SYNCOPE IN THE PEDIATRIC PATIENT
Identifieur interne : 001883 ( Main/Corpus ); précédent : 001882; suivant : 001884SYNCOPE IN THE PEDIATRIC PATIENT
Auteurs : Ronn E. Tanel ; Edward P. WalshSource :
- Cardiology Clinics [ 0733-8651 ] ; 1997.
Abstract
Syncope during childhood is common. A variable incidence has been reported, from 1 of 2000 emergency department visits,71 to 47% of interviewed college students.61 Driscoll and colleagues14 reported an overall incidence of 125 of 100,000 (0.125%) for pediatric patients seeking medical attention. Girls were seen for evaluation more commonly than boys, with the peak incidence occurring between ages 15 and 19 years. Despite its frequency, syncope generates an extraordinary amount of anxiety among patients, families, teachers, coaches, and physicians.In children and adolescents, the list of causes is generally similar to that described for adults, although the relative frequency and prognosis for the individual diagnoses are somewhat unique. Fortunately, most syncopal events in young patients are isolated and benign in nature. Driscoll's data14 revealed an association of sudden death and prior syncopal events that was not different from that of sudden death in the general population. This article describes the causes, diagnosis, and treatment of syncope in infants, children, and adolescents, focusing on the differences that must be identified when caring for the pediatric versus adult patient. Recommendations are presented for an economically efficient diagnostic workup and practical approach to treatment.
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DOI: 10.1016/S0733-8651(05)70336-2
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">SYNCOPE IN THE PEDIATRIC PATIENT</title><author><name sortKey="Tanel, Ronn E" sort="Tanel, Ronn E" uniqKey="Tanel R" first="Ronn E." last="Tanel">Ronn E. Tanel</name><affiliation><mods:affiliation>Department of Cardiology, Children's Hospital; and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</mods:affiliation></affiliation></author><author><name sortKey="Walsh, Edward P" sort="Walsh, Edward P" uniqKey="Walsh E" first="Edward P." last="Walsh">Edward P. Walsh</name><affiliation><mods:affiliation>Department of Cardiology, Children's Hospital; and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:72B4D003078254DE56EB523B535252BFB6227AD3</idno><date when="1997" year="1997">1997</date><idno type="doi">10.1016/S0733-8651(05)70336-2</idno><idno type="url">https://api.istex.fr/document/72B4D003078254DE56EB523B535252BFB6227AD3/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001883</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">SYNCOPE IN THE PEDIATRIC PATIENT</title><author><name sortKey="Tanel, Ronn E" sort="Tanel, Ronn E" uniqKey="Tanel R" first="Ronn E." last="Tanel">Ronn E. Tanel</name><affiliation><mods:affiliation>Department of Cardiology, Children's Hospital; and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</mods:affiliation></affiliation></author><author><name sortKey="Walsh, Edward P" sort="Walsh, Edward P" uniqKey="Walsh E" first="Edward P." last="Walsh">Edward P. Walsh</name><affiliation><mods:affiliation>Department of Cardiology, Children's Hospital; and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Cardiology Clinics</title><title level="j" type="abbrev">CCL</title><idno type="ISSN">0733-8651</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1997">1997</date><biblScope unit="volume">15</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="277">277</biblScope><biblScope unit="page" to="294">294</biblScope></imprint><idno type="ISSN">0733-8651</idno></series><idno type="istex">72B4D003078254DE56EB523B535252BFB6227AD3</idno><idno type="DOI">10.1016/S0733-8651(05)70336-2</idno><idno type="PII">S0733-8651(05)70336-2</idno><idno type="ArticleID">70336</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0733-8651</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Syncope during childhood is common. A variable incidence has been reported, from 1 of 2000 emergency department visits,71 to 47% of interviewed college students.61 Driscoll and colleagues14 reported an overall incidence of 125 of 100,000 (0.125%) for pediatric patients seeking medical attention. Girls were seen for evaluation more commonly than boys, with the peak incidence occurring between ages 15 and 19 years. Despite its frequency, syncope generates an extraordinary amount of anxiety among patients, families, teachers, coaches, and physicians.In children and adolescents, the list of causes is generally similar to that described for adults, although the relative frequency and prognosis for the individual diagnoses are somewhat unique. Fortunately, most syncopal events in young patients are isolated and benign in nature. Driscoll's data14 revealed an association of sudden death and prior syncopal events that was not different from that of sudden death in the general population. This article describes the causes, diagnosis, and treatment of syncope in infants, children, and adolescents, focusing on the differences that must be identified when caring for the pediatric versus adult patient. Recommendations are presented for an economically efficient diagnostic workup and practical approach to treatment.