Download Oncologic Emergencies, Part I: Spinal Cord Compression, Superior

Oncologic Emergencies, Part I:
Spinal Cord Compression, Superior Vena Cava Syndrome,
And Pericardial Effusion
A 65-year-old woman with a history of non-small-cell cancer is brought in
by her family to the emergency department (ED) with a chief complaint of
progressive lethargy for the past 2 days. According to the family, she had
2 weeks of cough and shortness of breath, and she was given antibiotics for
pneumonia a week ago in urgent care, with no improvement. She became
confused yesterday and is less interactive today. The family thinks that her
neck and arms are more swollen than usual, which you confirm by examining her driver’s license picture, taken last year. She is afebrile and has a
blood pressure (BP) of 160/95 mm Hg, heart rate of 70 beats per minute,
and respiratory rate of 24 breaths per minute with an oxygen saturation
of 98% on room air. She has intact cough and gag, but you can hear mild
stridor. An indwelling catheter in her left chest was used recently for chemotherapy. Although you consider superior vena cava syndrome, you are
not sure if you can put everything together with that diagnosis. As you try
to look up more on superior vena cava syndrome, a nurse grabs you, stating
that your patient’s respirations have increased to 36 breaths per minute.
Later in your busy shift, a 45-year-old man with altered mental status
is brought in by ambulance. At his bedside, a prehospital care provider tells
you that the patient is unable to provide a history and that the family is on
the way to the ED. The patient appears pale and lethargic and has labored
breathing. The ambulance crew reports that they administered 500 mL of
Ringer’s lactate in response to an initial blood pressure of 86/60 mm Hg. Editor-in-Chief
Andy Jagoda, MD, FACEP
Professor and Chair, Department
of Emergency Medicine, Mount
Sinai School of Medicine; Medical
Director, Mount Sinai Hospital, New
York, NY
Francis M. Fesmire, MD, FACEP
Director, Heart-Stroke Center,
Erlanger Medical Center; Assistant
Professor, UT College of Medicine,
Chattanooga, TN
University, Washington, DC; Director
of Academic Affairs, Best Practices,
Inc, Inova Fairfax Hospital, Falls
Church, VA
February 2010
Volume 12, Number 2
Authors
Michael T. McCurdy, MD
Assistant Professor of Emergency Medicine and Pulmonary
and Critical Care Medicine, University of Maryland School of
Medicine, Baltimore, MD
Tsuyoshi Mitarai, MD
Attending Physician, Emergency Department, Medical ICU,
Surgical ICU, Stanford Hospital; Clinical Instructor, Division
of Emergency Medicine, Department of Surgery, Stanford
University School of Medicine, Stanford, CA
Jack Perkins, MD
Associate Program Director, Franklin Square Hospital Internal
Medicine Residency; Attending Physician, Department of
Emergency Medicine, Baltimore, MD
Peer Reviewers
Kevin Reed, MD, FACEP, FAAEM
Assistant Professor of Clinical Emergency Medicine,
Georgetown University and Washington Hospital Center,
Washington, DC
Scott Weingart, MD, FACEP
Assistant Professor of Emergency Medicine, Mount Sinai
School of Medicine; Director of Emergency Critical Care,
Elmhurst Hospital Center, New York, NY
CME Objectives
Upon completion of this article, you should be able to:
1.
2.
3.
Describe common presenting signs and symptoms of
ESCC, SVCS, and malignant pericardial effusion.
Identify components of the history, physical
examination, and imaging for diagnosis of these 3
conditions.
Discuss appropriate treatment options for these 3
conditions.
Prior to beginning this activity, see “Physician CME
Information” on page 20.
Thomas Jefferson University,
Philadelphia, PA
Scott Silvers, MD, FACEP
Chair, Department of Emergency
Medicine, Mayo Clinic, Jacksonville,
FL
Keith A. Marill, MD
Assistant Professor, Department of
Emergency Medicine, Massachusetts
Corey M. Slovis, MD, FACP, FACEP
General Hospital, Harvard Medical
Editorial Board
Professor and Chair, Department
School, Boston, MA
William J. Brady, MD
of Emergency Medicine, Vanderbilt
Charles V. Pollack, Jr., MA, MD,
Professor of Emergency Medicine
University Medical Center, Nashville,
Michael A. Gibbs, MD, FACEP
FACEP
and Internal Medicine, Vice Chair
TN
Chief, Department of Emergency
Chairman,
Department
of
Emergency
of Emergency Medicine, University
Medicine, Maine Medical Center,
Jenny Walker, MD, MPH, MSW
Medicine, Pennsylvania Hospital,
of Virginia School of Medicine,
Portland, ME
Assistant Professor; Division Chief,
University of Pennsylvania Health
Charlottesville, VA
Family Medicine, Department
Steven A. Godwin, MD, FACEP
System, Philadelphia, PA
Peter DeBlieux, MD of Community and Preventive
Associate Professor, Associate Chair
Michael S. Radeos, MD, MPH
Professor of Clinical Medicine, LSU
Medicine, Mount Sinai Medical
and Chief of Service, Department
Assistant Professor of Emergency
Health Science Center; Director
Center, New York, NY
of Emergency Medicine, Assistant
Medicine, Weill Medical College of
of Emergency Medicine Services,
Dean, Simulation Education,
Ron M. Walls, MD
Cornell
University,
New
York,
NY.
University Hospital, New Orleans,
University of Florida COMProfessor and Chair, Department of
LA
Jacksonville, Jacksonville, FL
Robert L. Rogers, MD, FACEP,
Emergency Medicine, Brigham and
FAAEM, FACP
Wyatt W. Decker, MD
Women’s Hospital, Harvard Medical
Gregory L. Henry, MD, FACEP
Assistant
Professor
of
Emergency
Professor of Emergency Medicine,
School, Boston, MA
CEO, Medical Practice Risk
Medicine,
The
University
of
Mayo Clinic College of Medicine,
Assessment, Inc.; Clinical Professor
Scott Weingart, MD, FACEP
Maryland School of Medicine,
Rochester, MN
of Emergency Medicine, University
Assistant Professor of Emergency
Baltimore, MD
of Michigan, Ann Arbor, MI
Medicine, Mount Sinai School of
Alfred
Sacchetti,
MD,
FACEP
Medicine; Director of Emergency
John M. Howell, MD, FACEP
Assistant Clinical Professor,
Critical Care, Elmhurst Hospital
Clinical Professor of Emergency
Department of Emergency Medicine,
Center, New York, NY
Medicine, George Washington
Nicholas Genes, MD, PhD
Instructor, Department of Emergency
Medicine, Mount Sinai School of
Medicine, New York, NY
Research Editor
Lisa Jacobson, MD
Chief Resident, Mount Sinai School
of Medicine, Emergency Medicine
Residency, New York, NY
International Editors
Peter Cameron, MD
Chair, Emergency Medicine,
Monash University; Alfred Hospital,
Melbourne, Australia
Giorgio Carbone, MD
Chief, Department of Emergency
Medicine Ospedale Gradenigo,
Torino, Italy
Amin Antoine Kazzi, MD, FAAEM
Associate Professor and Vice Chair,
Department of Emergency Medicine,
University of California, Irvine;
American University, Beirut, Lebanon
Hugo Peralta, MD
Chair of Emergency Services,
Hospital Italiano, Buenos Aires,
Argentina
Maarten Simons, MD, PhD
Emergency Medicine Residency
Director, OLVG Hospital, Amsterdam,
The Netherlands
Accreditation: This activity has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education
(ACCME) through the sponsorship of EB Medicine. EB Medicine is accredited by the ACCME to provide continuing medical education for physicians. Faculty Disclosure: Dr.
McCurdy, Dr. Mitarai, Dr. Perkins, Dr. Reed, Dr. Weingart, and their related parties report no significant financial interest or other relationship with the manufacturer(s) of any
commercial product(s) discussed in this educational presentation. Commercial Support: This issue of Emergency Medicine Practice did not receive any commercial support.
Presenting vitals include a heart rate of 120 beats per
minute and a respiratory rate of 32 breaths per minute.
Oxygen saturation is 96% on 15 L of oxygen by nonrebreathing mask, and the patient is afebrile. His bedside
glucose measurement is 98 mg/dL. Physical examination
reveals a regular tachycardia with somewhat distant heart
sounds and clear lungs with shallow respirations. The
remainder of the examination is unremarkable. Concerned
that the patient will be unable to maintain an airway,
you prepare to intubate him. Meanwhile, you quickly run
through the differential for this patient with hypotension,
tachycardia, and altered mental status. The intubation
goes smoothly but the patient becomes more hypotensive
after the tube has been placed. The nurse hands you his
ECG and, appearing very concerned, asks, “What do you
think is going on?”
and identifying the transport destination that is best
prepared to manage the patient’s illness. Ideally,
each cancer patient should be taken to the hospital
with which his or her oncologist is affiliated; unfortunately, the available literature does not help
define the impact on outcome when the patient is
transported to a different hospital, and clearly more
research is needed on this topic.
Paramedics charged with caring for patients
with oncologic emergencies should be familiar with
the region-specific transport protocols and be aware
that the length of time that elapses before evaluation and treatment in the ED can significantly alter
outcomes. Gathering as much medical history as
possible from caregivers and resources at the scene,
including code status and advance directives, is extremely valuable to medical personnel who receive
the patient in the ED.
O
ncologic emergencies are not everyday occurrences in the ED, even at tertiary care centers.
Yet, because of the growing number of patients in
cancer treatment, those with problems related to their
disease and its treatment will inevitably present to
EDs. Since patients with cancer are at higher risk for
significant morbidity and mortality at baseline, the
potentially catastrophic complications of malignancy
can quickly turn lethal. Therefore, it is essential for
the emergency clinician to recognize these infrequent
presentations and be prepared to treat them. This
issue of Emergency Medicine Practice provides a review
of 3 important cancer-related complications: malignant epidural spinal cord compression, superior vena
cava syndrome, and malignant pericardial effusion
and tamponade. The March 2010 issue of Emergency
Medicine Practice, Oncologic Emergencies Part II, will
address the topics of neutropenic fever, tumor lysis
syndrome, and hypercalcemia of malignancy.
