric medicine at Ohio State University Medical Center. Dr. Brown is a clinical
instructor of emergency medicine at Ohio State University Medical Center.
Sharon E. Mace, MD, FACEP, reviewed “Hyperbaric Therapies.” Dr. Mace is professor of medicine
at the Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, director of the
Observation Unit and director of Pediatric Education and Quality Improvement at the Cleveland Clinic
Foundation, and faculty for the MetroHealth Medical Center Emergency Medicine Residency Program in
Cleveland, Ohio.
Frank LoVecchio, DO, MPH, FACEP, reviewed the questions for these lessons. Dr. LoVecchio is
research director at the Maricopa Medical Center Emergency Medicine Program and medical director of the
Banner Poison Control Center, Phoenix, Arizona, and a professor at Midwestern University/Arizona College
of Osteopathic Medicine in Glendale, Arizona.
Louis G. Graff IV, MD, FACEP, is Editor-in-Chief of Critical Decisions. Dr. Graff is professor of
traumatology and emergency medicine at the University of Connecticut School of Medicine in Farmington,
Connecticut.
Contributor Disclosures
In accordance with ACCME Standards and ACEP policy, contributors to Critical Decisions in Emergency Medicine must
disclose the existence of significant financial interests in or relationships with manufacturers of commercial products that
might have a direct interest in the subject matter. Authors and editors of these Critical Decisions lessons reported no such
interests or relationships.
Method of Participation
This educational activity consists of two lessons with a posttest and should take approximately 5 hours to complete.
To complete this educational activity as designed, the participant should, in order, review the learning objectives, read the
lessons, and complete the online posttest. Release date May 1, 2009. Expiration date April 30, 2012.
Accreditation Statement
The American College of Emergency Physicians (ACEP) is accredited by the Accreditation Council for Continuing
Medical Education (ACCME) to provide continuing medical education for physicians. ACEP designates this educational
activity for a maximum of 5 AMA PRA Category 1 Credits™. Physicians should only claim credit commensurate with
the extent of their participation in the activity. Approved by ACEP for 5 Category I credits. Approved by the American
Osteopathic Association for 5 hours of AOA Category 2-B credit (requires passing grade of 70% or better).
Target Audience
This educational activity has been developed for emergency physicians.
Critical Decisions in Emergency Medicine
Necrotizing Soft Tissue
Infections
Lesson 21
H. Edward Seibert, MD, FACEP, and Alexander Fernandez, MD
n Objectives
On completion of this lesson, you
should be able to:
1. Describe the different types of
necrotizing soft tissue infection
(NSTI).
2. Identify the bacterial causes of NSTI.
3. Discuss the variable clinical
presentations of NSTI.
4. Differentiate NSTI from other types of
skin and soft tissue infections.
5. Discuss the importance of early
surgical intervention in the treatment
of NSTI.
6. Identify the appropriate antibiotics
for the treatment of NSTI.
n From the EM Model
4.0 Cutaneous Disorders
4.4 Infections
Emergency department visits
for skin and soft tissue infections
are common and increasing in
frequency. Emergency physicians
encounter uncomplicated infections
like cellulitis and abscess on a
daily basis. Necrotizing soft tissue
infections (NSTIs) are an uncommon
but lethal subset of these infections.
NSTIs are characterized by extensive
inflammation, necrosis, and
thrombosis involving the dermis,
subcutaneous tissue, superficial
fascia, deep fascia, or muscle.
Necrotizing cellulitis, necrotizing
fasciitis, and myonecrosis are more
specific terms that denote the level of
soft tissue involvement.1,2
Hippocrates described NSTI in
the 5th century BC, “...the erysipelas
would quickly spread widely in
all directions. Flesh, sinews and
bones fell away in large quantities...
Fever was sometimes present and
sometimes absent... There were
many deaths. The course of the
disease was the same to whatever
part of the body it spread.”3 During
the Civil War, NSTIs were called
“hospital gangrene,” and the term
“necrotizing fasciitis” was coined
by Wilson in 1952. NSTIs share a
common pathophysiology, clinical
presentation, and prognosis and,
consequently, a common diagnostic
approach, treatment, and prognosis.4
Case Presentations
n Case One
A 50-year-old woman presents
to the emergency department with
2
pain in her left groin. She had been
recently discharged from the hospital
following a cardiac catheterization.
The pain began gradually but became
progressively more severe over the
course of 3 days. She reports a mild
fever but denies any other symptoms.
Her past medical history is significant
for diabetes mellitus, coronary artery
disease, and hypertension. Vital
signs are blood pressure 110/86,
pulse rate 68, respiratory rate 20,
and temperature 35.9°C (96.6°F).
Physical examination reveals an obese
woman in moderate discomfort. She
has tenderness to palpation of her
right lower quadrant, and a large
hematoma is present in her right
groin with surrounding erythema.
No purulent drainage is noted, but on
deep palpation of the site soft tissue
crepitus is appreciated.
n Case Two
A 41-year-old man who speaks no
English presents to the emergency
department with a chief complaint
of redness to his right upper thigh
and inability to urinate secondary
to extreme pain. Through family
members translating, he states that
he does not feel like himself. He
describes the pain as constant and
severe and says that makes it very
difficult to sit or lie in a comfortable
position. He reports having an oral
temperature of 38°C (100.4°F) about 2
days prior to arrival in the emergency
department and occasional chills. He
denies any past medical history or
current medication use. Vital signs are
July 2009 • Volume 23 • Number 11
Critical Decisions
• When should NSTI be suspected?
• How can NSTI be differentiated from other, less
life-threatening, soft tissue infections?
• What role do radiologic studies have in the diagnosis of
NSTI?
• What is the treatment for NSTI?
blood pressure 107/65, pulse rate 91,
respiratory rate 20, and temperature
36.6°C (97.8°F). Physical examination
reveals a slender man in obvious
distress because of pain. A large area
of erythema covers the anterior and
medial aspects of his right thigh.
Palpation of the affected area reveals
warm, tender, erythematous skin,
without any signs of crepitus. His
genital examination is normal.
n Case Three
A 55-year-old man with a history
of poorly controlled diabetes presents
to the emergency department with
scrotal swelling and pain that began
3 days ago while he was pushing
a car. He rates his pain as a 7 on
a scale of 10 and states that it has
been constant. He has not taken any
medicines for the pain. He denies
fever, dysuria, and penile discharge.
Vital signs are blood pressure 92/46,
pulse rate 128, respiratory rate 16,
and temperature 36.9°C (98.5°F).
Physical examination reveals a man
resting comfortably on his stretcher.
His scrotum is swollen and mildly
erythematous, with tenderness to
palpation diffusely, but greater on
the left. No crepitus or fluctuance is
palpated.
CRITICAL DECISION
When should NSTI be suspected?
Patient characteristics associated
with NSTI include diabetes mellitus,
peripheral vascular disease, alcohol
abuse, end-stage renal disease,
injection drug use, liver cirrhosis,
adrenal insufficiency, and cancer. In
approximately 15% of cases, however,
the patient has no comorbidities.1,5,6
Group A streptococcus, in particular,
• What antibiotics are appropriate for the treatment of
NSTI, and how has this changed with the emergence of
methicillin-resistant Staphylococcus aureus (MRSA)?
• What role do adjunct therapies play in the treatment of
NSTI?
is a cause of NSTI in young, otherwise
healthy patients.7
NSTI typically occurs following
some sort of break in the skin
that allows bacteria to enter the
subcutaneous tissue. NSTI can arise
at the site of surgical incisions and
decubitus ulcers. Often this skin
trauma is trivial, though, and NSTI
has been described following minor
abrasions, contusions, insect bites,
subcutaneous insulin injections, and
intravenous line placement. NSTI can
also occur without any apparent skin
defect or preceding event. In one case
series, less than half of patients with
NSTI had an identifiable portal of
entry.5,8 The most common location
for NSTI is the lower extremities,
although it can affect the upper
extremities, head and neck, trunk,
and perineum (Fournier gangrene) as
well.5,6
With necrotizing fasciitis, the
progression of skin findings reflects
the underlying pathology of the
disease. Bacterial proliferation occurs
within the superficial fascia (tissue
between the skin and deep fascia
overlying the muscles) causing
local inflammation. Although not
completely understood, it is thought
that the bacteria produce enzymes
like hyaluronidase, which degrade
the fascia and allow infection to
spread along fascial planes. This
corresponds to the early clinical
stage of necrotizing fasciitis, which is
characterized by erythema, swelling,
warmth, and tenderness. This
stage is generally indistinguishable
from severe cellulitis except that in
necrotizing fasciitis, the tenderness
can extend beyond the apparent
area of skin involvement. Patients
with necrotizing fasciitis can have
severe pain that is disproportionate
to cutaneous findings. Blood vessels
in the superficial fascia become
thrombosed resulting in ischemia
of the overlying skin. Subsequently,
blisters or bullae form in the
intermediate clinical stage, where skin
fluctuance and induration are also
seen.
In the late stages of necrotizing
fasciitis, advanced liquefactive
necrosis leads to the formation
of hemorrhagic bullae and dusky
discoloration of the skin that can
progress to frank gangrene.7,9 In
one case series, 100% of patients
who presented to the emergency
department with hemorrhagic bullae
had necrotizing fasciitis.10 Destruction
of subcutaneous nerves leads to skin
anesthesia (which might precede
signs of skin necrosis), and gasforming organisms can be present
(in approximately 30% of NSTIs),
resulting in crepitus.7,9 Fever is seen
in roughly half of patients with NSTI,
and hypotension in less than 20%.5
Table 1 summarizes clinical features
that should prompt further evaluation
or treatment for NSTI.
Critical Decision
How can NSTI be differentiated
from other, less life-threatening soft
tissue infections?
Sometimes, clinical features alone
can make the diagnosis of NSTI,
particularly the finding of crepitus
in the right clinical setting. More
commonly, however, other diagnostic
modalities are needed. Clinical
features that differentiate NSTI from
3
Critical Decisions in Emergency Medicine
more benign soft tissue infections like
cellulitis are not always present, and
the diagnosis is frequently missed,
resulting in delays in treatment.
Reported rates of correct diagnosis at
the time of admission range from as
low as 15% to as high as 60%.1,5,6
The LRINEC (Laboratory Risk
Indicator for Necrotizing Fasciitis)
score is a tool derived from
retrospective data to distinguish
necrotizing fasciitis from other soft
tissue infections (Table 2). In this
system, results from the patient’s
CBC, serum chemistry, and C-reactive
protein (CRP) are given a score
depending on a range that the value
falls into. The scores are then added
together. The score was 6 or higher
in more than 90% of the study
patients who had necrotizing fasciitis
diagnosed retrospectively, and less
than 6 in 97% of a group of randomly
selected patients with cellulitis that
was used as a cohort.11 The LRINEC
score is described in multiple
review articles but has never been
prospectively validated. Because of
this, a score less than 6 should not be
used to rule out NSTI if it is clinically
suspected. There does not seem to
be any harm, however, in using a
score of 6 or more to justify further
evaluation for NSTI. Currently, there
are no prospectively validated clinical
decision rules for predicting NSTI.
Other nonradiologic methods
for diagnosing NSTI include frozen
Table 1.
Clinical features associated with
NSTI8,9
Bullae – particularly
hemorrhagic bullae
Crepitus
Rapid spread
Severe pain disproportionate to
cutaneous findings
Skin anesthesia
Systemic toxicity
Tenderness extending beyond
the region of apparent skin
involvement
4
section biopsy and the “finger test.”
To obtain a frozen section biopsy,
a 1-cm3 piece of tissue is excised
from the suspected area under local
anesthesia and sent to a pathologist
for immediate examination. The
pathologist then determines whether
or not NSTI is present. The “finger
test” requires that a 2-cm incision
be made down to the level of the
deep fascia under local anesthesia,
followed by digital probing. Positive
test findings include lack of bleeding,
murky dishwater pus and minimal
tissue resistance to finger dissection.9
These methods of diagnosis would,
in most cases, require a surgeon at
the bedside to perform the test and,
for frozen section biopsy, a willing
pathologist.
Tissue oxygen monitoring with
near-infrared spectroscopy is a
noninvasive method to identify NSTI
that has shown promising results.
Wang and Hung found that tissue
oxygen saturation levels less than
70% over the suspected area of
infection were 100% sensitive and
97% specific for NSTI. The study
included only 19 patients with NSTI,
however, and excluded patients with
chronic venous stasis, peripheral
vascular disease, shock, and systemic
hypoxia.9,12 It is also unlikely that
many emergency departments have
this technology readily available.
CRITICAL DECISION
What role do radiologic studies have
in the diagnosis of NSTI?
Radiologic studies should not delay
definitive treatment for obvious NSTI.