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Ronn E. Tanel MD</name><affiliations><json:string>Department of Cardiology, Children's Hospital; and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</json:string></affiliations></json:item><json:item><name>Edward P. Walsh MD</name><affiliations><json:string>Department of Cardiology, Children's Hospital; and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</json:string></affiliations></json:item></author><articleId><json:string>70336</json:string></articleId><language><json:string>eng</json:string></language><abstract>Syncope during childhood is common. A variable incidence has been reported, from 1 of 2000 emergency department visits,71 to 47% of interviewed college students.61 Driscoll and colleagues14 reported an overall incidence of 125 of 100,000 (0.125%) for pediatric patients seeking medical attention. Girls were seen for evaluation more commonly than boys, with the peak incidence occurring between ages 15 and 19 years. Despite its frequency, syncope generates an extraordinary amount of anxiety among patients, families, teachers, coaches, and physicians.In children and adolescents, the list of causes is generally similar to that described for adults, although the relative frequency and prognosis for the individual diagnoses are somewhat unique. Fortunately, most syncopal events in young patients are isolated and benign in nature. Driscoll's data14 revealed an association of sudden death and prior syncopal events that was not different from that of sudden death in the general population. This article describes the causes, diagnosis, and treatment of syncope in infants, children, and adolescents, focusing on the differences that must be identified when caring for the pediatric versus adult patient. Recommendations are presented for an economically efficient diagnostic workup and practical approach to treatment.</abstract><qualityIndicators><score>7.78</score><pdfVersion>1.4</pdfVersion><pdfPageSize>504 x 719.759 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1323</abstractCharCount><pdfWordCount>9121</pdfWordCount><pdfCharCount>62176</pdfCharCount><pdfPageCount>18</pdfPageCount><abstractWordCount>190</abstractWordCount></qualityIndicators><title>SYNCOPE IN THE PEDIATRIC PATIENT</title><pii><json:string>S0733-8651(05)70336-2</json:string></pii><genre><json:string>research-article</json:string></genre><host><volume>15</volume><pii><json:string>S0733-8651(05)X7022-9</json:string></pii><pages><last>294</last><first>277</first></pages><issn><json:string>0733-8651</json:string></issn><issue>2</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><title>Cardiology Clinics</title><publicationDate>1997</publicationDate></host><publicationDate>1997</publicationDate><copyrightDate>1997</copyrightDate><doi><json:string>10.1016/S0733-8651(05)70336-2</json:string></doi><id>72B4D003078254DE56EB523B535252BFB6227AD3</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/72B4D003078254DE56EB523B535252BFB6227AD3/fulltext/pdf</uri></json:item><json:item><original>true</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/72B4D003078254DE56EB523B535252BFB6227AD3/fulltext/txt</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/72B4D003078254DE56EB523B535252BFB6227AD3/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/72B4D003078254DE56EB523B535252BFB6227AD3/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">SYNCOPE IN THE PEDIATRIC PATIENT</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1997</date></publicationStmt><notesStmt><note>Address reprint requests to Ronn E. Tanel, MD, Department of Cardiology, Children's Hospital, 300 Longwood Avenue, Boston, MA 02115</note><note>RET is currently supported by a research fellowship from the American Heart Association, Massachusetts Affiliate, Inc.</note><note type="content">Figure 1: A, A 12-lead ECG showing ventricular tachycardia at a rate of 226 beats per minute. This patient has Belhassen's tachycardia. Note the typical right bundle-branch pattern with a superior QRS axis. The ECG is recorded at half-standard amplitude. B, A 12-lead ECG showing sinus rhythm with salvos of slow ventricular tachycardia. The arrhythmia is due to an abnormal automatic focus in the right ventricular outflow tract. This is supported by the left bundle-branch pattern and inferior QRS axis.</note><note type="content">Figure 2: A, Supraventricular tachycardia in Wolff-Parkinson-White syndrome resulting from antegrade conduction over the atrioventricular node (AVN) and retrograde conduction over the accessory pathway (AP) yielding a normal narrow QRS complex. B, Supraventricular tachycardia in Wolff-Parkinson-White syndrome occurring in the reverse direction, antegrade over the AP and retrograde over the AVN. This results in a wide QRS complex. SAN = sinoatrial node.</note><note type="content">Figure 3: A 12-lead ECG from a newborn with congenital long Q-T syndrome. Note the sinus bradycardia and Q-Tc of 650 msec.</note><note type="content">Figure 4: Ambulatory Holter monitor recording from a patient with long Q-T syndrome. The recording shows sinus rhythm with ventricular premature beats followed by the induction of a polymorphic ventricular tachycardia (torsades de pointes).</note><note type="content">Figure 5: Ambulatory Holter monitor recording from a postoperative patient with electrocardiographic findings of sinus node dysfunction. The first beat is a conducted sinus beat followed by a sinus pause with a junctional escape beat. The fourth beat is an atrial premature beat followed by sinus arrest with another junctional escape beat.</note><note type="content">Figure 6: Ambulatory Holter monitor recording from a patient with congenital complete atrioventricular block. The ventricular rate is 45 beats per minute, and the sinus rate is 108 beats per minute. P = P wave; R = QRS complex.</note><note type="content">Table 1: CAUSES OF SYNCOPE</note><note type="content">Table 2: DIAGNOSTIC CRITERIA FOR LONG Q-T SYNDROME</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">SYNCOPE IN THE PEDIATRIC PATIENT</title><author><persName><forename type="first">Ronn E.</forename><surname>Tanel</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Cardiology, Children's Hospital; and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</affiliation></author><author><persName><forename type="first">Edward P.