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2 | Clinical for
PAGE 2|Guideline Policy:
the Critical December
December2010
PAGE
Issues In The
Management Evalua-
Of Acute Current
Current Guidelines
GuidelinesForForDiagnosis Volume
2009
Volume2,1,Number
Number122
tionChronic
And
Of
And Management
Adult
Pain In
Patients Pre-
Sickle Cell Disease.
And Management
Sickle Of Syncope In
Cell Disease:
Authors
Editor-In-Chief
Christopher R. Tainter, MD
II
Mount Sinai School of Medicine, New York, NY
Reuben J. Strayer, MD
With Syncope n this issue of EM Practice Guidelines Update, 2 practice guidelines ad- Assistant Professor of Emergency Medicine, Mount Sinai School of Medicine,
In this issue of EM Practice Guidelines Update, 2 guidelines Editorial Board
dressing the management of syncope are reviewed. Syncope is a brief, New York, NY
PAGE 4 | The Management
Annals of Medicine
of Emergency Sickle addressing
transient theconsciousness
loss of management of sickle cell
accompanied disease
by loss (SCD)
of postural are
tone, Andy Jagoda, MD, FACEP
Editorial Board
Professor and Chair, Department of Emergency Medicine
Cell Disease. National withreviewed.
spontaneous As recovery.
a result Itofisnumerous
attributed toSCD-related
global cerebralcomplications,
hypoperfusion, Nicole
MountC. Bouchard,
Sinai School ofMD, FRCPCNew York, NY
Medicine,
PAGE 4|Institutes of Health,
For National
Assistant Clinical Professor, Assistant Site Director; Director of Medical Toxicology,
Guidelines The distinct
patients from other
with SCD possible
havecauses of altered
significantly consciousness
diminished such as seizure
life expectancy. Erik
New Kulstad, MD,
York-Presbyterian MSColumbia University Medical Center, New York, NY
Hospital,
Heart Lung and Blood
Diagnosis And Man- or trauma. It is estimated to account for 1% to 1.5%
Although most patients will be followed by subspecialty of annual emergency
hema-
Research Director, Advocate Christ Medical Center
Andy Jagoda,
Department ofMD, FACEP Medicine, Oak Lawn, IL
Emergency
Institute.
agement Of Syncope department (ED) visits, and up to 6% of admissions. 1
tologists, SCD is fundamentally a “‘disease of emergencies.”’ Professor and Chair, Department of Emergency Medicine, Mount Sinai School of
Eddy S.
Medicine, NewLang,
York, NYMDCM, CCFP (EM), CSPQ
(Version 2009) Emergency
The prevalence clinicians
of syncope,should
thoughbenotfamiliar with the
well-reported, recommenda-
is high, on the order Associate Professor, McGill University, SMBD Jewish General
Erik Kulstad,
Hospital, MD, MS
Montreal, Canada
tions
of around
6.2-9.3 management
per 1000 person-years.of2,3acute SCD
Though thecomplications,
cause of syncopebecause
is often Research Director, Department of Emergency Medicine, Advocate Christ
LewisCenter,
Medical S. Nelson,
Oak Lawn,MDIL
European Heart Journal benign or unexplained, 2
a significant number of patients presenting
failure to appreciate the nuances of care in these brittle patients to the Director, Fellowship in Medical Toxicology, New York City Poison
Eddy S. Lang, MDCM, CCFP (EM), CSPQ
Control Center, Associate Professor, Department of Emergency
emergency department (ED) with syncope have a potentially
may place them at risk for short-term morbidity and mortality. The dangerous un- Senior Researcher, Alberta Health Services; Associate Professor, University of
Medicine, NYU Medical Center, New York, NY
PAGE 6| Editorial Comment derlying etiology, most of which have specific therapies. Syncope is therefore Calgary; Adjunct Professor, McGill University, Montreal, Quebec, Canada
methodology of these practice guidelines varies greatly–from Gregory
Lewis M. Press,
S. Nelson, MD MD, RDMS
aevidence-
cardinal, high-risk
based presentation for the emergency
to expert opinion–and clinician.