When there is suspicion for NSTI but
a paucity of physical examination
findings, radiologic studies can
actually expedite the diagnosis and
subsequent treatment by detecting
NSTI in its early stages. Plain
radiographs can be performed rapidly,
and if they show subcutaneous air in
the right clinical setting, no further
diagnostic studies are needed. The
absence of subcutaneous air does not
rule out NSTI, however. In one case
series, gas on plain radiographs was
only present in 17% of patients with
NSTI.5 The “flesh-eating bacteria,”
group A -hemolytic streptococci,
do not produce subcutaneous air
when they are the sole pathogen
causing NSTI.7 Plain radiographs
and ultrasonography are more
sensitive than clinical examination
for detecting subcutaneous air, and
computed tomography (CT) is more
sensitive than plain radiographs.13
Table 2.
Laboratory risk indicator for necrotizing fasciitis (LRINEC) score. From: Anaya D,
Dellinger EP. Necrotizing soft-tissue infection: diagnosis and management. Clin
Infect Dis. 2007;44:706. With permission from The University of Chicago Press.
Variable
C-reactive protein (mg/L)
WBC (per mm3)
Hemoglobin (g/dL)
Sodium (mmol/L)
Creatinine (mg/dL)
Glucose (mg/dL)
Value
>150
< or = 150
<15
15 to 25
>25
>13.5
11 to 13.5
<11
> or = 135
<135
< or = 1.6
>1.6
< or = 180
>180
Score
0
4
0
1
2
0
1
2
0
2
0
2
0
1
July 2009 • Volume 23 • Number 11
Bedside ultrasonography has
been used by emergency physicians
to diagnose Fournier gangrene
(typically a polymicrobial infection).
Ultrasonography will demonstrate
focal regions of high-amplitude
echoes with posterior acoustic
shadowing in the presence of
subcutaneous gas.14 It has also been
used to diagnose NSTI in the upper
and lower extremities using the
findings of “diffuse thickening of the
subcutaneous tissue accompanied by
a layer of fluid accumulation more
than 4 mm in depth along the deep
fascial layer, when compared with
the contralateral position on the
corresponding normal limb.”15 Even
for Fournier gangrene, though, CT
probably has greater specificity than
ultrasonography and is better for
demonstrating the extent of disease
involvement.16 In general, the role
of ultrasonography in diagnosing
NSTI is limited. However, emergency
physicians commonly use bedside
ultrasonography to evaluate soft
tissue infections for drainable fluid
collections; the presence of ultrasound
findings consistent with subcutaneous
gas in this setting should prompt
immediate treatment for NSTI.
The sensitivity and specificity
of CT for NSTI are unclear.
As mentioned, CT can detect
subcutaneous air better than plain
radiographs; it can also demonstrate
fascial thickening (a particularly
useful finding if the thickening is at
least twice that of the contralateral
side), fat infiltration or stranding
(linear soft tissue attenuation within
the fat), and focal fluid collections.
For NSTI of the trunk, CT can
reveal if the source of infection is
intraabdominal. Wysoki et al studied
CT characteristics of necrotizing
fasciitis in 20 patients with
pathologically proven necrotizing
fasciitis. Two of these patients had no
CT findings to suggest NSTI.13
Magnetic resonance imaging (MRI)
is not always an available option to
evaluate for NSTI and can be more
time consuming than CT, but it is
probably the most sensitive study.
Schmid et al evaluated the diagnostic
value of MRI in differentiating
necrotizing fasciitis from cellulitis.
MRI examinations performed over 4
years on 17 patients with clinically
suspected necrotizing fasciitis were
retrospectively reviewed. Final
diagnoses were necrotizing fasciitis
in 11 patients (proven surgically or at
autopsy) and cellulitis in 6 patients.
Thickening of the subcutaneous tissue
and an increase of signal intensity
on T2-weighted images and contrast
enhanced T1-weighted images were
seen on all 17 patients and, therefore,
do not differentiate cellulitis from
necrotizing fasciitis. They considered
the MRI to be positive for necrotizing
fasciitis only if deep fascial
involvement could be identified on
T2-weighted and contrast-enhanced
T1-weighted images. Using these
criteria, they identified all 11 cases
of necrotizing fasciitis and had one
false-positive; conferring a sensitivity
of 100% and specificity of 86%.17 Loh
et al demonstrated that the specificity
of MRI for NSTI is even lower than
this. They found that only 1 out of 22
patients with abnormally high signal
intensity on T2-weighted images
within deep fascial planes and 1
out of 13 patients with gadolinium
enhancement of the deep fascial
planes had necrotizing fasciitis. Most
of the patients had nonnecrotizing
cellulitis or abscess.18 Therefore,
MRI may be the best test for ruling
out NSTI due to its high sensitivity,
but can’t be used alone to make the
diagnosis. It must be interpreted in
the context of the clinical scenario
and physical examination. Of note,
MRI also tends to overestimate the
extent of infection compared to
surgical findings.17
The small numbers of patients in
even the largest studies evaluating
the use of radiologic imaging in
suspected NSTI make it difficult to
draw definitive conclusions regarding
which is best. The decision to use
one over another is, therefore, case
dependent, with many variables to
consider. It is important to remember
that the diagnosis of NSTI should be
made clinically, when possible, and
that radiologic studies should only
be ordered if they can be expected to
expedite the diagnosis and decrease
the time to definitive treatment.
Surgical consultation should not
be delayed when there is a strong
suspicion for NSTI.
CRITICAL DECISION
What is the treatment for NSTI?
The treatments for NSTI are
aggressive surgical débridement of
all necrotic tissue and intravenous
antibiotics. Treatment with antibiotics
alone, however, results in a mortality
rate approaching 100%, because
thrombosed blood vessels prevent
antibiotic delivery to the affected area.
Delays in surgery and incomplete
débridement are associated with
increased mortality. Necrotic tissue
should be debrided back until healthy,
bleeding tissue is seen at the wound
margins. In most cases, the patient is
brought back to the operating room
in 24 to 48 hours for reexploration of
the wound and further débridement,
if necessary. This process might
need to be repeated multiple times.
Frequently, large areas of skin must be
excised, and patients typically require
future skin grafting. Tissue cultures
should be obtained to guide antibiotic
therapy.4,5,8
CRITICAL DECISION
What antibiotics are appropriate for
the treatment of NSTI, and how has
this changed with the emergence of
MRSA?
Necrotizing fasciitis has
traditionally been divided into two
categories based on the bacteria
causing the infection. Type 1
necrotizing fasciitis is caused by
mixed aerobic and anaerobic bacteria.
It tends to begin at the site of surgical
incisions, mucosal tears, or where
skin breakdown is present in patients
with diabetes and peripheral vascular
disease. Type 1 necrotizing infections
are generally associated with
subcutaneous gas. Type 2 necrotizing
5
Critical Decisions in Emergency Medicine
fasciitis is caused by group A
streptococci, and can occur in young
patients without any comorbidities.
It has been described following
blunt trauma, muscle strain, and
chickenpox, as well as after surgery or
penetrating skin injury.19
More recent case series have
revealed the emergence of MRSA
as a cause of NSTI. MRSA was the
most common bacteria cultured from
patients with NSTI between 2001
and 2006 at a large urban hospital
in Texas. In most cases, MRSA was
the sole pathogen and thought to be
community acquired.20 Case series
from hospitals in California and
Taiwan have reported similarly high
incidences of MRSA in patients with
NSTI.6,21
Infectious Diseases Society of
America (IDSA) guidelines (from
2005) recommend antibiotic
therapy tailored to the specific
infection-causing pathogens. For
mixed infections (type 1), the
IDSA recommends ampicillinsulbactam plus clindamycin and
ciprofloxacin. A carbapenem as
a single agent is another option.
For patients with severe penicillin
hypersensitivity, they recommend
clindamycin or metronidazole
with an aminoglycoside or
fluoroquinolone with additional
coverage for staphylococcus if that
organism is present or suspected. For
streptococcus infection (type 2), the
IDSA recommends penicillin plus
clindamycin.19
Emergency physicians treating
NSTI do not typically know the
causative organism and must chose
antibiotics empirically. These
recommendations also do not take
into account the high incidence of
MRSA in NSTI that has been reported
since these guidelines came out.
More current recommendations
for empiric therapy are to use
vancomycin plus clindamycin and
piperacillin/tazobactam, or linezolid
plus piperacillin/tazobactam. A
carbapenem can be used in place of
piperacillin/tazobactam. Daptomycin
can be used in place of vancomycin.
Clindamycin and linezolid are
particularly efficacious because of
their ability to inhibit bacterial toxin
production.2 The use of clindamycin
is associated with decreased mortality
compared to other antibiotics in the
treatment of necrotizing fasciitis
caused by group A streptococcus.22
CRITICAL DECISION
What role do adjunct therapies play
in the treatment of NSTI?
Hyperbaric oxygen (HBO2) therapy
and intravenous immunoglobulin
(IVIG) have also been used as adjunct
therapies for treatment of NSTI.
There is no convincing evidence that
either treatment has any efficacy.
HBO2 therapy involves the delivery of
oxygen at increased pressure, which
can increase the oxygen saturation in
infected wounds by a thousand fold,
leading to a bactericidal effect and
enhanced wound healing. Several
retrospective studies have shown
no reduction in mortality or in the
number of débridements needed
with the use of HBO2 therapy.23,24
HBO2 therapy should never be a
consideration for the emergency
physician involved in the initial care
of patients with NSTI. Its only role, if
any, is as an adjunct therapy following
aggressive débridement. IVIG may
be beneficial to patients who have
developed streptococcal toxic shock
syndrome from group A streptococcal
infection.4,7
Figure 1.
Transverse (A) and longitudinal (B) magnetic resonance images of the right leg of a 41-year-old man with NSTI caused by
group A streptococci (the patient described in Case Two). The arrows point to areas of edema in the muscle, fascia, and
subcutaneous tissues.
A
6
B
July 2009 • Volume 23 • Number 11
Case Resolutions
n Case One
A surgeon was consulted
emergently, and empiric antibiotics
were initiated for suspected NSTI. The
patient’s WBC count was markedly
elevated, and radiographs of the
pelvis revealed a large amount of air
within the soft tissues extending from
the groin into the labia. She was taken
to the operating room for excision
of a large area of necrotic skin over
her abdomen and a vulvectomy
performed with the assistance of a
gynecologist. The patient continued
to receive intravenous antibiotics
and returned to the operating room
several times for autologous skin
grafting. She recovered and was
released from the hospital with home
wound care after 3 weeks.
n Case Two
Intravenous antibiotics were
initiated for suspected cellulitis. A
radiograph of the patient’s thigh and
pelvis was normal, with no evidence
of subcutaneous air. However,
initial laboratory results revealed
a WBC count of 25 and a lactate
level of 31. Because of the patient’s
severe discomfort, which seemed
disproportionate to his skin findings
on physical examination, an MRI of
his lower extremities was obtained to
evaluate for NSTI (Figure 1).
The MRI with contrast
demonstrated severe inflammation
affecting the musculature of the
medial compartment of the thigh,
with severe muscle swelling and
muscle edema. Interfascial and
marked subcutaneous edema
were also seen. The radiologist
concluded that these findings were
most suggestive of severe infectious
myositis, and that necrotizing
fasciitis remained possible despite
the absence of visible gas on MRI or
radiographs performed previously.
The patient was taken to the operating
room emergently for excision
and débridement. The fascia was
observed to be grossly swollen and
necrotic with pockets of purulence
running superiorly and inferiorly
on the muscle bellies of the thigh.
The fascia was stripped from the
involved muscles and debrided back
to clean healthy tissue. The patient
remained hospitalized for intravenous
antibiotics and required multiple
reexplorations and débridements for
continued spread of the infection.
-Hemolytic group A streptococcus
was cultured from tissue obtained
intraoperatively. He was eventually
discharged from the hospital with a
wound vacuum device, to return for
future skin grafting.
n Case Three
A urologist was consulted
immediately but was in the operating
room and unable to evaluate the
patient until finished with his case.
He questioned the presumptive
diagnosis of Fournier gangrene given
the lack of physical examination
findings and normal temperature and
insisted that a testicular ultrasound
be ordered to evaluate for testicular
torsion, epididymo-orchitis, or scrotal
abscess. Ultrasonography revealed
marked scrotal skin thickening
and gas bubbles within the scrotal
wall. The left testis was difficult to
visualize because of shadows from
the overlying gas. The urologist was
notified, and the patient transferred
to the operating room where he
underwent emergent débridement. He
was discharged from the hospital after
10 days with plastic surgery followup
for skin grafting.