Malignant Epidural Spinal Cord Compression
Malignant epidural spinal cord compression
(ESCC) is a serious complication of cancer, with
an incidence of 5% in the population with cancer2,3 and a median survival of only 6 months
after diagnosis.4,5 Although prompt recognition
and timely treatment will ensure good functional
outcomes in the majority of patients, diagnosis of
this complication is often delayed because the presentations are frequently varied and atypical and
clinicians’ index of suspicion is low. In a prospective, observational study of 310 patients, a delay
in diagnosis was the primary cause for postponing
treatment for a median of 2 months from the onset
of back pain and for a median of 2 weeks from the
onset of actual signs consistent with spinal cord
compression.6 Since the vast majority of cases of
malignant spinal cord compression result from
epidural (extradural) compression, it is the focus
of this review. Other less common causes include
intramedullary metastases (intradural involvement)7 and leptomeningeal metastases (dural
involvement).8,9
Critical Review Of The Literature
An Ovid MEDLINE® (www.ovid.com) and PubMed
(www.pubmed.gov) search was performed using the
terms malignant epidural spinal cord compression, superior vena cava syndrome, and malignant pericardial tamponade in articles published between 1966 and 2008.
The search yielded numerous studies ranging from
case series to randomized, double-blind, placebocontrolled trials; in addition, standard textbooks were
reviewed.1 Of the 3 topics, the literature on malignant
epidural spinal cord compression offered the best
evidence to support recommendations for its management. Evidence regarding management recommendations for the other 2 conditions was largely based on
case reports and observational cohort studies.
Etiology Of ESCC
Spinal cord compression is generally defined as
a condition in which thecal sac impingement is
evident on radiography but may or may not manifest clinical findings that correspond to the level of
impingement. Tumors invade the epidural space in
essentially 2 ways: (1) directly from vertebral bone
metastases, or (2) from extension through the neural
foramina from nearby structures, such as lymph
nodes or nerve bundles. Compression of the epidural sac and encasement of the spinal cord ensue,
causing an elevation in pressures within the venous
plexus that supplies the cord. Vasogenic edema occurs and leads to spinal cord ischemia.
Prehospital Care
Prehospital care is directed toward the presenting
complaint, with a focus on stabilizing the patient
Emergency Medicine Practice © 2010
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Approximately 90% of cases of ESCC are due
to extension of metastases in the vertebral bodies.10
Metastatic deposits in the vertebrae come primarily
from hematogenous (arterial and venous) sources.
The amount of arterial blood flow that a vertebra
receives depends on the volume of bone present.
Therefore, sections of vertebrae with more bone
volume (specifically the lumbosacral and thoracic
spine) have a greater likelihood of being seeded by
vascularly spread metastases.
In approximately 70% of patients with malignant
cord compression, the metastasis is located within
the thoracic spine, 20% are located in the lumbosacral
spine, and 10% in the cervical spine.11 The disproportionately greater percentage of cases of ESCC in the
thoracic region is thought to result from the relatively
smaller available free space within the thoracic canal,
which makes metastatic disease at this level more
frequently symptomatic.12 Though most metastases
are of arterial origin, many lumbosacral vertebral
metastases arise from venous sources. In general,
this is most likely due to the absence of valves in the
venous plexus that connects the lumbosacral spine
to organs such as the prostate. In the remaining 10%
of cases of ESCC, metastases gain access to the spinal
cord by penetrating the neural foramina.10 Although
less common, this mechanism of spinal cord compression is important because of the complete absence of
abnormalities associated with it on plain radiography,
as will be discussed later.
Since the majority of cases of ESCC are caused
by vertebral metastases, the likelihood of epidural
compression is related to both a tumor’s incidence
and its affinity for vertebral bone metastasis.13 Bone,
breast, lung, and prostate cancers account for 60%
of cases of ESCC.14 Approximately 25% of cases are
associated with non-Hodgkin’s lymphoma, renal cell
cancer, and multiple myeloma.15
often used to evaluate patients with cancer).17 Other
key features in the history can also provide insight
into the cause of a patient’s pain. For example, about
75% of patients with ESCC present with focal weakness,16 50% with bowel or bladder dysfunction,16 40%
to 90% with sensory abnormalities,13 and many others
with radicular pain or ataxia (due to impingement of
the spinocerebellar tract along the posterior aspect
of the spinal cord).18 Motor abnormalities typically
follow a sequential pattern of progressive weakness,
ataxia, and finally, paralysis.16
The emergency clinician should ask patients
about the following 6 subjects: (1) the type of cancer
they have and whether there are known metastases;
(2) whether they have undergone or are undergoing
radiation therapy or chemotherapy; (3) the results
of previous imaging studies; (4) recent trauma; (5)
risk factors that might point to other causes for
the symptoms; and (6) information about advance
directives and their wishes regarding workup and
treatment for possible oncologic complications.
Physical Examination For ESCC
The physical examination is a vital part of the evaluation for ESCC. Back tenderness is present in the
majority of patients with ESCC, and when localized
to the thorax, is thought to be more frequently associated with a malignant etiology. Sensory abnormalities are typically found as many as 5 levels below the
compressed cord.19 Reflexes below the level of the
cord lesion often become hyperresponsive as compression and neurologic injury progress. Although
no studies have specifically assessed the use of ED
ultrasound in this clinical situation, it may be a useful adjunct in evaluating urinary retention, which is
present in up to 50% of patients who present with
ESCC.16 Upon diagnosis, approximately 75% of
patients have weakness, which is generally due to
compression of the corticospinal tract located along
the anterior spinal cord.16 Lower extremity weakness
may be more suggestive of thoracic compression,20
and in 1 study of 310 patients with ESCC, over half
were nonambulatory at the time of diagnosis.6 An
important concept to remember is that the neurologic status of patients before treatment for ESCC is
the most important prognostic factor for neurologic
status after treatment.21
History For ESCC
Targeted questions during the patient interview
help stratify risk in individuals who present with
symptoms that suggest malignant ESCC. In patients
with a history of cancer, any suggestive symptoms
should be considered red flags for the presence of
ESCC, since back pain due to nerve damage, tumor
expansion, or vertebral collapse is the first symptom
in 95% of patients with ESCC,9 usually preceding all
other symptoms by up to 2 months.3,16 Although back
pain is a sensitive indicator of ESCC and is usually
what prompts a patient to seek medical attention, it
is rarely specific for the site of the lesion. The classic
teaching that pain worsens with recumbence was not
validated in a prospective series of 170 patients.17
Certain findings elicited on history-taking are associated with a higher risk for epidural compression;
these include pain at night and a low Karnofsky score
(a global assessment of independent function that is
February 2010 • EBMedicine.net
Diagnostic Studies For ESCC
The history and physical examination alone are
insufficient to diagnose or rule out ESCC. Radiologic
evidence of cord compression provides the basis for
the diagnosis of ESCC.
Laboratory Testing
Although there is no evidence to suggest that routine laboratory data aid in the diagnosis of malignant cord compression, such information may be
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Emergency Medicine Practice © 2010
Clinical Pathway For Evaluation Of Suspected Malignant
Epidural Spinal Cord Compression
Patient with back pain and
history of malignancy
Normal neurological exam
Abnormal neurological exam
Low suspicion of ESCC
High suspicion of ESCC
Administer empiric steroids
(see page 6 for dose) (Class II)
Excellent follow-up
Unreliable follow-up
Outpatient MRI or CT myelogram within
24 hours (Class III)
Emergent MRI or CT myelogram
(Class I)
No ESCC
ESCC
Admit; consult oncology, neurosurgery,
and radiation oncology as appropriate
Consider alternate diagnosis
Class Of Evidence Definitions
Each action in the clinical pathways section of Emergency Medicine Practice receives a score based on the following definitions.
Class I
• Always acceptable, safe
• Definitely useful
• Proven in both efficacy and
effectiveness
Level of Evidence:
• One or more large prospective
studies are present (with rare
exceptions)
• High-quality meta-analyses
• Study results consistently positive and compelling
Class II
• Safe, acceptable
• Probably useful
Level of Evidence:
• Generally higher levels of
evidence
• Non-randomized or retrospective studies: historic, cohort, or
case control studies
• Less robust RCTs
• Results consistently positive
Class III
• May be acceptable
• Possibly useful
• Considered optional or alternative treatments
Level of Evidence:
• Generally lower or intermediate
levels of evidence
• Case series, animal studies, consensus panels
• Occasionally positive results
Indeterminate
• Continuing area of research
• No recommendations until
further research
Level of Evidence:
• Evidence not available
• Higher studies in progress
• Results inconsistent, contradictory
• Results not compelling
Significantly modified from: The
Emergency Cardiovascular Care
Committees of the American
Heart Association and represen-
tatives from the resuscitation
councils of ILCOR: How to Develop Evidence-Based Guidelines
for Emergency Cardiac Care:
Quality of Evidence and Classes
of Recommendations; also:
Anonymous. Guidelines for cardiopulmonary resuscitation and
emergency cardiac care. Emergency Cardiac Care Committee
and Subcommittees, American
Heart Association. Part IX. Ensuring effectiveness of communitywide emergency cardiac care.
JAMA. 1992;268(16):2289-2295.
This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient’s individual
needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright © 2010 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Practice, LLC.
Emergency Medicine Practice © 2010
4
EBMedicine.net • February 2010
helpful in the management of comorbidities and
in preparing for further invasive interventions (eg,
platelet count prior to lumbar puncture, or serum
creatinine levels prior to contrast-enhanced imaging studies). In rare cases, cerebrospinal fluid (CSF)
analysis to detect leptomeningeal metastasis may
be performed, and an alternative diagnosis may be
found to explain a patient’s presentation.
sion, as evidenced by 27% of the 280 patients with
ESCC mentioned earlier whose sensory levels were
either 4 vertebral segments below or 2 vertebral
segments above the MRI-confirmed area of compression.25 Contrast-enhanced images with gadolinium
provide better visualization of the less-common leptomeningeal metastases and intramedullary tumors,
but the evaluation of epidural spinal cord compression does not require intravenous (IV) contrast.31
Plain Radiography
Clinicians should not rely on plain radiography as the
only tool for diagnosing cord compression. Vertebral
compression cannot be visualized unless there has
been bone loss of up to 50%.9 Ten percent of cases of
ESCC are caused by neuroforamen invasion without
significant bone destruction. In fact, even when vertebral collapse is evident on an x-ray film, the overall
sensitivity of plain radiography for ESCC is approximately 75%,3 which drops to 66% in patients with lymphoma.22 In the absence of other available radiographic
modalities, x-ray evidence of compression coupled
with clinical findings that are consistent with that level
of sensory abnormality can aid in the diagnosis and
management of clinically relevant ESCC.17,23
Computed Tomography With Myelography
Myelography is an inherently invasive imaging modality in which a lumbar puncture is performed and
contrast dye is injected into the spinal canal during
fluoroscopy to highlight any existing flow obstructions that may indicate spinal cord compression. For
many years, it was the standard imaging modality
used in the assessment of patients suspected of having ESCC. Although myelography was useful for
detecting blockages in the spinal canal, it was not
particularly helpful in assessing the degree of cord
injury or other anatomic abnormalities proximal to
the obstruction.
