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BOOTH #105
Las Vegas, NV
April 25-27

Syncope In Pediatric Patients:
A Practical Approach To Differential
Diagnosis And Management In The
Emergency Department

Colleen Fant, MD, MPH
Department of Emergency Medicine, Ann and Robert H. Lurie
Children's Hospital of Chicago, Chicago, IL
Ari Cohen, MD, FAAP
Chief of Pediatric Emergency Medicine Services, Massachusetts
General Hospital; Instructor in Pediatrics, Harvard Medical School,
Boston, MA
Peer Reviewers

Syncope is a condition that is often seen in the emergency department.
Most syncope is benign, but it can be a symptom of a life-threatening
condition. While syncope often requires an extensive workup in
adults, in the pediatric population, critical questioning and simple,
noninvasive testing is usually sufficient to exclude significant or lifethreatening causes. For low-risk patients, resource-intensive workups
are rarely diagnostic, and add significant cost to medical care. This
issue will highlight critical diseases that cause syncope, identify highrisk “red flags,” and enable the emergency clinician to develop a costeffective, minimally invasive algorithm for the diagnosis and treatment
of pediatric syncope.


April 2017

Volume 14, Number 4

Andrew Dixon, MD, FRCPC
Associate Professor, Faculty of Medicine, Department of Pediatrics,
Division of Emergency Medicine, Stollery Children’s Hospital,
Edmonton, AB, Canada
Sabrina Guse, MD
Attending Physician, Emergency Medicine & Trauma Center,
Children’s National Health System; Assistant Professor of Pediatrics
& Emergency Medicine, The George Washington University School
of Medicine, Washington, DC
Timothy Rupp, MD, MBA, FACEP, FAAEM
Emergency Medicine Physician, Dallas, TX
Prior to beginning this activity, see “Physician CME Information”
on the back page.

Ilene Claudius, MD
Associate Professor, Department
of Emergency Medicine and
Pediatrics, USC Keck School of
Medicine, Los Angeles, CA

Alson S. Inaba, MD, FAAP
Garth Meckler, MD, MSHS
Pediatric Emergency Medicine
Associate Professor of Pediatrics,
Specialist, Kapiolani Medical Center
University of British Columbia;
for Women & Children; Associate
Division Head, Pediatric Emergency
Professor of Pediatrics, University
Medicine, BC Children's Hospital,
of Hawaii John A. Burns School of
Vancouver, BC, Canada
Ari Cohen, MD, FAAP
Chief of Pediatric Emergency Medicine
Joshua Nagler, MD, MHPEd
Services, Massachusetts General
Madeline Matar Joseph, MD, FACEP, Assistant Professor of Pediatrics,
Hospital; Instructor in Pediatrics,

Harvard Medical School; Fellowship
Associate Editor-in-Chief
Harvard Medical School, Boston, MA
Professor of Emergency Medicine
Director, Division of Emergency
Medicine, Boston Children’s
Vincent J. Wang, MD, MHA
Marianne Gausche-Hill, MD, FACEP,
Director, Pediatric Emergency
Hospital, Boston, MA
Professor of Pediatrics, Keck
Medicine Division, University
School of Medicine of the
Medical Director, Los Angeles
James Naprawa, MD
MedicineUniversity of Southern California;
County EMS Agency; Professor of
Attending Physician, Emergency
Jacksonville, Jacksonville, FL
Associate Division Head, Division
Clinical Medicine and Pediatrics,
Department USCF Benioff
of Emergency Medicine, Children's
David Geffen School of Medicine at Stephanie Kennebeck, MD
Children's Hospital, Oakland, CA
Hospital Los Angeles, Los Angeles,
UCLA, Los Angeles, CA
Associate Professor, University of
Joshua Rocker, MD
Michael J. Gerardi, MD, FAAP,
Associate Chief, Division of
Cincinnati, OH
FACEP, President
Pediatric Emergency Medicine,
Editorial Board
Associate Professor of Emergency
Anupam Kharbanda, MD, MS
Cohen Children's Medical Center;
Jeffrey R. Avner, MD, FAAP
Medicine, Icahn School of Medicine Chief, Critical Care Services
Assistant Professor of Emergency
Professor of Pediatrics and Chief
at Mount Sinai; Director, Pediatric
Children's Hospitals and Clinics of
Medicine and Pediatrics, Hofstra
of Pediatric Emergency Medicine,
Emergency Medicine, Goryeb
Minnesota, Minneapolis, MN
Northwell School of Medicine, New
Albert Einstein College of Medicine,
Children's Hospital, Morristown
Hyde Park, NY
Tommy Y. Kim, MD, FAAP, FACEP
Children’s Hospital at Montefiore,
Medical Center, Morristown, NJ
Associate Professor of Pediatric
Steven Rogers, MD
Bronx, NY
Sandip Godambe, MD, PhD
Emergency Medicine, University of
Associate Professor, University of
Steven Bin, MD
Vice President, Quality & Patient
California Riverside School of Medicine,
Connecticut School of Medicine,
Associate Clinical Professor
Safety, Professor of Pediatrics and
Riverside Communtiy Hospital,
Attending Emergency Medicine
of Emergency Medicine and
Emergency Medicine, Attending
Department of Emergency Medicine,
Physician, Connecticut Children's
Pediatrics, UCSF School of
Physician, Children's Hospital of the
Riverside, CA
Medical Center, Hartford, CT
Medicine; Medical Director, UCSF
King's Daughters Health System,
Melissa Langhan, MD, MHS
Christopher Strother, MD
Benioff Children's Hospital, San
Norfolk, VA
Associate Professor of Pediatrics and Assistant Professor, Emergency
Francisco, CA
Ran D. Goldman, MD
Emergency Medicine; Fellowship
Medicine, Pediatrics, and Medical
Richard M. Cantor, MD, FAAP,
Professor, Department of Pediatrics,
Director, Director of Education,
Education; Director, Undergraduate
University of British Columbia;
Pediatric Emergency Medicine, Yale
and Emergency Department
Professor of Emergency Medicine
Research Director, Pediatric
University School of Medicine, New
Simulation; Icahn School of Medicine
and Pediatrics; Director, Pediatric
Emergency Medicine, BC Children's
Haven, CT
at Mount Sinai, New York, NY
Emergency Department; Medical
Hospital, Vancouver, BC, Canada
Robert Luten, MD
Director, Central New York Poison
Professor, Pediatrics and
Control Center, Golisano Children's
Emergency Medicine, University of
Hospital, Syracuse, NY
Florida, Jacksonville, FL
Adam E. Vella, MD, FAAP
Associate Professor of Emergency
Medicine, Pediatrics, and Medical
Education, Director Of Pediatric
Emergency Medicine, Icahn School
of Medicine at Mount Sinai, New
York, NY

Click on the

David M. Walker, MD, FACEP, FAAP
Director, Pediatric Emergency
Medicine; Associate Director,
Department of Emergency Medicine,
New York-Presbyterian/Queens,
Flushing, NY

International Editor
Lara Zibners, MD, FAAP, FACEP
Honorary Consultant, Paediatric
Emergency Medicine, St. Mary's
Hospital Imperial College Trust,
London, UK; Nonclinical Instructor
of Emergency Medicine, Icahn
School of Medicine at Mount Sinai,
New York, NY

Pharmacology Editor
Aimee Mishler, PharmD, BCPS
Emergency Medicine Pharmacist,
Maricopa Medical Center, Phoenix,

Quality Editor
Steven Choi, MD
Assistant Vice President, Montefiore
Network Performance Improvement;
Director, Montefiore Institute for
Performance Improvement; Assistant
Professor of Pediatrics, Albert
Einstein College of Medicine, Bronx,

CME Editor
Deborah R. Liu, MD
Assistant Professor of Pediatrics,
Keck School of Medicine of USC;
Division of Emergency Medicine,
Children's Hospital Los Angeles,
Los Angeles, CA

icon for a closer look at tables and figures.

Case Presentations

peaking in patients aged between 15 and 19 years.
Fifty percent of people report an episode of syncope
during adolescence.1 Syncope accounts for 1% to 3%
of emergency department (ED) visits, with an overall incidence in the pediatric population of 0.1% to
0.5%.2,3 Syncope must be distinguished from all other
causes of loss of consciousness, such as seizures, head
trauma, and psychiatric causes.
There are many ways to classify syncope, but
the simplest is to divide the causes of syncope into
2 groups: cardiac and noncardiac etiologies. While
cardiac causes represent the minority of syncope
cases, they should not be missed,1 as they can result
in sudden death.4 As many as 1% to 5% of syncopal
events may be related to underlying cardiac disease.5 This issue of Pediatric Emergency Medicine Practice will help emergency clinicians develop a broad
differential diagnosis, use a classification scheme to
identify the causes of syncope, and determine appropriate evaluation of the patient. Most importantly,
this issue will help emergency clinicians identify the
red flags for etiologies that must not be missed in the
evaluation of pediatric syncope in the ED.

A 10-year-old previously healthy boy presents after
“passing out” and experiencing chest pain while playing
basketball with friends earlier that evening. The patient
reports occasional chest pain with exertion. Today, he also
had chest pain while running, collapsed, and had a loss
of consciousness for 4 to 5 seconds. He then returned to
baseline. He has no prior history of syncope and no recent
infections. He denies drug use. On physical examination,
there is no evidence of acute distress, and he has normal
pulmonary and cardiac examinations. You immediately
order an ECG. Do you also need to obtain troponins, Ddimer, or coagulation studies? Does he also need an echocardiogram? You want the patient to see a cardiologist,
but does this need to happen in the middle of the night?
A 16-year-old previously healthy adolescent girl
presents with multiple episodes of syncope over the last 24
hours. Her preceding symptoms include the sensation that
her heart was racing, seeing spots in her visual fields, and
feeling short of breath. She had been feeling unwell for 4
days with a dry cough, but no other cold-like symptoms.
The first episode of syncope occurred the previous night
after getting up from seated position and walking. Her
second episode of syncope was this morning, again, after
getting up and walking. She had her third episode of
syncope today while seated on a couch. This episode was
witnessed by friends who state she was unconscious for a
few seconds. She denies any pain with these episodes. She
currently has no chest pain, but feels short of breath. She
has no risk factors for pulmonary embolism and no family
history of early cardiac death or clotting disorders. Her
last menstrual period was 2 weeks ago. As you order an
ECG and a pregnancy test, you think about what else you
need to do for this patient.
An 18-year-old previously healthy adolescent girl
presents after fainting. She was standing and waiting
for the subway when she "felt the room closing in” and
the “world going dark.” The next thing she remembers
is lying on the ground with people looking down at her.
The patient reports recent cold symptoms and decreased
appetite. She denies the use of drugs or alcohol. She denies
pregnancy. This has happened one other time, several
years ago. Now she feels she has returned to her baseline.
What diagnostic testing is helpful in the diagnosis of this
patient? What further evaluation does she need, if any?
How should she be managed? Does she need admission?

Critical Appraisal Of The Literature
A literature search was performed in PubMed using
the terms syncope, fainting, blackout, and vasovagal.
The search was limited to articles published since
1960 that involved patients aged 0 to 18 years. The
term emergency department was also included in
a subsequent search. This search was limited by
age, English language, and human subjects. These
searches identified several thousand articles that
were screened by title, which resulted in approximately 150 articles that were considered for inclusion. The Cochrane Database of Systematic Reviews,
Evidence-Based Medicine Reviews: Best Evidence
(American College of Physicians), Database of Abstracts of Reviews of Effectiveness (DARE), and the
National Guideline Clearinghouse were all queried
for articles related to syncope in adults or children.
The results of these queries produced more than 130
articles that were reviewed in full.