</forename><surname>Walsh</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Cardiology, Children's Hospital; and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</affiliation></author></analytic><monogr><title level="j">Cardiology Clinics</title><title level="j" type="abbrev">CCL</title><idno type="pISSN">0733-8651</idno><idno type="PII">S0733-8651(05)X7022-9</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1997"></date><biblScope unit="volume">15</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="277">277</biblScope><biblScope unit="page" to="294">294</biblScope></imprint></monogr><idno type="istex">72B4D003078254DE56EB523B535252BFB6227AD3</idno><idno type="DOI">10.1016/S0733-8651(05)70336-2</idno><idno type="PII">S0733-8651(05)70336-2</idno><idno type="ArticleID">70336</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1997</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Syncope during childhood is common. A variable incidence has been reported, from 1 of 2000 emergency department visits,71 to 47% of interviewed college students.61 Driscoll and colleagues14 reported an overall incidence of 125 of 100,000 (0.125%) for pediatric patients seeking medical attention. Girls were seen for evaluation more commonly than boys, with the peak incidence occurring between ages 15 and 19 years. Despite its frequency, syncope generates an extraordinary amount of anxiety among patients, families, teachers, coaches, and physicians.In children and adolescents, the list of causes is generally similar to that described for adults, although the relative frequency and prognosis for the individual diagnoses are somewhat unique. Fortunately, most syncopal events in young patients are isolated and benign in nature. Driscoll's data14 revealed an association of sudden death and prior syncopal events that was not different from that of sudden death in the general population. This article describes the causes, diagnosis, and treatment of syncope in infants, children, and adolescents, focusing on the differences that must be identified when caring for the pediatric versus adult patient. Recommendations are presented for an economically efficient diagnostic workup and practical approach to treatment.</p></abstract></profileDesc><revisionDesc><change when="1997">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier doc found" wicri:toSee="Elsevier, no converted or simple article"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 5.0.1//EN//XML" URI="art501.dtd" name="istex:docType"><istex:entity SYSTEM="f027701" NDATA="IMAGE" name="f027701"></istex:entity><istex:entity SYSTEM="f027702" NDATA="IMAGE" name="f027702"></istex:entity><istex:entity SYSTEM="f027703" NDATA="IMAGE" name="f027703"></istex:entity><istex:entity SYSTEM="f027704" NDATA="IMAGE" name="f027704"></istex:entity><istex:entity SYSTEM="f027705" NDATA="IMAGE" name="f027705"></istex:entity><istex:entity SYSTEM="f027706" NDATA="IMAGE" name="f027706"></istex:entity></istex:docType><istex:document><article docsubtype="fla" version="5.0" xml:lang="en"><item-info><jid>CCL</jid><aid>70336</aid><ce:pii>S0733-8651(05)70336-2</ce:pii><ce:doi>10.1016/S0733-8651(05)70336-2</ce:doi><ce:copyright type="other" year="1997">W. B. Saunders Company</ce:copyright></item-info><ce:floats><ce:figure id="f1"><ce:label>Figure 1</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0010"><ce:italic>A,</ce:italic> A 12-lead ECG showing ventricular tachycardia at a rate of 226 beats per minute. This patient has Belhassen's tachycardia. Note the typical right bundle-branch pattern with a superior QRS axis. The ECG is recorded at half-standard amplitude. <ce:italic>B,</ce:italic> A 12-lead ECG showing sinus rhythm with salvos of slow ventricular tachycardia. The arrhythmia is due to an abnormal automatic focus in the right ventricular outflow tract. This is supported by the left bundle-branch pattern and inferior QRS axis.</ce:simple-para></ce:caption><ce:link locator="f027701"></ce:link></ce:figure><ce:figure id="f2"><ce:label>Figure 2</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0015"><ce:italic>A,</ce:italic> Supraventricular tachycardia in Wolff-Parkinson-White syndrome resulting from antegrade conduction over the atrioventricular node (AVN) and retrograde conduction over the accessory pathway (AP) yielding a normal narrow QRS complex. <ce:italic>B,</ce:italic> Supraventricular tachycardia in Wolff-Parkinson-White syndrome occurring in the reverse direction, antegrade over the AP and retrograde over the AVN. This results in a wide QRS complex. SAN = sinoatrial node.</ce:simple-para></ce:caption><ce:link locator="f027702"></ce:link></ce:figure><ce:figure id="f3"><ce:label>Figure 3</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0020">A 12-lead ECG from a newborn with congenital long Q-T syndrome. Note the sinus bradycardia and Q-T<ce:inf loc="post">c</ce:inf> of 650 msec.</ce:simple-para></ce:caption><ce:link locator="f027703"></ce:link></ce:figure><ce:figure id="f4"><ce:label>Figure 4</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0025">Ambulatory Holter monitor recording from a patient with long Q-T syndrome. The recording shows sinus rhythm with ventricular premature beats followed by the induction of a polymorphic ventricular tachycardia (torsades de pointes).</ce:simple-para></ce:caption><ce:link locator="f027704"></ce:link></ce:figure><ce:figure id="f5"><ce:label>Figure 5</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0030">Ambulatory Holter monitor recording from a postoperative patient with electrocardiographic findings of sinus node dysfunction. The first beat is a conducted sinus beat followed by a sinus pause with a junctional escape beat. The fourth beat is an atrial premature beat followed by sinus arrest with another junctional escape beat.</ce:simple-para></ce:caption><ce:link locator="f027705"></ce:link></ce:figure><ce:figure id="f6"><ce:label>Figure 6</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0035">Ambulatory Holter monitor recording from a patient with congenital complete atrioventricular block. The ventricular rate is 45 beats per minute, and the sinus rate is 108 beats per minute. P = P wave; R = QRS complex.