Summary
NSTIs are a rare but frequently
fatal form of soft tissue infection. The
indolent nature of early NSTI and its
nonspecific clinical signs in the early
stages of infection can considerably
delay the diagnosis. Emergency
physicians should be aware of this
disease and always consider it in
the differential diagnosis of an acute
cellulitis. When differentiating
cellulitis from NSTI, clinical suspicion
alone could warrant early surgical
evaluation. There are no prospectively
validated clinical decision rules for
NSTI.
The diagnosis of NSTI should be
made clinically whenever possible,
but in early cases, in which the
patient might have severe pain
but minimal physical examination
findings and normal vital signs,
Pearls
• Severe pain out of proportion to
physical examination findings
should raise suspicion for NSTI.
• Hemorrhagic bullae, crepitus,
and skin anesthesia are very
specific but insensitive physical
examination findings for NSTI.
• NSTI in a young, otherwise
healthy patient without
significant skin trauma is
typically caused by group
A streptococcus.
• NSTI should be considered
in patients with a LRINEC
of 6 or greater.
• Aggressive surgical
débridement is the mainstay
of therapy for NSTI.
• Clindamycin inhibits bacterial
toxin production and is
associated with decreased
mortality compared to
other antibiotics in patients
with NSTI caused by
group A streptococcus.
Pitfalls
• Assuming that the absence
of subcutaneous gas on plain
radiographs rules out NSTI.
• Delaying surgical consultation
to order radiologic studies
when signs of NSTI are obvious
on physical examination.
• Assuming that absence of
fever rules out NSTI.
• Not accounting for MRSA
when choosing empiric
antibiotic therapy for NSTI.
7
Critical Decisions in Emergency Medicine
for example, radiologic studies can
expedite care. Plain radiographs can
be performed quickly but are often
negative in patients with NSTI and
should never be used to rule out the
disease. MRI is the most sensitive
radiologic test for NSTI but may not
be available, is often time consuming,
and is nonspecific.
Early and aggressive surgical
débridement decreases mortality in
NSTI. Intravenous antibiotics have
an important role as well, but are
ineffective without débridement. Any
antibiotic regimen should include
clindamycin, which is associated with
decreased mortality in patients with
NSTI due to group A streptococci.
MRSA is now a common pathogen in
NSTI, and empiric antibiotic coverage
should account for this.
References
1. Frazee BW, Fee C, Lynn J, et al. Community-acquired
necrotizing soft tissue infections: a review of 122 cases
presenting to a single emergency department over 12
years. J Emerg Med. 2008;34:139-146.
2. Abrahamian FM, Talan DA, Moran GJ. Management
of skin and soft-tissue infections in the emergency
department. Infect Dis Clin North Am.
2008;22:89-116.
3. Descamps V, Aitken J, Lee MG. Hippocrates on
necrotising fasciitis. Lancet. 1994;344:556.
4. Anaya D, Dellinger EP. Necrotizing soft-tissue
infection: diagnosis and management. Clin Infect Dis.
2007;44:705–710.
5. Wong CH, Chang HC, Pasupathy S, et al. Necrotizing
fasciitis: clinical presentation, microbiology, and
determinants of mortality. J Bone Joint Surg Am.
2003;85:1454-1460.
6. Hsiao CT, Weng HH, Yuan YD, et al. Predictors of
mortality in patients with necrotizing fasciitis. Am J
Emerg Med. 2008;26:170-175.
7. Levine EG, Manders SM. Life-threatening necrotizing
fasciitis. Clin Dermatol. 2005;23:144-147.
8. Stevens DL, Bisno AL, Chambers HF, et al. Practice
guidelines for diagnosis and management of skin and
soft-tissue infections. Clin Infect Dis. 2005;41:13731406.
9. Wong CH, Wang YS. The diagnosis of necrotizing
fasciitis. Curr Opin Infect Dis. 2005;18:101-106.
10. Hsiao CT, Lin LJ, Shiao CJ, et al. Hemorrhagic
bullae are not only skin deep. Am J Emerg Med.
2008;26:316-319.
11. Wong CH, Khin LW, Heng KS, et al. The LRINEC
(Laboratory Risk Indicator for Necrotizing Fasciitis)
score: a tool for distinguishing necrotizing fasciitis
from other soft tissue infections. Crit Care Med.
2004;32:1535-1541.
12. Wang TL, Hung CL. Role of tissue oxygen saturation
monitoring in diagnosing necrotizing fasciitis of the
lower limbs. Ann Emerg Med. 2004;44:222-228.
13. Wysoki MG, Santora TA, Shah RM, et al. Necrotizing
fasciitis: CT characteristics. Radiology.
1997;203:859-863.
14. Morrison D, Blaivas M, Lyon M. Emergency diagnosis
of Fournier’s gangrene with bedside ultrasound. Am J
Emerg Med. 2005:23;544-547.
15. Yen ZS, Wang HP, Ma HM, et al. Ultrasonographic
screening of clinically-suspected necrotizing fasciitis.
Acad Emerg Med. 2002;9:1448-1551.
16. Levenson R, Singh AK, Novelline RA. Fournier
gangrene: role of imaging. Radiographics.
2008;28:519-528.
8
17. Schmid MR, Kossmann T, Duewell S. Differentiation
of necrotizing fasciitis and cellulitis using MR imaging.
AJR Am J Roentgenol. 1998;170:615-620.
18. Loh NN, Ch’en IY, Cheung LP, et al. Deep fascial
hyperintensity in soft-tissue abnormalities as revealed
by T2-weighted MR imaging. AJR Am J Roentgenol.
1997;168:1301-1304.
19. Stevens DL. Necrotizing fasciitis, gas gangrene,
myositis and myonecrosis. In: Cohen J, Powderly
WG, eds. Infectious Diseases. 2nd ed. St Louis, MO:
Elsevier; 2004.
20. Lee TC, Carrick MM, Scott BG, et al. Incidence
and clinical characteristics of methicillin-resistant
Staphylococcus aureus necrotizing fasciitis in a large
urban hospital. Am J Surg. 2007;194:809-813.
21. Miller LG, Perdreau-Remington F, Rieg G, et al.
Necrotizing fasciitis caused by community-associated
methicillin-resistant Staphylococcus aureus in Los
Angeles. N Engl J Med. 2005;352:1445–1453.
22. Kaul R, McGeer A, Low ED, et al. Population-based
surveillance for group A streptococcal necrotizing
fasciitis: clinical features, prognostic indicators, and
microbiologic analysis of seventy-seven cases. Am J
Med. 1997;103:18-24.
23. George ME, Rueth NM, Skarda DE, et al. Hyperbaric
oxygen does not improve outcome in patients with
necrotizing soft tissue infection. Surg Infect (Larchmt).
2008 Nov 8 [Epub ahead of print].
24. Brown DR, Davis NL, Lepawsky M, et al. A multicenter
review of the treatment of major truncal necrotizing
infections with and without hyperbaric oxygen
therapy. Am J Surg. 1995;169:187-188.
The Drug Box
Vancomycin
By Michelle D Walters, MD; Summa Health System Emergency Medicine Residency
The use of the antibiotic vancomycin has become more common as the
prevalence of methicillin-resistant Staphylococcus aureus (MRSA) has
increased. Vancomycin must be administered slowly to decrease the
risk of histamine release (“red man” syndrome), and the dose must be
adjusted for patients with renal dysfunction. Use of vancomycin should be
avoided in patients with inflammatory bowel disease because it can cause
pseudomembranous colitis. Co-administration of aminoglycosides should also
be avoided because it increases the risk of ototoxicity.
Vancomycin
Mechanism of
Action
Indications
Dosing
Side Effects
Estimated Cost
to Hospital and
Patienta
Contraindication/
Precautions
a
Binds precursor units of bacterial cell walls inhibiting cell wall
synthesis. Inhibits RNA synthesis in gram-positive bacteria
Skin infections, pneumonia, bone/joint infections, endocarditis,
bacteremia, septicemia, urinary tract infection, and peritonitis
Oral treatment of colitis due to Clostridium difficile or
Staphylococcus aureus
Intravenous: 15 mg/kg every 12 hrs; blood levels must be
checked to maintain appropriate intravenous dosing; administer
no faster than 10 mg/min to avoid infusion-related reactions
Oral: 125-500 mg every 6 hrs for 7-10 days
Anaphylaxis; histamine release (flushing, hypotension,
tachycardia, wheezing, dyspnea, urticaria, pruritus, muscle
spasms, paresthesias); neutropenia; thrombocytopenia;
eosinophilia; leukopenia; vasculitis; exfoliative dermatitis;
Stevens-Johnson syndrome
$4.50 per 1,000 mg PO
Contraindicated in patients with known hypersensitivity
to vancomycin or corn products; must be renally dosed to
decrease ototoxicity and nephrotoxicity; administer slowly,
less than 10 mg/min, to avoid histamine release; avoid in
patients with irritable bowel disease as this could predispose
to pseudomembranous colitis; risk of ototoxicity when
administered with aminoglycosides
Oral preparation is pregnancy category B; intravenous
preparation is pregnancy category C
Cost data provided by Summa Health System Pharmacy
Feature Editor: Michael S. Beeson, MD, FACEP
July 2009 • Volume 23 • Number 11
The LLSA Literature Review
“The LLSA Literature Review” summarizes articles from ABEM’s “2010 Lifelong Learning and Self-Assessment Reading List.”
Many of these articles are available online in the ACEP LLSA Resource Center (www.acep.org/llsa) and on the ABEM web site.
bacterial peritonitis is suggested if the polymorphonuclear
cell count is greater than 250 cells/mm3.
Article 5
Highlights
Paracentesis
• Perform paracentesis in patients with new-onset ascites or
suspected spontaneous bacterial peritonitis or to alleviate
the discomfort of tense ascites.
Reviewed by Alisha Perkins Garth, MD, and J. Stephen Bohan,
MD, MS, FACEP; Harvard Affiliated Emergency Medicine
Residency; Brigham and Women’s Hospital
• The incidence of clinically significant bleeding complications
is low.
Thomsen TW, Shaffer RW, White B, Setnik GS. Paracentesis. New Engl J
Med. 2006;355(19):e21.
Abdominal paracentesis is indicated for patients with newonset ascites of unclear etiology, for those with suspected
spontaneous bacterial peritonitis, and to alleviate discomfort
or respiratory compromise in patients with tense ascites.
This procedure is contraindicated in patients with disseminated intravascular coagulation. It should be used with
caution in patients who are pregnant or who have organomegaly, bowel obstruction, adhesions, or a distended bladder.
It should not be done through the site of a skin or soft tissue
infection, engorged vessel, surgical scars, or hematoma. Patients can have underlying coagulopathy or thrombocytopenia, but the incidence of significant bleeding complications
from paracentesis is low. Routine use of fresh-frozen plasma
or platelets is not recommended.
To perform the procedure, begin by placing the patient in
the supine position with the head of the bed slightly elevated.
The recommended sites for needle insertion are 2 cm below
the umbilicus in the midline or in the right or left lower quadrant 2 to 4 cm medial and cephalad to the anterior superior
iliac spine. Use ultrasonography, if it is available, to mark the
appropriate site. Use sterile technique. Anesthetize the area
using a 22- or 25-gauge, 1.5-inch needle and 1% to 2% lidocaine. Place a wheal of anesthetic in the epidermis, and
then continue along the anticipated trajectory of the catheter
injecting anesthetic. Remove the needle and make a small incision at the insertion site to facilitate advancement of the
catheter. Insert the catheter device at a 45-degree angle to the
skin, and advance it until ascitic fluid returns. Immediately
stop advancing the needle and guide the catheter over the
needle. Remove the needle, and collect fluid as desired.
Place the fluid in specimen tubes and send for analysis.
The serum-albumin gradient can be calculated; if it is greater
than 1.1 g/dL portal hypertension is indicated. Spontaneous
• Use caution when performing paracentesis in patients
who have organomegaly, bowel obstruction, adhesions, or
distended urinary bladder or who are pregnant.
• Recommended needle-insertion sites are 2 cm below the
umbilicus or in the right or left lower quadrant 2 to 4 cm
medial and cephalad to the anterior superior iliac spine.
9
Critical Decisions in Emergency Medicine
The LLSA Literature Review
“The LLSA Literature Review” summarizes articles from ABEM’s “2010 Lifelong Learning and Self-Assessment Reading List.”
Many of these articles are available online in the ACEP LLSA Resource Center (www.acep.org/llsa) and on the ABEM web site.
Article 6
Transient Ischemic Attack: Risk
Stratification and Treatment
Reviewed by Alisha Perkins Garth, MD, and J. Stephen Bohan,
MD, MS, FACEP; Harvard Affiliated Emergency Medicine
Residency; Brigham and Women’s Hospital
Cucchiara B, Ross M. Transient ischemic attack: risk stratification and
treatment. Ann Emerg Med. 52(2):2008;52(2):S27-S39.