Etiology And Pathophysiology
Syncope, while technically an ICD (International
Statistical Classification of Diseases) diagnosis, is the
presenting symptom of relative cerebral hypoperfusion that is the result of neurocardiogenic, cardiac,
neurologic, metabolic, toxin-mediated, or psychiatric
etiologies. With respect to the pediatric population,
syncope is more common in the adolescent population (ages 13 to 18 years) and is more common in
girls than boys. In the adolescent population, syncope most commonly results from a benign etiology
and is most often neurocardiogenic in nature. Young

Syncope is defined as a transient loss of consciousness
and postural tone due to an alteration in cerebral perfusion, usually associated with spontaneous recovery.
In pediatric patients, syncope is most often a brief episode with complete recovery, without sequelae. These
typical episodes, however, must be differentiated
from those with rare, life-threatening etiologies. Syncope is most common in teenagers, with the incidence
Copyright © 2017 EB Medicine. All rights reserved.



children rarely present with syncope, except in the
setting of breath-holding spells, seizures, and cardiac
dysrhythmias.5 In young children, unless the history
is classic for a breath-holding spell, additional evaluation is warranted.

simple historical and physical examination features
can aid the emergency clinician in distinguishing
between cardiac and noncardiac syncope. Table 1
notes various etiologies of syncope.

Pathophysiology Of Neurocardiogenic
(Vasovagal) Syncope

Hypertrophic Cardiomyopathy
Hypertrophic cardiomyopathy (HCM) is a rare,
genetic, structural heart condition that has received
substantial public attention. One of the most famous
cases was the sudden unexpected death of basketball player Reggie Lewis in 1993; additional cases
in other famous athletes have occurred since then.
HCM is the most commonly identified cause of sudden death in athletes. It is frightening, as it can afflict
athletes or young adults in their prime. Despite the
public perception of its high mortality rate, the actual prevalence of this disease is relatively low. The
true prevalence of HCM in the pediatric population
is not certain, but some studies have identified the
prevalence in young adults to be 1 in 500.13

HCM is defined as an asymmetric, hypertrophied, and nondilated left ventricle without other
underlying cardiac disease.14 It is caused by disorganized, irregular, and hypertrophied cardiac myocytes. When these myocytes undergo necrosis, they
are replaced by fibrotic tissue, which creates hypertrophy of the left ventricular wall that is typically
asymmetric and preferentially affects the septum or
apex. Once this hypertrophy becomes larger, it can
cause left ventricular outflow tract (LVOT) obstruction. Heart function becomes preload-dependent
to overcome the obstruction. Persistent obstruction
can lead to additional ventricular hypertrophy due

Neurocardiogenic syncope (NCS), or vasovagal
syncope, is the most common cause of pediatric syncope, accounting for 60% to 80% of syncope cases.5
The loss of consciousness caused by NCS is due
to cerebral hypoperfusion. In NCS, cerebral perfusion decreases 30% to 50% from baseline.3 The body
has multiple compensatory measures to prevent
this drop. When standing from a sitting or lying
position, the decreased venous return results in a
decreased stroke volume. In order to compensate
for this subsequent drop in mean arterial pressure,
high-pressure receptors in the aortic arch and carotid
sinus, as well as low-pressure receptors in the lungs
and heart, are activated. This activation of the sympathetic nervous system results in a compensatory
increase in heart rate and blood pressure. Additionally, venous return is increased through muscle
contraction in the distal extremities, which increases
peripheral vascular resistance. If these compensatory
measures are engaged, cerebral perfusion is maintained and syncope is prevented. When these measures are altered or are insufficient, syncope occurs.

Cerebral hypoperfusion occurs in the setting of
autonomic dysregulation with inappropriate withdrawal of sympathetic stimulation and increased
vagal stimulation.2,6 This manifests in 3 ways: (1) inadequate compensatory tachycardia, (2) insufficient
vascular tone, and (3) decreased cardiac output.5,7

Cerebral vascular perfusion is particularly sensitive to changes because, in the standing position,
the mean cerebral pressure is only slightly above the
lower limit of cerebral autoregulation. The most important sympathetic receptors in preventing syncope
are those in the carotid sinus that affect peripheral
vascular resistance, where 60% of the body’s blood
volume resides.8

Differential Diagnosis
Differentiating cardiogenic syncope from the other
causes can be especially challenging for the emergency clinician. Several highly publicized cases
have drawn attention to life-threatening diagnoses
such as hypertrophic cardiomyopathy (HCM) and
cardiac dysrhythmias.1 Although these make up a
small proportion of syncope cases that present to the
ED, they account for the vast majority of morbidity
and mortality in the pediatric population. Extensive
evaluation of children presenting with syncope is
low-yield and often costly.9-12 Fortunately, several
April 2017 •

Cardiogenic Etiologies Of Syncope

Table 1. Etiologies Of Syncope
Cardiac Causes

Noncardiac Causes

• Hypertrophic cardiomyopathy
• Anomalous coronary artery*
• Myocarditis*
• Pericarditis*
• Valvular dysfunction*

• Neurocardiogenic/vasovagal
(most common)
• Postural orthostatic
tachycardia syndrome
• Psychogenic pseudosyncope
• Drugs and toxins*
• Metabolic derangements,
• Breath-holding spells
• Seizure
• Trauma
• Pregnancy
• Pulmonary hypertension*
• Pulmonary embolism*

• Commotio cordis*
• Long QT syndrome
• Wolff-Parkinson-White
• Supraventricular tachycardia
• Brugada syndrome
• Short QT syndrome*
• Heart block
• Sick sinus syndrome*
• Arrythmogenic right
ventricular dysplasia*

*Not discussed in detail in this article.

3 Copyright © 2017 EB Medicine. All rights reserved.

to the increased force needed by the left ventricle to
overcome the LVOT obstruction, and these cellular
changes can generate dysrhythmias, heart failure,
and sudden death. The dysrhythmias associated
with HCM and sudden death are ventricular tachycardia and ventricular fibrillation. There are over
450 genetic mutations that have been found to be
associated with HCM. Of patients with an identified
genotype, 70% have a mutation in either the betamyosin heavy chain or the myosin-binding protein
in cardiac myocytes. Pathogenic mutations are inherited in an autosomal-dominant pattern.13,14

There are varying types of HCM that can present
with different degrees of obstruction and symptomatology. Many patients with HCM can live for years
without symptoms. For adults, the mortality rates
range from 1% to 6% per year. Higher mortality is
associated with HCM in patients aged < 20 years.
Sudden death in the setting of HCM is more prevalent in the younger population (< 30 years) and is
equal between genders. In the pediatric population,
HCM tends to be associated more with a syndromic
phenotype, such as underlying genetic or neuromuscular syndrome, whereas in the adult population,
HCM tends to be a primary disease.

HCM causes sudden death in approximately 5%
of cases, but in cases of sudden cardiac death among
athletes and young people, it is the most common
identified cause. Sudden death is often the first clinical manifestation of HCM. In a study by Maron et al,
HCM was the identifiable cause in 36% of cases of
sudden pediatric death.15

Patients with HCM who do not present with
sudden death typically present for evaluation of
an incidental murmur or positive family history;
this includes most patients. Patients presenting
in distress, however, are likely to have symptoms
such as heart failure, syncope, arrhythmias, or
cardiac arrest. Patients who present with these
symptoms have a poorer prognosis.13

Of those patients who present with syncope to
the pediatric ED, the number of patients identified
as having HCM is exceptionally low, but could be
determined by taking a thorough family history of
cardiac disease and sudden death, and by abnormal
ECG findings. For a patient with HCM, the physical
examination may be notable for a systolic murmur
that increases during maneuvers that decrease
cardiac preload, which causes the LVOT obstruction to increase. These maneuvers include moving
from supine to standing/sitting, or from squatting
to standing.

In the setting of a high clinical suspicion for
HCM, an echocardiogram should be ordered as the
diagnostic study of choice. In order to diagnose
ventricular hypertrophy on echocardiogram, the left
ventricle wall thickness must be > 2 standard
deviations above the mean. ECG is abnormal in 75%
Copyright © 2017 EB Medicine. All rights reserved.

to 95% of patients with HCM and usually shows left
ventricular hypertrophy.13 (See Figure 1, page 5. )

Long QT Syndrome
Long QT syndrome is a potentially fatal cardiac
dysrhythmia that can be either acquired or congenital.
For children with long QT syndrome, there is an
alteration in cardiac cell membrane ion channel
permeability that results in prolonged depolarization
that is seen on ECG as a prolonged QT interval. (See
Figure 2, page 6. ) This abnormality has varying
degrees of clinical manifestation, but usually presents
between the ages of 9 and 15 years, with seizures,
syncope, or sudden death. The most commonly
described dysrhythmia associated with long QT
syndrome is a polymorphic ventricular dysrhythmia,
or torsades de pointes, which describes the oscillating
QRS axis. The diagnosis of long QT syndrome is
based on an abnormal 12-lead ECG obtained at rest.16
The QTc (corrected for heart rate) interval can be
calculated by dividing the QT interval by the square
root of the preceding R-R interval. If this value is >
460 milliseconds, it is considered abnormal or prolonged.17,18 Dysrhythmias are most often associated
with a QTc interval > 500 milliseconds.19

Congenital long QT syndrome is associated
with 2 syndromes: Jervell and Lange-Nielson
syndrome (which is also associated with congenital
deafness and higher rates of sudden death) and
Romano-Ward syndrome.20 The genetic risk associated with these syndromes makes obtaining
a family history a crucial aspect of the syncope
evaluation. Women are known to have an increased
likelihood of recurrent cardiac events and are at an
increased risk of developing syncope or sudden
death, especially during menses.20-23

The frequency of a medication-induced long QT
interval is uncertain but tends to be associated with
cumulative QT-prolonging medications or an
underlying risk of long QT syndrome. (See Table 2,
page 7. ) Because many QT-prolonging medications are regularly administered in the ED, providers
must be aware of the potential for the cumulative
effect of these medications in prolonging the QT
interval, in addition to any home medications. It
may be prudent to use these medications with
caution in patients with a history of syncope or to
consider obtaining an ECG prior to administration.
Wolff-Parkinson-White Syndrome And Narrow QRS
Complex Tachycardia
Wolff-Parkinson-White (WPW) syndrome is an
accessory pathway-induced re-entrant tachycardia,
either anterograde (90%) or retrograde (10%). The
typical WPW pattern on ECG (a short PR interval
and associated ventricular pre-excitation as seen by
the delta wave) (see Figure 3, page 8 ), is found in
approximately 0.2% of the population, but only a


small proportion of these patients will be symptomatic.24 Not all patients with WPW syndrome will have
the classic ECG findings, unless the accessory pathway is activated. The accessory pathway is most
likely to be activated during periods of tachycardia.
In a prospective study published in 2013, 446 children
from a cardiology database were identified as having
WPW. Of this identified cohort, 4% were diagnosed
after presenting with syncope.25 Although WPW is a
rare cause of syncope, it is often identifiable by
screening ECG. In fact, 25% of the patients within the
previously mentioned cohort were diagnosed with
WPW based on an incidental ECG finding.25

The most common tachydysrhythmia in WPW
is anterograde atrioventricular re-entrant tachycardia, which produces a narrow QRS complex
tachycardia that can evolve into a ventricular
tachycardia. (See Figure 4, page 8. ) There is
also the less-common retrograde conduction from
the atrioventricular node to the atria, generating a
wide QRS complex tachycardia that is difficult to
distinguish from polymorphic ventricular tachycardia.26 Santinelli et al assessed 184 asymptom-

atic children with WPW who were diagnosed by
screening ECG in Italy, and 10% had a potentially
treatable dysrhythmia. These identified dysrhythmias had a variety of presenting symptoms that
ranged from cardiac arrest or syncope to mild or
atypical symptoms such as gastrointestinal distress.27 This study helped to emphasize the significant morbidity and mortality of WPW. The current
interventional cardiology practice includes more
aggressive attempts to induce and ablate these
accessory pathways.28
Supraventricular Tachycardia
Supraventricular tachycardia (SVT) is the most common symptomatic pediatric dysrhythmia. SVT is
defined as a narrow QRS complex tachycardia, with
a rate > 220 beats/min in infants or > 180 beats/min
in children and adolescents. In addition, P waves are
absent and there is a lack of beat-to-beat variability.
The compromised cardiac output that can result
from SVT may lead to syncope. SVT can be induced
by caffeine intake, which has become increasingly
common in adolescents, given that energy drinks

Figure 1. Hypertrophic Cardiomyopathy On Electrocardiogram

Normal sinus rhythm, left anterior hemiblock, left ventricular hypertrophy, right ventricular hypertrophy, nonspecific T-wave abnormalities in anterior (V3,
V4), and lateral leads (V5-V6).
Image courtesy of Manuella Lahoud-Rahme, MD and Joseph Spinner, MD.