</ce:simple-para></ce:caption><ce:link locator="f027706"></ce:link></ce:figure><ce:table id="cetable1" frame="topbot" colsep="1" rowsep="0"><ce:label>Table 1</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0040">CAUSES OF SYNCOPE</ce:simple-para></ce:caption><tgroup cols="1" rowsep="0" colsep="0"><colspec colnum="1" colname="col1" colwidth="100*"></colspec><tbody><row><entry colname="col1">Cardiac syncope</entry></row><row><entry colname="col1"> Outflow obstruction</entry></row><row><entry colname="col1"> Valvular aortic stenosis</entry></row><row><entry colname="col1"> Hypertrophic cardiomyopathy</entry></row><row><entry colname="col1"> Primary pulmonary hypertension</entry></row><row><entry colname="col1"> Eisenmenger's syndrome</entry></row><row><entry colname="col1"> Myocardial dysfunction</entry></row><row><entry colname="col1"> Primary ventricular dysfunction</entry></row><row><entry colname="col1"> Dilated cardiomyopathy</entry></row><row><entry colname="col1"> Neuromuscular disorders (i.e., Duchenne muscular dystrophy, Becker muscular dystrophy)</entry></row><row><entry colname="col1"> Secondary ventricular dysfunction</entry></row><row><entry colname="col1"> Inflammatory disease</entry></row><row><entry colname="col1"> Acute myocarditis</entry></row><row><entry colname="col1"> Kawasaki disease</entry></row><row><entry colname="col1"> Ischemia</entry></row><row><entry colname="col1"> Anomalous coronary artery</entry></row><row><entry colname="col1"> Kawasaki disease</entry></row><row><entry colname="col1"> Arrhythmias</entry></row><row><entry colname="col1"> Ventricular tachycardia</entry></row><row><entry colname="col1"> No congenital heart disease</entry></row><row><entry colname="col1"> Postoperative congenital heart disease</entry></row><row><entry colname="col1"> Supraventricular tachycardia (i.e., Wolff-Parkinson- White)</entry></row><row><entry colname="col1"> Long Q-T syndrome</entry></row><row><entry colname="col1"> Sinus node dysfunction</entry></row><row><entry colname="col1"> Atrioventricular block</entry></row><row><entry colname="col1"> Arrhythmogenic right ventricular dysplasia</entry></row><row><entry colname="col1">Noncardiac syncope</entry></row><row><entry colname="col1"> Seizure disorder</entry></row><row><entry colname="col1"> Breath-holding spells</entry></row><row><entry colname="col1"> Orthostatic hypotension</entry></row><row><entry colname="col1"> Migraine</entry></row><row><entry colname="col1"> Drug/toxic exposure</entry></row><row><entry colname="col1"> Metabolic abnormality</entry></row><row><entry colname="col1"> Hyperventilation</entry></row><row><entry colname="col1"> Situational syncope (i.e., cough, micturition, defecation, stretch, hair grooming)</entry></row><row><entry colname="col1"> Dysautonomia</entry></row><row><entry colname="col1"> Hysteria</entry></row><row><entry colname="col1"> Carotid sinus hypersensitivity</entry></row><row><entry colname="col1">Neurocardiogenic syncope</entry></row></tbody></tgroup></ce:table><ce:table id="cetable2" frame="topbot" colsep="1" rowsep="0"><ce:label>Table 2</ce:label><ce:caption><ce:simple-para view="all" id="simple-para.0045">DIAGNOSTIC CRITERIA FOR LONG Q-T SYNDROME</ce:simple-para></ce:caption><tgroup cols="2" colsep="0" rowsep="0"><colspec colnum="1" colname="col1" colwidth="75*"></colspec><colspec colnum="2" colname="col2" colwidth="25*"></colspec><tbody><row><entry colname="col1">Family history</entry><entry colname="col2" align="char" char="."></entry></row><row><entry colname="col1"> Family members with definite long Q-T syndrome</entry><entry colname="col2" align="char" char=".">1</entry></row><row><entry colname="col1"> Unexplained sudden cardiac death < age 30 among immediate family members</entry><entry colname="col2" align="char" char=".">0.5</entry></row><row><entry colname="col1">Symptoms</entry><entry colname="col2" align="char" char="."></entry></row><row><entry colname="col1"> Syncope<ce:cross-ref refid="cetablefn1">*</ce:cross-ref></entry><entry colname="col2" align="char" char="."></entry></row><row><entry colname="col1"> With stress</entry><entry colname="col2" align="char" char=".">2</entry></row><row><entry colname="col1"> Without stress</entry><entry colname="col2" align="char" char=".">1</entry></row><row><entry colname="col1"> Congenital deafness</entry><entry colname="col2" align="char" char=".">0.5</entry></row><row><entry colname="col1">Electrocardiographic findings Q-Tc</entry><entry colname="col2" align="char" char="."></entry></row><row><entry colname="col1"> >480 msec</entry><entry colname="col2" align="char" char=".">3</entry></row><row><entry colname="col1"> 460–470 msec</entry><entry colname="col2" align="char" char=".">2</entry></row><row><entry colname="col1"> 450 msec (in males)</entry><entry colname="col2" align="char" char=".">1</entry></row><row><entry colname="col1"> Torsades de pointes<ce:cross-ref refid="cetablefn1">*</ce:cross-ref></entry><entry colname="col2" align="char" char=".">2</entry></row><row><entry colname="col1"> T-wave alternans</entry><entry colname="col2" align="char" char=".">1</entry></row><row><entry colname="col1"> Notched T wave in 3 leads</entry><entry colname="col2" align="char" char=".">1</entry></row><row><entry colname="col1"> Low heart rate for age</entry><entry colname="col2" align="char" char=".">0.5</entry></row><row><entry colname="col1"> Prominent U waves</entry><entry colname="col2" align="char" char=".">1</entry></row><row><entry colname="col1"> Miscellaneous</entry><entry colname="col2" align="char" char=".">1</entry></row><row><entry namest="col1" nameend="col2">Total score: 0 – 2 = unaffected; 2.5–4.0 = indeterminate; ≥ 4.5 = affected.</entry></row></tbody></tgroup><ce:table-footnote id="cetablefn1"><ce:label>*</ce:label><ce:note-para>Mutually exclusive.</ce:note-para></ce:table-footnote></ce:table></ce:floats><head><ce:article-footnote><ce:note-para><ce:italic>Address reprint requests to</ce:italic> Ronn E. Tanel, MD, Department of Cardiology, Children's Hospital, 300 Longwood Avenue, Boston, MA 02115</ce:note-para><ce:note-para>RET is currently supported by a research fellowship from the American Heart Association, Massachusetts Affiliate, Inc.