Evaluation and management of patients with transient
ischemic attacks (TIAs) in the emergency department is difficult. Currently, three clinical risk scores have been developed
and validated: the ABCD, the California, and the ABCD². All
three scores aim to identify patients at high risk for stroke
up to 90 days after a TIA. Points are assigned for clinical
features, and the sum of the points determines whether the
patient fits in a higher-risk group. Clinical factors shown to
have predictive value include age older than 60 years, diabetes, symptoms lasting longer than 10 minutes, symptoms of
unilateral weakness or speech impairment, and an elevated
blood pressure. Validation of these scores has shown them
to be helpful to clinicians but not a replacement for clinical
judgment.
In addition to risk scores, diffusion-weighted magnetic
resonance imaging may also be important for risk stratification. Patients who have lesions consistent with cerebral
ischemia on imaging are at high-risk. Similarly, patients who
have large vessel disease confirmed on vascular imaging are
at a higher short-term risk of stroke.
Disposition of these patients in the emergency department
is challenging, and this review found limited clinical data on
the benefit of hospitalization. The best guidelines cited are the
2006 National Stroke Association guidelines, which recommend hospitalization for patients with crescendo symptoms,
duration of symptoms for more than 1 hour, symptomatic
carotid stenosis greater than 50%, known cardiac embolic
source, hypercoagulable state, or an appropriate score from
the California or ABCD scores.
Treatment options for TIAs include basic supportive care
to optimize cerebral blood flow with positioning the head of
10
the bed flat, permissive hypertension, and isotonic fluid administration to maintain intravascular volume. Additionally,
once hemorrhage has been excluded antithrombotic therapy
with aspirin should be given. Currently there are no data
supporting the use of clopidogrel, ticlopidine, heparin, or
low-molecular-weight heparin alone or in combination with
aspirin in the acute management of TIAs. Long-term prevention and management must, however, be based on the underlying etiology of the cerebrovascular event.
Highlights
• Patients with high short-term risk of stroke after TIA include
older patients and those with hypertension, diabetes,
symptom duration more than 10 minutes, and symptoms of
weakness or speech impairment.
• Magnetic resonance imaging and vascular imaging may be
tools to help risk stratify patients with TIA.
• Immediate treatment should include positioning the patient
with the head of the bed flat, isotonic fluids, permissive
hypertension, and aspirin (once hemorrhage has been ruled
out by imaging).
• Long-term treatment and prevention must be tailored to the
individual patient.
Critical Decisions in Emergency Medicine
Hyperbaric Therapies
Lesson 22
Colin G. Kaide, MD, FACEP, UHM; Sorabh Khandelwal, MD, UHM;
and Erica Brown, MD
n Objectives
On completion of this lesson, you
should be able to:
1. Illustrate the mechanisms by which
hyperbaric oxygen exerts its effect.
2. List the emergency conditions for
which hyperbaric oxygen has a role
in the treatment process.
3. Identify patients who may benefit
from hyperbaric oxygen therapy.
4. Identify conditions that may warrant
emergent transfer to a hyperbaric
facility.
5. List the contraindications to
hyperbaric oxygen therapy.
n From the EM Model
6.0 Environmental Disorders
6.2 Dysbarism
In 1976, an evidence-guided list
of indications for hyperbaric therapy
was developed by a multispecialty
subcommittee of the Undersea
and Hyperbaric Medicine Society
(UHMS).1,2 As of the most recent
revision of the hyperbaric guidelines
(2003), there are 13 conditions for
which hyperbaric oxygen therapy
has been shown to be an effective
treatment modality (Table 1).2
Hyperbaric oxygen (HBO2) therapy
involves the exposure of the entire
body to 100% oxygen at a pressure
greater than one atmosphere absolute
(ATA), in either a single-patient
hyperbaric chamber (monoplace)
or in a larger chamber capable of
providing treatment to many patients
simultaneously (multiplace chamber).
Under normobaric conditions,
humans live under the downward
pressure exerted by the weight of the
atmosphere above. This pressure is
usually measured in millimeters of
mercury (mm Hg). At sea level, one
atmosphere is 760 mm Hg (14.7 lbs/
in2, 760 Torr). In dive medicine, a
branch of hyperbaric medicine that
deals with scuba diving and other
situations involving the breathing of
compressed gasses, it is customary
to refer to pressure in terms of feet of
seawater. One atmosphere is equal to
the pressure exerted at a depth of 33
feet (10 meters) of seawater. Under
hyperbaric treatment conditions,
the body is exposed to pressures
that are typically in the range of 2 to
3 ATA—one atmosphere from the
earth’s atmosphere plus an additional
one to two atmospheres exerted by
pressurizing the hyperbaric chamber.
All of the physiologic effects of
HBO2 are based on the ideal gas
laws. The Dalton law states that the
total pressure of a mixture of gases
is equal to the sum of the partial
pressures of each of the individual
gases.3,4 The air we breathe is 21%
oxygen, 78% of nitrogen and 1%
trace gases. The Henry law states
that the amount of gas that dissolves
in a liquid is proportional to the
pressure exerted on the surface
of the liquid.3,5 Therefore, as the
partial pressure of the gas above a
liquid increases, the amount of the
gas that dissolves in the liquid also
increases. Conversely, when the
partial pressure of the gas decreases,
dissolved gases will come out of
solution and return to the gaseous
state. HBO2 therapy capitalizes on the
Henry law by significantly increasing
the ambient pressure of oxygen,
causing a dramatic increase in the
amount of dissolved oxygen carried
by the blood. As the partial pressure
of oxygen reaches 100 mm Hg,
hemoglobin becomes fully saturated.
Under normobaric conditions,
the dissolved oxygen is negligible,
representing only 0.3 mL of oxygen
per 100 mL of blood (called volumes
percent—vol%), compared to 20
vol% carried by hemoglobin. Under
hyperbaric conditions the Pao2 at 3
ATA is above 2,200 mm Hg. This is
high enough to generate 5.4 vol% of
dissolved oxygen, which can sustain
basal metabolic functions in the
11
Critical Decisions in Emergency Medicine
Critical Decisions
• When is HBO2 therapy indicated for acute carbon
monoxide (CO) poisoning?
• What clinical presentations and signs and symptoms
should raise suspicion for air embolism?
• What treatments should be undertaken as soon as the
diagnosis of air gas embolism is suspected?
complete absence of any hemoglobin
(Table 2).
Hyperoxygenated plasma can
transport oxygen to areas that are
inaccessible to red cells, delivering
oxygen to relatively hypoxic tissues
in proportion to the oxygen tension
of the plasma. This is especially
important in areas of the body that
are deprived of blood flow when
arteries are blocked by gas bubbles
and in tissue that has experienced a
hypoxic insult (Table 3).
The only absolute
contraindications to HBO2 therapy
are untreated pneumothorax and
concurrent or recent (within 7
days) use of doxorubicin. Relative
Table 1.
Approved indications for HBO2
therapy2
1. Air embolism
2. Decompression sickness
3. CO poisoning
4. Crush injury, compartment
syndrome, and other acute
ischemias
5. Exceptional blood loss, anemia
6. Delayed radiation injury
(osteo and soft-tissue)
7. Skin grafts and flaps
8. Thermal burns
9. Enhancement of healing in
selected problem wounds
10. Necrotizing soft tissue
infections
11. Clostridial myositis and
myonecrosis (gas gangrene)
12. Osteomyelitis (refractory),
includes malignant otitis externa
13. Intracranial abscesses
12
• What signs and symptoms should prompt an emergency
physician to consider decompression sickness?
• How does the physician distinguish between type I and
type II decompression sickness?
• What therapies should be initiated in patients with
decompression sickness?
contraindications are listed in Table 4.
They should not preclude the use of
HBO2 therapy in emergency situations
in which it is considered the primary
and possibly only effective treatment
modality.
Case Presentations
n Case One
A 28-year-old woman was
found with a depressed level of
consciousness by her husband upon
his return home from work. He called
911, and the woman was transported
to the emergency department on highflow oxygen via nonrebreathing face
mask. The house was being heated by
a wood-burning stove. The patient’s
husband states that his wife is 32
weeks pregnant and has no medical
problems. Her carboxyhemoglobin
(HbCO) level in the emergency
department is 30%.
n Case Two
A 35-year-old woman with a
history of Crohn disease presents
with complaints of abdominal
pain that is typical of a Crohn
exacerbation. After multiple attempts
at intravenous access, a triple-
lumen central venous catheter is
placed into the internal jugular vein
under ultrasound guidance without
complication. Frustrated at the
wait for assistance when she calls
for help going to the bathroom, she
disconnects the catheter from the
IV drip, leaving the distal port open
to air. Seated on the commode, she
breathes deeply to strain for a bowel
movement and collapses, falling
off the commode. A nearby patient
hears the fall and calls for help. The
patient is discovered on the floor,
cyanotic and with agonal respirations.
She is immediately transferred to a
resuscitation room.
Physical examination findings
after the event reveal an unconscious,
cyanotic patient in severe distress.
Vital signs are blood pressure
60/palpable, heart rate 130,
respiratory rate 6, and temperature
36.8°C (98.2°F). The patient’s pupils
are mid-position and sluggishly
reactive. The lungs are clear bilaterally
to auscultation (post-intubation),
and heart sounds are obscured by a
“churning” sound of the precordium.
The abdomen is soft. The extremities
show cyanosis with absent pedal
Table 2.
Oxygen content equation
Normobaric Conditions
Oxygen content = oxygen carried by hemoglobin + oxygen dissolved in plasma
Arterial oxygen content = 1.34 (Hgb)(%Sat) + .003 (Pao2)
= 1.34 (15)(100%) + .003 (100)
= 20.1 + 0.3
= 20.4 Vol%
Hyperbaric conditions—3 ATA
Arterial oxygen content = 1.34 (15)(100%) + .003 (2,200)
= 20.1 + 6.6 Vol%
July 2009 • Volume 23 • Number 11
pulses. A formal neurologic
examination is not possible; however
the un-paralyzed patient does not
make any attempt at movement.
The patient is immediately
intubated and placed on a ventilator
and turned on her left side with her
head down in Trendelenburg position.
She is given a bolus of normal saline
and an arterial line is placed. The
presumptive diagnosis of venous air
embolism is made, and the emergency
physician on call for hyperbaric
medicine is immediately contacted.
A chest radiograph is unremarkable,
and an ECG shows sinus tachycardia
with right bundle-branch block. On
preliminary evaluation, a computed
tomography (CT) scan of the head
appears normal (Figure 1).
n Case Three
A 32-year-old woman presents
to the emergency department
complaining of progressive lower
extremity pain and weakness. She
had been in the surgical waiting area
of the hospital where her son was
having an urgent appendectomy. She
states she and her husband had been
on a scuba diving trip off the coast of
Oregon when she received word that
her son was going to have surgery.
She and her husband had returned
home that same day.
The couple had spent most of
the past week doing two dives per
day, and her last dive was early this
morning. She went to a depth of
38 m (125 feet), and owing to what
she believed to be a dive computer
malfunction, her bottom time could
only be estimated at 25 minutes,
with a total dive lasting 40 minutes
(this exceeds the maximum allowable
bottom time). She had a slow ascent
and made all the appropriate safety
stops. The couple received word about
their son’s illness, and they flew home
7 hours after surfacing.
She had fainted on the return
flight and seemed to be out for 5
minutes. The couple attributed this to
stress and declined transport by EMS
after landing. She states that during
the flight she did have some mild
leg pain in addition to her fainting
spell. Since landing, she continued
to have persistent leg pain. While
awaiting the completion of her son’s
Table 3.
Effects of HBO2 therapy
Mechanical Effects of Increased Pressure
Reduction in the size and shape of gas bubbles in proportion to the increase in
pressure
Effects of Increased Partial Pressure of Dissolved Oxygen
Delivery of increased amounts of oxygen to tissues
Vasoconstriction/edema reduction
Increased healing of hypoxic wounds
Antimicrobial effects
Antibiotic synergism
Anti-anaerobic organism effects
Enhanced efficacy of leukocyte-mediated killing
Reduced production of clostridial alpha toxin
Suppression of bacterial growth in hyperoxygenated tissues
Toxic oxygen radical modulation
Blunting of ischemic-reperfusion injury
Antagonizing lipid peroxidation of cellular membranes
Generation of reactive oxygen scavengers
Bubble size reduction
Diffusion of oxygen into mixed gas bubbles
procedure, she tried to stand up and
said she “almost collapsed because
her legs were so weak.” At that time,
her husband insisted she come to
the emergency department. She is
otherwise healthy, and her only
medication is a birth control pill.
Her physical examination reveals
an age-appropriate, anxious woman.