With the advent of MRI and computed tomography (CT), imaging quality has been greatly
enhanced, allowing for much better anatomic detail
of the spine. Since spinal CT alone (with or without
contrast) does not adequately image the spinal cord
Magnetic Resonance Imaging
If ESCC seems likely, based on history and physical
examination, the diagnostic evaluation should proceed directly to magnetic resonance imaging (MRI).
(See Figure 1.) Despite slight variations in readings,
and depending on the experience of the radiologist,
the overall accuracy of MRI for ESCC is high (93%
sensitivity, > 97% specificity, > 95% positive predictive value).24-26 Additional benefits of MRI, including
its noninvasive nature, cost-effectiveness, and ability
to image the entire spine to look for compression,
intramedullary lesions, and bone metastases, make
this modality the study of choice for suspected
ESCC.27 Approximately one-third of all patients
diagnosed with ESCC have multiple sites of epidural metastases, so being able to image the entire
spine is extremely valuable.23,25,28-30 If MRI is unavailable or if the patient cannot tolerate the lengthy
imaging time, focused imaging of those areas that
arouse clinical suspicion is a reasonable temporary
alternative.23 In a study of 280 patients with confirmed ESCC, if clinical findings were suspicious for
thoracic or lumbar cord injury, less than 1% of the
patients had cervical lesions.25
Therefore, it is probably safe to forgo MRI of the
cervical spine if plain films initially verify thoracic or
lumbar cord compression which is then corroborated
on the clinical examination. Nevertheless, careful
imaging of the thoracic and lumbar spine should be
performed in all ESCC patients to rule out multiple
epidural metastases. Overall, it is important to note
that the sensory level affected does not necessarily
correspond to the area of suspected cord compresFebruary 2010 • EBMedicine.net
Figure 1. MRI Showing Spinal Cord
Compression At C5
Reprinted with permission from Michael McCurdy, MD, and the University of Maryland Medical Center.
5
Emergency Medicine Practice © 2010
itself or the epidural space, it is not recommended
in the evaluation of ESCC. However, in the absence
of available MRI or CT myelography, noncontrast
spinal CT could be used to evaluate the vertebrae
for possible compression fractures or cortical bone
discontinuity that could suggest cord compression.32
CT imaging is very useful when used in conjunction with myelography. In fact, when the flow
of contrast in the CSF is not halted by a completely
occluded spinal canal, CT myelography allows
good-quality visualization of paraspinal and spinal masses, with sensitivity and specificity that is
comparable to those of MRI (both over 95%) in the
evaluation of ESCC.33,34 The invasive nature of CT
myelography often prohibits its use in many cancer
patients, who are often severely thrombocytopenic.
Moreover, patients with complete subarachnoid
blockage may neurologically decompensate when
lumbar puncture reduces CSF pressure below the
block; no studies have been carried out to determine
what risk factors might predict this rare occurrence.
Despite its risks, CT myelography is a worthwhile
and proven alternative to MRI when the latter is
unavailable or contraindicated.
Corticosteroids
Vasogenic edema of the spinal cord associated with
ESCC can be mitigated by the use of corticosteroids, a mainstay of treatment that should be started
in the ED. The benefits of steroids are generally
well-accepted. In the most-quoted randomized
controlled trial of corticosteroids for patients with
myelography-confirmed ESCC treated with radiation therapy, high-dose dexamethasone (IV bolus of
96 mg, followed by 24 mg orally 4 times daily for 3
days, and then tapered over the next 10 days) was
compared with no steroid therapy.38 The 3-month
post-radiation evaluation demonstrated a significantly higher rate of ambulation in the group treated
with steroids (81% of patients) vs the group without
steroid therapy (63%).
The safety of high-dose vs low-dose steroids is
still a matter of controversy. One case-control study
compared high-dose dexamethasone (same regimen
as noted above) with a low-dose regimen (10 mg IV
bolus, then 4 mg IV daily, tapered over 2 weeks).
Although the 2 regimens had similar efficacy rates,
the high-dose regimen was associated with many
side effects.39 Despite inconclusive evidence regarding the proper steroid dose for ESCC, expert recommendations are to administer high-dose steroids
(dexamethasone, 100 mg IV bolus, with a rapid
taper, halving the total daily dose every 3 days if the
patient is stable) for patients with myelopathy or
abnormal neurologic findings on examination, and
low-dose steroids (dexamethasone, 10 mg IV bolus
with 4 mg IV doses daily, tapered over 2 weeks)
for all other patients, such as those in whom only
radiographic evidence of ESCC exists in the absence
of corresponding clinical findings.9,40 Large-scale
studies are needed to determine the most appropriate dose of steroids for ESCC.
Bone Scintigraphy
More efficient, accurate, and comprehensive radiographic modalities have largely supplanted the
bone scan in the detection of ESCC. However, when
both MRI and CT myelography are contraindicated
or not available, bone scintigraphy can still be of
value. Plain radiographs in conjunction with bone
scintigraphy have been reported to have a sensitivity
as high as 98% for ESCC.35 In these difficult cases,
consultation with the radiation oncologist, neurosurgeon, or primary oncologist is recommended.
Treatment For ESCC
Surgery
The generally accepted indications for surgical
decompression include spinal instability (defined by
gross spinal deformity or bony retropulsion into the
canal), previous radiation therapy in the compressed
area, a need for tissue diagnosis of a primary malignancy, disease progression despite radiation and
steroids, and the presence of radioresistant tumors
(eg, melanoma, sarcoma, or renal cell carcinoma).20,41
The debate over the appropriate criteria for selecting surgery and/or radiation therapy is ongoing.
Various retrospective studies report similar neurologic outcomes in patients who undergo radiation
plus laminectomy and those who receive radiation
only,6,42 with some studies demonstrating slightly
improved outcomes with the latter.43 As previously
discussed, the majority of cases of malignant ESCC
originate from the vertebral bodies. However, in
earlier studies (mostly in the 1980s), the surgical arm
involved posterior laminectomy, which conceptually
would relieve pressure within the epidural space
The neurologic status of patients before treatment
for ESCC is the most important prognostic factor for
neurologic status after treatment.21 The timing of a
patient’s presentation may also have prognostic value, with 1 prospective study failing to demonstrate
any improvement in neurologic status if a patient’s
deficits developed rapidly within the 48-hour period
prior to presentation.36 The emergency clinician
must understand the significant prognostic implications of the patient’s presenting neurologic status,
and treatment goals for each individual patient
should be well-defined before therapy is initiated.
It is imperative to involve the appropriate consultants in the early and definitive management of
patients with ESCC. In most circumstances, the goals
are to improve or maintain a patient’s pretreatment
neurologic function, to control local tumor growth,
to stabilize the spine, and to control pain.37 Standard treatment typically involves a combination of
steroids, surgery, and/or radiation.
Emergency Medicine Practice © 2010
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EBMedicine.net • February 2010
itself without addressing the site of metastasis. A
more recent large, prospective, randomized trial
assigned patients to either radiation therapy alone
or to radical surgical decompression (involving only
the anterior vertebral body in 60% of cases) followed by postoperative radiation. Ambulation time
was significantly longer for the group treated with
surgery plus radiation than for those treated with
radiation alone (median time = 126 vs 35 days).44
The conclusions reached in this study and in similar
studies have made surgical management a much
more attractive initial treatment option for patients
who present with ESCC, although formal guidelines
from specialty societies have not yet been issued.45
neurologic function is normal will remain ambulatory regardless of the type of treatment.46
Summary Of ESCC
A delay in the diagnosis of malignant ESCC often
results in significant morbidity. Therefore, early
suspicion, diagnosis, and treatment are paramount in
obtaining the best neurologic outcome. Back pain is
usually the earliest symptom, and MRI is the diagnostic test of choice, although CT myelography is a
reasonable alternative. Imaging of the entire spine
is recommended, since patients can have multiple
sites of metastasis. Initiation of steroids in the ED is
indicated, after which most patients with ESCC are
treated with either radiation alone or surgical decompression along with radiation therapy. Pretreatment
ambulatory status is the most important determinant
of posttreatment ambulation and should therefore be
well-documented at the time of diagnosis.
Radiation Therapy
Radiation therapy is of benefit in patients with
ESCC who have already undergone radical spinal
decompression,44,45 who have no spinal compression
or instability, who have subclinical cord compression (radiographically evident but without clinical
signs or symptoms consistent with compression),21
and who are not eligible for surgery. Although the
value of radiation therapy in these circumstances
has been well-proven, the ideal dosages and schedule regimens for the treatment of ESCC have still
not been determined. The poor survival rates of
patients treated with radiation (median = 6 months)
is thought to be associated with the severity of the
underlying malignancy rather than with the radiation therapy. Intuitively, it is assumed that radiation would be more successful in the recovery of
neurologic function in patients with radiosensitive
tumors (eg, lymphoma, myeloma, breast, prostate,
and small-cell lung cancers) than in patients with
radioresistant ones (eg, melanoma, sarcoma, and
renal cell carcinoma). Nearly half of all patients who
receive radiation therapy and who are still alive 1
year after the procedure maintain their ability to
ambulate.13 Further clarification is needed to identify
which subgroups benefit from particular combinations of radiation therapy and surgery.
Disposition Of Patients With ESCC
Patients who are diagnosed in the ED with ESCC
should be admitted to the hospital for pain control,
frequent neurologic assessments, and definitive
treatment. The involvement of all the appropriate
specialties (eg, neurosurgery, radiation oncology,
and oncology) is critical to ensure the most effective
level of care.