April 2017 •

5 Copyright © 2017 EB Medicine. All rights reserved.

can have > 200 mg of caffeine in 1 to 2 ounces of volume.29 Questions about caffeine use as well as illicit
drug use should be part of the history taken for all
children presenting with syncope.

Complete heart block is the most common cause of
symptomatic bradycardia in children and infants.30 In
children, acquired heart block can be due to an infectious cause. Heart block can also occur as a result of
iatrogenic causes such as medications or as a result of
prior heart surgery. Additionally, it can be associated
with a syndrome such as lupus erythematosus.
  Delayed conduction from any form of heart
block can result in symptomatic bradycardia that can
decrease cardiac output enough to cause syncope.31
High-degree heart block (ie, second-degree type II
or third-degree) is more dangerous than low-degree
heart block (first-degree or second-degree type I),
with high-degree heart block more likely to evolve
into ventricular dysrhythmias and sudden death.

Heart Block
Heart block occurs in several forms and may also
cause syncope. (See Figure 5, page 9. ) First-degree
heart block, or PR prolongation without dropped ventricular beats, is often asymptomatic. Second-degree
heart block is either Mobitz I or II, with the latter
being more likely to progress to third-degree or
complete heart block. Mobitz I is characterized by
gradual lengthening of the PR interval until a ventricular beat is dropped, whereas Mobitz II exhibits
stable PR intervals and ventricular beats are dropped
in a specified ratio to P waves that are conducted (eg,
3:1, 4:1, etc). Third-degree or complete heart block
occurs when there is atrioventricular node dysfunction and the electrical activity of the atria is no longer
communicating with the ventricles and the ventricular beats are generated from the ventricle itself.

Heart block can be either congenital or acquired.

Brugada Syndrome
Brugada syndrome was first described in 1992 as a
cause of sudden cardiac death. It is a rare, autosomal-dominant disease, with an estimated pediatric
prevalence of 0.0098% in one study population32 and
0.0005% in the general population in another study.33
Overall, Brugada syndrome has a poorly defined

Figure 2. Long QT Syndrome On Electrocardiogram




Distance between the Q wave and the T wave is noted. The QTc (corrected for heart rate) interval can be calculated by dividing the QT interval by the
square root of the preceding R-R interval.
Image courtesy of Manuella Lahoud-Rahme, MD and Joseph Spinner, MD.

Copyright © 2017 EB Medicine. All rights reserved.



prevalence in children. Since the classic ECG findings are only intermittently present, the true prevalence is unknown.33 The syncope and sudden death
that results from symptomatic disease may occur at
rest, during sleep, or with hyperpyrexia, large meals,
cocaine use, or excessive alcohol consumption. In
the pediatric population, fever is a well-documented
precipitant of cardiac events, and it is recommended
that children with Brugada syndrome be treated
early with antipyretics and brought to the hospital
for cardiac evaluation, ECG, and cardiac monitoring
during febrile episodes.32 Although age of onset is
typically in the third to fourth decade of life, neonatal and pediatric cases of Brugada syndrome are well

Brugada syndrome is defined by ECG findings of
ST-segment elevations of at least 2 mm in at least 2 of
3 right precordial leads with a “coved morphology,”
followed by a negative T wave with little or no
isoelectric separation (type 1) or a saddle-back
appearance with a high take-off ST segment followed
by a gradually descending ST segment (type 2). Type
3 may have either a coved or saddleback appearance
with < 1 mm of ST-segment elevation.33 (See Figure 6,
page 13. ) In the largest pediatric study to date, with
30 children aged < 16 years, syncope was the most
common presenting symptom in one-third of the
cases.32 Thirteen percent of the patients had associated atrial fibrillation or flutter, which are very
uncommon pediatric dysrhythmias. Half of the cases
in this study were detected by family screening.

Table 2. Medications That Prolong The QT
Medication Type

Drugs Commonly Used In The
Pediatric Population

Macrolides (account for 77% of
antimicrobial-induced torsades
de pointes)

• Azithromycin
• Erythromycin
• Clarithromycin


• Levofloxacin
• Moxifloxacin


• Voriconazole
• Fluconazole
• Ketoconazole

Gastrointestinal agents

• Ondansetron
• Metoclopramide

Psychiatric medications


• Trimethoprimsulfamethoxazole
• Tacrolimus
• Methadone
• Chloroquine


April 2017 •

Patients with spontaneous (not medication-induced)
type 1 ECG findings and patients with syncope are at
high risk for malignant dysrhythmias.32,37,38
Other Cardiogenic Etiologies
Additional cardiogenic causes of syncope include
anomalous left coronary artery, commotio cordis,
myocarditis, and pericarditis. These topics have been
covered in previous issues of Pediatric Emergency
Medicine Practice. For more information regarding the
management of these conditions, please see the following Pediatric Emergency Medicine Practice issues:
• “Congenital Heart Disease In Pediatric Patients:
Recognizing The Undiagnosed And Managing
Complications In The Emergency Department,”
May 2016, available at:
• “Emergency Management Of Blunt Chest Trauma In Children: An Evidence-Based Approach,”
November 2013, available at:
• “Myocarditis And Pericarditis In The Pediatric
Patient: Validated Management Strategies,” July
2015, available at:

Noncardiac Etiologies Of Syncope That
Require Further Evaluation
Pregnancy And Ectopic Pregnancy
Pregnant adolescents make up a small proportion of
pediatric ED visits (< 1%),39 but adolescent pregnancy accounts for significant morbidity in the pediatric
population, with an incidence of teen pregnancy of
57.4 per 1000 adolescents in the United States. Syncope and near-syncope are common in pregnancy,
particularly during the third trimester.3 Of all pregnant women, 5% experience syncope and almost
30% of pregnant women experience presyncope.40

Menstrual history should be obtained and documented in all adolescent girls; however, it should not
be used to determine whether testing will be performed, as adolescent sexual history can be unreliable. Given the unpredictable nature of adolescent
menstrual cycles, the high risk of missing a pregnancy, and low-cost, noninvasive testing methods
(point-of-care urine analysis), a urine human chorionic gonadotropin (HCG) pregnancy test is indicated in all girls of reproductive age.3,5 Because the age
of menarche is variable, and a patient can become
pregnant during her first cycle, assessment of Tanner
staging is useful when determining a patient’s potential for pregnancy. Menarche does not occur until
late in Tanner stage III.41 All patients with appropriate Tanner staging could, theoretically, be pregnant.

Ectopic pregnancy occurs at a rate of 19.7 per
1000 pregnancies; a ruptured ectopic pregnancy can
be life-threatening.42 Pregnancy-associated syncope
can occur with ectopic pregnancy and ruptured
ectopic pregnancy, resulting in hemorrhage and
7 Copyright © 2017 EB Medicine. All rights reserved.

hemodynamic instability as well as pulmonary embolism due to the prothrombotic state of pregnancy.
While syncope itself is not a common presentation of
pregnant pediatric patients in the ED, hemorrhage in
early pregnancy is the second most common presentation of pregnant pediatric patients to the ED,
accounting for 16% of pregnancy-associated visits, in
one study.39 Early recognition is critical, as hemodynamic instability can lead to syncope and additional
morbidity and mortality.

mia as a cause of syncope in the pediatric population
is uncertain, but, in one study of adults by Massin et
al, the combined incidence was < 3 per 226. (However, hypoglycemia was not specifically separated
out from other causes.)9 Because syncope is, by
definition, a transient phenomenon, it is unlikely
to be due to hypoglycemia,44 which would cause
persistent symptoms until the hypoglycemia was reversed. In the 2009 European Society of Cardiology
guidelines on syncope, hypoglycemia was not even
included as a cause.43 Hypoglycemia is most common in diabetic patients and, within that subgroup,
it is more common among the elderly – not pediatric
patients.44 Standard testing of glucose is therefore
not recommended in routine syncope evaluation

Syncope in the setting of hypoglycemia is rare in the
adult population, comprising approximately 1%, in
one study population.43 The incidence of hypoglyce-

Figure 3. Delta Waves On Electrocardiogram Consistent With Wolff-Parkinson-White Syndrome


Arrow indicates the upslanting delta wave. Note the shortened PR interval.
Image courtesy of Manuella Lahoud-Rahme, MD and Joseph Spinner, MD.

Figure 4. Atrioventricular Re-Entrant Tachycardia In Wolff-Parkinson-White Syndrome

Wide QRS complex tachycardia noted on electrocardiogram.
Used with permission from

Copyright © 2017 EB Medicine. All rights reserved.



Figure 5. Types Of Heart Block On Electrocardiogram
A. First-degree heart block

Arrow indicates the buried P wave.

B. Second-degree Mobitz I heart block

Oval indicates the P wave without a subsequent QRS complex in a random fashion.

C. Second-degree Mobitz II heart block

Ovals indicate the lack of a QRS complex after the P wave in specific intervals.

D. Third-degree heart block

Independent P waves and QRS complexes indicative of ventricular beats generated from the ventricles.
All images used with permission from

April 2017 •

9 Copyright © 2017 EB Medicine. All rights reserved.

Clinical Pathway For The Management Of Pediatric Patients With Syncope
Patient presents to ED
for episode of syncope

• Obtain historyb (Class II)
• Perform physical examinationc
(Class II)


Patient returned to baseline?

• Obtain additional historyb
• Perform physical examinationc
(Class II)



• Follow PALS guidelines
• Perform primary assessment
• Obtain focused historya (Class II)

Spontaneous return to consciousness?

• Abnormal cardiac or neurologic
• Known cardiac disease?


Obtain cardiology or neurology
specialist examination
to determine disposition

Initiate care as warranted


Obtain ECG (Class II-III)

Abnormal findings?d (Class II)




Pregnancy possible?


Obtain urine HCG testing


• Perform obstetric assessment, rule
out ectopic pregnancy, involve OB as
indicated, discharge if stable
• Refer to obstetrician/gynecologist
• Consider social services involvement

• Administer supportive care
• IV fluids if symptomatic hypovolemia
• Consider review of ECG by pediatric

• Discharge if no red flags and patient
is asymptomatic
• Recommendations to patient and



Ensure adequate oral intake

Avoid provoking events

Recognize vasovagal symptoms

Focused history: onset of symptoms, details of events, underlying medical problems, allergies,
medications, last meal.
History to determine etiology: personal or family history of seizures, metabolic disease, or diabetes;
history of medication or toxic ingestion, history of recurrent syncope, menstrual history in females,
history of trauma. See Table 3, page 12, for additional history details.
Physical examination: general appearance, full set of vital signs, injuries, neurologic examination
(intracranial injury, seizure), cardiac examination (heart rate, regularity, murmurs, and other sounds
such as rubs or gallops).
Positive findings of any one of the following is indicative of a cardiac etiology: (1) any syncope that
surrounded activity, (2) a family history of cardiac disease or sudden death, (3) physical examination
findings suggestive of cardiac disease, and (4) an abnormal ECG.
Red flags: Multiple episodes of syncope in a short time period, syncope associated with chest pain,
syncope occurring during exercise or while sitting, syncope in patients with a family history of cardiac
disease, deafness, or sudden death.
Abbreviations: ECG, electrocardiogram; ED, emergency department; HCG, human chorionic
gonadotropin; IV, intravenous; OB, obstetrician; PALS, pediatric advanced life support.