Her vital signs are blood pressure
126/74, pulse rate 97, respiratory
rate 14, and oral temperature 36.8°C
(98.2°F). She has clear, bilateral
breath sounds. Heart has a regular
rate and rhythm without murmurs,
gallops, or rubs. Her skin is without
rash, and there is no evidence of
subcutaneous emphysema. Her
neurologic examination reveals
normal cranial nerves and normal
Table 4.
Relative contraindications to HBO2
therapy*
Surgical Procedures
A history of recent thoracic
surgery
Recent retinal repair
Reconstructive ear surgery
Untreated Conditions
Congestive heart failure
Severe claustrophobia
Uncontrolled high fever
Untreated acidosis
Severe obstructive lung disease
Past Medical Problems
History of optic neuritis
History of spontaneous
pneumothorax
Current Medical Conditions
Pulmonary lesions on CT scan or
chest radiograph
Seizure disorder
Acute viral infections
Congenital spherocytosis
Other
Presence of hydrocarbon-based
ointments and gels on the skin
(spontaneous ignition hazard).
They can be cleaned off of the
skin and this removes the risk
*None of these conditions should preclude
hyperbaric treatment in an emergency
situation, especially if it is the primary or
only effective treatment modality
13
Critical Decisions in Emergency Medicine
strength in the upper extremities.
She has 3/5 strength in her lower
extremities bilaterally and is unable to
stand. She has decreased sensation in
her feet, and 3+ patellar reflexes.
Her chest radiograph, laboratory
studies, and ECG are essentially
normal.
Carbon Monoxide
Poisoning
Carbon monoxide (CO) is the
leading cause of poisoning in the
United States and the most common
cause of injury and death from
poisoning in the world.6,7 CO toxicity
develops from CO-induced tissue
hypoxia and direct CO-mediated
cellular damage.
Tissue Hypoxia
The tissue hypoxia from CO
results from its competitive binding
of hemoglobin, with an affinity
230 to 270 times stronger than that
of oxygen. Additionally, binding
of CO to hemoglobin shifts the
oxyhemoglobin dissociation curve
to the left (Haldane effect) resulting
in decreased tissue oxygen delivery
and, ultimately, cellular hypoxia.
Tissue hypoxia prompts an increase
in minute ventilation, which in turn
causes a respiratory alkalosis. This
further exaggerates the leftward shift
Figure 1.
Cerebral air on CT. Image
courtesy of Colin Kaide, MD.
14
of the oxyhemoglobin dissociation
curve, perpetuating a vicious cycle of
worsening hypoxia.
The deleterious effects of CO are
potentiated when CO binds to skeletal
and cardiac myoglobin, the affinity
of which is three times stronger than
that for hemoglobin.8 This increased
affinity results in a slow dissociation
and delayed release of CO from those
tissues. The reintroduction of the
dissociated CO into the circulation
can cause a deleterious rebound effect
when CO again binds to hemoglobin.9
CO poisoning in the fetus involves
additional complexities; CO is bound
more tightly to fetal hemoglobin than
to hemoglobin A. This, in conjunction
with the naturally leftward-shifted
fetal oxyhemoglobin dissociation
curve, intensifies tissue hypoxia in
the fetus. The consequence of this
physiology is that a CO level that
could be nonfatal in an adult can be
deadly in a fetus.10,11
Cellular Damage
Although tissue hypoxia can
explain most of the cardiac and
neurologic symptoms commonly
seen with acute CO poisoning,
additional effects develop as the
result of direct CO-mediated cellular
damage. Peripheral oxygen utilization
and oxidative phosphorylation are
hindered because of CO’s interaction
with a variety of cellular proteins
including myoglobin, cytochromes,
and triphosphopyridine nucleotide
reductase.12
Tissue perfusion is decreased
through several CO-mediated
mechanisms including myocardial
depression, ventricular arrhythmias,
and peripheral vasodilation.13 As
tissue perfusion is reestablished,
postischemic reperfusion injury, brain
lipid peroxidation, and subsequent
demyelization of central nervous
symptom lipids can develop.14 These
CNS effects are mediated mainly by
leukocytes.15 Finally, CO-induced
oxidative stress on cells can lead to
generation of oxygen free radicals that
can exacerbate cellular damage.16,17
Clinical Manifestations
Acutely, CO leads to injury of the
brain, heart, and other organs as
manifested by myocardial ischemia,
syncope, and metabolic acidosis.
A well-recognized syndrome that
develops in survivors of severe
CO poisoning, delayed neurologic
sequelae (DNS), manifests after a
latent period of 2 to 21 days and has
an incidence that ranges from 12% to
68%. Symptoms include, but are not
limited to, memory loss, impairments
of concentration and language,
parkinsonism, and affective changes
such as depression.18
The rationale for the use of HBO2
therapy for CO poisoning has two
main principles. First, HBO2 therapy
provides a more rapid detoxification
than normobaric oxygen (HbCO halflife is 300 minutes at atmospheric
conditions, 100 minutes with 100%
Fio2, and less than 30 minutes at
3 ATA). Second, it decreases the
incidence of DNS.
There is good scientific literature
available that discusses how
hyperbaric oxygen mitigates the
mechanisms of CO toxicity.9,10
However, the debate over HBO2
therapy for CO poisoning has been
ongoing in the literature for many
years, with arguments both in
support of and against its use.8,12
The American College of Emergency
Physicians’ “Clinical Policy on Critical
Issues in the Management of Adult
Patients Presenting to the Emergency
Department with Carbon Monoxide
Poisoning”18 includes two Level C
recommendations (Table 5).
The authors judge the best study
to date is the randomized, controlled
trial by Weaver et al, published in
2002.13 This is the only randomized,
controlled trial that addresses
long-term neurologic sequelae after
CO poisoning. It demonstrated a
statistically significant reduction in
the incidence of DNS measured at
6 weeks, 6 months, and 1 year after
treatment.
July 2009 • Volume 23 • Number 11
CRITICAL DECISION
When is HBO2 therapy indicated for
acute CO poisoning?
The exact criteria for the use of
HBO2 therapy in CO poisoning is
still a matter of controversy. It clearly
should not be used in everyone with
CO poisoning. It makes sense to look
at the specific patient population
that derived benefit from this
therapy in the study by Weaver et
al. The UHMS published its current
recommendations for the treatment
of CO poisoning in 2008 (Table 6).
HBO2 therapy should be initiated in
those with a loss of consciousness,
metabolic acidosis (as defined by a
base deficit of more than -2 mmol/
liter), and HbCO of more than 25%.19
Many hyperbaric physicians and
toxicologists would also suggest
that HBO2 therapy be considered
in patients with any neurologic
abnormality, patients with evidence of
cardiac dysfunction, pregnant women
with HbCO levels of more than 15%,
patients with unresolved neurologic
symptoms despite normobaric
oxygen therapy, and patients with
neuropsychometric deficits.
Given the controversial aspects and
indications for HBO2 therapy, it seems
reasonable to seek guidance from a
hyperbaric physician or a toxicologist
who is familiar with the literature and
the clinical application of HBO2.
Air Embolism
Air embolism occurs when
bubbles of air are introduced into
the circulatory system, either as
Table 5.
Management of adult patients
with CO poisoning18
HBO2 is a therapeutic option for
CO-poisoned patients
No clinical variables, including
HbCO levels, identify a subgroup
of CO-poisoned patients for
whom HBO2 therapy is most
likely to provide benefit or cause
harm
a consequence of a dive-related
accident or as the result of a medical
procedure. Iatrogenic introduction
of air into the circulatory system
represents the most common cause
of cerebral arterial gas embolism
(CAGE).20 It has occurred in almost
all medical specialties and settings
including during cardiac bypass,
cardiac catheterization, open lung
procedures, craniotomy, head and
neck surgeries, dialysis, relatively
simple procedures such as the
placement of a central line,21 and as
the result of vaginal insufflation with
air in pregnant women during oral
sex.22
Air embolism can occur either on
the venous side or the arterial side of
the circulatory system. Additionally, a
paradoxical arterial air embolism can
develop when a venous air embolism
travels to the arterial system by way of
an intra-pulmonary shunt or through
a patent foramen ovale.
Venous Air Embolism
A small venous air embolism or
even a large volume of air delivered
slowly (30 mL/minute) is likely to
be filtered by the pulmonary system
and remain asymptomatic.23 Large
boluses of air introduced into the
venous system all at once are capable
of causing a complete obstruction
of flow through the heart, resulting
in immediate circulatory collapse.24
Between 100 and 300 mL of air is
sufficient to cause cardiac arrest, and
up to 100 mL per second of air can be
injected through a 14-gauge needle.25
The mechanism by which the
cardiovascular collapse develops
begins with the arrival of the air
bolus to into the right ventricle. It
may remain in the right ventricle
and cause a mechanical obstruction
or move distally into the pulmonary
vessels causing a progressive increase
in pulmonary vascular resistance.
This, in turn, leads to a decrease in
pulmonary venous return and left
ventricular preload. If the obstruction
is large enough, cardiac output can
drop to a level at which complete
cardiovascular collapse could
develop.20,24,25
Arterial Air Embolism
It is estimated that up to 30% of
otherwise healthy patients can have
a patent foramen ovale.26 When air
from the venous system is present in
a large enough quantity, increased
pressures in the right ventricular
outflow tract can force air from the
right side to the left side of the heart
via the foramen ovale. Additionally, a
massive volume of air delivered to the
pulmonary vasculature can force air
through other intrapulmonic shunts.20
This movement of venous air to the
arterial side is called a paradoxical air
embolism.
Scuba diving accidents are a
significant cause of arterial air
embolism. As a scuba diver begins
to ascend, the gas in his lungs
expands. If the diver continues
to breathe in and out during the
assent, problems rarely develop. If,
on the other hand, the diver takes
a breath of air and holds it while
Table 6.
Indications for HBO2 therapy for acute CO poisoning ­— recommendations of
the UHMS2
Recommended HBO2 therapy
regardless of CO levels if:
Consider HBO2 therapy if:
Transient or prolonged unconsciousness
Cardiovascular disfunction
Severe metabolic acidosis
Duration of exposure to CO is 24 hours or
more, even if intermittent
HbCO level 25% to 30%
Neuropsychological test results are abnormal
15
Critical Decisions in Emergency Medicine
continuing to ascend, the air will
expand to exceed the maximum
lung volume and eventually cause
severe lung injury. Injuries can
range from pneumothorax and
pneumomediastinum to entry of
the gas into the pulmonary venous
system. This air is then delivered to
the left ventricle and ultimately to the
rest of the body.
The consequences of an arterial gas
embolism depend on which organs
receive the gas and how well they
tolerate an acute vascular occlusion.
Muscle, connective tissue, and skin
tolerate small emboli well; however,
small bubbles of air entering the
coronary arteries can precipitate an
acute coronary syndrome. When
air enters the carotid arteries and
ultimately the brain, the symptoms
that develop depend on which part of
the brain is affected. Symptoms can
include motor or sensory problems,
confusion and altered mental status,
hemiparesis, seizures, and coma.27
As little as 0.5 mL of blood-air foam
arriving at the brainstem can be
fatal.20
Bubbles produce injury by multiple
mechanisms. The first, most obvious
problem is acute arterial occlusion.
Bubbles also cause damage to the
endothelium of blood vessels. This
can produce leukocyte activation,
release of inflammatory mediators,
and activation and aggregation of
platelets.20 Additionally, a reperfusiontype injury can develop when the
mechanical obstruction caused by the
bubbles is relieved. A phenomenon
called “no-reflow” can occur in which
microvascular perfusion is impaired
in the postischemic state. The cause
of this is not well understood but is
believed to involve factor VIII and an
interaction with prostaglandins and
leukocytes.28
CRITICAL DECISION
What clinical presentations and
signs and symptoms should raise
suspicion for air embolism?
Because the symptoms can mimic
an acute cerebrovascular accident,
16
epilepsy, or any other acute neurologic
condition, CAGE can be difficult
to diagnose if taken out of clinical
context. A diver who surfaces with
immediate neurologic symptoms
should be assumed to have CAGE
until it is proved otherwise. Air
embolism with paradoxical passage of
venous air into the arterial side of the
system should be strongly considered
in patients who develop CNS
symptoms in the context of a new
central line placement or who have
a complication of an existing central
line. The development of an acute
coronary syndrome in these contexts
also suggests arterial air embolism,
although the usual causes of acute
coronary syndrome must still be
considered. Acute coronary syndrome
developing concomitantly with
CAGE in the appropriate context very
strongly suggests an air embolism.
During the workup for arterial
embolism, a CT scan of the brain
might occasionally show air in
the cerebral vessels; however this
finding is variable and can be
difficult to recognize. Imaging
with CT or MRI may be useful in
some, less clear-cut cases to help
exclude a cerebrovascular accident
or intracerebral hemorrhage that
developed via the usual mechanisms.