thus must be Because
applied theto Assistant
Associate Professor,
Professor DirectorMedicine,
of Emergency of Emergency
New YorkUltrasound, Emergency
University School of
Ultrasound Fellowship
FellowshipDirector,
in MedicalDepartment ofYork
Emergency
City PoisonMedicine,
PAGE 7| Clinical Pathway For syncope evaluation itself can be costly and can subject the patient to a host Medicine; Director, Toxicology, New Control
emergency practice with caution and pragmatism. University of Texas
Center, New York, NY at Houston Medical School, Houston, TX
Syncope of risks, a careful balance must be maintained between under- and over- Maia Rutman,
Gregory M. Press,MD MD, RDMS
utilization of resources. These guidelines have been developed to assist the MedicalProfessor,
Assistant Director,Director
Pediatric Emergency
of Emergency Services,
Ultrasound, Dartmouth-
Emergency Ultrasound
Hitchcock Medical Center;ofAssistant Professor
Medicine, of Pediatric
clinician
Practice in planning an appropriate
Guideline Impactassessment.
Fellowship Director, Department Emergency University of Texas at
PAGE 8| References Emergency Medicine, Dartmouth
Houston Medical School, Houston, TX Medical School, Lebanon, NH
• In the management of acute SCD pain crises, bolus normal Scott
Maia S. M. Silvers,
Rutman, MD MD
Practice
saline Guideline Impact unless the patient is hypovolem-
is not recommended
Chair, Director,
Medical Department of Emergency
Pediatric Medicine
Emergency Services, Dartmouth-Hitchcock Medical
MayoAssistant
Center; Clinic, Jacksonville, FL
Professor of Pediatric Emergency Medicine, Dartmouth
• ic. In euvolemic
Syncope patients,
is a distinct intravenous
clinical entity hydration
that must shouldfrom
be differentiated not Medical School, Lebanon, NH
Scott Weingart, MD FACEP
Editor’s Note: To read more about this publication Scott M. Silvers,
Assistant MD Department of Emergency Medicine, Elmhurst
Professor,
and the background and methodologies for practice exceed
other 1.5 times
causes maintenance
of altered with D5 ½ NS.
states of consciousness and transient events. Hospital
Chair, Center,ofMount
Department SinaiMedicine,
Emergency School Mayo
of Medicine, New York,FLNY
Clinic, Jacksonville,
guideline development, go to:
http://www.ebmedicine.net/introduction • The initial evaluation of patients with syncope should always include Scott Weingart, MD, FACEP
• In the management of acute SCD pain crises, specific rec- Prior to Professor,
Assistant beginningDirector
this activity,
of thesee “Physician
Division CME Information”
of Emergency Critical Care,on
an electrocardiogram (ECG). Laboratory and additional testing should page 9. of Emergency Medicine, Mount Sinai School of Medicine,
ommendations exist with regard to opiate choice and adju-
be performed as directed by the history and physical examination.
Department
New York, NY
vant medications.
• Patients with ECG abnormalities; older age and associated comor-
Editor’s
Prior Note: To
to beginning thisread more
activity, seeabout
“CME this publication
Information” on page 9.
• bidities; hematocrit
In patients with SCD< 30 and
(if obtained);
suspectedhistory or presence
infection, of heart
criteria exist to and the background and methodologies for practice
failure, coronary artery disease, structural
identify candidates for outpatient treatment. heart disease, and other guideline development, http://www.ebmedicine.net/
content.php?action=showPage&pid=107&cat_id=16
high-risk factors are more likely to have short-term adverse outcomes
• Separate
and algorithms
therefore exist
require more for the evaluation
extensive diagnosisand/or
and treatment
admission.of
stroke in adults and children with SCD.
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T
his document was developed by a subcommittee and com- Critical Question 1: What history and physical examination data
mittee organized by the American College of Emergency help to risk-stratify patients with syncope?