Copyright © 2017 EB Medicine. All rights reserved.



for children. However, if on careful history there is
report of prolonged fasting, drug ingestion, diabetes,
or metabolic disease, point-of-care glucose testing
may be useful to guide treatment.9

Outside of the hospital, hypoglycemia is often
diagnosed in the field with a fingerstick glucose
measurement by emergency medical services (EMS)
providers and is treated prior to arrival to the ED.
Unless the patient is still symptomatic (ie, with
lethargy or confusion), routine glucose testing in
the ED is unlikely to be diagnostic, as glucose levels
will have likely normalized. A study by Salins et al
showed that while patients may experience transient
hypoglycemia during a syncopal episode, their glucose levels returned to normal after the event once
their symptoms subsided.45
Other Noncardiac Etiologies
Syncope may also be caused by ingestion of drugs or
toxins, but would present with signs and symptoms
related to the associated toxidromes. It is possible for
syncope to occur in the setting of metabolic derangements, but since metabolic derangements are not
typically transient, they are more likely to cause
altered mental status, lethargy, or coma than the
transient loss of consciousness that defines syncope.
The routine testing of electrolytes in the workup of
syncope has not been shown to contribute to diagnosis or management.46

Noncardiac, Non–Life-Threatening Etiologies
Of Syncope
Neurocardiogenic Syncope
NCS is the most common cause of pediatric syncope,
and it is benign.5 NCS tends to present in 3 phases:
prodrome, loss of consciousness, and recovery.3
Often, a good history of prodromal symptoms can
elucidate the diagnosis. Typical triggers for NCS can
include postural changes, prolonged sitting or standing, or noxious stimuli.5 NCS can occur in otherwisehealthy patients in the setting of exercise (due to venous pooling), hyperthermia, hypovolemia or dehy-

dration, and hyperventilation. These key historical
findings must be distinguished from syncope that
occurs during exertion (“mid-stride” syncope) that
is more worrisome for a cardiac etiology and would
not have the same prodromal symptoms. Associated
prodromal symptoms for NCS include lightheadedness, headache, vision or hearing changes, pallor,
nausea, and diaphoresis, and they are more likely to
occur with NCS than with syncope from a cardiac
etiology.47 The neurologic symptoms of headache,
visual changes, and lightheadedness are thought to
be directly related to the transient cerebral hypoperfusion that occurs during syncope.

The environment and preceding events are also
key to taking a prodromal history. In a study by Tretter
and Kavey, a history of prolonged standing prior to a
syncopal episode was present in 82% of NCS patients,
but was not present in any patients who experienced
cardiac syncope.47 In addition, fewer patients with
NCS had loss of consciousness during activity or during peak activity as opposed to patients with cardiac
syncope.47 Acute stressors such as anxiety, pain, and
strong emotions can also trigger syncope. This stress
response is postulated to trigger a parasympathetic
firing of the autonomic nervous system, resulting in
syncope. A detailed history to document volume status
to assess for hypovolemia as a contributing factor can
also support the diagnosis of NCS.

The second phase of NCS is the transient loss of
consciousness. Typically, once the patient is supine,
cerebral hypoperfusion is reversed and symptoms
resolve in seconds to minutes, with complete resolution in 1 to 2 minutes.3,8 Most of the morbidity of
NCS occurs during the loss-of-consciousness phase,
particularly if the patient sustains a head injury
or injures another body part. Cases of traumatic
injuries have been reported. In a study by Johnson
et al, 12% of patients had injury with syncope.48 A
detailed history, particularly from bystanders, is
helpful to determine whether additional injury was
sustained during the syncopal event. During the
loss-of-consciousness phase, the patient may appear

Class Of Evidence Definitions
Each action in the clinical pathways section of Pediatric 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

Class II
• Safe, acceptable
• Probably useful

Level of Evidence:
• Generally higher levels of evidence
• Nonrandomized or retrospective studies:
historic, cohort, or case control studies
• Less robust randomized controlled trials
• Results consistently positive

Class III
• May be acceptable
• Possibly useful
• Considered optional or alternative treatments

Level of Evidence:
• Generally lower or intermediate levels of
• Case series, animal studies,
consensus panels
• Occasionally positive results

• Continuing area of research
• No recommendations until further

Level of Evidence:
• Evidence not available
• Higher studies in progress
• Results inconsistent, contradictory
• Results not compelling

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 © 2017 EB Medicine. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Medicine.

April 2017 •

11 Copyright © 2017 EB Medicine. All rights reserved.

pale, diaphoretic, or clammy, and may even have
abnormal movements. The patient typically does not
remember this phase of the event.3

In the third, recovery phase of NCS, the patient
returns to baseline over the subsequent 5 to 30 minutes, and during this time the patient may experience
symptoms of headache, nausea, weakness, or fatigue.

Often, NCS can be recurrent. Evaluation and
diagnosis in the ED should include a thorough
history of the event with emphasis on the typical
prodromal symptoms described previously. A history negative for red flags (see Table 3) (including a
family history of cardiac disease, syncope occurring
during exertion or while sitting, and associated chest
pain) is also key to the diagnosis of NCS. Physical
examination should be thorough and should focus
on pertinent negatives, as patients with NCS have
a normal physical examination, barring any trauma
sustained during the episode. Normal vital signs,
neurologic examination, and cardiac examination
are reassuring. While used in the past, the head-up
tilt-table test is not necessary for the diagnosis of
NCS.48 Particularly in the ED setting, this test is time
and labor-intensive and does not add value over a
thorough history and physical examination.

Seizure is often high on the differential diagnosis of
syncopal events. Syncope from various causes can
be convulsive, with transient stiffening, clonus, or
myoclonus due to the transient cerebral hypoxia that
suppresses the limbic and cortical structures. These
movements occur after the loss of consciousness. In
contrast, during a seizure, the abnormal movements
occur before or at the onset of loss of consciousness.
The abnormal movements during syncope tend to
be few or brief rather than sustained tonic-clonic
seizure activity. Furthermore, the prodrome prior to
typical NCS is different from the symptoms associat-

ed with seizure. The associated symptoms more consistent with seizure include supine posture; warm,
flushed, or cyanotic skin; loss of bowel function or
bladder function; and tongue biting. Additionally,
a true seizure will have a postictal phase, characterized by lethargy or confusion, while syncope may
be followed by headache, nausea, or weakness—a
subtle, yet important, distinction.3

Breath-Holding Spells
Breath-holding spells are a common cause of syncope
in toddlers. Breath-holding typically occurs in young
children who begin to cry either after injury or while
frightened or frustrated. In the setting of this crying
episode, the child then becomes quiet and cyanotic or
pallid and goes limp, often with loss of consciousness.
The pathophysiology is unclear. Initial episodes most
often occur before 2 years of age and are most often
not associated with other developmental abnormalities. The child usually stops crying in full expiration
with mouth open. Loss of consciousness lasts for < 1
minute. The patient should then return to baseline.
These episodes can be associated with posturing,
body “jerks,” or incontinence. In general, workup is
not required if the history is consistent. Reassurance
is the best treatment, although since anemia has been
associated with these episodes,49 complete blood cell
count testing may be considered either in the ED or as
an outpatient.
Postural Orthostatic Tachycardia Syndrome
Postural orthostatic tachycardia syndrome (POTS) is
similar to NCS in that they can both result in syncope
and presyncope through the presumed mechanisms
of cerebral hypoperfusion. Distinct from NCS, however, POTS does not produce observed changes in
blood pressure. In POTS, symptoms are characterized
by sympathetic activation with palpitations, chest
pain, vasomotor symptoms, or tremulousness elicited
by orthostatic changes. When standing, patients can
also experience symptoms of orthostatic intolerance,
such as syncope and near-syncope, dizziness, lightheadedness, visual changes, weakness, headache, and
nausea. Patients may also have chronic fatigue. In patients with POTS, orthostatic changes elicit a change
in heart rate by > 30 beats/min or an absolute systolic
blood pressure > 120 mm Hg within 10 minutes of
active standing. These changes may cause presyncope and syncope in patients with POTS, but unlike
patients with NCS, there is no associated orthostatic
hypotension, or only modest hypotension. The
diagnosis is based on the chronicity of sympathetic
activation symptoms such as palpitations, chest pain,
or tremulousness, as well as the subjective symptoms
of orthostatic intolerance.50

The estimated prevalence of POTS in adults is
170 per 100,000,51 but the incidence is unknown in
the pediatric population. Patients with POTS are
most commonly aged between 12 and 40 years,

Table 3. “Red Flags” And “Green Lights” In
Patients With Syncope
Red Flags

Green Lights

• Multiple episodes in a short
time period
• Associated chest pain
• Episode occurred during
exercise or while sitting
• Family history of cardiac
disease, deafness, or sudden

• Episode occurred
during standing, in a hot
environment, after poor oral
intake, or while ill
• Normal electrocardiogram
and negative pregnancy test
• Normal physical examination
• Patient is at baseline on
• Preceding symptoms include
dizziness, visual changes,
nausea, or diaphoresis

Red flags are worrisome aspects of the history. Green lights are
reassuring aspects of the history that suggest neurocardiogenic

Copyright © 2017 EB Medicine. All rights reserved.



and there is a 4:1 female-to-male prevalence. In a
study by Jajour of adolescents with POTS, the most
common symptoms were chronic fatigue, nausea,
and disordered sleeping. Patients with POTS may
present to the ED with syncope and presyncope. A
thorough history of the chronicity of the symptoms
as well as vital sign abnormalities are sufficient to diagnose this syndrome.50 Given that ED presentations
represent only a snapshot in time, however, multiple
presentations with syncope and presyncope may occur prior to diagnosis.
Psychogenic Pseudosyncope
Psychogenic pseudosyncope is defined as an apparent transient loss of consciousness without hav-

ing true loss of consciousness. It is associated with
chronicity and progressive worsening of symptoms,
causing disability and impaired quality of life. While
poorly characterized, particularly in the pediatric
population, it has been estimated to account for 0%
to 8% of patients presenting with syncope.52 Typically, the patient history is notable for a stressor around
the time of onset of these symptoms. Occasionally,
these patients go on to present with subsequent
alternative pseudoneurologic disorders that are not
attributed to an organic etiology. In patients with
psychogenic pseudosyncope, a thorough history
is key to the diagnosis. As compared with patients
who experience true loss of consciousness with
syncope, these patients tend to have longer periods

Figure 6. Brugada Syndrome Patterns On Electrocardiogram

Precordial leads of a resuscitated patient with Brugada syndrome. Arrows indicate coved ST segment changes. Note the dynamic electrocardiogram
(ECG) changes over time. All 3 patterns are shown. Arrows denote the J wave. The left panel shows a clear type 1 ECG. Between 7–2-99 and 13–299, types 2 and 3 are shown. Calibrations are given.
Arthur A.M. Wilde, Charles Antzelevitch, Martin Borggrefe et al. Proposed Diagnostic Criteria for the Brugada Syndrome. Circulation. 106(19):25142519. DOI: Reprinted with permission from Wolters Kluwer Health, Inc.

April 2017 •

13 Copyright © 2017 EB Medicine. All rights reserved.

of “unconsciousness” lasting minutes, and may have
multiple episodes a day.53 Patients with psychogenic
pseudosyncope are more likely to be young women
who report worsening episodes of “syncope” for the
previous 6 months. Patients with syncope have an
open, glassy-eyed appearance, while patients with
psychogenic pseudosyncope tend to have closed eyes.

Diagnosing psychogenic pseudosyncope can be
challenging for the ED clinician, but fortunately, like
most common forms of pediatric syncope, it is not
life-threatening. In general, a history that is devoid
of typical autonomic disturbances associated with
cerebral hypoperfusion supports the diagnosis of
psychogenic pseudosyncope. While no specific testing is warranted to support this diagnosis, the suggestibility of this patient population makes it more
likely that they will experience a pseudosyncopal
event during testing.52

with ventilations being most important for hypoxic/
asphyxial arrest versus sudden cardiac arrest. As 70%
of pediatric arrests are respiratory in etiology, current
recommendations still strongly support ventilations
and compressions, due to increased survival rates.58,59
If ventilations are not possible or cannot be performed
safely, then compressions alone are preferable to no
CPR. The use of automated external defibrillators has
become the standard of care, with improved outcomes for pediatric and adult out-of-hospital arrests
that occur in schools and public spaces.60-62

If a patient has experienced syncope but has regained consciousness by the time of arrival of EMS,
then care is largely supportive and dependent on
history and physical examination. If the patient has
ongoing mental status changes, a fingerstick glucose
measurement should be obtained and acted upon, if
abnormal. In the asymptomatic patient, monitoring
is often the only required intervention prior to ED

Prehospital Care

Emergency Department Evaluation

Prehospital care may differ widely depending on
the specific type of syncope. If a patient had a brief
syncopal event in a public area, bystanders may
have been present to help minimize injury (eg, fall
prevention or securing the location of the patient).
Depending on the length of the loss of consciousness, the patient may or may not have returned to
baseline by the time of arrival of medical providers,
specifically EMS.