CRITICAL DECISION
What treatments should be
undertaken as soon as the diagnosis
of air embolism is suspected?
Primary treatments for venous
embolism may include aspiration
of large air pockets in the ventricle,
treatment with oxygen, and
hemodynamic support. Immediately
placing patients in the left-lateral
decubitus position is advocated for
patients with venous air embolism
with the goal of trapping air in the
right ventricle and decreasing the
risk of paradoxical embolization and
passage more distally into the lungs.
This is usually ineffective by the time
the patient is seen in the emergency
department, because venous air has
already been distributed to the lungs
and through any shunts and may be
gone from the right ventricle.
In cases of venous air embolism,
HBO2 therapy is usually considered
an adjunctive therapy, unless a
paradoxical arterial air embolism
develops concomitantly. HBO2
therapy may be useful for patients
with venous gas embolism who
remain symptomatic, especially with
pulmonary edema.20,28
The only definitive treatment
for an acute arterial embolism is
recompression in a hyperbaric
chamber.20,21,23,27-29 The faster the
patient receives HBO2 therapy, the
more likely the chance for complete
neurologic recovery. For this reason,
rapid recognition of an arterial gas
embolism as the cause of the patient’s
symptoms is essential.
When arterial gas embolism is
suspected, the patient should be
immediately placed on oxygen at
the highest possible concentration.
A tight-fitting nonrebreathing mask
with a reservoir, on 15 L of oxygen
per minute will typically deliver
about 72% oxygen. High-flow oxygen
serves to not only treat hypoxia
but also to help create a diffusion
gradient across existing bubbles that
favors the movement of inert gases
(nitrogen) out of the bubble and back
into solution, thereby reducing bubble
size.20,21,23,27-29 If the head-down
position is used for a short time, the
patient should be returned to the
supine position, which will be more
helpful in resuscitative efforts.29
Although there are no data in
humans, multiple animal studies have
shown that the administration of
lidocaine seems to improve cerebral
blood flow, reduce infarct size
and edema, and lower intracranial
pressure in CAGE. Given the low risk
of lidocaine use and the potential
benefit, it is recommended in cases of
CAGE at the dose of 1.5 mg/kg bolus,
followed by infusion at typical cardiac
dosing of 2 to 4 mg/minute.20,21,29,32,33
Patients should be transferred
as quickly as possible to a
hyperbaric chamber for immediate
July 2009 • Volume 23 • Number 11
recompression therapy. The current
recommendations from the UHMS
in the Hyperbaric Oxygen Therapy
Committee Report are for patients
to be treated using the US Navy
recommendations (Figure 2).
This treatment regimen involves
compression with 100% oxygen at
pressures between 2 ATA to 2.82
ATA with at least 60 minutes spent
at 2.82 ATA. Time extensions at
both the higher and lower pressures
can be added depending on the
patient’s response to the treatment.
Some patients will require additional
treatments in the hyperbaric chamber
to facilitate more complete resolution
of symptoms.
Decompression Sickness
Decompression sickness develops
from the formation of bubbles of inert
gases (mainly nitrogen) in the tissues
and/or blood in volumes large enough
to impair organ function.3-5,34-38
Bubbles can form when the ascent
from diving (or from a compressed
air environment) is too rapid and/
or when unpressurized flying takes
place soon after a patient surfaces
from a dive.34 It is necessary to
discuss the basic properties of
gases, the physiology of diving, and
the mechanism by which bubble
formation occurs to understand the
pathophysiology of decompression
sickness.
of taking on more nitrogen with
increased depth is called “ongassing” or supersaturation.34,35 As a
diver ascends, the ambient pressure
decreases and the partial pressure of
the inspired nitrogen is less than the
partial pressure of nitrogen dissolved
in the blood. Because gases move
from areas of higher concentration
to areas of lower concentration, the
nitrogen accumulated in the body
tissues during descent begins to move
from the tissue to the blood and from
the blood out through the lungs. This
is called off-gassing.34,35
Bubble Formation
During a proper ascent, nitrogen
should remain in solution as it moves
from the tissues to the blood stream
and should not reform into the
gaseous phase until it reaches the
lungs.34 The reformation of gaseous
nitrogen in tissues and/or blood (prior
to arrival at the lungs) causes bubbles
to develop in the blood and tissues.
This forms the basis for the problems
seen in decompression sickness.3-5,34-38
Bubbles can be generated if the ascent
is too rapid for the given amount of
dissolved nitrogen to move from the
tissues to the lungs before returning
to the gaseous phase.4,34-36
When the diver surfaces, the
amount of nitrogen in the body is
still elevated, and off-gassing is still
taking place, although not in the
form of pathologic bubbles.3,34 For
this reason, air travel shortly after
diving can be problematic. Most
commercial aircraft are pressurized
to the ambient pressure at 8,000 feet
(2,440 m) (about 0.73 atmospheres),
not to the pressure found at sea level.
A diver’s continued rapid ascent to
this new, lower ambient pressure
can further facilitate the formation
of bubbles in the blood and tissue
that were previously off-gassing well,
resulting in an increased chance of
decompression sickness.34,35,37 Some
newer aircraft and most private
jets now pressurize to sea level,
eliminating this concern.
When a diver follows the standard
US Navy dive tables or uses a dive
computer, the maximum depth
allowed and the length of time at that
depth do not usually allow for enough
nitrogen to accumulate to cause
nitrogen bubble formation (Table 7).
Figure 2.
US Navy recommendations for duration of HBO2 therapy following dives at
various depths (US Navy Diving Manual, Volume 5, Table 6)
Diving Physiology
As a diver descends under water,
the ambient pressure increases and
it becomes harder for the diver to
expand his/her chest. Scuba gear is
designed to address this problem
by sensing the external pressure
and delivering air through the
regulator at the ambient pressure so
as to overcome the increased work
of breathing.34 A rise in air pressure
increases the total pressure of the
inspired gas and thereby the partial
pressures of the component gasses
(nitrogen and oxygen). As the partial
pressure of nitrogen rises, the amount
dissolved in the blood and transferred
to the tissues also rises. This concept
17
Critical Decisions in Emergency Medicine
Mechanism of Damage
There are two major mechanisms
by which the bubbles in blood/tissues
cause decompression sickness. The
first is mechanical occlusion of vessels
causing tissue hypoxia and prevention
of further off-gassing. The second
is the blood-bubble interaction that
can damage endothelium, resulting
in leakage of plasma into tissues,
activation of clotting factors and
cytokines, and platelet aggregation.5,35
These serve to worsen tissue hypoxia.5
The blood-bubble interactions can
be the most detrimental factors in
patients with decompression sickness
because the effect can continue long
after the removal of the bubbles
from tissues. Tissue hypoxia and
inflammation cause the symptoms of
decompression illness.5,35
Table 7.
Time and depth limits at which
decompression is not required
Depth
(Feet)
10
15
20
25
30
35
40
50
60
70
80
90
100
110
120
130
140
150
160
170
180
190
18
(Meters)
3.0
4.6
6.1
7.6
9.1
10.7
12.2
15.2
18.2
21.3
24.4
27.4
30.5
33.5
36.6
39.6
42.7
45.7
48.8
51.8
54.8
59.9
Time
(Minutes)
310
200
100
60
50
40
30
25
20
15
10
10
5
5
5
5
5
CRITICAL DECISION
What signs and symptoms should
prompt an emergency physician to
consider decompression sickness?
Decompression sickness is a
clinical diagnosis. The history and
physical examination will usually
make the diagnosis. Most patients
will present with sensory symptoms
that began within 1 to 3 hours after
they surfaced from a dive.36 One study
reports that 50% of patients will
have symptoms within 10 minutes
of surfacing, 85% within 1 hour, and
90% within the first 24 hours.35 It is
unlikely for symptoms to arise after
24 hours.4 Joint pain and paresthesias
are the most common complaints,
occurring in 40% of patients with
decompression sickness.35 Symptoms
occur along a spectrum and can
range from a simple rash to shock and
cardiopulmonary arrest.35,36
Once decompression sickness
has been considered as the cause
of a patient’s symptoms, a detailed
history of the dive should be
obtained, including the maximum
depth, length of time at that depth,
characteristics of the ascent, and
any increase in altitude shortly after
surfacing.3,5,36 The maximum depth
and length of time spent at that depth
are used to determine if the diver
exceeded depth/time limits. The risk
of decompression sickness in divers
who exceed depth and time limits
approaches 100%.35 It is important
to note however, that decompression
sickness can still occur in divers who
adhere strictly to decompression
tables.3 The type of dive is also
important.3 Decompression sickness
is less likely in breath-holding dives
than in dives in which scuba gear is
used and on-gassing (supersaturation)
takes place.34,35
The physical examination
should focus on vital signs and
cardiopulmonary, skin, and
neurologic examinations. The
cardiopulmonary examination
can reveal signs of pneumothorax,
pneumomediastinum, or
subcutaneous emphysema, all of
which can be present. The presence
of pneumothorax is especially
important, as it will require
management prior to any definitive
treatment in a hyperbaric chamber.
The skin should be thoroughly
examined for rashes. The most
common rash is a marbled, pruritic
rash also known as cutis marmorata.4
A complete neurologic examination
should be done, including assessment
of sensory/motor/cerebellar function.
The neurologic examination can often
reveal subtle deficits that the patient
may not have noticed.
CRITICAL DECISION
How does the physician distinguish
between type I and type II
decompression sickness?
Decompression sickness is
categorized by symptoms into type I
(mild) and type II (serious).4 Patients
can, however, have both types
concurrently.
Type I decompression sickness is
characterized by pain, itching, fatigue,
pitting edema, and skin rash.3,34,36
Pain in or near a joint is often referred
to as the “bends.” Pruritus or “skin
bends” can also manifest as a burning
sensation and rash. The pitting edema
is often painless and is a sign of
lymphatic involvement.3,34,36
Type II decompression sickness
is characterized by central nervous
system (CNS) dysfunction,
cardiopulmonary symptoms, or any
symptoms of type I decompression
sickness occurring while the diver
is still under water.3,34 The CNS
symptoms can include loss of
consciousness, ataxia, paresthesias,
paresis, paralysis, urinary/bowel
incontinence, and mental status
changes.3,4,36 The pulmonary
symptoms are also referred to as the
“chokes” and include burning with
inspiration, nonproductive cough, and
respiratory distress. Cardiac effects
include vasomotor instability and
shock.3,4,36
July 2009 • Volume 23 • Number 11
CRITICAL DECISION
What therapies should be initiated
in patients with decompression
sickness?
As with all emergency department
patients, care should be taken
to address any cardiopulmonary
instability by ensuring the patient’s
airway is intact. Some patients
may require intubation if they are
obtunded or cannot protect their
airway. Supplemental oxygen should
be given at the highest attainable
concentration.5,38 All patients should
be hydrated, given aspirin, and
transferred to a hyperbaric facility as
soon as possible.5 Although patients
with type I or mild type II illness
may dramatically improve with 100%
oxygen, this should not prevent their
transfer to a hyperbaric facility; these
patients will often have recurrence
of symptoms and worse outcomes if
HBO2 therapy is delayed.
Recompression using HBO2
therapy is the only definitive
treatment for decompression
sickness.3-5,34-38 HBO2 therapy
reduces bubble size by compressing
the gas in the bubble, facilitating its
passage to more distal parts of the
circulation. Also, by increasing the
pressure gradient, oxygen diffuses
into the bubble and causes nitrogen to
diffuse out and back into the plasma
and into solution. Finally, tissue
hypoxia is corrected, reperfusion
injury is blunted, and cerebral edema
is reduced. All these actions result
in reversal of the mechanical cause
of decompression sickness and
amelioration of the resultant tissue
injury.5,36,37
Aspirin prevents platelet
aggregation that is caused by
interaction of bubbles with
endothelium. There are no studies
regarding the dose of aspirin,
although cardiac dosing is commonly
used.5 The use of early steroids in
decompression sickness has only been
shown to be useful in those patients
with evidence of spinal cord ischemia
and injury. The recommended dose is
methylprednisolone 30 mg/kg within
the first 8 hours of injury.5,38
It is essential to understand that
patients who seem to experience only
mild type I symptoms could manifest
concomitant type II symptoms that
initially might be very subtle. Some of
these patients will develop full-blown
type II decompression sickness over
time. For this reason, all patients
who develop decompression sickness
of any kind should be evaluated
for immediate recompression in a
hyperbaric chamber.