Superior Vena Cava Syndrome
Superior vena cava syndrome (SVCS) is a rare but
potentially serious complication of an underlying malignancy. Throughout the second half of the 20th century, the condition was almost exclusively limited to
malignancy-related obstruction of the superior vena
cava. However, with the growing number of patients
dependent on dialysis, the incidence of catheter-related thrombosis as a cause of SVCS has increased significantly. SVCS is generally considered an “urgency”
rather than emergency related to cancer.47
Epidemiology Of SVCS
Special Circumstances: Malignant ESCC In
Children
SVCS, which affects approximately 15,000 people
per year in the United States,48 was first described
in 1757 by Hunter in a case report of a patient with
syphilis in whom a thoracic aortic aneurysm was
compressing the superior vena cava. Until the 1950s,
SVCS was most commonly associated with syphilis
and tuberculosis.48,49 In the late 20th century, however, 85% to 97% of SVCS cases are caused by malignancy.50 Approximately 80% of these cases result
from lung cancer (most commonly bronchogenic),
10% from lymphoma (mostly non-Hodgkin’s), and
10% from metastatic disease (eg, breast cancer).
Interestingly, only a small fraction of patients with
lung cancer (3% to 5%) will have SVCS during the
course of their illness.48 Nonmalignant causes of
The prevalence and management of particular
malignancies in children differ from those in adults.
Pediatric malignant ESCC most frequently arises
from paravertebral tumors that invade the epidural
space through the neuroforamen, leaving spinal
bone intact. Ewing’s sarcoma and neuroblastoma are
the 2 most common causes of ESCC in children. Ewing’s and other sarcomas are best treated by surgical
decompression alone or in conjunction with postoperative medical therapy. However, neuroblastomas,
Hodgkin’s disease, and germ cell tumors are best
treated with chemotherapy, with or without radiation. Two-thirds of children whose pretreatment
February 2010 • EBMedicine.net
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Emergency Medicine Practice © 2010
neck, and upper-extremity swelling, especially when
they are lying down or bending over. Dyspnea,
cough, facial flushing, and hoarseness often occur,
but frank airway obstruction from laryngeal edema
is rare. Patients may also experience headache,
confusion, or lethargy as venous drainage from the
intracranial space becomes compromised. In the
case series by Rice et al, the most common signs
and symptoms were face or neck swelling (82%),
upper-extremity swelling (62%), dyspnea at rest
(53%), cough (50%), and dilated chest veins (38%).49
Interestingly, certain symptoms were significantly
more common in SVCS due to cancer than in SVCS
due to other causes; these included dyspnea at rest
(64% vs 35%), cough (70% vs 19%), and chest or
shoulder pain (28% vs 2%). These findings suggest
that the symptoms attributed to SVCS may actually
be caused by the underlying cancer.47,50,53
SVCS include infection (eg, histoplasmosis, tuberculosis, syphilis, actinomycosis, mediastinitis), vascular problems (eg, aortic aneurysm), and trauma and
local thromboses related to central venous catheters
and pacemaker wires.48 In their retrospective case
series, Rice et al found that of 78 patients with SVCS,
40% of cases were due to causes other than cancer,
with the majority stemming from catheters inserted
for chemotherapy access and dialysis.49
Pathophysiology Of SVCS
SVCS results from the occlusion of the superior vena
cava (SVC) due to either external compression or
internal obstruction. A short review of the relevant
anatomy will help to explain its pathophysiology.
The SVC is formed by the junction of the brachiocephalic veins. Before entering the right atrium, it
merges posteriorly with the azygos venous system.
It is a low-pressure vessel with thin walls surrounded by right paratracheal, perihilar, and subcarinal
lymph nodes; the ascending aorta; and other mediastinal structures such as the trachea, right bronchus, pulmonary artery, and thymus.47,51 Significant
enlargement of any of these structures can compress
the SVC. The surrounding lymph nodes drain
mostly from the right side of the lung, which may
explain why right-sided lung cancer is 4 times more
common than left in patients with SVCS due to lung
cancer.47 If the obstruction is above the level of the
azygos vein, this vein can partially accommodate an
increase in venous flow from the head, neck, and upper extremities. If the obstruction is below the azygos attachment, the venous flow has to go through
the abdominal venous system. Owing to the abdomen’s more limited capacity to shunt venous flow,
the symptoms of obstruction can be more severe.51
Diagnosis Of SVCS
Clinical suspicion for SVCS depends on a thorough
history and physical examination. Many patients
present to the ED more than once before the true
etiology is uncovered. Imaging studies are needed to
confirm the clinician’s suspicion and can elucidate the
cause, exact location, and extent of the obstruction.
Plain Radiography
A chest radiograph can provide clues to the diagnosis. In a retrospective case series involving 125
patients, Armstrong et al found that 78% of patients
with SVCS had an abnormal chest radiograph (59%
with a superior mediastinal mass and 19% with a
right hilar mass).54
Chest CT
This modality is preferred in the emergency setting
for several reasons: it is widely available, provides
anatomic details of both the extent of obstruction and
collateral flow, and can potentially identify causes of
the syndrome (eg, compression vs indwelling catheter-related disease). The presence of any collateral
veins in the abdomen and thorax on CT is an accurate
predictor of SVCS (sensitivity 96%, specificity 92%).47
In a retrospective review of 19 patients with pathologically confirmed SVCS, 94.7% had at least 1 enlarged
collateral vein at or below the level of the diaphragm
that was apparent on abdominal CT scans.55 No reports in the literature specifically address the sensitivity or specificity of CT for SVCS nor are there any contraindications to the use of this modality other than
those inherent in the use of contrast-enhanced media.
Clinical Presentation Of SVCS
The severity of symptoms of SVCS varies, depending on the site of obstruction relative to the azygos
vein. Incomplete occlusion may be asymptomatic,
whereas complete and extensive occlusion involving the collateral circulation can cause significant
morbidity. In addition to the location and extent of
obstruction, its acuity plays an important role. When
obstruction occurs rapidly, there is not enough time
for collateral circulation to develop. In general, sudden presentations are the exception. Delayed presentations tend to be the rule, making diagnosis more
difficult. More than 75% of patients have signs and
symptoms of SVCS for longer than 1 week before
seeking medical attention.52 It is not uncommon for
patients to complain of SVCS-related symptoms for
weeks, or even months.53
The symptoms and findings on examination
reflect the underlying venous congestion. Symptoms
tend to be worse upon awakening and improve as
the day progresses. Patients typically have facial,
Emergency Medicine Practice © 2010
MRI
Although MRI is considered the diagnostic modality
of “choice” because of the excellent anatomic detail
it provides, it may not be routinely available in EDs,
and its use may be limited by the presence of incom8
EBMedicine.net • February 2010
patible metals within a patient, the inability to lie flat
for an extended amount of time, or an allergy to or
contraindication to the use of gadolinium. Hansen et
al found that MRI detected thoracic venous obstruction with 94% sensitivity and 100% specificity.56
patients with SVCS associated with non-small-cell
carcinoma (NSCC), 60% had relief of the SVC occlusion following chemotherapy and/or radiation
therapy, and the rate of recurrence for occlusion was
19%.57 In general, surgical bypass is reserved for
patients with nonmalignant causes of SVCS, whose
better long-term prognosis justifies an invasive approach.47,53 On the other hand, endovascular stent is
a less invasive and yet very effective alternative for
cancer-related SVCS. This procedure is especially
useful among patients with acute and severe symptoms for whom immediate treatment is needed, and
for whom radiation or chemotherapy has failed.53 In
the study of NSCC patients, placement of an endovascular SVC stent relieved SVC occlusion in 95% of
patients, with a recurrence rate of 11%.57
The emergency clinician must bear in mind
various key elements when caring for patients who
present with malignancy-induced SVCS. Addressing the “ABCs” is always the priority, and particular
attention should be paid to the patency of airway. In
extreme cases, patients can lose their airway secondary to cerebral edema or stridor from SVCS. Elevating the patient’s head and providing supplemental
oxygen are 2 simple measures that are generally
recommended despite the lack of quality evidence to
support their benefit.50 Diuretics often result in dehydration in this setting and have not been proven
to be efficacious; therefore, they are not recommended for patients with SVCS. In addition, no evidence
supports the use of empiric corticosteroids, and
they should not be routinely administered in the ED
(although they may be considered if a tissue diagnosis has been established and the tumor is known
to be responsive to steroids). Consultation with the
primary oncologist is recommended to assist with
this decision.
If the SVCS is caused by the large acute or subacute thrombosis, the emergency clinician should
consult with an interventional radiologist, who can
give thrombolytic therapy directly into the thrombus
by infusion catheters that are centered in the thrombus. The literature has not addressed the issue of the
ideal location for IV access in patients with SVCS,
but the authors recommend obtaining femoral access
if a central line is needed. Internal jugular and subclavian central lines may further complicate SVCS
with local thrombosis; however, since many of these
patients only have partial SVC obstruction, and
since those with complete obstruction usually have
some degree of collateral circulation, upper-extremity peripheral venous access is generally sufficient.
Contrast Venography
CT, MRI, and nuclear imaging have largely replaced
this invasive procedure; however, contrast venography is still considered a useful adjunctive modality
for patients being evaluated for surgical or radiologic interventions.
Radionuclide Venography
This test requires nuclear tracers and a significant
amount of time, thus limiting its usefulness in the
ED setting. It is less invasive than contrast venography but also less specific in defining patency and
flow.47 If a patient has a contraindication to both CT
and MRI, this study is a viable option to diagnose
SVCS. Discussion with a radiologist is encouraged
when choosing the optimal imaging modality for the
individual patient.
Treatment Of SVCS
The cause of SVCS should be determined before
initiating treatment for the following reasons:
1. The syndrome is usually insidious, so one typically has time to make a diagnosis.
2. There is no role for empiric radiation or chemotherapy in nonmalignant causes of SVCS.
3. Different cancers have variable sensitivities to
radiation and chemotherapy.
4. In SVCS caused by cancer, patients do not usually die from SVCS itself, but rather from progression of the underlying malignancy, and the
prognosis depends on the type of tumor.
Since the long-term prognosis for patients with
malignancy-related SVCS is generally poor, treatment should focus on improving quality of life.