If a patient is unconscious or unresponsive on
EMS arrival, then the PALS or APLS guidelines
should be followed with evaluation and support
of airway, breathing, circulation, and disability
(ABCD). Depending on the level of consciousness,
airway support may not be required or may range
from noninvasive with placement of oxygen to
advanced airway management. For the layperson
caring for a patient who is unconscious and unresponsive, the 2011 PALS guidelines recommend cardiopulmonary resuscitation (CPR). The guidelines
have been updated for both bystanders (laypersons)
and medical providers, because it has been found
that only 30% of victims of sudden death receive
bystander CPR.54 Current recommendations support
the hands-only (compression-only) option, especially for layperson CPR, as this is easier to perform,
requires no equipment, and is simpler to instruct
over the phone.54-56 In adult studies of mostly cardiac syncopal events, survival rates have been found
to be similar or better without rescue breathing, but
no definitive pediatric trial of compression-only CPR
has been conducted.57

Modification of the classic A-B-C training for
resuscitation to the current model of C-A-B emphasizes the circulation aspect of CPR even for children.
For trained providers, ventilations and compressions
are the preferred mode of CPR to increase survival,
Copyright © 2017 EB Medicine. All rights reserved.

Initial Management
The evaluation for syncope in the ED depends on
whether or not the patient has returned to baseline or
remains unconscious or has continued altered mental
status. All patients who have altered mental status
or are unconscious should be treated using standard
PALS guidelines, with an evaluate-identify-intervene
continuous cycle of assessment with primary and secondary assessments taking place in a rapid fashion.
Of note, if the patient does not have a spontaneous
return to consciousness within seconds to minutes
and remains unconscious, then this should no longer
be treated as syncope; the treatment of the obtunded
patient is beyond the scope of this review.

Initial history in a patient with altered mental status
should be brief and focused toward pertinent information such as onset of symptoms, details of events,
and underlying medical problems.63 Additional
pieces of history that are useful to the emergency
clinician in the acute setting may be obtained using
the “SAMPLE” mnemonic (Signs and Symptoms,
Allergies, Medications, Past medical history, Last
meal, and surrounding Events).

Additional history that is useful in patients
with syncope who present either unconscious then
recover or for patients who have already returned
to baseline focuses on delineating the underlying
cause of the syncope. History should be focused
on worrisome and reassuring aspects. See Table 3,
page 12 for “red flags” (worrisome aspects of the
history) and "green lights" (reassuring aspects of
the history that suggest NCS). Other aspects of the
history that may elucidate the etiology of syncope


can include a personal or family history of seizures,
metabolic diseases, and diabetes. Additionally, a
history of medication or toxic ingestion would be
relevant,3 as well as history of recurrent syncope,
menstrual history and risk of pregnancy, and possible trauma history.

Physical Examination
Physical examination in the patient who has recovered from syncope should focus on general appearance, evaluation for injuries, and an overall cursory
examination of the patient. Special attention should
be directed toward the neurologic and cardiac
examinations. A full set of vital signs should also be
obtained in patients who have experienced syncope.
Abnormal neurologic findings may indicate intracranial injury or seizure and would warrant additional
directed evaluation that may include EEG or head
imaging.9 A cardiac examination is also warranted in
each patient to evaluate for rate, regularity, murmurs, and other adventitious sounds such as rubs or
gallops. Any abnormality would require additional
cardiac evaluation9 unless the emergency clinician is
confident that the patient has a benign flow murmur.
In NCS, the neurologic and cardiac examinations
will be normal.

Diagnostic Studies
Vasovagal syncope/NCS is a largely clinical diagnosis. Because the biggest challenge for the emergency
clinician is to evaluate whether or not a patient’s syncope is from a benign or vasovagal etiology or from
a more concerning cause such as cardiac syncope,
the most useful test is an ECG (though they are only
diagnostic a small portion of the time). While there
are no definitive data to suggest that a normal ECG
ensures a patient’s syncope is vasovagal, the majority
of current algorithms in the literature include an ECG
as part of the evaluation of syncope. More specifically,
in several current algorithms to evaluate for syncope, a normal ECG is a common branch point when
distinguishing between vasovagal syncope and other
more concerning etiologies. In studies that attempt
to distinguish cardiac versus noncardiac causes of
syncope, an ECG is used in both decision rules and
algorithms.2,3,5,10,11,47,63-65 Additionally, there are no
studies that have specifically demonstrated the negative predictive value of a normal ECG in the evaluation of routine syncope, but there are multiple studies
that have evaluated the negative predictive value of
a normal ECG in cardiac syncope.46,47 Because of the
low cost and noninvasive nature of an ECG, it is recommended to include a screening ECG in the evaluation of routine syncope.

In a retrospective review that compared pediatric cardiology clinic patients with vasovagal syncope
to a 10-year chart review of cardiogenic causes of
April 2017 •

syncope, Tretter and Kavey devised a simple screening rule to identify patients who require cardiology
referral.47 The study showed that a 4-part screen
had a sensitivity of 100% and a specificity of 60% for
identifying a cardiac cause of syncope in that patient
population. The screening consisted of: (1) a history
of exertional syncope, (2) a family history of known
cardiac disease or unexplained sudden death, (3) an
abnormal physical examination supporting a cardiac
diagnosis, or (4) an abnormal finding on ECG. Using a similar screen, a study of 480 children with
syncope identified 21 of 22 patients with a cardiac

In addition to an ECG, urine testing should be
considered if pregnancy is possible. These noninvasive, low-cost tests, as well as a thorough physical
examination, make up most ED evaluations.

Evidence Against Routine Testing
When pediatric patients present to the ED after a
syncopal event, they often undergo unnecessary and
expensive evaluations without additional diagnostic yield. In a study by Goble et al, 90% of patients
had electrolytes checked, 58% had head computed
tomography (CT) scans, and 37% had chest x-rays.
Diagnostic tests are costly and have not been shown
to be helpful in the workup of routine syncope.46 In
contrast, the majority of guidelines reviewed for this
paper have recommended ECG as part of routine
workup, yet only 58% to 85% of patients with routine syncope had ECG studies performed.2,46

In the ED, following standardized clinical pathways has been shown to be effective and produce
significant cost savings by preventing unnecessary
low-yield testing and admissions.11,66,67 In spite of
this, workup for routine syncope in the pediatric
population remains an area that needs improvement in more effective resource utilization.68 Routine
use of additional testing, including but not limited
to, head-up tilt-table testing, orthostatic vital signs,
head imaging, EEG, laboratory testing (such as
electrolytes), echocardiograms, and x-rays, is not
indicated and has been shown by multiple analyses
to be low-yield in determining cause and management of pediatric syncope. Special cases, based on
history and initial evaluation (including ECG and
urine HCG), may require additional diagnostic tests
as outlined above, but these should be obtained on
an individual basis rather than a routine basis.
Head-Up Tilt-Table Test
The head-up tilt-table test is neither efficient nor
necessary for the diagnosis of NCS. In one protocol,
the test is performed in more than 30 minutes. A
test is considered positive for NCS if it results in
age-specific bradycardia, hypotension, or dysrhythmia, such as sinus or atrioventricular node block or
transient asystole. In one study, as many as 13% of
15 Copyright © 2017 EB Medicine. All rights reserved.

patients with syncope received head-up tilt-table
testing, but the data have shown consistently that
this type of testing does not provide additional
information beyond that obtained from the history,
physical examination, and ECG, nor is it helpful
to predict outcomes.48,69 The specificity of head-up
tilt-table testing has been estimated to be between
48% and 100%, and in one study, 87% of patients
with NCS were diagnosed without results of headup tilt-table testing.11

tients, but this study was costly ($1100 to $1500 per
scan), and all CT scans were normal in the absence
of abnormal neurologic findings.46 Based on these
results, the use of CT in the setting of routine syncope is costly, low-yield, and also subjects patients to
unnecessary radiation. Radiologic imaging should
only be obtained if there is significant concern for
intracranial bleeding.
Cardiac Enzymes
Cardiac enzymes for routine pediatric syncope
should not be obtained unless there is a suspicion
for aberrant coronary artery or myocarditis. As these
are very rare causes in the pediatric population,
this type of testing should only be performed in the
setting of chest pain or history of chest pain with
suggestive ECG findings.68 Despite this recommendation, the National Hospital Ambulatory Medical
Care Survey from 2005 to 2007 showed that 15% of
patients had such testing performed.2

Orthostatic Vital Sign Measurements
Orthostatic vital sign abnormalities were defined in
1995 by the American Autonomic Society, but they are
not correlated with symptomatology.70 Orthostatic vital signs are often obtained in the ED setting, but their
clinical significance is unclear in pediatric patients
with syncope. In large studies of healthy schoolage children, significant variations in heart rate and
blood pressure were detected.71 In a study by KoziolMcLain et al of adults in an ED, 43% of presumed
euvolemic patients met criteria for being orthostatic.72
In healthy adolescent volunteers, 44% had significant
orthostasis.73 Since so many nonsyncopal children can
have “positive” or abnormal results, the diagnostic
value is questionable. The sensitivity and specificity
of pulse change in adolescents has been shown to be
61% and 56%, respectively. Even with known volume
depletion from blood loss, sensitivity was shown to
be < 30% for heart rate and blood pressure change.74
Any patient with persistent symptoms of orthostasis
(ie, lightheadedness with sitting or standing), regardless of change in heart rate or blood pressure, should
be evaluated and treated.

Supportive care is the primary treatment for the
vast majority of pediatric patients presenting to the
ED with syncope, as most syncope is neurocardiogenic. For those patients who have symptomatic
hypovolemia, fluids are indicated. Up to 90% of patients with syncopal symptoms will improve with
adequate fluid and salt intake. Intravenous fluid
is a common treatment for patients who present
with persistent symptoms or who have evidence of
dehydration and cannot readily hydrate orally. In
addition, anticipatory guidance should be given to
patients regarding adequate oral intake at home,
avoiding provoking events, and early identification
of vasovagal symptoms to adjust behaviors and
prevent syncope.
All cases with a suspected cardiac etiology
should have a pediatric cardiac consultation and
close pediatric cardiology follow-up. If a patient is
to be discharged home after discussion with cardiology, exercise limitation is warranted until follow-up
is obtained. Cardiac events or sudden cardiac death
can occur at any time and often occur at rest, but
physical activity increases the risk.75 As symptomatology cannot always be predicted in patients with
presumed cardiac syncope, patients discharged to
home must be limited in their exercise and competitive sport participation until evaluated by cardiology. ECG interpretation by a pediatric cardiologist
can be helpful if the results are being used to determine disposition.46 In some studies, it has been
documented that pediatric emergency clinicians
may underappreciate significant ECG findings, or
conversely, be unnecessarily concerned about QT
intervals.76,77 ECG review by pediatric cardiology
may be useful in determining patient disposition,

Electroencephalogram And Computed Tomography 
Head imaging is frequently performed as part of the
syncope evaluation. In the setting of neurologic deficit or trauma, imaging is warranted, but in a study
by Massin et al of routine syncope evaluation, EEG
and head imaging did not contribute to diagnosis
of any patients.9 While EEG may be a useful evaluation tool in diagnosing seizures, it is very low-yield
for routine use as part of a syncope evaluation. In
the Massin et al study, there was a positive yield for
EEG in < 1 in 300 instances.9 An EEG would only be
useful to rule out seizure in the setting of concerning
history (as noted in the "Seizure" section, page 12) or
postictal state on examination. Additionally, even if
there is history to suggest that a seizure has occurred
but has since stopped, the utility of an EEG in the
ED versus inpatient or outpatient settings is variable. If seizure is suspected, then consultation with
neurology is indicated to determine the appropriate
timing of the EEG (eg, the need for admission for
EEG or deferral to outpatient evaluation).

CT scanning was found to be performed as part
of routine syncope evaluation in 58% of pediatric paCopyright © 2017 EB Medicine. All rights reserved.