Transport to a hyperbaric facility
can often entail travel of some
distance. In these cases, patients
should be transported via ground to
avoid worsening of their condition by
altitude. If the patient must go by air,
he or she should be transported in an
aircraft that can be pressurized to sea
level or by helicopter with flight level
below 300 m.3,5
Case Resolutions
n Case One
The pregnant 28-year-old
woman responded to high-flow
normobaric oxygen with improving
mental status. The obstetrics service
was immediately consulted, and
fetal monitoring was initiated
demonstrating decreased short-term
and long-term heart rate variability
suggestive of fetal hypoxia. A decision
was made to treat with HBO2 at
3 ATA. After completion of the
treatment, repeat fetal monitoring
demonstrated good tracing. The
patient was admitted to the obstetrical
service and monitored overnight. She
did well and eventually delivered a
healthy baby at 39 weeks by cesarean
section.
n Case Two
On arrival of the hyperbaric
physician, the patient’s vital
signs had stabilized. The patient
was immediately placed in the
supine position and taken out of
Trendelenburg position. The patient
still remained comatose and made
no effort at movement. The history,
laboratory findings, and imaging
were reviewed. A second look at
the patient’s head CT demonstrated
intracranial air. This finding is
virtually pathognomonic for CAGE.
The patient was given 100 mg of
lidocaine (approximately 1.5 mg/
kg). The hyperbaric physician
performed a bilateral myringotomy.
The patient was transported to the
hyperbaric department (adjacent to
the emergency department) and was
placed in the monoplace hyperbaric
chamber with cardiac monitor, IV
access, and arterial line in place. She
was connected to the hyperbaric
ventilator. Treatment was initiated
following the US Navy Treatment
Table 6 protocol. During the first hour
of treatment at 2.8 ATA, the patient
became agitated and developed a brief
tonic-clonic seizure. She received
2 mg of lorazepam intravenously,
and a 1 mg/kg bolus of propofol was
delivered followed by a continuous
infusion. The patient’s agitation
was controlled, and no further
complications developed. The patient
awoke during the last 30 minutes
of the treatment and was following
commands. She was transported to
the ICU where she remained in stable
condition. She was extubated the
following morning. She made two
additional trips to the hyperbaric
chamber for residual neurologic
symptoms. After her third treatment
was completed, she appeared to
have returned to baseline neurologic
function. Detailed cognitive testing
revealed some mild deficits with
regard to memory and mathematical
processing. A echocardiogram with
a bubble study performed during
her hospitalization revealed a patent
foramen ovale.
n Case Three
The patient was presumed to
have decompression sickness type
II precipitated by altitude closely
following a dive, which clearly
violated the “no decompression”
dive limits. She was placed on
100% oxygen and given intravenous
19
Critical Decisions in Emergency Medicine
fluids and 325 mg of aspirin.
Because of the neurologic deficits
and concern for spinal cord injury,
methylprednisolone (30 mg/kg IV)
was given. The local hyperbaric
center was contacted, and she was
transported via ambulance to that
facility. She was immediately placed
in a hyperbaric chamber and treated
using US Navy Treatment Table 6
protocol. Her leg pain completely
resolved after the first treatment,
and she was able to stand; however
she continued to have some leg
weakness. She received two additional
treatments, after which her weakness
completely resolved.
Summary
HBO2 therapy has 13 approved
applications recommended by the
Undersea and Hyperbaric Medical
Society. Of these, CO poisoning, gas
embolism, and decompression illness
are most likely to be encountered in
emergency medicine.
CO poisoning must be considered
in patients who present with loss of
consciousness and acute neurologic
deficits from environments with
potential exposure to CO. Although
HBO2 treatment in CO poisoning is
controversial, we feel that there is
ample evidence to justify treatment
of selected individuals. At the least,
a referral or consultation should be
made to a knowledgeable hyperbaric
physician or toxicologist.
HBO2 treatment in air embolism
cases can be life-saving. The diagnosis
of air embolism is difficult; it should
be considered in divers and those
undergoing venous or arterial
vessel manipulation who suffer a
cardiovascular or neurologic event.
HBO2 therapy is the only definitive
treatment for decompression sickness.
The symptoms of decompression
sickness are varied, and emergency
physicians must maintain a high
degree of suspicion for the diagnosis
when confronted with a patient who
has recently been diving.
2. Gesell LB, ed. Hyperbaric Oxygen Therapy Indications.
12th ed. Durham, NC: Undersea and Hyperbaric
Medical Society; 2008.
References
14. Thom SR. Carbon monoxide-mediated brain lipid
peroxidation in the rat. J Appl Physiol.
1990;68:997-1003.
1. Kindwall E. A history of hyperbaric medicine. In:
Kindwall EP, Wheelan HT, eds. Hyperbaric Medicine
Practice. 3rd ed. Flagstaff, AZ: Best Publishing
Company; 2008:5-22.
3. Schockley LW. Scuba diving and dysbarism. Marx JA,
Hockberger RS, Walls RM, eds. Rosen’s Emergency
Medicine: Concepts and Clinical Practice. 6th ed. St
Louis, MO: Mosby; 2006:2279-2295.
4. Kindwall EP, Wheelan HT. Hyperbaric Medicine
Practice, 3rd ed. Flagstaff, AZ: Best Publishing
Company; 2008. (Comprehensive review.)
5. Tetzlaff K, Shank ES, Muth CM. Evaluation and
management of decompression illness—an
intensivist’s perspective. Intensive Care Med.
2003:29:2128-2136.
6. Gasman JD, Varon J, Gardner JP. Revenge of the
barbecue grill. Carbon monoxide poisoning. West J
Med. 1990;153: 656-657.
7. Thom SR, Keim LW. Carbon monoxide poisoning:
a review epidemiology, pathophysiology, clinical
features, and treatment options including hyperbaric
therapy. J Toxicol Clin Toxicol. 1989;27:141-156.
8. Coburn RF. The carbon monoxide body stores. Ann
NY Acad Sci. 1970;174:11-22.
9. Anderson GK. Treatment of carbon monoxide
poisoning with hyperbaric oxygen. Mil Med.
1978;143:538-541.
10. Farrow JR, Davis GJ, Roy TM, et al. Fetal death due to
nonlethal maternal carbon monoxide poisoning.
J Forensic Sci. 1990;35:1448-1452.
11. Longo LD, Hill EP. Carbon monoxide uptake and
elimination in fetal and maternal sheep. Am J Physiol.
1977;232:H324-H330.
12. Hardy KR, Thom SR. Pathophysiology and treatment
of carbon monoxide poisoning. J Toxicol Clin Toxicol.
1994;32:613-629.
13. Zhang J, Piantadosi CA. Mitochondrial oxidative stress
after carbon monoxide hypoxia in the rat brain. J Clin
Invest. 1992;90:1193-1199.
15. Thom SR. Leukocytes in carbon monoxide-mediated
brain oxidative injury. Toxicol Appl Pharmoacol.
1993;123:234-247.
16. Penny DG. Acute carbon monoxide poisoning: animal
models: a review. Toxicology. 1990;62:123-160.
Pearls and Pitfalls
• HBO2 therapy should not be given to patients with
untreated pneumothorax or patients with current
or recent (within 7 days) doxorubicin treatment.
• CO poisoning can be subtle, manifesting only as a
headache, with minimal additional symptoms.
• When patients present with headache, vomiting,
lethargy, confusion, nonspecific dizziness, or
afebrile viral-like illnesses lacking symptoms of
an upper respiratory infection, this should trigger
the question, “Why isn’t this CO poisoning?”
• Although controversy exists with HBO2 treatment in
CO poisoning, we feel that there is ample evidence
to justify treatment of selected individuals. At the
least, a referral or consultation should be made to a
knowledgeable hyperbaric physician or toxicologist.
• Air embolism should be considered in patients
who have just completed a scuba dive and in those
who have had procedures involving access to the
pulmonary or venous system who develop sudden
cardiovascular collapse or severe CNS problems.
• Although the patient may be placed in the headdown position initially, the value of the Trendelenburg
20
•
•
•
•
position is refuted by studies suggesting it does
little to prevent or ameliorate the symptoms of
CAGE and may even promote cerebral edema.
The only definitive treatment for an acute arterial
embolism is recompression in a hyperbaric chamber.
The faster the patient receives HBO2 therapy, the more
likely the chance for complete neurologic recovery.
The diagnosis of decompression sickness
should be considered in any patient with
acute onset of pain, paresthesias, or loss of
consciousness who has recently been diving.
Diagnostic testing in patients with possible decompression
sickness should be minimal, as definitive HBO2 therapy
should not be delayed. Patients should be stabilized,
placed on the highest amount of oxygen available, receive
a chest radiograph (to rule out pneumothorax), and
transferred to a hyperbaric facility as soon as possible.
Do not withhold HBO2 therapy from patients with
decompression sickness who improve with 100% oxygen.
These patients may develop more serious problems (type II)
or have a recurrence if they do not receive HBO2 therapy.
July 2009 • Volume 23 • Number 11
17. Thom SR. Dehydrogenase conversion to oxidase and
lipid peroxidation in brain after carbon monoxide
poisoning. J Appl Physiol. 1992;73:1584-1589.
18. Wolf SW, Lavonas EJ, Sloan EP, et al. Clinical policy:
critical issues in the management of adult patients
presenting to the emergency department with
acute carbon monoxide poisoning. Ann Emerg Med.
2008;51:138-152.
19. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric
oxygen for acute carbon monoxide poisoning. N Engl J
Med. 2002;347:1057-1067.
20. Kindwall EP. Gas Embolism. In: Kindwall EP, Wheelan
HT, eds. Hyperbaric Medicine Practice, 3rd ed.
Flagstaff, AZ: Best Publishing Company;
2008:519-534.
21. Muth CM; Shank ES. Gas Embolism. N Engl J Med.
2000;342:476-482.
22. Fyke FE 3rd, Kamier FJ, Harms RW. Venous air
embolism: life-threatening complication of orogenital
sex during pregnancy. Am J Med. 1985;78:333-336.
23. Van Allen CM, Hrdina LS, Clark J. Air embolism from
the pulmonary vein. Arch Surg. 1929;19:567-599.
24. Durant TM, Long J, Oppenheimer MJ. Pulmonary
(venous) air embolism. Am Heart J. 1947;33:269-81.
25. Palmon SC, Moore LE, Lundberg J, et al. Venous air
embolism: a review. J Clin Anesth. 1997;9:251-257.
26. Lynch JJ, Schuchard GH, Gross CM, et al. Prevalence
of right-to-left atrial shunting in a healthy
population: detection by Valsalva maneuver contrast
echocardiography. Am J Cardiol. 1984;53:1478-1480.
27. Smith RM, Van Hoesen KB, Neuman TS. Arterial gas
embolism and hemoconcentration. J Emerg Med.
1994;12:147-153.
28. Francis TJ, Mitchell SJ. Pathophysiology of
decompression sickness. In Bove AA, ed. Bove and
Davis’ Diving Medicine. 4th ed. Philadelphia, PA:
Elsevier; 2004:164-183. (Comprehensive review of dive
medicine.)
29. Moon RE. Treatment of decompression illness. In Bove
AA, ed. Bove and Davis’ Diving Medicine. 4th ed.
Philadelphia, PA: Elsevier; 2004:195-223.
30. Van Liew HD, Conkin J, Burkard ME. The oxygen
window and decompression bubbles: estimates and
significance. Aviat Space Environ Med.
1993;64:859-865.
31. Butler BD, Laine GA, Leiman BC, et al. Effects of
Trendelenburg position on the distribution of arterial
air emboli in dogs. Ann Thorac Surg.
1988;45:198-202.
32. Fukaya E, Hopf HW. HBO and gas embolism. Neurol
Res. 2007;29:142-145.
33. McDermott JJ, Dutka AJ, Evans DE, et al. Treatment
of experimental cerebral air embolism with lidocaine
and hyperbaric oxygen. Undersea Biomed Res.
1990;17:525-534.
34. Bookspan J. Diving Physiology in Plain English.
Kensington, MD: Undersea and Hyperbaric Medical
Society, Inc; 1995.
35. Bove AA, ed. Bove and Davis’ Diving Medicine. 4th ed.
Philadelphia, PA: Elsevier; 2004.
36. Freiberger JJ, Lyman SJ, Denoble PJ, et.al. Consensus
factors used by experts in the diagnosis of
decompression illness. Aviat Space Environ Med.
2004;75(12):1023-1028. (Study about factors used to
make diagnosis of DCS.)
37. Freiberger JJ, Denoble PJ, Pieper CF, et al. The relative
risk of decompression sickness during and after air
travel following diving. Aviat Space Environ Med.
2002;73:980-984. (Risk of flying after diving.)
38. Moon RE. Treatment of diving emergencies. Crit Care
Clin. 1999;15:429-456.
The Critical Image
A previously healthy 40-year-old man presenting with a 4-week history of cough, sputum production,
subjective fever, and mild dyspnea. He had been seen 2 weeks previously in the emergency department and
treated with moxifloxacin for a possible atypical pneumonia. A chest x-ray was performed (B). The patient
was diagnosed by the emergency physician with bronchitis and discharged.