Tissue diagnosis and definitive treatment typically begin after the patient has been admitted to
the hospital. Coordination of subspecialties such
as oncology, radiation oncology, interventional
radiology, and pulmonology is often necessary to
develop an appropriate therapeutic regimen. Once
a malignant cause has been established, decisions
regarding potential chemotherapy, radiation treatment, or even endovascular stent placement can be
addressed. Multiple factors will affect this process,
including a patient’s clinical stability, comorbidities,
functional status, personal preference, and possible
hospice status. In patients with SVCS associated
with small-cell lung carcinoma, nonrandomized
trials have demonstrated that chemotherapy and/
or radiation therapy relieves SVC occlusion in 77%
of patients, with a recurrence rate of only 17%.57 For
February 2010 • EBMedicine.net
SVCS Summary
The clinical signs and symptoms of SVCS are often
subtle and subacute, and can easily divert the ED
clinician from the true diagnosis. Consequently, it is
not unusual for a patient with SVCS to present many
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Emergency Medicine Practice © 2010
times before the correct diagnosis is established. The
clinician must be astute and focus on the relative
chronicity of symptoms in order to entertain the
infrequent diagnosis of SVCS. Once the diagnosis is
suspected, it can be confirmed by CT or MRI. Treatment in the ED should focus on an assessment of
the patient’s airway and coordination of care with
appropriate subspecialties to ensure the lowest morbidity and mortality after hospital admission.
Cardiac tamponade is one of the true emergencies
in emergency medicine. The list of causes of cardiac
tamponade is long and ranges from trauma to malignancy. With increased awareness of this complication
and relatively easy access to bedside echocardiography, it is likely that emergency clinicians will be diagnosing more cases of malignant pericardial effusion
and tamponade in the future. Although it is not necessary to diagnosis every case of pericardial effusion
in the ED, it is crucial to identify cardiac tamponade
promptly, since early intervention can be lifesaving.
estimated to be 2 months; only about 25% of patients
live for an additional 2 years.60 Metastatic pericardial involvement is approximately 16 times more common than are primary tumors of the pericardium.61
Theoretically, any cancer can metastasize to the
pericardium. Cancers originating above the diaphragm are the most common sources of metastatic
pericardial disease, with lung and breast cancer
accounting for about half of all cases. Lymphoma,
leukemia, and melanoma account for an additional
25% of metastatic disease.62 It is generally believed
that the majority of patients with pericardial metastases have a known underlying cancer with
metastatic disease in other organ systems. However,
in a small case series of 23 patients with cardiac
tamponade, Haskell et al found that 8 patients had
cardiac tamponade as the first clinical manifestation
of previously undiagnosed cancer.63 Seven patients
were seen by a physician prior to the ultimate diagnosis of tamponade, and 6 patients were incorrectly
diagnosed as having bronchitis, congestive heart
failure, or pneumonia despite abnormal findings on
chest radiograph that should have raised suspicion
for malignancy. These findings reinforce the need
for clinicians to consider pericardial effusion and
tamponade in patients who present with signs and
symptoms of concern.
Patients with an underlying malignancy can
have a pericardial effusion that is not caused by the
cancer. In addition to malignancies of idiopathic origin, other etiologies include radiation, medications,
hypothyroidism, infection, end-stage renal disease,
and autoimmune disorders. In roughly 20% to 40%
of malignant pericardial effusions, the results of
cytologic analysis are negative62; therefore, experts
recommend that a pericardial fluid sample be tested
for protein, lactic dehydrogenase, hematocrit, glucose, cell count, and culture to aid in the diagnosis.
Epidemiology Of Malignant Pericardial
Effusion And Tamponade
Pathophysiology Of Malignant Pericardial
Effusion And Tamponade
Disposition Of SVCS Patients
Patients with respiratory compromise are best
managed in the intensive care unit (ICU) setting.
Coordination with other specialties (eg, radiation
oncology) is essential before considering intervention to relieve the obstruction. Most patients will be
clinically stable and can be given a regular floor bed
on the appropriate medical service. In select cases,
discharge may be appropriate if the primary doctor
(eg, oncologist) is aware of the diagnosis of SVCS
but judges that admission is not indicated (eg, for a
hospice patient).
Malignant Pericardial Effusion And Cardiac
Tamponade
Pericardial effusion is the most common complication associated with metastases to the heart and
pericardium. One might believe that metastasis to
the pericardium is a relatively uncommon phenomenon, but an autopsy series of patients with cancer
reported by DeLoach and Haynes showed that 15%
to 20% of patients had metastases to the heart and
pericardium.58 The majority of these patients did not
have a history of metastatic burden; in most cases,
this complication remains clinically silent during a
patient’s lifetime. Of the 137 patients with cardiac
metastases, 22 had pericardial effusions but only
2 had symptoms attributable to the effusions.58 In
contrast, another case series reported by Thurber et
al demonstrated that 55 of 189 (29%) patients with
pericardial metastases had symptoms believed to be
related to the effusion.59 Once a malignant pericardial effusion has been diagnosed, median survival is
Emergency Medicine Practice © 2010
The pericardium consists of 2 membranes: parietal
and visceral. The visceral membrane is composed
of a single layer of mesothelial cells that adhere
to the myocardium, and the parietal membrane
is a fibrous layer surrounding the heart. The fluid
between these 2 membranes (up to 50 mL) functions
as a physiologic lubricant. In order for a significant
pericardial effusion to arise from a malignant lesion,
3 conditions must be present: (1) neoplastic invasion
of the mediastinal or hilar lymph nodes; (2) local
obstruction of lymphatic flow; and (3) implantation
of the tumor on the serosal surface of the pericardial
membranes, with subsequent exudation of fluid into
the pericardial space.64
Kline et al demonstrated that the sequence of
events begins with mediastinal lymph node metastases from primary tumor sites. Retrograde migration
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EBMedicine.net • February 2010
of cancer cells through the lymphatic system into the
pericardium follows, with subsequent fluid production and accumulation within the pericardial sac.65
The shared lymphatic drainage of the chest structures into the hilar and mediastinal lymph nodes
may explain why lung and breast cancers are the
most common causes of pericardial metastases. Direct invasion and hematogenous metastases are also
potential sources of cardiac and pericardial metastases and are associated with a significantly increased
risk of dysrhythmia or tamponade.66
The development of clinical symptoms depends
on the time course of fluid accumulation. Patients
can develop symptoms with as little as 200 mL of
pericardial fluid if accumulation is rapid — a situation typically seen in the setting of trauma.67 Symptomatic malignant effusions occur more insidiously,
allowing the parietal pericardium to accommodate
a greater volume of fluid. In a minority of patients,
several liters of fluid may accumulate without subsequent tamponade, although the literature is not clear
regarding the percentage of patients in whom such
large effusions develop.64
Cardiac tamponade occurs when the pericardial
fluid begins to impede cardiac diastolic filling, resulting in inadequate cardiac output. Unfortunately,
no single sign or symptom has sufficient sensitivity
or specificity to confirm or exclude this diagnosis.
Patients may present in extremis or even in cardiac
arrest due to tamponade.
Patients with cardiac tamponade may deteriorate rapidly; the emergency clinician must have a
high index of suspicion for this diagnosis to facilitate its early recognition. The literature describes
a “last-drop phenomenon,” in which the pressure
exerted on the cardiac chambers by the accumulation of pericardial fluid reaches a critical level. The
“last drop” is the tipping point at which just a small
amount of additional fluid in the pericardial space
causes sudden clinical deterioration because the
cardiac chambers can no longer adequately fill to
sustain the necessary cardiac output.67
toms (eg, cachexia, weight loss), thyroid disease,
end-stage renal disease, autoimmune disease (eg,
systemic lupus erythematosus, rheumatoid arthritis),
infectious disease (eg, HIV infection, tuberculosis), a
history of chest irradiation, and current medications.
Physical Examination For Malignant
Pericardial Effusion And Tamponade
The majority of patients with pericardial effusion
will present with relatively preserved blood pressure
and variable symptoms and signs, including dyspnea, tachypnea, and tachycardia. Guberman et al
reviewed the charts of 56 patients seen between 1963
and 1980 for cardiac tamponade of nontraumatic
etiology (eg, malignancy, myocardial infarction).69
Almost two-thirds of the patients had an average
systolic arterial blood pressure greater than 100 mm
Hg, and almost all patients were stable and provided a thorough history. Contrary to common medical
school teaching, these same authors reported that
most patients with a gradual onset of tamponade
did not present with Beck’s triad (hypotension,
distant heart sounds, and jugular venous distention).69 This triad is found in less than 20% of cases
of tamponade unrelated to trauma.
Pulsus paradoxus is an exaggeration of the normal variations in systolic blood pressure during the
inspiratory component of respiration. It remains a
key bedside diagnostic test for pericardial tamponade. (See Table 1.) In the Guberman study cited
earlier, 53 of 56 patients with tamponade exhibited
a documented decrease in systolic blood pressure of more than 10 mm Hg during inspiration.69
The mean drop in systolic blood pressure in the
study group as a whole was 49 mm Hg; however,
clinicians should be aware that pulsus paradoxus
occurs in conditions other than tamponade, such
as asthma, pulmonary embolus, obesity, and mitral
stenosis. In a meta-analysis, Roy et al found the
pooled sensitivity of pulsus paradoxus to be 82%
for cardiac tamponade.70 In a retrospective review
of 19 patients, Bishiniotis et al found that the most
common signs of pericardial tamponade in women
with breast cancer were pulsus paradoxus (79%),
tachycardia (74%), jugular venous distention
History For Malignant Pericardial Effusion
And Tamponade
The most common symptom in malignant pericardial effusion, by far, is dyspnea (91%). Thurber
et al reported other common symptoms: cough
(65%), thoracic pain (47%), and orthopnea (38%).59
Bishiniotis et al reviewed 19 patients with confirmed
malignant pericardial effusion causing cardiac tamponade. Common symptoms were dyspnea (95%),
orthopnea (58%), cough (47%), chest pain (42%), and
peripheral edema (36%).68
If the patient is clinically stable, a thorough
search should be undertaken to determine the underlying cause. Questions should specifically target
a possible history of cancer or cancer-related sympFebruary 2010 • EBMedicine.net
Table 1. Detecting Pulsus Paradoxus When
Using A Manual Sphygmomanometer
Step 1: Note SBP when Korotkoff sounds are audible during expiration
only.
Step 2: Note SBP when Korotkoff sounds are audible during both expiration and inspiration.
Step 3: Pulsus paradoxus present if: (SBP on expiration only) - (SBP
on inspiration and expiration) > 10 mm Hg
Abbreviation: SBP, systolic blood pressure.
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Emergency Medicine Practice © 2010
(68%), hepatomegaly (63%), distant heart sounds
(58%), and hypotension (53%).68 Kussmaul’s sign
(26%) and friction rub (16%) were rare. In another
study, the most common findings were evidence
of pleural effusion (53%), hepatomegaly (51%),
cyanosis (35%), and leg edema (31%).59 It is interesting to note that a friction rub and distant heart
sounds were each found in only 1 patient (1.8%).