Risk Management Pitfalls In Pediatric Patients With Syncope
1. “The teenage patient assured me that she could
not be pregnant, so I did not order an HCG
Ensuring that adolescent patients have a chance
to speak with providers without their parents
present is an expected part of adolescent
medicine and often allows capture of sensitive
information. The emergency clinician must
verify that teenage girls who report no sexual
intercourse are really not pregnant. Results
should be provided in a confidential manner
based upon individual state law.
2. “It was such a classic story for neurocardiogenic syncope, except for the family history of
sudden death, that I did not perform an ECG.”
Cardiac abnormalities can easily be overlooked.
Most of the rules regarding limiting extensive
testing presume a normal ECG. A family history
of sudden death could suggest a genetically
inherited cause of cardiac syncope.
3. “I asked if there were any medical problems
that run in the family, but the patient didn’t
tell me that her sister is deaf.”
Many families do not recognize deafness as a
reportable medical problem, so this must be
asked specifically. This is also true for sudden
unexplained deaths in the family. Patients may
not offer this information unless it is explicitly
4. “The coach, parents, and patient all told me
he was just overexerted while running. They
think he can play in the state championship
game tomorrow.”
Don’t be swayed by elite athletes, coaches,
or family members minimizing symptoms.
The primary goal is to ensure the safety of the
patient. If syncope occurred during activity,
then the patient should refrain from strenuous
activity until cleared by cardiology.
5. “The patient had a history and physical examination consistent with neurocardiogenic
syncope without any evidence of injury. The
mother was very concerned about a brain tumor, so I obtained a CT scan to reassure her.”
Sometimes the path of least resistance can do
more harm than good. Do not unnecessarily
irradiate pediatric patients, as this exposes them
to radiation that increases their long-term risk of
April 2017 •

6. “I looked at the ECG quickly to check for ischemic changes as I do for my adult patients and
was reassured by the ECG.”
Remember ECG analysis in pediatric patients
is not primarily to assess for myocardial
infarctions, and emergency clinicians must
change their point of reference and concentrate
on cardiac abnormalities that can cause syncope
in children (eg, prolonged QT, Wolff-ParkinsonWhite syndrome, Brugada syndrome, or
7. “The nurse checked orthostatic vitals. I knew
the patient could not be volume depleted, so
we discharged her without fluid resuscitation.”
Orthostatic vitals have been shown to be neither
sensitive nor specific for volume depletion.
Patients who are orthostatic by symptom
description should be hydrated and reassessed
prior to discharge.
8. “The patient had known congenital cardiac
disease, but the episode sounded neurocardiogenic so I sent him home.”
Children with underlying cardiac disease
warrant consultation with pediatric cardiology
prior to discharge to ensure that the syncope is
not related to their underlying condition.
9. “A pediatrician referred this patient with classic syncope to the ED. His ECG was normal,
but the primary care physician wanted him
admitted for overnight observation.”
Routine admission for a patient who has
returned to baseline, has no cardiac risk factors,
and has a normal ECG is unnecessary and not
cost-effective. To date, there are no data that
show that routine admission after a syncopal
event alters morbidity or mortality, and
admission increases healthcare costs and may
expose patients to additional risks.84
10. “I know the patient had no cardiac risk factors, but I wanted to be thorough, so I ordered
electrolytes, an EEG, an echo, and head-up tilttable testing.”
Extensive testing in low-risk groups rarely
improves diagnostic yield and results in
unnecessary medical expenses.

17 Copyright © 2017 EB Medicine. All rights reserved.

particularly if the ECG is abnormal.

Table 4 summarizes management approaches
for various etiologies of syncope.

ther workup. The Canadian Cardiovascular Society
made similar recommendations. The incidence of
heart disease in children is estimated to be 0.7% to
1%.11,81 At this time, there are no clear guidelines
about routine admission for pediatric patients.

Factors that would dictate additional evaluation
or admission in these patients include their repair
status, current functionality or disease, and any existing known residual defects. At this time, any patient
with known cardiac history presenting to the ED
would warrant cardiology evaluation. In addition to

Special Populations
Patients With Known Cardiac Disease
In the European Society of Cardiology syncope
guidelines (for adult patients), it is recommended
that all patients with syncope who have known
structural heart disease should be admitted for fur-

Table 4. Management Of Various Etiologies Of Syncope
Cardiac Etiology



Long QT syndrome

• Therapy is aimed at reducing sympathetic activity to the heart.
• Treat patients with torsades de pointes with IV magnesium sulfate (25-50 mg/kg, maximum of 2000 mg), betablockers,a and/or temporary cardiac transcutaneous pacing.78
• Provide specific instructions both verbally and in writing to patients and parents when discharging patients from the
ED with cardiology follow-up. Patients should be advised to:

Management is supportive.
Follow the PALS or APLS algorithm for persistent dysrhythmias and to treat any underlying heart failure.
Advise restriction from all competitive athletics to reduce the risk of sudden death.
In an otherwise asymptomatic patient, activity restriction, adequate hydration, and urgent cardiac evaluation are
• For high-risk patients, treatment may include medical management, surgical myectomy, or the use of implantable

Avoid competitive sports, although possible participation in specific recreational activities may be allowed.b




Drink electrolyte-rich fluids and eat potassium-rich foods during exercise in hot environments.20
Be aware of QT-prolonging medications and avoid them, if possible.


• Treatment of these patients in the ED depends on their presenting symptoms and their ECG findings.
• All patients with WPW ECG morphology will need cardiology evaluation. Consider electrophysiologic consultation to
induce and ablate the accessory pathways.31
• Treat any persistent dysrhythmia per established PALS guidelines with immediate electrical cardioversion for
unstable patients.
• For patients presenting with irregular wide QRS complex tachycardias, the emergency clinician must differentiate
WPW-induced atrial fibrillationc from polymorphic VT, which is mostly a concern for the adult population.

Supraventricular tachycardia

• Follow the PALS or APLS algorithm, with emphasis on early cardioversion in an unstable patient.
• Vagal maneuvers are appropriate for the stable patient who is normotensive and without signs or symptoms of
cardiorespiratory compromise.
• For infants, a slurry of ice water to the face, and for older children, valsalva maneuvers (bearing down as if to
defecate or blowing through an obstructed straw) can be effective in aborting the dysrhythmia.
• If vagal maneuvers are not effective, the appropriate next treatment for a stable patient is a rapid push of adenosine
(0.1 mg/kg with a maximum of 6 mg given as a rapid IV bolus) using the IV line closest to the heart. A second dose
of 0.2 mg/kg of adenosine (with a maximum of 12 mg) may be given, if needed.
• If the patient becomes unstable or shows signs of cardiorespiratory compromise, the treatment of choice is
synchronized cardioversion with 0.5-1 J/kg.

Heart block

• For symptomatic bradycardia, treat with supportive measures (eg, oxygen, IV fluids).
• For cardiorespiratory compromise, administer epinephrine (0.01 mg/kg IV, every 3-5 minutes) to increase the
patient’s heart rate. Atropine (0.02 mg/kg IV, can be repeated once) can also be given if there are concerns about
primary AV node dysfunction.
• In the unstable patient with cardiorespiratory compromise, external pacing is warranted after addressing airway and
breathing with airway adjuncts and oxygen. This should be done while addressing the underlying cause, if one is
• A cardiology consultation is warranted in patients with syncope who have an identified heart block on ECG (see
Figure 5, page 9), because the presence of syncope implies that the patient is having symptomatic heart block.

Brugada syndrome

• Recommend exercise restriction79 and that the patient avoid medications including antidysrhythmics,
antiarrhythmics, tricyclic antidepressants, local anesthetics (eg, bupivacaine), and opioids.33
• Cardiology consultation is warranted if a Brugada pattern is identified on ECG in the ED.

Copyright © 2017 EB Medicine. All rights reserved.



the baseline ECG, these patients may be more likely
to require additional testing such as echocardiogram,
chest x-ray, or laboratory studies. While in the ED,
these patients should remain on a cardiac monitor.

Controversies And Cutting Edge
The use of pharmacologic agents in the treatment of
NCS is controversial. Fludrocortisone has been used
in patients with recurrent syncope and presyncope

associated with hypotension. Fludrocortisone is a
mineralocorticoid agent that raises blood pressure
by stimulating renal sodium and fluid retention.
Side effects and treatment-limited effects include
hypertension, hypokalemia, and hypomagnesemia.
Fludrocortisone tends to be the first-line pharmacologic treatment for recurrent NCS, but recent
data suggest that fludrocortisone is not effective at
preventing NCS and is not better than placebo. The
data, however, are generally limited, and it is difficult to draw conclusive recommendations.8,82

Table 4. Management Of Various Etiologies Of Syncope
Noncardiac Etiology



• Early referral to obstetric services, as well as to social work for additional support, is recommended.
• Ultrasound may be indicated to confirm intrauterine pregnancy, if there are additional symptoms of vaginal bleeding
or abdominal pain when urine HCG is positive.


• IV glucose is recommended with glucose-containing fluids to provide 0.5-1 g/kg of glucose. The fluids can also be
taken orally (if the patient is able).

Neurocardiogenic syncope

• Treatment is largely supportive. In general, patients who are diagnosed with NCS do not require any specific
treatment. However, there are several pharmacologic agents used for recurrent NCS with limited supporting data;
these are discussed in detail in the “Controversies And Cutting Edge” section, page 19.
• Correcting fluid deficits in a dehydrated patient may be useful.d
• To prevent recurrent NCS, exercise has also been recommended to increase orthostatic tolerance.
• Patient education should be provided on ways to minimize the risk of future episodes through behavioral
modifications (eg, staying hydrated, avoiding prolonged standing or time spent in the supine position, and
increasing salt intake).
• Additionally, advising patients to recognize the syncope prodrome and encouraging them to lower themselves to
the ground prior to loss of consciousness may minimize potential injuries associated with syncope.


• History alone is sufficient to distinguish most cases of syncope from seizure; but rarely, for cases when true seizure
is unclear, neurology referral or EEG may be useful.e

Breath-holding spells

• Treatment with iron has been shown to decrease subsequent episodes, but it is unclear whether treatment is
effective if the child is not anemic.49
• As breath-holding episodes can recur until the child reaches school age, expectant guidance and reassurance that
there are no long-term sequelae are recommended.

Postural orthostatic
tachycardia syndrome

• If a patient is suspected of having POTS, then referral to a specialist should be considered to establish the
• Treatment for POTS is controversial, but the mainstays of therapy include increased fluid intake (to 2 to 2.5 L per
day) and increased salt intake.
• Reconditioning, exercise, and avoiding circumstances that may worsen the symptoms are also important.
• Pharmacologic treatments include fludrocortisone, low-dose beta blockers, and midodrine, but there are currently
no United States Food and Drug Administration-approved treatments for pediatric patients with POTS.


• No additional management is necessary other than reassurance.
• Avoid excessive testing, but psychiatry referral may be of the most benefit to these patients.


For maintenance management of long QT syndrome, beta blockers are generally considered the first line of therapy, and have been shown to decrease
mortality from 71% to 6% and to eliminate dysrhythmia in 60% of patients.21-23,80
A complete list with the degree of risk can be found in the American Heart Association consensus statement published in 2004.79
With atrial fibrillation, the ECG will more likely reveal an irregular, wide QRS complex tachycardia that has beat-to-beat variation. This finding, in
conjunction with a faster ventricular rate (can exceed 300 beats/min), can be more suggestive of atrial fibrillation due to WPW.26
Drinking water profoundly affects sympathetic tone and increases heart rate in patients with autonomic failure, and it is possible that this may be
extrapolated to patients with NCS.
EEG has not, however, been shown to be an efficacious component of a routine syncope workup.9 In patients who have been referred to pediatric
neurology for evaluation of seizure, up to 20% do not have epileptic seizures, and NCS is a common finding in this population.7
The diagnostic evaluation for POTS is often extensive and may involve testing for metabolic and hematologic abnormalities as well as potentially
performing autonomic function tests. This evaluation is not appropriate in an ED setting, and while POTS does cause significant personal distress for
patients, there is no additional management that is necessary in the ED. A referral to a provider who specializes in POTS may be useful.
Abbreviations: APLS, Advanced Pediatric Life Support; AV, atrioventricular; ECG, electrocardiogram; ED, emergency department; EEG,
electroencephalogram; HCG, human chorionic gonadotropin; IV, intravenous; PALS, Pediatric Advanced Life Support; VT, ventricular tachycardia.

April 2017 •

19 Copyright © 2017 EB Medicine. All rights reserved.

Time- And Cost-Effective Strategies

Alpha-1 agonists, such as midodrine, have also
been used to increase blood pressure in patients with
primary autonomic failure, and the effects of this
may be extrapolated to patients with recurrent NCS.
The data, however, are still inconclusive. A study of
26 children with recurrent syncope demonstrated
that patients with NCS who were taking midodrine
hydrochloride had a lower recurrence of events.83
Low-dose beta blockers have also been used to treat
recurrent NCS.83 Despite some promising early data,
in general, there is no definitive treatment for recurrent NCS beyond management of symptoms.