A
B
C
This case illustrates several important points:
• When prior x-rays are available, always compare them with the current x-ray to detect subtle changes.
• In this case, comparison of the current x-ray (B) with the one obtained 2 weeks previously (A) would have revealed an
increase in heart size to more than half of the right-left chest diameter. In addition, an increase in pulmonary vascular
markings in the upper lung fields is notable. This redistribution of vascular markings is called cephalization and is an
early finding of pulmonary edema.
The patient returned again 7 days later (20 days after his initial presentation), and another chest x-ray was obtained
(C). He continued to complain of cough, and his vital signs were notable for tachycardia to 130 and a temperature of
38.3°C (100.9°F). On this visit, the emergency physician noted an interval increase in heart size on the chest x-ray, and
a viral cardiomyopathy was suspected. Within days, the patient required a left ventricular assist device. He underwent
heart transplant surgery and recovered.
Feature Editor: Joshua S. Broder, MD, FACEP
Images courtesy of Emergency Medicine Picture Archiving & Communication System (www.empacs.org).
21
Critical Decisions in Emergency Medicine
CME Questions
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 I Credits™, and 5 AOA Category 2-B credits for answering the following
questions. To receive your certificate, go to www.acep.org/criticaldecisionstesting and submit your answers online. You
will immediately receive your score and printable CME certificate. You may submit the answers to these questions at any
time within 3 years of the publication date. You will be given appropriate credit for all tests you complete and submit
within this time. Answers to this month’s questions will be published in next month’s issue.
1. Which radiologic study is most sensitive for NSTI?
A. CT scan
B. MRI
C. plain films
D. ultrasonography
E. V/Q scan
2. For suspected necrotizing fasciitis, which of the following
antibiotic combinations is recommended?
A. clindamycin, piperacillin/tazobactam
B. imipenem
C. vancomycin, clindamycin, piperacillin/tazobactam
D. vancomycin, piperacillin/tazobactam
E. vancomycin, rifampin, piperacillin/tazobactam
3. A 35-year-old woman presents with warmth, swelling, and
erythema at the site of her incision from a recent cesarean
section. Crepitus is present. What is the next step in her
care?
A. emergent gynecology consultation
B. MRI
C. radiographs
D. transfer to a center for hyperbaric oxygen
E. ultrasonography
4. A 23-year-old woman presents with severe buttock
pain after a fall from standing 3 days ago. She is febrile,
hypotensive, and has necrotic-appearing skin over her left
buttock and into her vulva that is draining foul-smelling
fluid. There is no crepitus. What is the most likely causative
organism?
A. Escherichia coli
B. Haemophilus
C. Neisseria
D. Streptococcus
E. Vibrio
5. The mortality rate for NSTI treated only with antibiotics is:
A. 15%
B. 25%
C. 50%
D. 75%
E. approaching 100%
6. Which of the following is an advantage of CT over
ultrasonography in assessing suspected NSTI that involves
the trunk?
A. can be performed at bedside
B. can always be performed more quickly
C. may show an intraabdominal source
D. may show fluid along the deep fascia
E. may show subcutaneous gas
22
7. A 70-year-old man with peripheral vascular disease
develops NSTI at the site of an existing skin ulcer. What is
the most likely causative organism?
A. Candida
B. a mixture of aerobic and anaerobic bacteria
C. Pseudomonas
D. Streptococcus
E. Vibrio
8. In what subset of patients with NSTI might IVIG be useful?
A. patients with Fournier gangrene
B. patients with group A streptococcus infection and shock
C. patients with high fever
D. patients with NSTI of the head and neck
E. young adult patients
9. What is the role of radiologic studies in evaluating NSTI?
A. assist surgeon with operative approach
B. confirm a clinical diagnosis
C. accurately evaluate the extent of disease
D. expedite care for patients with a paucity of clinical findings
E. identify drainable fluid collections
10. Which of the following antibiotics inhibits protein
synthesis and, therefore, toxin production in bacteria
causing NSTI?
A. ciprofloxacin
B. clindamycin
C. penicillin
D. tobramycin
E. vancomycin
11. A diver presents, having just surfaced from a 37-meter dive
that lasted for 29 minutes, complaining of intense right
foot pain and itching along his abdomen. He states that
the symptoms started halfway through his ascent. He has a
marbling rash over the epigastric area of his abdomen and
a normal neurologic examination. This patient has which
of the following conditions?
A. air embolism
B. allergic reaction and musculoskeletal pain
C. barotrauma
D. decompression sickness type I
E. decompression sickness type II
12. Which of the following factors makes it less likely that a
patient’s symptoms are caused by decompression sickness?
A. breath-holding dive
B. exceeding depth and time limits for a given dive
C. flying within the first 24 hours after surfacing from a dive
D. rapid ascent
E. scuba diving
July 2009 • Volume 23 • Number 11
13. Which of the following patients is most likely to benefit
from acute hyperbaric oxygen treatment?
A. a patient presenting with an itchy skin rash 3 days after a scuba
diving trip
B. a patient with a sudden collapse after a central line placement
who recovers to a normal blood pressure over 15 minutes with
no neurologic deficits
C. a patient who develops sudden hemiparesis immediately after
an open lung biopsy
D. a scuba diver who lost consciousness immediately after making
a rapid emergency ascent from 45 feet while holding his
breath. He has been in cardiopulmonary arrest with ACLS in
progress for 1 hour
E. an 80-year-old hypertensive scuba diver with an acute
intraventricular hemorrhage on cranial CT
14. Which of the following statements best characterizes the
role of HBO2 therapy in patients presenting with an acute
venous air embolism?
A. it is a first-line therapy and should be initiated immediately in
all patients in whom the diagnosis of venous air embolism is
considered
B. it is a first-line therapy in patients with venous embolism
who present with hypotension, hypoxia, and a new focal
neurological deficit
C. it is an unproven therapy in all cases of venous air embolism
D. it is most effective in venous air embolism when delivered at an
Fio2 of 21% at 3 ATA for 60 minutes
E. it should be initiated only after definitive confirmation of a
paradoxical arterial embolism in a patient with a suspected
venous air embolism
15. Which of the following is a contraindication to HBO2
therapy?
A. a history of a traumatic pneumothorax, 3 years ago
B. a history of a pneumothorax with a chest tube in place
C. a small apical pneumothorax less than 15%
D. a history of severe claustrophobia
E. chemotherapy with rituximab 1 year ago
16. Tissue hypoxia from CO is a result of competitive binding
of hemoglobin. This shifts the oxyhemoglobin dissociation
curve to:
A. downward
B. the left
C. no shift; CO affects oxygenation via a different mechanism
D. the right
E. upward
17. A CO level that is not fatal in an adult can be deadly in a
fetus because:
A. CO binds less tightly to fetal hemoglobin; more free CO causes
more damage to tissues
B. CO binds less tightly to fetal hemoglobin, shifting the
oxyhemoglobin dissociation curve farther to the left
C. CO binds more tightly to fetal hemoglobin; less free CO causes
more damage to tissues
D. CO binds more tightly to fetal hemoglobin, shifting the
oxyhemoglobin dissociation curve farther to the left
E. CO binds more tightly to fetal hemoglobin, shifting the
oxyhemoglobin dissociation curve farther to the right
18. The most common cause of air embolism is:
A. introduction of air during a case of untreated tension
pneumothorax
B. introduction of air during an invasive surgical or medical
procedure
C. introduction of air from oral-vaginal sexual activity
D. introduction of air via a scuba diving accident
E. introduction of air via explosive decompression in a
compromised aircraft at altitude
19. Bubbles cause injury to tissues by all of the following
mechanisms except:
A. activation and aggregation of platelets
B. damage to the endothelium of blood vessels producing
leukocyte activation, release of inflammatory mediators
C. hypoxia from acute arterial occlusion
D. initiation of secondary reperfusion injury
E. maximal distention of arterioles and capillaries producing
vascular burst phenomena
20. Which of the following patients with CO exposure has the
best indication for HBO2 therapy?
A. a patient with a CO level of 20 and a severe headache
B. a patient with chest pain, ST-segment depression, and a CO
level of 29
C. a pregnant smoker with a CO level of 10
D. a smoker with headache, cough, muscle aches, fever, and a CO
level of 7
E. an unresponsive patient pulled from a house fire 30 minutes
ago on oxygen via nonrebreathing mask with a CO level of 6
and coma
Answer key for June 2009, Volume 23, Number 10
1
C
2
B
3
B
4
E
5
D
6
A
7
C
8
D
9
C
10
B
11
B
12
B
13
A
14
E
15
B
16
A
17
C
18
A
19
B
20
E
The American College of Emergency Physicians makes every effort to ensure that contributors to College-sponsored publications are knowledgeable authorities in their fields. Readers are nevertheless advised that the statements
and opinions expressed in this series are provided as guidelines and should not be construed as College policy unless specifically cited as such. The College disclaims any liability or responsibility for the consequences of any
actions taken in reliance on those statements or opinions. The materials contained herein are not intended to establish policy, procedure, or a standard of care.
23
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July 2009 • Volume 23 • Number 11
Critical Decisions in Emergency Medicine is the official
CME publication of the American College of Emergency
Physicians. Additional volumes are available to keep
emergency medicine professionals up-to-date on relevant
clinical issues.
Editor-in-Chief
Louis G. Graff IV, MD, FACEP
Professor of Traumatology and Emergency Medicine,
Professor of Clinical Medicine, University of
Connecticut School of Medicine; Farmington,
Connecticut
Section Editor
J. Stephen Bohan, MS, MD, FACEP
Executive Vice Chairman and Clinical Director,
Department of Emergency Medicine, Brigham &
Women’s Hospital; Instructor, Harvard Medical School,
Boston, Massachusetts
Feature Editors
Michael S. Beeson, MD, MBA, FACEP
Program Director, Department of Emergency Medicine, Summa Health System, Akron, Ohio; Professor,
Clinical Emergency Medicine, Northeastern Ohio
Universities College of Medicine, Rootstown, Ohio
The Critical ECG
A 63-year-old woman with generalized weakness.
Joshua S. Broder, MD, FACEP
Assistant Clinical Professor of Surgery, Associate
Residency Program Director, Division of Emergency
Medicine, Duke University Medical Center, Durham,
North Carolina
Amal Mattu, MD, FACEP
Program Director, Emergency Medicine
Residency Training Program,
Co-Director, Emergency Medicine/Internal Medicine
Combined Residency Training Program, University of
Maryland School of Medicine, Baltimore, Maryland
Associate Editors
Daniel A. Handel, MD, MPH
Director of Clinical Operations, Department of Emergency
Medicine, Oregon Health & Science University, Portland,
Oregon
Frank LoVecchio, DO, MPH, FACEP
Research Director, Maricopa Medical Center Emergency
Medicine Program; Medical Director, Banner Poison
Control Center, Phoenix, Arizona; Professor, Midwestern
University/Arizona College of Osteopathic Medicine,
Glendale, Arizona.
Sharon E. Mace, MD, FACEP
Associate Professor, Department of Emergency
Medicine, Ohio State University School of Medicine;
Faculty, MetroHealth Medical Center/Cleveland Clinic
Foundation Emergency Medicine Residency Program;
Director, Pediatric Education/Quality Improvement
and Observation Unit, Cleveland Clinic Foundation,
Cleveland, Ohio
Robert A. Rosen, MD, FACEP
Medical Director, Culpeper Regional Hospital,
Culpeper, Virginia
George Sternbach, MD, FACEP
Sinus rhythm with second-degree atrioventricular block type 1 (Mobitz I,
Wenckebach), rate 80. This is an example of a slowly progressing Mobitz I rhythm with
only one nonconducted P wave on the ECG. The P-P intervals remain constant, and
there is very slight PR-interval prolongation from one complex to the next, although
the PR-interval prolongation becomes more evident just prior to the nonconducted P
wave.
Feature Editor: Amal Mattu, MD, FACEP
From: Mattu A, Brady W. ECGs for the Emergency Physician. London: BMJ Publishing;
2003:100,140. Available at www.acep.org/bookstore. Reprinted with permission.
Clinical Professor of Surgery
(Emergency Medicine), Stanford University
Medical Center, Stanford, California
Editorial Staff
Mary Anne Mitchell, ELS
Managing Editor
Mike Goodwin
Creative Services Manager
Mary Hines
Editorial Assistant
Lilly E. Friend
CME and Subscriptions Coordinator
Marta Foster
Director and Senior Editor
Educational and Professional Publications
Critical Decisions in Emergency Medicine is a trademark
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of Emergency Physicians, PO Box 619911, Dallas TX
75261-9911. Send address changes to Critical Decisions
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