Physicians (ACEP). The policy targets physicians working in Level A Recommendations: Use history or physical examination
hospital-based EDs. Panel members are listed but their affiliations findings consistent with heart failure to help identify patients at higher
and qualifications are not. The source of funding is ACEP. Conflict-of- risk of an adverse outcome.
interest disclosures were not reported. Level B Recommendations:
1. Consider older age, structural heart disease, or a history of coro-
The group identified 3 critical questions and utilized an explicit strat- nary artery disease as risk factors for adverse outcome.
egy for their literature search and review. Evidence was evaluated for 2. Consider younger patients with syncope that is nonexertional,
quality according to predefined criteria and sorted into 4 classes (I, II, without history or signs of cardiovascular disease, a family history
III, or X-fatally flawed). Recommendations were made based on the of sudden death, and without comorbidities to be at low risk of
strength of evidence for each question. adverse events.
• Level A recommendations: Generally accepted principles for Critical Question 2: What diagnostic testing data help to risk-
patient management that reflect a high degree of clinical certainty. stratify patients with syncope?
• Level B recommendations: Recommendations for patient man- Level A Recommendations: Obtain a standard 12-lead ECG in
agement that may identify a particular strategy or range of man- patients with syncope.
agement strategies that reflect moderate clinical certainty. Level C Recommendations: Laboratory testing and advanced
• Level C recommendations: Other strategies for patient manage- investigative testing such as echocardiography or cranial computed
ment based on preliminary, inconclusive, or conflicting evidence, or tomography (CT) scanning need not be routinely performed unless
in the absence of any published literature, based on panel consen- guided by specific findings in the history or physical examination.
sus.
Critical Question 3: Who should be admitted after an episode of
The guideline applies to adult patients presenting to the ED with syncope of unclear cause?
syncope. Pediatric patients are excluded, as are patients in whom the Level B Recommendations:
episode of syncope is thought to be secondary to another disease 1. Admit patients with syncope and evidence of heart failure or
process such as seizures, chest pain, headache, abdominal pain, structural heart disease.
dyspnea, hemorrhage, hypotension, or a new neurologic deficit. 2. Admit patients with syncope and other factors that lead to stratifica-
tion as high-risk for adverse outcome. (See Figure, Factors That
Lead To Stratification As High-Risk For Adverse Outcome, page 3.)
T
his document was developed by a task force assembled by the Class I, Level C: Arrythmia-related syncope is diagnosed by ECG
European Society of Cardiology in collaboration with the Euro- when the following are present:
pean Heart Rhythm Association (EHRA), Heart Failure Associa- • Repetitive sinoatrial block; persistent sinus bradycardia < 40
tion (HFA), and Heart Rhythm Society (HRS). A funding source is not beats/minute; or sinus pauses ≥ 3 seconds
identified. Conflict of interest disclosures for all authors and reviewers • Mobitz II second-degree or third-degree atrioventricular block
were reported separately. • Alternating left and right bundle branch block
• Ventricular tachycardia or rapid paroxysmal supraventricular
Evidence was evaluated for quality based on criteria specified in the tachycardia
preparation document and sorted into 3 levels of evidence (A, B, C). • Non-sustained episodes of polymorphic ventricular tachycardia
Recommendations were graded based on the strength of evidence and long or short QT interval
for each question. Class I: evidence or agreement as beneficial/use- • Malfunction of pacemaker or implantable cardioverter defibrillator
ful/effective; Class IIa: conflicting evidence in favor of usefulness/ with cardiac pauses
efficacy; Class IIb: usefulness/efficacy less well established; Class
III: evidence/agreement not useful/effective or may be harmful. The When is carotid sinus massage an appropriate diagnostic
guidelines are designed for “all physicians who are interested in the maneuver?
field [of cardiology].” Only recommendations that pertain to emergen- Class I, Level B: Carotid sinus massage is indicated for patients
cy medicine are summarized here. greater than 40 years of age who have syncope of unknown etiology
after initial evaluation.