To help explain this phenomenon, researchers have
suggested that heart sounds may be preserved by
neoplastic bridges between the visceral and the
parietal pericardium.61
effusion and tamponade, Bishiniotis et al reported
that 95% of patients had a cardiothoracic ratio
above 0.5. As shown in Figure 3, this is the ratio
of the transverse diameter of the heart (distance
from A to B) to the greatest internal diameter of the
thorax (distance from C to D) on a posteroanterior
chest film.68 They also identified pleural effusions
and malignant parenchymal disease in 68% and
42% of patients, respectively.
Electrocardiography
Patients who present with pericardial effusions and
tamponade frequently have abnormal electrocardiographic findings. In 1962, a retrospective autopsy
review of 189 patients showed that 27 with obtainable ECGs had “significant” pericardial metastatic
lesions; for those patients with metastatic lesions
in the pericardium, the findings included T-wave
abnormalities in 25 (93%), low QRS voltage in 22
(88%), and sinus tachycardia in 15 (56%).59
Direct tumor invasion of the atria can lead to
atrial fibrillation, atrial flutter, and premature atrial
contractions. Note that these dysrhythmias may be
resistant to typical medical therapy. Electrical alternans — ie, beat-to-beat variations in the direction,
amplitude, or duration of any component of the ECG
— has classically been associated with pericardial
effusion and tamponade, but may also be found in
other conditions, such as hypertrophic cardiomyopathy. (See Figure 4.) Total electrical alternans, in which
Diagnostic Studies For Malignant Pericardial
Effusion And Tamponade
Plain Radiography
Chest radiographs are often abnormal in patients
with cardiac effusions and may be the first sign
to suggest this diagnosis. An enlarged cardiomediastinal silhouette on posteroanterior and lateral
radiographs can correlate with as little as 250 mL of
pericardial fluid.71 Two studies involving a total of
139 patients reported this sign in 71% to 95% of patients with pericardial effusions.69,72 Other findings
may include a globular (ie, “water-bottle”) heart
shadow, irregular and nodular contours of the
cardiac chambers, a pericardial fat stripe, mediastinal widening, hilar adenopathy, or a hilar mass.61,72
(See Figure 2.) In a study of malignant pericardial
Figure 2. Chest X-Ray Of Pericardial
Effusion Showing The Classic “WaterBottle” Heart
Figure 3. The Cardiothoracic Ratio
Reproduced with permission from Serhat Yalcinkaya, Ahmet Hakan
..
Vural, Hakan Ozkan: Lung Adenocarcinoma Causing Pericardial Tamponade. The Internet Journal of Thoracic and Cardiovascular Surgery.
2004. Volume 6 Number 2. www.ispub.com.
Emergency Medicine Practice © 2010
Reprinted from Journal of Cardiology, Vol. 54(1), Kunihisa Miwa and
Masatoshi Fujita, Cardiac function fluctuates during exacerbation and
remission in young adults with chronic fatigue syndrome and “small
heart.” Pages 29-35, Copyright 2009, with permission from Elsevier.
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EBMedicine.net • February 2010
the P wave, QRS complex, and T wave all exhibit
beat-to-beat variability, is rare (5% to 10%) and is seen
most commonly with large pericardial effusions.61
nal area should be sterilized with povidone-iodine
or chlorhexadine while the drainage materials are
being prepared. A 16- or 18-gauge spinal needle
attached to a 60-mL syringe is used to enter the
pericardial space between the xiphoid process and
the left costal margin and should be aimed at a 15°
angle and advanced toward the left shoulder until
blood or other fluid is aspirated without resistance.67
Although blind attempts at pericardiocentesis can
be complicated by ventricular laceration, coronary
artery puncture, and pneumothorax (7% to 15%),
52 consecutive blind pericardiocenteses in 1 study
resulted in only 1 fatality.62
To prevent accidental ventricular puncture with
the spinal needle, ECG guidance can be used by
attaching 1 alligator clip to the proximal aspect of
the needle and the other to the V1 lead of the ECG
machine. The needle is then inserted and advanced,
as described above, while the clinician monitors the
ECG in real time for any pattern of myocardial injury pattern. Usually such injury is in the form of STsegment elevation, ventricular dysrhythmias, or premature ventricular complexes if the needle contacts
or penetrates the heart.74 If such an injury pattern is
seen, the needle should be withdrawn in 1- to 2-mm
increments until the ECG pattern disappears. Pericardial fluid is then aspirated, as described above. In
1 study, inadvertent ventricular needle puncture occurred in only 6 of 40 patients (15%) who underwent
this procedure.75 ECG-guided pericardiocentesis was
popular before the widespread use of 2-dimensional
echocardiography in the ED.
Given the obvious advantage of 2-dimensional
echocardiography for visualizing the effusion and
Echocardiography
The standard diagnostic tool for confirming cardiac
tamponade is echocardiography (a Class I recommendation by the American College of Cardiology).73 (See Figure 5.) A growing number of emergency clinicians are now facile using ultrasound to
detect pericardial effusion; however, the presence
of a pericardial effusion does not always equal a
diagnosis of cardiac tamponade. Echocardiographic
findings suggestive of cardiac tamponade include
early diastolic collapse of the right ventricle and
late diastolic collapse of the right atrium.73 Experienced echocardiographers may visualize abnormal
diastolic movement of the anterior mitral valve
leaflet. One great benefit of using sonography in
the ED setting is that if the clinician is confident
that the pericardium has been adequately visualized, absence of an effusion may be enough to rule
out this diagnosis.
Treatment For Malignant Pericardial Effusion
And Tamponade
The initial management of a patient suspected of
having cardiac tamponade begins immediately,
with the insertion of 2 large-bore IV lines for aggressive volume resuscitation using normal saline or
Ringer’s lactate. Patients with tamponade become
preload-dependent, so agents that reduce preload
(eg, nitroglycerin) should be strictly avoided. If
volume resuscitation is not immediately successful
in stabilizing the patient, pericardiocentesis should
be performed.
Figure 5. Echocardiogram Of Large
Pericardial Effusion With Tamponade
Pericardiocentesis
For patients in imminent danger of cardiac arrest,
pericardiocentesis may be done blindly. The ster-
Effusion
Figure 4. ECG Showing Electrical Alternans
In A Patient With Pericardial Effusion
LV
RV
Abbreviations: RV, right ventricle; LV, left ventricle.
ECG of patient with pericardial effusion showing tachycardia,
low voltage, and electrical alternans (adapted by permission from
www.askdrwiki.com)
February 2010 • EBMedicine.net
Reprinted with permission from Michael McCurdy, MD, and the University of Maryland Medical Center.
13
Emergency Medicine Practice © 2010
the track of the needle, it is prudent to choose this
method whenever possible (a Class IIa recommendation by the American College of Cardiology).72
Echocardiography-guided pericardiocentesis appears to be the safest approach, with no fatalities
reported during more than 600 attempts, according
to a study by Callahan et al.76 In another study of
32 such procedures, the success rate was 97%, with
a complication rate of 12.5% (generally due to cases
of pneumothorax or ventricular lacerations).77 An
added benefit of ultrasound is that the Seldinger
technique can be used to insert a catheter to allow continuous drainage once the location of the
needle is confirmed to be within the pericardial sac.
Although no studies have formally assessed the
usefulness of this technique, a triple-lumen central
venous catheter can be placed to facilitate drainage
if a pericardial drain kit is unavailable. If a patient
with cardiac tamponade or pericardial effusion
suffers a cardiac arrest, emergent pericardiocentesis
may revive the patient and restore circulation.78
ate symptoms or improve the patient’s hemodynamic
status, the clinician should consider the possibility
of an alternative diagnosis or procedural failure (eg,
improper placement of the catheter in the pericardial
space). When mechanical ventilation is being considered or has already been instituted for possible cardiac tamponade, the emergency clinician should be
aware that positive-pressure ventilation may impede
venous return and further reduce preload.67
Once the patient has been stabilized, consultation with other hospital services — oncology
(in cases of known malignancy), cardiology, and
surgical services — is advised to thoroughly plan
any intervention. Whenever pericardiocentesis is
the sole treatment modality, malignant effusions are
reported to recur at a rate of 56%, often within 24 to
48 hours.62,78 Consequently, these patients should
be offered other interventions that may reduce the
recurrence rate. The patient’s oncologist and the consulting surgeon may base their decision for intervention on the patient’s functional status, the specific
characteristics of the tumor, and overall prognosis.
Procedures that are usually considered include thoracotomy with pericardectomy; thoracotomy with a
pericardial, subxiphoid, or transcutaneous-balloon
pericardial window; local infiltration of sclerosing
agents or chemotherapeutic agents; systemic chemotherapy; and radiation therapy. Minimally invasive
approaches should be considered for patients with
poor functional status.
The success of any of these procedures is measured by the 30-day survival rate and the absence of
pericardial effusion during those 30 days. Given the
relatively poor prognosis associated with malignant
pericardial effusion, a thorough discussion with the
family and the patient should be undertaken by the
consulting services to ensure that invasive or risky
operative interventions are warranted.
Examination Of The Pericardial Fluid
Pericardiocentesis should be considered both
a diagnostic and a therapeutic procedure in all
patients with nontraumatic tamponade. As much
fluid as possible should be aspirated to improve
the patient’s hemodynamic status and to maximize
yield for cytologic examination to detect malignant
cells. Cytology is believed to be positive in 60%
to 80% of patients with a malignant pericardial
effusion.62 Cytology will assist in the determination of a primary cancer and will therefore indicate
the patient’s prognosis. For example, breast cancer
patients diagnosed with a pericardial effusion may
survive 10 to 13 months, whereas patients with an
effusion associated with lung cancer may survive
less than 6 months.78
In addition to cytologic analysis, routine studies
of the pericardial fluid should include a cell count
and differential, hematocrit, bacterial culture, and levels of protein, glucose, and lactic dehydrogenase. The
color of the pericardial fluid sample is not an accurate
predictor of the cause of the effusion. Malignant effusions may be serous, serosanguineous, or grossly
bloody. If bloody, the fluid should not easily form a
clot, and the fluid hematocrit should be lower than
the serum hematocrit. If the fluid clots easily and the
hematocrit is similar to the serum hematocrit, consider the possibility that an intracardiac sample was
inadvertently obtained. If the patient is stable enough
to allow echocardiogram-guided pericardiocentesis, a
catheter should be inserted and left in the pericardial
space to allow continued drainage.73 After the catheter is sutured to the skin, it may be affixed to a 3-way
valve or Hemovac®. Sterile technique should always
be used to avoid infectious complications.