</ce:note-para></ce:article-footnote><ce:title>SYNCOPE IN THE PEDIATRIC PATIENT</ce:title><ce:author-group><ce:author><ce:given-name>Ronn E.</ce:given-name><ce:surname>Tanel</ce:surname><ce:degrees>MD</ce:degrees></ce:author><ce:author><ce:given-name>Edward P.</ce:given-name><ce:surname>Walsh</ce:surname><ce:degrees>MD</ce:degrees></ce:author><ce:affiliation><ce:textfn>Department of Cardiology, Children's Hospital; and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</ce:textfn></ce:affiliation></ce:author-group><ce:abstract class="author"><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0050">Syncope during childhood is common. A variable incidence has been reported, from 1 of 2000 emergency department visits,<ce:cross-ref refid="bib71"><ce:sup loc="post">71</ce:sup></ce:cross-ref> to 47% of interviewed college students.<ce:cross-ref refid="bib61"><ce:sup loc="post">61</ce:sup></ce:cross-ref> Driscoll and colleagues<ce:cross-ref refid="bib14"><ce:sup loc="post">14</ce:sup></ce:cross-ref> reported an overall incidence of 125 of 100,000 (0.125%) for pediatric patients seeking medical attention. Girls were seen for evaluation more commonly than boys, with the peak incidence occurring between ages 15 and 19 years. Despite its frequency, syncope generates an extraordinary amount of anxiety among patients, families, teachers, coaches, and physicians.</ce:simple-para><ce:simple-para view="all" id="simple-para.0055">In children and adolescents, the list of causes is generally similar to that described for adults, although the relative frequency and prognosis for the individual diagnoses are somewhat unique. Fortunately, most syncopal events in young patients are isolated and benign in nature. Driscoll's data<ce:cross-ref refid="bib14"><ce:sup loc="post">14</ce:sup></ce:cross-ref> revealed an association of sudden death and prior syncopal events that was not different from that of sudden death in the general population. This article describes the causes, diagnosis, and treatment of syncope in infants, children, and adolescents, focusing on the differences that must be identified when caring for the pediatric versus adult patient. Recommendations are presented for an economically efficient diagnostic workup and practical approach to treatment.</ce:simple-para></ce:abstract-sec></ce:abstract></head><body view="all"><ce:sections><ce:section id="cesec1" view="all"><ce:section-title>CAUSE</ce:section-title><ce:para view="all" id="para.0010">Syncope can be classified into three categories: cardiac, noncardiac, and neurocardiogenic (or vasovagal) <ce:cross-ref refid="cetable1">(Table 1)</ce:cross-ref><ce:float-anchor refid="cetable1"></ce:float-anchor>. For young patients, neurocardiogenic events clearly account for the majority of episodes, but the goal of all evaluations must be the accurate identification of the rare individual with potentially serious pathology.</ce:para><ce:section id="cesec2" view="all"><ce:section-title>Cardiac Syncope</ce:section-title><ce:para view="all" id="para.0015">Cardiac syncope results from an obstruction to flow, myocardial dysfunction, or cardiac arrhythmia. Any of these disorders may be congenital and are sometimes familial. In addition, the pediatric cardiologist frequently evaluates syncope in older children and young adults who have previously undergone surgical repair or palliation of congenital heart disease. These patients have potential for acquired or residual structural lesions, myocardial dysfunction, and supraventricular or ventricular arrhythmias. The medical evaluation of syncope in a patient with a history of prior cardiac surgery is often challenging.</ce:para><ce:section id="cesec3" view="all"><ce:section-title>Obstruction to Flow</ce:section-title><ce:para view="all" id="para.0020">Syncope related to an obstruction to flow often occurs in association with exertion or exercise and is generally classified into categories of (1) fixed or dynamic obstruction owing to a structural cardiac lesion or (2) obstruction owing to pulmonary vascular disease.</ce:para><ce:section id="cesec4" view="all"><ce:section-title>Valvular Aortic Stenosis.</ce:section-title><ce:para view="all" id="para.0025">Valvular aortic stenosis, a fixed obstructive lesion, is a common congenital defect frequently associated with a bicuspid aortic valve. A more severe form of the disease may include a unicommissural or severely dysplastic valve, which presents with secondary myocardial dysfunction and congestive heart failure in the newborn period. Approximately 20% of patients have associated cardiac anomalies<ce:cross-ref refid="bib7"><ce:sup loc="post">7</ce:sup></ce:cross-ref> (e.g., coarctation of the aorta<ce:cross-ref refid="bib84"><ce:sup loc="post">84</ce:sup></ce:cross-ref>), particularly common in girls with Turner's syndrome. Children with malformed aortic valves generally develop thickening of the leaflets, which contributes to the obstructive gradient and symptoms. In contrast to adults, children seldom develop valvular calcification.<ce:cross-ref refid="bib3"><ce:sup loc="post">3</ce:sup></ce:cross-ref></ce:para><ce:para view="all" id="para.0030">Pediatric patients with valvular aortic stenosis do not usually have symptoms but are recognized by the presence of a murmur and systolic ejection click. Symptomatic children may develop syncope as well as chest pain, dyspnea on exertion, and poor exercise tolerance. Children with severe valvular aortic stenosis may develop exertional syncope as a result of reduced cardiac output and decreased cerebral blood flow during activity.<ce:cross-ref refid="bib7"><ce:sup loc="post">7</ce:sup></ce:cross-ref> A history of symptoms<ce:cross-ref refid="bib30"><ce:sup loc="post">30</ce:sup></ce:cross-ref> and symptoms during strenuous exercise<ce:cross-ref refid="bib41"><ce:sup loc="post">41</ce:sup></ce:cross-ref> contribute to the greatest risk for sudden death.