What are the diagnostic criteria with initial evaluation of patients Class III, Level C: Carotid sinus massage should be avoided in
presenting with syncope? patients with previous transient ischemic attack or stroke within 3
Class I, Level C: Vasovagal syncope is diagnosed if syncope is as- months or carotid bruits unless carotid Doppler studies exclude sig-
sociated with typical prodrome and precipitated by orthostatic stress nificant stenosis.
or emotional distress.
Class I, Level C: Situational syncope is diagnosed if syncope occurs What testing is indicated for suspected orthostatic hypotension?
during or immediately after coughing, sneezing, exercising, eating, Class I, Level B: When orthostatic hypotension is suspected, manual
gastrointestinal stimulation, micturition, or other precipitating events. intermittent determination of blood pressure (both supine and during
Class I, Level C: Orthostatic syncope is diagnosed when syncope active standing for 3 minutes) with sphygmomanometer is indicated
occurs after the patient stands up. There must be documentation of as initial evaluation.
orthostatic hypotension.
When is ECG monitoring or electrophysiology evaluation When is exercise testing indicated in the evaluation of syncope?
indicated in the evaluation of syncope? Class I, Level C: In patients who experience syncope during or
Class I, Level B: ECG monitoring or electrophysiology evaluation is shortly after exertion, exercise testing is indicated.
indicated for patients who have clinical or ECG features that suggest
arrythmic syncope, such as: When is neurological evaluation indicated in the evaluation of
• Bifascicular block syncope?
• QRS duration ≥ 120 milliseconds Class I, Level C: In patients in whom transient loss of consciousness
• Mobitz I second-degree atrioventricular block is suspected to be epilepsy, neurologic evaluation is indicated.
• Asymptomatic sinus bradycardia (< 50 beats/minute), sinoatrial Class I, Level C: When syncope is due to autonomic failure, neuro-
block, or sinus pause ≥ 3 seconds not attributable to medication logical evaluation is indicated to evaluate the underlying disease.
• Non-sustained ventricular tachycardia Class III, Level B: Unless a non-syncopal cause of transient loss of
• Pre-excitated QRS complexes consciousness is suspected, electroencephalography, ultrasound of
• Long or short QT intervals the neck arteries, and computed tomography or magnetic resonance
• Early repolarization imaging of the brain are not indicated.
• Brugada syndrome
• ECG evidence of arrhythmogenic right ventricular cardiomyopathy What treatment is indicated for reflex causes of syncope?
• Q-waves suggesting myocardial infarction Class I, Level C: For all patients, explanation of the diagnosis, pro-
vision of reassurance, and an explanation of the risks of recurrence
When is echocardiography indicated in the evaluation of are indicated.
syncope? Class I, Level B: In patients with prodrome, isometric physical coun-
Class I, Level B: In patients who are suspected of having structural terpressure maneuvers are indicated. ■
heart disease, echocardiography is indicated for diagnosis and risk
stratification.
Moya A, Sutton R, Ammirati F, et al. Task Force for the Diagnosis
and Management of Syncope of the European Society of Cardiology
(ESC). Guidelines for the diagnosis and management of syncope
(version 2009). Eur Heart J. 2009;30:2631-2671. By permission of
European Society of Cardiology.
Editorial Comment
S
yncope as a presenting complaint may be anxiety-provoking induced orthostatic hypotension, and volume depletion), and cardio-
for both patients and ED providers. While most causes are genic syncope (including arrhythmia and structural heart disease).3 A
benign, syncope is well-recognized to signal a variety of variety of dangerous non-cardiac conditions can also initially manifest
life-threatening conditions, including cardiac dysrhythmias or isch- as syncope, including pulmonary embolism, subarachnoid hemor-
emia, subarachnoid hemorrhage, pulmonary embolism, or anemia. rhage, and any occult blood loss such as gastrointestinal hemor-
In addition, syncope must be differentiated from other causes of rhage, ruptured ectopic pregnancy, or ruptured abdominal aortic
altered consciousness. aneurysm. These conditions, unlike the primary syncope syndromes,
are not episodic; a history and physical examination directed at ex-
Several guidelines have emerged to assist the clinician with evaluation cluding them is therefore usually adequate if no suggestive features
of the patient with syncope.1,3-7 Many of these guidelines focus on an (focal pain, signs of hypovolemia, etc.) are present.