Ensuring that the appropriate questions are asked to
rule out red flags and capture green lights is a costefficient and effective way to avoid missing a critical
cardiac etiology of syncope. Extensive workups do
not generally provide more information for the routine case of pediatric syncope. Screening with lowcost, noninvasive tests such as ECG and pregnancy
testing (when indicated) is the most reasonable approach to most pediatric patients with syncope.

Admission rates tend to be high and are often
based on ECG findings. When considering admission based on ECG findings, a review by a pediatric
cardiologist is warranted. Given the underappreciation of significant ECG findings by emergency
clinicians and unnecessary concern about prolonged
QT syndrome that is diagnosed by emergency clinicians but not deemed concerning by cardiology, this
process should happen early in the course of treatment.76,77 Such a practice pathway could decrease
unnecessary admissions and ensure that critical
findings are not missed.

Head CT scans and chest x-rays are often obtained in pediatric patients presenting with syncope.
In one study in a community ED, of the 113 pediatric
patients seen, 58% had head CT scans and 37% had
chest x-rays. None of the CT scans had positive findings, but this resulted in a large percentage of patients being deemed high-resource utilizers.46 Other
studies have assessed noncardiac testing and found
low utility and high average patient costs.9,11 Having standardized algorithms and clinical pathways
has been shown to increase diagnostic yield, reduce
admissions, and decrease overall costs.66

Admission is rarely indicated for patients presenting
with syncope. After evaluation and stabilization in
the ED, the vast majority of patients with syncope
who have no red flags and are asymptomatic can be
discharged home safely with supportive management and explanation of risk factors for future episodes. For patients with concerning cardiac findings,
consulting cardiology from the ED is indicated to
help establish safe disposition and further workup.
The decision of inpatient admission, outpatient
specialist referral, or discharge home with reassurance is dependent on the individual etiologies.
Patients with NCS can be discharged home safely
with instructions to watch for warning signs of a
more worrisome syncopal etiology (ie, red flags
for cardiac etiology), and to follow up with their
primary care provider. Additionally, patients should
receive instructions about adequate hydration and
early identification of vasovagal symptoms. Routine
inpatient evaluation of syncope is not warranted
unless a specific etiology is being considered and
is either dependent on further workup that cannot
be performed in the ED (eg, echocardiograms at
some institutions), or if their specific etiology (eg,
myocarditis, dysrhythmias) pose significant risk of
anticipated morbidity or mortality. When considering admission based on ECG findings, a review by
a pediatric cardiologist may be useful; such practice
may decrease unnecessary admissions.76,77

Patients with likely seizure should have a neurology consultation and likely early follow-up as an
outpatient, unless there is a high enough index of
suspicion for an infectious etiology or if the patient
does not return to baseline in an acceptable period
of time. Patients with positive pregnancy tests do
not require routine admission, but should be evaluated for possible ectopic pregnancy and assessed by
obstetrics and social work, if indicated.

In cases where the patient is clinically unstable,
unable to maintain adequate hydration, or has a concerning history or physical examination and requires
continued monitoring or evaluation that cannot be
performed as an outpatient, admission is warranted.
Copyright © 2017 EB Medicine. All rights reserved.

Syncope in the pediatric population is a common
presenting complaint to EDs. Etiologies can range
from life-threatening cardiac causes to more benign
etiologies. There are certain red flags that require
careful attention, but most cases can be safely and
efficiently managed with screening ECGs and pregnancy screening. Extensive and expensive workups
have not been shown to be useful or diagnostic,
unless there are specific signs and symptoms to
suggest the need for in-depth testing. Establishing a
care algorithm for these patients has been shown to
improve efficiency and decrease cost and length of
stay. The causes of pediatric syncope and syncope in
adults are often different. The evaluation of pediatric
patients who have had a syncopal event must be
tailored to the individual patient.



Case Conclusions
Multiple red flags existed for the 10-year-old who collapsed on the basketball court. You immediately suspected
cardiac causes due to the event occurring during vigorous
exercise. In addition to his screening ECG, cardiology
was consulted from the ED and the patient had an urgent
echocardiogram. The patient’s echocardiogram showed a
significantly thickened interventricular septum with outflow obstruction. The patient was started on beta blockers,
but later had a recurrent episode and had an implantable
cardiac defibrillator placed. The patient was put on exercise limitation and was restricted from competitive sports.

The case of the 16-year-old girl demonstrated many
red flags for a cardiac etiology of her syncope. She had
multiple episodes during activity with persistent symptoms of shortness of breath. The patient’s ECG showed
sinus tachycardia at 164 beats/min with low voltages,
right-axis deviation, and diffuse 1-mm ST elevations. You
ordered a chest x-ray that did not show cardiomegaly,
infiltrate, or edema. You called for an emergent cardiology
consultation, and the patient had an initial echocardiogram that showed a small pericardial effusion and normal
ejection fraction. While in bed, the patient had a presyncopal sensation and then had a generalized seizure with
hypoxia and relative bradycardia at 100 beats/min. After
receiving lorazepam, the patient’s symptoms resolved.
Cardiology was called again, and repeat echocardiogram
showed poor ejection fraction. During the echocardiogram, the patient went into a 2:1 AV block and became
pulseless. Immediate CPR resulted in return of spontaneous circulation and the ECMO team was mobilized. The
patient was cannulated in the ED and transported to the
pediatric ICU. She remained on ECMO for 9 days and
was discharged from the hospital after 1 month with the
diagnosis of influenza myocarditis. On follow-up echocardiogram 9 months after her admission, she continued to
have normal cardiac function and was given approval to
return to normal activity levels.

The 18-year-old girl had a normal ECG, but had a
positive HCG test. The patient denied abdominal pain
or bleeding and had an ultrasound that showed a 7-week
estimated gestational age intrauterine pregnancy. Social
work was consulted, and reassurance and support information was provided. No further testing was performed.
After tolerating oral intake and demonstrating ability
to ambulate, she was discharged home with obstetrician
follow-up information.

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
April 2017 •

reference, pertinent information about the study, such
as the type of study and the number of patients in the
study is included in bold type following the references,
where available. The most informative references cited
in this paper, as determined by the authors, are noted
by an asterisk (*) next to the number of the reference.

Driscoll DJ, Jacobsen SJ, Porter CJ, et al. Syncope in children
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(Retrospective population-based analysis)

2.* Anderson JB, Czosek RJ, Cnota J, et al. Pediatric syncope:
National Hospital Ambulatory Medical Care survey results.
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627,489 ED visits)

Fischer JW, Cho CS. Pediatric syncope: cases from the emergency department. Emerg Med Clin North Am. 2010;28(3):501516. (Review article)


Liberthson RR. Sudden death from cardiac causes in children
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Moodley M. Clinical approach to syncope in children. Semin
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6.* Fu Q, Levine BD. Pathophysiology of neurally mediated syncope: role of cardiac output and total peripheral resistance.
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Mastrangelo M, Mariani R, Ursitti F, et al. Neurocardiogenic
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Medow MS, Stewart JM, Sanyal S, et al. Pathophysiology,
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Massin MM, Bourguignont A, Coremans C, et al. Syncope
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10. Zhang Q, Du J, Wang C, et al. The diagnostic protocol in
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12. Drezner JA, Fudge J, Harmon KG, et al. Warning symptoms
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20. Vincent GM. The molecular genetics of the long QT syndrome: genes causing fainting and sudden death. Annu Rev
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40. Yarlagadda S, Poma PA, Green LS, et al. Syncope during
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21. Moss AJ, Schwartz PJ, Crampton RS, et al. The long QT
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41. Tenore JL. Ectopic pregnancy. Am Fam Physician.
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42. World Health Organization. Antiretroviral Therapy for HIV
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43. Lagi A, Cencetti S, Lagi F. Incidence of hypoglycaemia associated with transient loss of consciousness. A retrospective
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consciousness, 39 with transient hypoglycemia)

24. Kulig J, Koplan BA. Cardiology patient page. Wolff-Parkinson-White syndrome and accessory pathways. Circulation.
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26. Fengler BT, Brady WJ, Plautz CU. Atrial fibrillation in the
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(Case reports, review article)

45. Salins PC, Kuriakose M, Sharma SM, et al. Hypoglycemia as
a possible factor in the induction of vasovagal syncope. Oral
Surg Oral Med Oral Pathol. 1992;74(5):544-549. (Prospective
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27. Santinelli V, Radinovic A, Manguso F, et al. The natural history of asymptomatic ventricular pre-excitation a long-term
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J Am Coll Cardiol. 2009;53(3):275-280. (Prospective study; 184

46.* Goble MM, Benitez C, Baumgardner M, et al. ED management
of pediatric syncope: searching for a rationale. Am J Emerg
Med. 2008;26(1):66-70. (Retrospective cohort; 140 patients)
47.* Tretter JT, Kavey RE. Distinguishing cardiac syncope
from vasovagal syncope in a referral population. J Pediatr.
2013;163(6):1618-1623.e1. (Retrospective cohort; 106 patients)

28. Campbell RM, Strieper MJ, Frias PA, et al. Survey of current practice of pediatric electrophysiologists for asymptomatic Wolff-Parkinson-White syndrome. Pediatrics.
2003;111(3):e245-e247. (Survey, retrospective; 66 pediatric

48. Johnson ER, Etheridge SP, Minich LL, et al. Practice variation
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29. Comsumer reports. The buzz on energy-drink caffeine. 2012;
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org/cro/magazine/2012/12/the-buzz-on-energy-drinkcaffeine/index.htm. (Magazine atricle)

49. Daoud AS, Batieha A, al-Sheyyab M, et al. Effectiveness of iron therapy on breath-holding spells. J Pediatr.
1997;130(4):547-550. (Randomized controlled study; 67

30. Gewitz MH, Woolf PK. Textbook of Pediatric Emergency Medicine. In: Fleisher GR, Ludwig, S. eds. 6th ed. Philadelphia:
Wolters Kluwer/Lippencott Williams & Wilkins Health;
2010:701-706. (Textbook chapter)

50. Jarjour IT. Postural tachycardia syndrome in children and
adolescents. Semin Pediatr Neurol. 2013;20(1):18-26. (Review

31. Caughey RW, Humphrey JM, Thomas PE. High-degree atrioventricular block in a child with acute myocarditis. Ochsner J.
2014;14(2):244-247. (Case report; 1 patient)

51. Low PA, Sandroni P, Joyner M, et al. Postural tachycardia
syndrome (POTS). J Cardiovasc Electrophysiol. 2009;20(3):352358. (Review article)

32. Probst V, Denjoy I, Meregalli PG, et al. Clinical aspects and
prognosis of Brugada syndrome in children. Circulation.
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52. Raj V, Rowe AA, Fleisch SB, et al. Psychogenic pseudosyncope: diagnosis and management. Auton Neurosci. 2014;184:6672. (Review article)

33. Rossenbacker T, Priori SG. The Brugada syndrome. Curr
Opin Cardiol. 2007;22(3):163-170. (Review article)

53. Chen L, Zhang Q, Ingrid S, et al. Aetiologic and clinical
characteristics of syncope in Chinese children. Acta Paediatr.
2007;96(10):1505-1510. (Retrospective cohort; 154 children)

34. Zaidi AN. An unusual case of Brugada syndrome in
a 10-year-old child with fevers. Congenit Heart Dis.
2010;5(6):594-598. (Case report; 1 patient)

54. Sayre MR, Berg RA, Cave DM, et al. Hands-only (compression-only) cardiopulmonary resuscitation: a call to action for
bystander response to adults who experience out-of-hospital
sudden cardiac arrest: a science advisory for the public from
the American Heart Association Emergency Cardiovascular
Care Committee. Circulation. 2008;117(16):2162-2167. (Consensus guidelines)

35. De Marco S, Giannini C, Chiavaroli V, et al. Brugada syndrome unmasked by febrile illness in an asymptomatic child.
J Pediatr. 2012;161(4):769-769.e1. (Case report; 1 child)
36. Skinner JR, Chung SK, Nel CA, et al. Brugada syndrome masquerading as febrile seizures. Pediatrics.
2007;119(5):e1206-e1211. (Case report; 1 patient)