<ce:cross-ref refid="bib33"><ce:sup loc="post">33</ce:sup></ce:cross-ref> The mechanism of sudden death may be related to an acute rise in intracavitary ventricular pressure, causing a reflex hypotensive syncopal event, acute ischemia, and ventricular fibrillation.<ce:cross-ref refid="bib31"><ce:sup loc="post">31</ce:sup></ce:cross-ref> Patients with valvular aortic stenosis who undergo transcatheter or surgical intervention, generally for valve gradients 50 mmHg or greater, may have a reduced frequency of syncope and sudden death.<ce:cross-ref refid="bib38"><ce:sup loc="post">38</ce:sup></ce:cross-ref></ce:para></ce:section><ce:section id="cesec5" view="all"><ce:section-title>Hypertrophic Cardiomyopathy.</ce:section-title><ce:para view="all" id="para.0035">Hypertrophic cardiomyopathy can result in a combination of dynamic and fixed subvalvular obstruction. The disease may be sporadic but more recently has been recognized as an autosomal dominant pattern of inheritance, with specific genetic defects involving at least four gene loci.<ce:cross-refs refid="bib27 bib80 bib85"><ce:sup loc="post">27,80,85</ce:sup></ce:cross-refs> Echocardiographic studies have shown that 60% of affected individuals have an affected first-degree relative; however, the 20% to 25% reported incidence of obstructive disease demonstrates phenotypic heterogeneity among genotypes.<ce:cross-refs refid="bib51 bib52"><ce:sup loc="post">51,52</ce:sup></ce:cross-refs> Hypertrophic cardiomyopathy is more common in some clinical disorders, such as Noonan's syndrome, Friedreich's ataxia, and LEOPARD syndrome.</ce:para><ce:para view="all" id="para.0040">Syncope is reported in 15% to 25% of adult patients with hypertrophic cardiomyopathy<ce:cross-ref refid="bib56"><ce:sup loc="post">56</ce:sup></ce:cross-ref> but appears to be much less common in pediatric patients. When syncope does occur in children, however, it is an ominous finding.<ce:cross-ref refid="bib55"><ce:sup loc="post">55</ce:sup></ce:cross-ref> The most important risk factor in pediatric patients with hypertrophic cardiomyopathy is age of onset for symptoms, with infants having the poorest prognosis. One study found that 9 of 11 symptomatic infants died by 1 year of age.<ce:cross-ref refid="bib54"><ce:sup loc="post">54</ce:sup></ce:cross-ref> In addition, infants seem to have a much different presentation from older children and adults, marked by symptoms of congestive heart failure and cyanosis. In addition, affected infants and young children frequently have obstruction to right ventricular outflow, which occurs together with subaortic obstruction. The subpulmonic obstruction, more commonly of the fixed type, often has a gradient of equal or greater amplitude than the subaortic obstruction.<ce:cross-ref refid="bib54"><ce:sup loc="post">54</ce:sup></ce:cross-ref> In general, the pattern of left ventricular hypertrophy seems to be a contributing factor for the development of clinical symptoms, but the specific echocardiographic measurements of left ventricular mass and wall thickening do not allow the prediction of a more severe clinical course.<ce:cross-ref refid="bib53"><ce:sup loc="post">53</ce:sup></ce:cross-ref></ce:para><ce:para view="all" id="para.0045">Beta-blockers and calcium channel blockers have both been shown to improve symptoms, and calcium channel blockers may improve survival. Calcium channel blockers should be used cautiously, especially in infants less than 1 year of age.<ce:cross-ref refid="bib16"><ce:sup loc="post">16</ce:sup></ce:cross-ref> Surgical myectomy provides many patients with relief of symptoms, even though annual mortality statistics do not appear to change following the procedure, which is accompanied by high operative morbidity and mortality.<ce:cross-ref refid="bib51"><ce:sup loc="post">51</ce:sup></ce:cross-ref> Dual-chamber pacing is another controversial form of therapy currently being evaluated by a pediatric multicenter randomized trial. Automatic implantable cardioversion-defibrillators are becoming accepted as an effective form of therapy, particularly in larger patients with syncope, documented arrhythmias, or a family history of sudden death.</ce:para></ce:section><ce:section id="cesec6" view="all"><ce:section-title>Primary Pulmonary Hypertension.</ce:section-title><ce:para view="all" id="para.0050">Pulmonary vascular disease may cause syncope because of the inability of the structurally normal heart to maintain an adequate cardiac output. Primary pulmonary hypertension is a disease of young adults, sometimes presenting during adolescence. Because patients may have unrecognized disease for years as a result of compensatory hypertrophy, shortness of breath, dyspnea on exertion, and syncope may be the first presenting symptoms at advanced degrees of vascular pathology. Chest pain, fatigue, palpitations, and other nonspecific symptoms are common. Symptomatic disease may alternatively present at young ages and has been reported at less than 6 months of age.<ce:cross-ref refid="bib75"><ce:sup loc="post">75</ce:sup></ce:cross-ref> Familial cases are known, and inheritance appears to be in an autosomal dominant pattern with variable penetrance.<ce:cross-ref refid="bib87"><ce:sup loc="post">87</ce:sup></ce:cross-ref></ce:para><ce:para view="all" id="para.0055">Syncope is present in up to 55% of patients.<ce:cross-ref refid="bib91"><ce:sup loc="post">91</ce:sup></ce:cross-ref> Syncope occurs as a result of low cardiac output and may be discerned from other causes by the presence of a narrow pulse pressure, peripheral cyanosis, pallor, dyspnea, and tachypnea. These symptoms are present in the setting of an increased right ventricular impulse, loud second heart sound, systolic murmur with ejection click, and diastolic murmur of pulmonary regurgitation. Electrocardiographic findings include right ventricular hypertrophy, right atrial enlargement, right axis deviation, and right ventricular conduction delay, whereas the chest radiograph usually shows a normal heart size with large pulmonary arteries. Patients are also prone to both supraventricular and ventricular arrhythmias, which are other causes for syncope and sudden death in the affected patient.