If drainage of the pericardial fluid does not alleviEmergency Medicine Practice © 2010
Summary For Malignant Pericardial Effusion
And Tamponade
Although the presentation in the ED of a patient with
acute cardiac tamponade can be a frightening event,
most cases of nontraumatic cardiac tamponade tend to
be more insidious. Medical histories are often vague,
and the “typical” complaints of dyspnea, cough, and
orthopnea generate a broad differential diagnosis. Findings on physical examination that are suggestive of, but
not definitive for, cardiac tamponade include pulsus
paradoxus, tachycardia, jugular venous distention,
hepatomegaly, distant heart sounds, and hypotension.
The serious consideration of tamponade within the
differential diagnosis is the first step in diagnosing and
managing this oncologic emergency. Routine laboratory
tests are of little help in this process, but the ECG and
chest film are of value. Low-voltage or electrical alternans on the ECG, coupled with a markedly enlarged
cardiac silhouette on a chest film, should prompt the
14
EBMedicine.net • February 2010
emergency clinician to perform or request urgent bedside echocardiography. Although many emergency clinicians are capable of detecting a large pericardial effusion and signs of tamponade, a cardiologist’s interpretation is often necessary to confirm a subtle diagnosis
of tamponade by means of formal echocardiography.
If a patient with a pericardial effusion becomes markedly unstable or if tamponade is grossly visible on the
echocardiogram, the clinician needs to be familiar with
the equipment, supplies, and steps required to perform
pericardiocentesis. It is important to reiterate that for all
stable patients, consultation with other hospital services
(cardiology, oncology [if appropriate], and surgery) will
allow the team to thoroughly coordinate any interventions and inpatient care.
tamponade. You wheel over the bedside ultrasound
equipment, and the echocardiogram reveals an extremely
large pericardial effusion with what appears to be very
restricted ventricular activity. The patient’s hypotensive
state improves within 10 minutes after bedside pericardiocentesis yields 400 mL of bloody fluid. The cardiothoracic surgeon arrives at the bedside and consults with
the family regarding the possible creation of a pericardial
window to more definitively treat his condition. Your
high level of suspicion for this catastrophic complication of malignancy and quick actions averted what could
have been a lethal situation.
Disposition Of Patients with Malignant
Pericardial Effusion And Tamponade
The presentation and management of oncologic
emergencies are infrequently encountered by
most emergency clinicians; however, what were
once thought to be relatively rare presentations
in the ED are now becoming more common as
patients with cancer are living longer and receiving a broad array of treatments. The presentation
of SVCS can be subtle and easily missed if the
physician does not suspect this diagnosis. Patients
with epidural metastases and cardiac tamponade
may present in a more dramatic fashion and will
require prompt intervention to achieve a favorable outcome. It is important to remember that
such patients often have other serious comorbidities that contribute to their poor clinical status. In
conclusion, this review highlights the importance
of obtaining a thorough history, maintaining a
high index of suspicion for these 3 complications,
and acting quickly on these concerns for cancer
patients who present to the ED.
Summary
All patients who are diagnosed with cardiac tamponade in the ED should be admitted to the ICU
for close monitoring until definitive treatment can
be delivered. Prior to admission to the ICU, some
patients may be sent directly to surgery or to the
angiography department for interventional treatment. Any patient who undergoes pericardiocentesis
in the ED will require intensive care to monitor for
signs of decompensation. Patients who are believed
to have a stable pericardial effusion without cardiac
tamponade can be considered for admission to the
medical floor if no coexisting conditions dictate a
higher level of care.
Case Conclusions
During the emergent intubation of your patient with
SVCS, laryngeal edema was evident. Her post-intubation
chest x-ray shows opacity, likely representing her underlying tumors. Her head CT shows diffuse cerebral edema
without herniation or abnormality, and her chest CT with
intravenous contrast reveals a tumor compressing the
SVC and an extensive clot burden within the vessel. The
patient is admitted to the ICU, and specialists in radiation
oncology and interventional radiology are consulted. On
the same day, the patient is taken to the interventional
radiology suite where a local thrombolytic agent is infused
at the site of thrombosis and a stent is placed in the SVC.
Within 24 hours of the intervention, her facial and arm
swelling improves significantly. A few days later, the
patient’s mental status and laryngeal edema has improved
to the extent that she can be extubated. Her quality of life
was improved with this treatment of SVCS and her palliative chemotherapy was continued, to maximize valuable
time with her loved ones.
The family of your 45-year-old male arrives and
states that he has a history of lung cancer. The ECG
demonstrates low-voltage amplitudes in all leads. This
finding, in conjunction with this patient’s clinical
presentation and history, makes you suspect cardiac
February 2010 • EBMedicine.net
Acknowledgments
The authors thank Linda Kesselring for her assistance in the preparation of this article, and Anis
Frayha, MD for helping to acquire the images.
Practice Recommendations
Available Online!
You asked and we listened! The one-page EvidenceBased Practice Recommendations sheet that accompanies your monthly issue is now available online
instead of in print. To download your copy, visit
http://www.ebmedicine.net/topics, click the title
of the article, and click “Practice Recommendations
(key points from the issue)” in the Table of Contents
below the Abstract.
15
Emergency Medicine Practice © 2010
References
3.
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are
equally robust. The findings of a large, prospective,
randomized, and blinded trial should carry more
weight than a case report.
To help the reader judge the strength of each
reference, pertinent information about the study,
such as the type of study and the number of patients
in the study, will be included in bold type following
the reference, where available. In addition, the most
informative references cited in this paper, as determined by the authors, will be noted by an asterisk (*)
next to the number of the reference.
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Risk Management Pitfalls For Oncologic Emergencies (continued on page 17)
1. “Even though the patient whom I just diagnosed with malignant spinal cord compression
wasn’t able to walk into the ED, I’m going to
tell the family that he should be all right once
treatment is initiated.”
The neurologic status of patients before treatment for ESCC is the most important prognostic
factor for neurologic status after treatment. Understanding the significant prognostic implications of the patient’s presenting neurologic
status should help guide your discussions with
patients and their families.
with ESCC, and it usually predates all other
symptoms by up to 2 months.
4. “I know he had lung cancer, but his back pain
doesn’t seem too bad. I’ll just get an x-ray and
send him home with some acetaminophen if
it’s normal.”
Not seriously considering ESCC in the differential diagnosis in any cancer patient with
back pain is a recipe for disaster. Also, relying
on a plain radiograph alone for the diagnosis of
ESCC is inadequate. Since plain radiography is
only 75% sensitive for ESCC even when vertebral collapse is evident, MRI is the study of
choice.
2. “This lady has ESCC. She needs to get radiation now!”
Radiation therapy is not indicated in all patients.
Its greatest benefits are seen in the following
situations: recurrences following surgical decompression, no spinal compression or instability, subclinical cord compression, radiosensitive
tumors, or in patients who are not candidates for
surgery.
5. “I couldn’t tell the patient’s face was swollen.
I’ve never seen him before and I thought he
always looked like that.”
Although facial swelling is often obvious, it can
be overlooked by one who is not familiar with
the patient’s usual appearance. The emergency
clinician must obtain a thorough history to elicit
important clues, such as worsening of the swelling in the morning or a sense of facial fullness
when bending down. Consider involving family
or friends for their opinion or look at a patient’s
driver’s license for comparison.
3. “He said his back has been hurting for 2
months, making it difficult for him to walk,
but he appeared fine to me in the ED and had a
normal x-ray.”
A new diagnosis of an underlying malignancy
is made in 20% of patients who present with
ESCC, so clinical suspicion must always remain
high for any patient with relevant symptoms.
Back pain is the first symptom in 95% of patients
Emergency Medicine Practice © 2010
6. “I knew that the patient had SVCS, but it was
subacute and I thought that she could follow up with her oncologist to take care of it. I
16
EBMedicine.net • February 2010
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Risk Management Pitfalls For Oncologic Emergencies (continued from page 16)
didn’t know that it could progress to stridor or
cerebral edema.”
Their exact incidence is not known, but the 2
most feared complications of this syndrome are
upper-airway obstruction and cerebral edema,
both of which are attributable to diminished
venous return to the head and neck. Even if the
presentation is subacute, treatment should be
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Given the coordination required among multiple disciplines, it is reasonable to admit most
patients with SVCS.
alerts physicians to the possibility of this diagnosis, but the lack of this finding is insufficient
to rule out the diagnosis.
9. “After the pericardiocentesis, my patient was
doing so well. He said he could follow up with
his oncologist a week later, so I let him go
home. I didn’t realize that fluid could reaccumulate that quickly!”
When pericardiocentesis is the sole treatment modality for a malignant pericardial effusion, it can
recur at a rate of 56%, often within 24 to 48 hours.
Patients should be admitted for close observation
and a repeat echocardiogram. In cases of recurrent malignant pericardial effusions, more definitive treatment, such as a subxiphoid pericardial
window, should be considered in consultation
with the cardiothoracic surgery team.
7. “There is no facial edema and the chest film is
normal — this patient doesn’t have SVCS.”
About 20% of patients with SVCS have no facial
or neck edema, and about 20% have normal
chest films. When abnormal radiographic findings are present, they usually include evidence
of lung masses. Further imaging is warranted if
SVCS continues to be suspected.
10. “But the patient initially had a stable blood
pressure. Nobody would have suspected cardiac tamponade.”
Initially, many patients with nontraumatic cardiac tamponade present with preserved blood
pressure; however, they can deteriorate quickly
because of the “last drop” phenomenon. Beck’s
triad is rarely present in such patients. For any
patient with a pulmonary malignancy (primary
tumor or metastasis) who presents with heart
failure-like symptoms, cardiac tamponade is
often detected only by emergency clinicians who
are alert for this possible diagnosis.
8. “A chest x-ray without an enlarged cardiac
silhouette essentially rules out a pericardial
effusion.”