inpatient- or outpatient-based comprehensive evaluation to determine
a cause of the event. Despite this, the etiology remains unknown in ap- A systematic approach can be used to guide ED management. (See
proximately 40% of patients.2 The concern of the emergency clinician Clinical Pathway For Syncope, page 7.) As always, the emergency
is to determine the need for immediate intervention as well as the most clinician must first address the ABCs and any dangerous effects of
appropriate setting for further evaluation, if indicated. the transient loss of consciousness, eg, head trauma from a fall. The
next priority is to distinguish syncope from its mimics. When syncope
Syncope is, by definition, brief and transient, with spontaneous is established as the working diagnosis, all patients should receive an
resolution. This makes syncope distinct from metabolic disturbances ECG and a history and physical examination directed at determining
such as hypoglycemia or hypoxia, which persist until intervened the underlying cause. Elements of the history that may help delineate
upon. In order to cause a loss of consciousness, transient ischemic the etiology include the report of a prodrome (“sudden” syncope is
attack must either involve both cerebral hemispheres (a distinctly rare more concerning for a cardiogenic etiology), medications and envi-
event), or involve the reticular activating system, in which case other ronmental exposures which may precipitate syncope, a family history
signs of posterior circulation insufficiency should have been present of cardiac disease (especially sudden cardiac death), and syncope
(ataxia, dysarthria, dysphagia, diplopia, vertigo). that occurs with exertion. The physical examination should give care-
ful attention to dangerous non-cardiac causes of syncope, as well as
Seizure is the chief syncope mimic; a careful history will usually dif- evidence of heart failure or the presence of a murmur.
ferentiate the two, particularly if a reliable witness can assist. Helpful
clinical features to elicit include duration (syncope will generally last Although a definition of change in systolic blood pressure of ≥ 20 mm
less than 5 minutes), tonic-clonic activity (syncope can be associated Hg or diastolic ≥ 10 mm Hg is widely quoted as evidence of orthos-
with myoclonic twitches, but generally less than 15 seconds),7 neuro- tatic hypotension, this definition was determined by consensus,8 not
logic aura, prolonged postictal period, incontinence, or tongue-biting. based on measured physiologic data, and thus may not produce ho-
mogenous symptoms in patients presenting to the ED with orthostatic
There are 3 main classifications of syncope: reflex syncope (including syncope. Therefore, it may be prudent to use symptomatic response
vasovagal syncope, situational syncope, and carotid sinus hypersen- to positional changes instead of numeric values when assessing for
sitivity), orthostatic hypotension (including autonomic failure, drug- orthostatic syncope. (Editorial Comment continued on page 8.)
Perform: Is there evidence to suggest that the transient loss of con- Are there features to suggest a structural or arrhythmic
• History sciousness was a seizure? cardiac etiology?