</ce:para><ce:para view="all" id="para.0060">There is no cure for primary pulmonary hypertension, so goals of therapy include reduction of pulmonary artery pressure, treatment of arrhythmias, and improvement of right heart congestive failure and cardiac output. Clinical trials with intravenous vasodilators, such as acetylcholine, are frequently used as a predictor for the subgroup of patients who would benefit from long-term therapy with oral agents, such as nifedipine. Other supportive therapy includes supplemental oxygen, digoxin, diuretics, and anticoagulation. Patients with syncope or other evidence of poor cardiac output may benefit from atrial septostomy as an interventional method for improving systemic output.<ce:cross-ref refid="bib64"><ce:sup loc="post">64</ce:sup></ce:cross-ref></ce:para></ce:section><ce:section id="cesec7" view="all"><ce:section-title>Eisenmenger's Syndrome.</ce:section-title><ce:para view="all" id="para.0065">Eisenmenger's syndrome describes pulmonary hypertension and elevated pulmonary vascular resistance in combination with a cardiac shunt, which becomes right-to-left at its terminal stages. The rate at which pulmonary hypertension progresses depends on the associated cardiac lesion (atrial septal defect, ventricular septal defect, or patent ductus arteriosus). Patients are less likely to have had symptoms of congestive heart failure during infancy and therefore may not have a diagnosed cardiac lesion until symptoms of pulmonary hypertension and cor pulmonale are noticed.</ce:para><ce:para view="all" id="para.0070">Syncope may occur in up to nearly half of patients with Eisenmenger's syndrome. The mechanism of syncope is usually low cardiac output. Other symptoms include chest pain, shortness of breath, and hemoptysis, and the physical examination may reveal an increased right ventricular impulse, palpable second heart sound, cyanosis, and clubbing. Patients usually become most symptomatic in early adulthood, but presentation and death may occur during childhood, 27% among 26 young patients in one study.<ce:cross-ref refid="bib95"><ce:sup loc="post">95</ce:sup></ce:cross-ref> Sudden death is due to Eisenmenger's syndrome in up to 15% of patients and is commonly attributed to an arrhythmia.<ce:cross-ref refid="bib41"><ce:sup loc="post">41</ce:sup></ce:cross-ref> This seems to be a reasonable explanation because these patients usually have ventricular hypertrophy, marked hypoxemia, and right ventricular pressure overload. The experience at Texas Children's Hospital, however, does not entirely support this notion because two patients who were wearing 24-hour ambulatory Holter monitors at the time of death demonstrated progressive sinus bradycardia and asystole without ventricular arrhythmia.<ce:cross-ref refid="bib19"><ce:sup loc="post">19</ce:sup></ce:cross-ref> Treatment of patients with Eisenmenger's syndrome is supportive and similar to that of patients with primary pulmonary hypertension.</ce:para></ce:section></ce:section><ce:section id="cesec8" view="all"><ce:section-title>Myocardial Dysfunction</ce:section-title><ce:para view="all" id="para.0075">Myocardial dysfunction is rarely a direct cause of syncope but usually results in syncope when there are associated cardiac arrhythmias. The causes for primary ventricular dysfunction in children are numerous, but they are usually related to a more general myopathy or specific inflammatory or ischemic event. The neuromuscular disorders, including Duchenne muscular dystrophy, Becker muscular dystrophy, and Emery-Dreifuss syndrome, are associated with a high incidence of arrhythmias. Examples of myocardial inflammation and ischemia in the pediatric population include viral myocardiitis, Kawasaki disease, and anomalous left coronary artery from the pulmonary artery. Recognition of these disorders is of primary importance and can usually be identified by clinical examination and electrocardiogram (ECG). Viral myocarditis and Kawasaki disease respond well to intravenous gamma globulin, if the child is treated early. The anomalous left coronary artery can be treated surgically, with generally good long-term results.</ce:para></ce:section><ce:section id="cesec9" view="all"><ce:section-title>Arrhythmias</ce:section-title><ce:para view="all" id="para.0080">Arrhythmias as a cause of syncope in children with structurally normal hearts are unusual but probably represent the one item in the differential diagnosis that deserves the most attention. Most instances of supraventricular arrhythmias result in symptoms of palpitations rather than syncope or sudden death, with the exception of Wolff-Parkinson-White syndrome, with rapid conduction of atrial flutter or fibrillation. Symptoms related to ventricular arrhythmias vary widely depending on the mechanism.</ce:para><ce:section id="cesec10" view="all"><ce:section-title>Ventricular Arrhythmias in a Normal Heart.</ce:section-title><ce:para view="all" id="para.0085">Sudden cardiac death resulting from ventricular arrhythmias in patients with no structural heart disease has a variable incidence of 0 to 13%.<ce:cross-refs refid="bib11 bib18"><ce:sup loc="post">11,18</ce:sup></ce:cross-refs> Ventricular tachycardia in children with normal hearts is typically due to an abnormal automatic focus, usually in the right ventricular outflow tract. Occasional young patients can also be identified with Belhassen's tachycardia, a ventricular tachycardia that arises near the left posterior fascicle and is probably due to a reentry mechanism <ce:cross-ref refid="f1">(Fig. 1</ce:cross-ref><ce:float-anchor refid="f1"></ce:float-anchor><ce:italic>A</ce:italic>). This arrhythmia has an electrocardiographic appearance that is different from the typical right ventricular outflow tract automatic focus <ce:cross-ref refid="f1">(Fig. 1</ce:cross-ref><ce:italic>B</ce:italic>). Some infants with incessant ventricular tachycardia because of an automatic focus have undergone surgical excision of hamartomas of Purkinje cell origin,<ce:cross-ref refid="bib22"><ce:sup loc="post">22</ce:sup></ce:cross-ref> but in most cases there is no demonstrable pathology.