55. Kern KB. Cardiopulmonary resuscitation without ventilation. Crit Care Med. 2000;28(11 Suppl):N186-N189. (Review

37. Hermida JS, Jandaud S, Lemoine JL, et al. Prevalence of
drug-induced electrocardiographic pattern of the Brugada syndrome in a healthy population. Am J Cardiol.
2004;94(2):230-233. (Prospective cohort; 1000 patients)

56. Hupfl M, Selig HF, Nagele P. Chest-compression-only versus
standard cardiopulmonary resuscitation: a meta-analysis.
Lancet. 2010;376(9752):1552-1557. (Meta-analysis; 3 randomized trials)

38. Belhassen B, Glick A, Viskin S. Efficacy of quinidine in
high-risk patients with Brugada syndrome. Circulation.

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57. Bobrow BJ, Spaite DW, Berg RA, et al. Chest compressiononly CPR by lay rescuers and survival from out-of-hospital
cardiac arrest. JAMA. 2010;304(13):1447-1454. (Prospective
observational cohort study; 5272 patients)
58. Kitamura T, Iwami T, Kawamura T, et al. Bystander-initiated
rescue breathing for out-of-hospital cardiac arrests of noncardiac origin. Circulation. 2010;122(3):293-299. (Prospective
study; 43,246 bystander-witnessed out-of-hospital cardiac
59. Kitamura T, Iwami T, Kawamura T, et al. Conventional and
chest-compression-only cardiopulmonary resuscitation by
bystanders for children who have out-of-hospital cardiac
arrests: a prospective, nationwide, population-based cohort
study. Lancet. 2010;375(9723):1347-1354. (Prospective cohort;
5170 children)
60. Drezner JA, Rao AL, Heistand J, et al. Effectiveness of emergency response planning for sudden cardiac arrest in United
States high schools with automated external defibrillators.
Circulation. 2009;120(6):518-525. (Retrospective cohort; 1710
schools, 36 sudden cardiac arrest victims)
61. Kovach J, Berger S. Automated external defibrillators and
secondary prevention of sudden cardiac death among
children and adolescents. Pediatr Cardiol. 2012;33(3):402-406.
(Review article)
62. Ramaraj R, Ewy GA. Rationale for continuous chest
compression cardiopulmonary resuscitation. Heart.
2009;95(24):1978-1982. (Review article)
63. Marcdante K, Kliegman R. Syncope. Nelson Essentials of Pediatrics. 7th ed: Saunders; 2015:486-487. (Book chapter)
64. Ritter S, Tani LY, Etheridge SP, et al. What is the yield of
screening echocardiography in pediatric syncope? Pediatrics.
2000;105(5):E58. (Retrospective cohort; 480 patients)
65. Delgado C. Syncope. In: Fleisher, ed. Textbook of Pediatric
Emergency Medicine. 6th ed.2010:593. (Textbook)
66. Brignole M, Ungar A, Bartoletti A, et al. Standardizedcare pathway vs. usual management of syncope patients
presenting as emergencies at general hospitals. Europace.
2006;8(8):644-650. (Prospective controlled multicenter
study; 1674 patients)
67.* Raucci U, Scateni S, Tozzi AE, et al. The availability and
the adherence to pediatric guidelines for the management of syncope in the emergency department. J Pediatr.
2014;165(5):967-972.e1. (Retrospective cohort; 1073 patients)
68. Kessler C, Tristano JM, De Lorenzo R. The emergency
department approach to syncope: evidence-based guidelines and prediction rules. Emerg Med Clin North Am.
2010;28(3):487-500. (Review article)
69. Ikiz MA, Cetin, II, Ekici F, et al. Pediatric syncope: is detailed
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Pediatr Emerg Care. 2014;30(5):331-334. (Prospective cohort;
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70. Kaufmann H. Consensus statement on the definition of orthostatic hypotension, pure autonomic failure and multiple
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71. Tanaka H, Thulesius O, Borres M, et al. Blood pressure
responses in Japanese and Swedish children in the supine
and standing position. Eur Heart J. 1994;15(8):1011-1019.
(Prospective cohort; 131 children)

clinical examination. Is this patient hypovolemic? JAMA.
1999;281(11):1022-1029. (Meta-analysis; 14 studies)
75. Pilmer CM, Kirsh JA, Hildebrandt D, et al. Sudden cardiac
death in children and adolescents between 1 and 19 years of
age. Heart Rhythm. 2014;11(2):239-245. (Retrospective cohort;
116 cases of sudden cardiac death)
76. Wathen JE, Rewers AB, Yetman AT, et al. Accuracy of ECG
interpretation in the pediatric emergency department. Ann
Emerg Med. 2005;46(6):507-511. (Prospective analysis; 1653
ECGs, 1501 patients)
77. Hue V, Noizet-Yvernaux O, Vaksmann G, et al. ED management of pediatric syncope. Am J Emerg Med. 2008;26(9):10591060. (Prospective cohort)
78. Salen P, Nadkarni V. Congenital long-QT syndrome: a
case report illustrating diagnostic pitfalls. J Emerg Med.
1999;17(5):859-864. (Case report; 1 patient)
79. Maron BJ, Chaitman BR, Ackerman MJ, et al. Recommendations for physical activity and recreational sports participation for young patients with genetic cardiovascular diseases.
Circulation. 2004;109(22):2807-2816. (Review article)
80. Schwartz PJ. Idiopathic long QT syndrome: progress and
questions. Am Heart J. 1985;109(2):399-411. (Review article)
81. Marelli AJ, Ionescu-Ittu R, Mackie AS, et al. Lifetime prevalence of congenital heart disease in the general population
from 2000 to 2010. Circulation. 2014;130(9):749-756. (Retrospective cohort; 107,559 patients)
82. Salim MA, Di Sessa TG. Effectiveness of fludrocortisone and
salt in preventing syncope recurrence in children: a doubleblind, placebo-controlled, randomized trial. J Am Coll Cardiol.
2005;45(4):484-488. (Double-blind randomized controlled
trial; 33 children)
83. Qingyou Z, Junbao D, Chaoshu T. The efficacy of midodrine
hydrochloride in the treatment of children with vasovagal
syncope. J Pediatr. 2006;149(6):777-780. (Randomized controlled trial; 26 children)
84. Morag RM, Murdock LF, Khan ZA, et al. Do patients with
a negative emergency department evaluation for syncope
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(Prospective cohort; 45 patients)

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72. Koziol-McLain J, Lowenstein SR, Fuller B. Orthostatic vital
signs in emergency department patients. Ann Emerg Med.
1991;20(6):606-610. (Prospective cohort; 132 patients)
73. Stewart JM. Transient orthostatic hypotension is common
in adolescents. J Pediatr. 2002;140(4):418-424. (Prospective
cohort; 23 healthy adolescents)
74. McGee S, Abernethy WB 3rd, Simel DL. The rational

April 2017 •

23 Copyright © 2017 EB Medicine. All rights reserved.

6. Which of the following is more likely associated with psychogenic syncope?
a. Episodes lasting for several seconds
b. Closed eyes
c. The event does not recur during evaluation
d. A patient who is a boy

1. A teenager feels the “world going dark” and
then collapses while standing. What is the
most likely cause of her syncope?
a. Neurocardiogenic
b. Hypertrophic cardiomyopathy
c. Psychogenic pseudosyncope
d. Breath-holding spell

7. In the setting of syncope due to traumatic
cardiac arrest on the ball field, what is the most
effective measure for reducing morbidity and
a. Being located near a hospital
b. Having an automated external defibrillator
c. Having oxygen available
d. Having a doctor at all games

2. A 17-year-old deaf patient with a history of
syncope presents to the ED for cough, nausea,
and vomiting and is found to have pneumonia
on chest x-ray. Which of the following medications could be prescribed without an ECG?
a. Cefuroxime
b. Levofloxacin
c. Azithromycin
d. Ondansetron

8. What is the most useful screening test for children who present with syncope?
a. Electrolytes
b. ECG
c. Head CT
d. Fingerstick glucose

3. Which of these findings is reassuring that a
patient most likely has vasovagal syncope?
a. QTc of > 500 milliseconds
b. Family history of sudden cardiac death
c. Prodrome of nausea, diaphoresis, and
d. Event occurred while running

9. A teenager collapses while sprinting during
football tryouts. He wants to go back to practice tomorrow. When should he be allowed to
a. As soon as he is asymptomatic
b. Once he is cleared by cardiology
c. The next day, if his ECG is normal
d. After 1 week without recurrent symptoms

4. A teenager collapsed while playing basketball
and had some “shaking” movements. He has a
history of syncope with lightheadedness when
having his blood drawn and has a family history of syncope. Which of the findings would
heighten your concern for an underlying cardiac etiology of his syncope?
a. Syncope is associated with lightheadedness
b. The patient’s mother experienced syncope
as a teenager
c. Syncope occurred while running at
basketball practice
d. Rhythmic shaking during the loss-ofconsciousness phase

10. What follow-up should be arranged for a patient who presents with syncope and has a QTc
on ECG of 500 milliseconds who is currently
a. Emergent pediatric cardiology referral in the
b. Admission to the hospital
c. Primary care physician follow-up within the
d. Competitive sports limitations until
outpatient pediatric cardiology appointment

5. While seated playing a video game, a 10-yearold has an episode of unresponsiveness with
loss of tone followed by several minutes of
shaking movements of his upper extremities.
There was no loss of continence. What is the
most likely cause of this altered mental status?
a. Neurocardiogenic
b. Psychogenic pseudosyncope
c. Breath-holding spell
d. Seizures

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A Quick-Read

Review Of Key

Points & Clinic

al Pearl

s, July 2016
Pediatric Severe
Traumatic Brain
An Evidence-Ba
sed Review

Cervical artery
dissections involv
vertebral arterie
e the carotid or
s. An intimal
tear creates a
dolumen with
Cervical artery
later lead to vessel ural hematoma, which
dissections can
occlusion, throm
with minor traum
tion, embolus,
a or spontaneous occur
pseudoaneurysm, bus formaly.
Cervical artery
or rupture.
dissections from
Maintain a high
caused by direct
blunt trauma
index of suspic
blow to the neck,
artery dissections
ion of
sion or contra
hyperextenin patients presen cervical
lateral rotatio
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n, intraoral traum
or skull-base
any concerning
occur spontaneous es. However, they can also
average, sympt
trauma. On
Early administratio
oms occur 2 to
n of antiplatelet
3 days after the
traumatic event.
significantly reduce agents or
• Cervical artery
stroke in cervica
s the risk of
dissections may
headache, facial
present with
pain, or neck
pain and may
associated with
Cervical artery
dissection is not
symptoms, dysgeu
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cation for throm
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Risk factors includ s, or cervical radiculopath
ic stroke.
vascular abnorm e connective tissue diseas
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dissection is not
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for thrombolytic
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High-risk findin
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cal deficits, Glasgo include lateralizing neurol
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s safely even
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crepitus, anisoc
Horner syndro
telet agents and
me, cervical spine
tion should be
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fracture, and
delayed for 24

• Though digital
ts diagnosed
with a cervica
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l artery dissec
gold standard
raphy is the
admitted and
for diagnosis
closely monito
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sections, compu
g is needed to
progression in
assess disease
an accepted choice tomographic angiography
7 to 10 days.
• Due to the
and 95% to 100% , with 98% to 100% sensitivity
lack of data, blood
specificity while
pressure manag
ment targets
risks and delays
having fewer
are up to indivi
ecompared to angiog
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is also an alterna
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Issue Author
ve for vertebral
• Early admin
artery dissect
Rhonda Cadena
with antiplatelet n of antithrombotic therap
Assistant Professo , MD
agents (eg, aspirin
r, Departments
Emergency Medicine
of Neurology,
lants (eg, hepari
, University of
n) has been shown ) or anticoaguand
North Carolina,
Points & Pearls
reduce the risk
Chapel Hill, NC
of stroke in cervica to significantly
tions. There is
l artery dissecJeremy Kim,
no clear benefi
Department of
t of one agent
another, but many
Emergency Medicine
Sinai, New York,
prefer heparin
, Icahn School
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an acute throm
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to antithrombot
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July 2016 • Emerg
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Date of Original Release: April 1, 2017. Date of most recent review: March 15, 2017.
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