• Physical examination • Neurological aura NO • Concerning ECG
• ECG, specifically assessing for: • Tonic-clonic movements > 15-30 seconds • Occurred during exertion or supine
l Arrhythmia • Tongue biting • Family history of sudden cardiac death
l Ischemia • Incontinence • Absence of prodrome
l Pre-excitation • Prolonged post-event confusion or lethargy • Preceded by palpitations or chest pain
l Brugada syndrome • New murmur
l Hypertrophic obstructive cardiomyopathy YES NO
l Corrected QT interval > 500 ms YES NO
YES NO
EM
EM Practice
Practice Guidelines
Guidelines Update
Update © 2010
© 2010 2 7 ebmedicine.net
ebmedicine.net •• December
December 2010
2010
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(Editorial Comment continued from page 6.) Patients with evident reflex-mediated syncope may benefit from
learning physical isometric counterpressure maneuvers, which are
The ECG is an essential component in the evaluation of syncope, as employed at the onset of symptoms and increase systemic vascular
it may demonstrate rare but potentially life-threatening pathologies. In resistance, possibly averting subsequent loss of consciousness.10
addition to dysrhythmias and ischemia, particular attention should be
paid to screening for pre-excitation syndromes, Brugada, and a long- After an appropriate ED evaluation, the cause of syncope often
QT interval, as well as evidence of hypertrophic cardiomyopathy (left remains uncertain. In these cases, disposition is determined by the
ventricular hypertrophy and deep, narrow Q-waves, particularly in the presence of features that predict short-term adverse events, as pre-
inferior and lateral leads).9 sented in the ACEP clinical policy. (See Figure, page 3.) ■
References
1. Huff JS, Decker WW, Quinn JV, et al. American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and man-
agement of adult patients presenting to the emergency department with syncope. Ann Emerg Med. 2007;49:431-444. (Systematic review)
2. Soteriades ES, Evans JC, Larson MG, et al. National Heart, Lung, and Blood Institute Framingham Heart Study. Incidence and prognosis of
syncope. N Engl J Med. 2002;347(12):878-885. (Prospective, sub-group analysis; 7814 patients)
3. Moya A, Sutton R, Ammirati F, et al. Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology
(ESC). Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J. 2009;30:2631-2671. (Systematic review)
4. Linzer M, Yang E, Mark Estes NA III, et al. The Clinical Efficacy Assessment Project of the American College of Physicians. Clinical guide-
line: diagnosing syncope: part I: value of history, physical examination, and electrocardiography. Ann Intern Med.1997;126:989-996. (Sys-
tematic review)
5. Linzer M, Yang E, Mark Estes NA III, et al. The Clinical Efficacy Assessment Project of the American College of Physicians. Clinical guide-
line: diagnosing syncope: part II: unexplained syncope. Ann Intern Med. 1997;127:76-86. (Systematic review)
6. Strickberger SA, Benson W, Biaggioni I, et al. American Heart Association Councils on Clinical Cardiology, Cardiovascular Nursing, Car-
diovascular Disease in the Young, and Stroke, and the Quality of Care and Outcomes Research Interdisciplinary Working Group; and the
American College of Cardiology Foundation: In Collaboration With the Heart Rhythm Society: Endorsed by the American Autonomic Society.
AHA/ACCF scientific statement on the evaluation of syncope. Circulation. 2006;113:316-327. (Review)
7. Westby M, Davis S, Bullock I, et al. NHS National Institute for Health and Clinical Excellence. National Clinical Guideline Centre for Acute
and Chronic Conditions, Royal College of Physicians. Transient loss of consciousness ("blackouts") management in adults and young
people. http://www.nice.org.uk. Accessed October 15, 2010. (Review)
8. Kaufmann H. Consensus statement on the definition of orthostatic hypotension, pure autonomic failure and multiple system atrophy. Clin
Auton Res.1996;6(2):125-126. (Consensus statement)
9. Dovgalyuk J, Holstege C, Mattu A, et al. The electrocardiogram in the patient with syncope. Am J Emerg Med. 2007;25:688-701. (Review)
10. van Dijk N, Quartieri F, Blanc JJ, et al. Effectiveness of physical counterpressure maneuvers in preventing vasovagal syncope. J Am Coll
Cardiol. 2006;48(8);1652-1657. (Prospective, randomized; 223 patients)
Discussion of Investigational Information: As part of the newsletter, faculty may be presenting investi-
gational information about pharmaceutical products that is outside Food and Drug Administration-approved
Opinions expressed are not necessarily those of this publication. Mention of prod- labeling. Information presented as part of this activity is intended solely as continuing medical education
ucts or services does not constitute endorsement. This publication is intended as a and is not intended to promote off-label use of any pharmaceutical product.
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In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty for this CME activity
were asked to complete a full disclosure statement. The information received is as follows: Dr. Tainter,
The materials contained herein are not intended to establish policy, procedure, or
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