In the case of malignant pericardial effusion, the
effusion is usually large in volume, owing to the
subacute nature of the fluid accumulation. The
pericardium therefore has enough time to stretch
and accommodate a large amount of fluid without affecting hemodynamic status. The classic
“water-bottle” heart on chest x-ray certainly
February 2010 • EBMedicine.net
17
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72. Eisenberg MJ, Dunn MM, Kanth N, et al. Diagnostic value of
chest radiography for pericardial effusion. J Am Coll Cardiol
1993;22:588-93. (Retrospective study; 83 patients)
73. Cheitlin MD, Armstrong WF, Aurigemma GP, et al. ACC/
AHA/ASE 2003 guideline update for the clinical application of echocardiography: a report of the American College
of Cardiology/American Heart Association Task Force on
Practice Guidelines (ACC/AHA/ASE Committee to Update
the 1997 Guidelines for the Clinical Application of Echocardiography). 2003. American College of Cardiology Web Site.
Available at: www.acc.org/clinical/guidelines/echo/index.
pdf. (Society guidelines)
74. Reichman EF, Simon RR. Emergency Medicine Procedures.
York, PA: McGraw-Hill; 2004. (Textbook)
75. Bishop LH, Estes EH, McIntosh HD: The electrocardiogram
as a safeguard in pericardiocentesis. JAMA 1956; 162:264-265.
(Prospective, observational study; 40 patients)
76. Callahan J, Seward J. Pericardiocentesis guided by two-dimensional echocardiography. Echocardiography. 1997;14:497504. (Retrospective study; 610 patients)
77. Ozer HO, Davutoglu V, Cakici M, et al. Echocardiographyguided pericardiocentesis with the apical approach. Turk
Kardiyol Dern Ars. 2009; 37(3):177-181. (Prospective, observational study; 32 cases)
78. Vaitkus P, Herrmann H, LeWinter M. Treatment of malignant pericardial effusion. JAMA. 1994;272(1):59-64. (Review
article)
February 2010 • EBMedicine.net
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1. What is the most important prognostic factor for
neurologic outcome in a patient with ESCC?
a. Back pain on recumbency
b. Bladder dysfunction
c. Night pain
d. Pre-treatment neurologic function
e. Type of cancer
2. Which of the cancers listed below least frequently involves the bones?
a. Breast b. Lung
c. Pancreas
d. Prostate
e. Multiple myeloma
3. What is the diagnostic modality of choice for
suspected malignant ESCC?
a. Bone scintigraphy
b. CT scan
c. MRI
d. Physical examination
e. Plain radiography
4. What initial steroid type and dose is used for
ESCC without evidence of myelopathy on
examination?
a. Dexamethasone, 10 mg IV
b. Dexamethasone, 50 mg IV
c. Dexamethasone, 100 mg IV
d. Prednisone, 40 mg PO
e. Prednisone, 60 mg PO
5. What is the most common tumor for malignancy-related SVCS?
a. Breast
b. Esophageal
c. Head and neck
d. Lung
e. Lymphoma
19
Emergency Medicine Practice © 2010
Physician CME Information
6. What is the diagnostic mode of choice for
SVCS?
a. Chest CT scan with IV contrast
b. Chest CT scan without IV contrast
c. Chest MRI
d. Chest x-ray
e. Physical examination
Date of Original Release: February 1, 2010. Date of most recent review: December
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7. What is the next appropriate clinical step following a new diagnosis of SVCS due to a previously undiagnosed cancer?
a. Consultation to assist with a tissue diagnosis prior to definitive treatment
b. Consult oncologist for emergency chemotherapy
c. Consult radiation oncologist for emergency radiation treatment
d. Consult thoracic surgeon for bypass surgery
8. What is the most common symptom in patients
with malignant pericardial effusions?
a. Chest pain
b. Cough
c. Dyspnea
d. Lightheadedness
e. Palpitations
9. What percentage of patients with a malignant
pericardial effusion have a positive result on
pericardial fluid cytology?
a. 20% to 40%
b. 60% to 80%
c. 100%
10. What is the recurrence rate of malignant pericardial effusions following pericardiocentesis?
a. 0% to 10%
b. 30% to 40%
c. 40% to 50%
d. 50% to 60%
e. 80% to 90%
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The materials contained herein are not intended to establish policy, procedure, or standard of care. Emergency Medicine Practice is a trademark of EB Practice, LLC. Copyright © 2010 EB
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Emergency Medicine Practice © 2010
20
EBMedicine.net • February 2010
EVIDENCE-BASED practice RECOMMENDATIONS
Oncologic Emergencies, Part I: Spinal Cord Compression, Superior Vena Cava Syndrome, And
Pericardial Effusion
McCurdy M, Mitarai T, Perkins J. February 2010, Volume 12; Number 2
This issue of Emergency Medicine Practice provides a review of 3 important cancer-related complications that present to emergency
departments. For a more detailed discussion of this topic, including figures and tables, clinical pathways, and other considerations not
noted here, please see the complete issue on the EB Medicine website at www.ebmedicine.net/topics.
Key Points
Comments
Early suspicion of epidural spinal cord compression (ESCC) is
fundamental in timely diagnosis and treatment, as clinical outcomes
are dependent on the functional status of the patient at the time of
diagnosis.
Neurologic status of a patient prior to treatment for ESCC is the
most important prognostic factor for neurologic status after treatment.19
MRI of the entire spine is appropriate in most circumstances for the
diagnosis of ESCC.
The added benefits of a non-invasive modality, cost efficiency,21
and the ability to image the entire spine for ESCC, intramedullary
lesions, and bony metastases make MRI the study of choice for patients with suspected ESCC. Imaging the entire spine is considered
extremely valuable because approximately one-third of all patients
diagnosed with ESCC have multiple sites of epidural metastases.22,23,66,68,77
Patients with superior vena cava syndrome (SVCS) often present
with subacute complaints, and diagnosis can be further delayed
without careful history and examination.
In general, sudden presentations are the exception, making the diagnosis more difficult. Delayed presentations are more of the rule, with
more than 75% of patients having signs and symptoms of SVCS for
greater than 1 week before seeking medical attention.42 Furthermore,
it is not uncommon for patients to complain of SVCS-related symptoms for weeks, or even months.43
The preferred ED radiographic modality to diagnose SVCS is a
chest CT with IV contrast.
This modality is preferred in the emergency setting for multiple
reasons: it has wide availability, it provides both anatomic details
of the extent of obstruction and collateral flow, and it can potentially identify causes of the syndrome (compression vs in-dwelling
catheter-related disease).
Most malignant pericardial effusions are asymptomatic.
In DeLoach’s case series of 137 patients with cardiac metastases,
22 developed pericardial effusions, but only 2 of the patients had
symptoms attributable to the effusions.48
Breast and lung cancers account for about half of pericardial metastases.
Theoretically, any cancer can metastasize to the pericardium.
Cancers originating above the diaphragm are the most common
sources of metastatic pericardial disease, with lung and breast cancer
accounting for about half of all cases. Lymphoma, leukemia, and
melanoma account for an additional 25% of metastatic disease.52
Bedside echocardiography is a key instrument for both diagnostic
and therapeutic use in cases of cardiac tamponade.
Echocardiographic findings suggestive of cardiac tamponade include
right ventricular early diastolic collapse and right atrial late diastolic
collapse.62 More experienced echocardiographers may visualize
abnormal diastolic movement of the anterior mitral valve leaflet. A
great benefit of the use of sonography in the ED setting is that if a
physician is confident that adequate visualization of the pericardium
has been obtained, then the absence of a pericardial effusion may
“rule out” this diagnosis.
See reverse side for reference citations.
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REFERENCES
These
references are
excerpted from
the original
manuscript.
For additional
references and
information on
this topic, see
the full text
article at
ebmedicine.net.
19. Posner JB. Neurologic Complications of Cancer. Philadelphia, PA: FA Davis; 1995. (Textbook)
21. Maranzano E, Latini P. Effectiveness of radiation therapy without surgery in metastatic spinal cord compression:
final results from a prospective trial. Int J Radiat Oncol Biol Phys. 1995;32:959-967. (Prospective, nonrandomized study; 209 patients)
22. Haddad P, Thaell JF, Kiely JM, et al. Lymphoma of the spinal extradural space. Cancer. 1976;38:1862-1866. (Retrospective chart review; 94 patients)
23. Cook AM, Lau TN, Tomlinson MJ, et al. Magnetic resonance imaging of the whole spine in suspected malignant
spinal cord compression: impact on management. Clin Oncol (R Coll Radiol) 1998;10:39-43. (Prospective, observational study; 127 patients)
42. Young RF, Post EM, King GA. Treatment of spinal epidural metastases. Randomized prospective comparison of
laminectomy and radiotherapy. J Neurosurg. 1980;53:741-748. (Prospective, randomized study; 29 patients)
43. Gilbert RW, Kim JH, Posner JB. Epidural spinal cord compression from metastatic tumor: diagnosis and treatment.
Ann Neurol. 1978;3:40-51. (Retrospective study; 235 patients)
48. Schindler N, Vogelzang R. Superior vena cava syndrome: experience with endovascular stents and surgical therapy.
Surg Clin North Am. 1999;79(3):683-694. (Review article)
52. Yellin A, Rosen A, Reichert N, et al. Superior vena cava syndrome. The myths – the facts. Am Rev Respir Dis.
1990;141:1114-1118. (Retrospective study; 63 patients)
62. Buzaid A, Garewal H, Greenberg B. Managing malignant pericardial effusion. West J Med. 1989;150(2):174-179.
(Review article)
66. Hill GJ, Cohen BI. Pleural pericardial window for palliation of cardiac tamponade due to cancer. Cancer.
1970;26:81-93. (Retrospective study; 5 patients)
68. Bishiniotis TS, Antoniadou S, Katseas G, et al. Malignant cardiac tamponade in women with breast cancer treated
by pericardiocentesis and intrapericardial administration of triethylenethiophosphoramide (Thiotepa). Am J Cardiol. 2000;86:362-364. (Prospective study; 19 patients)
77. Ozer HO, Davutoglu V, Cakici M, et al. Echocardiography-guided pericardiocentesis with the apical approach. Turk
Kardiyol Dern Ars. 2009; 37(3):177-181. (Prospective, observational study; 32 cases)
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Emergency Medicine Practice (ISSN Print: 1524-1971, ISSN Online: 1559-3908) is published monthly (12 times per year) by EB Practice, LLC. 5550 Triangle Parkway, Suite 150,
Norcross, GA 30092. Opinions expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as
a general guide and is intended to supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific
medical decisions. The materials contained herein are not intended to establish policy, procedure, or standard of care. Emergency Medicine Practice is a trademark of EB Practice, LLC.
Copyright © 2010 EB Practice, LLC. All rights reserved.