</ce:para><ce:para view="all" id="para.0090">Idiopathic ventricular tachycardia is rare in infants and increases gradually with age.<ce:cross-ref refid="bib40"><ce:sup loc="post">40</ce:sup></ce:cross-ref> Some of the ventricular tachycardias that present in early childhood<ce:cross-ref refid="bib90"><ce:sup loc="post">90</ce:sup></ce:cross-ref> are self-limited and spontaneously resolve,<ce:cross-refs refid="bib69 bib96"><ce:sup loc="post">69,96</ce:sup></ce:cross-refs> but patients with exercise-induced ventricular tachycardia may be at risk for syncope or sudden death.<ce:cross-ref refid="bib11"><ce:sup loc="post">11</ce:sup></ce:cross-ref> Any child or adolescent who presents with syncope and idiopathic ventricular tachycardia<ce:cross-refs refid="bib11 bib48 bib76"><ce:sup loc="post">11,48,76</ce:sup></ce:cross-refs> usually receives a thorough evaluation, including echocardiogram; 24-hour ambulatory Holter monitor; exercise test; and sometimes cardiac catheterization for biopsy, angiography, and provocative electrophysiologic stimulation. Unfortunately, no single test or combination of tests provides an adequate recognition of which patients are at greatest risk for sudden cardiac death. Therefore, depending on symptoms, degree of ectopy, and ventricular function, treatment with antiarrhythmic medications, catheter ablation, or implantable cardioversion-defibrillators may be indicated.</ce:para><ce:para view="all" id="para.0095">Some ventricular arrhythmias are associated with minor structural heart disease. For example, adult patients with mitral valve prolapse have a higher incidence of syncope and sudden death than the general population. Although sudden death in children with mitral valve prolapse is essentially unreported, high-grade ventricular ectopy was present in 8% of 24-hour ambulatory Holter monitors in pediatric patients in one study.<ce:cross-ref refid="bib37"><ce:sup loc="post">37</ce:sup></ce:cross-ref> Ebstein's malformation of the tricuspid valve is also associated with ventricular arrhythmias. Up to 25% of unoperated patients may be affected.<ce:cross-ref refid="bib65"><ce:sup loc="post">65</ce:sup></ce:cross-ref></ce:para></ce:section><ce:section id="cesec11" view="all"><ce:section-title>Wolff-Parkinson-White Syndrome.</ce:section-title><ce:para view="all" id="para.0100">The overall prevalence of Wolff-Parkinson-White syndrome is estimated at 0.1% to 0.3% among the general population,<ce:cross-ref refid="bib10"><ce:sup loc="post">10</ce:sup></ce:cross-ref> but it is more common in patients with Ebstein's malformation of the tricuspid valve, ventricular inversion, and hypertrophic cardiomyopathy. This diagnosis is usually apparent on ECG when a patient presents with syncope. Supraventricular tachycardia typically occurs with reentry involving antegrade conduction over the atrioventricular node and retrograde conduction over the accessory pathway (orthodromic), yielding a normal QRS complex <ce:cross-ref refid="f2">(Fig. 2</ce:cross-ref><ce:float-anchor refid="f2"></ce:float-anchor><ce:italic>A</ce:italic>). In young children, tachycardia rarely results from reentry in the opposite direction (antidromic) causing a wide QRS complex <ce:cross-ref refid="f2">(Fig. 2</ce:cross-ref><ce:italic>B</ce:italic>). Orthodromic reentry may be rapid in young children, sometimes up to 300 beats per minute, and may result in an acute hemodynamic decompensation or syncope. The highest risk for syncope and sudden death, however, exists in patients who can conduct rapidly (1:1 atrioventricular conduction) over the accessory pathway during atrial fibrillation or atrial flutter.</ce:para><ce:para view="all" id="para.0105">Atrial fibrillation and atrial flutter and the possibility for rapid ventricular conduction are extremely rare before adolescence. This may be due to the lack of substrate necessary to sustain atrial arrhythmias, especially fibrillation, in the physically small heart. As patients approach young adulthood, however, atrial flutter and atrial fibrillation become more common, and the risk for syncope and sudden death increases. Fortunately, radiofrequency catheter ablation now provides a safe, effective method for treating this disease.<ce:cross-ref refid="bib83"><ce:sup loc="post">83</ce:sup></ce:cross-ref> Syncope is considered to be a clear indication for ablation in a child of any age with Wolff-Parkinson-White syndrome.</ce:para></ce:section><ce:section id="cesec12" view="all"><ce:section-title>Long Q-T Syndrome.</ce:section-title><ce:para view="all" id="para.0110">The long Q-T syndrome can be either an inherited or acquired condition that results in a prolonged Q-T interval on the surface ECG <ce:cross-ref refid="f3">(Fig. 3)</ce:cross-ref><ce:float-anchor refid="f3"></ce:float-anchor> and abnormal ventricular repolarization at the cellular level. Inherited forms include the Romano-Ward syndrome, which has an autosomal dominant genetic pattern, and the Jervell and Lange-Nielsen syndrome, which has an autosomal recessive pattern and is associated with congenital nerve deafness. Several groups have reported genetic linkage analyses attributing the hereditary long Q-T syndrome to four loci on chromosomes 11,<ce:cross-ref refid="bib39"><ce:sup loc="post">39</ce:sup></ce:cross-ref> 3, 7,<ce:cross-ref refid="bib32"><ce:sup loc="post">32</ce:sup></ce:cross-ref> and 4.<ce:cross-ref refid="bib78"><ce:sup loc="post">78</ce:sup></ce:cross-ref> The responsible mutations have been reported in the presumed cardiac potassium and sodium ion channel genes. Children may also acquire a long Q-T interval as the result of electrolyte abnormalities or exposure to some medications and toxins.</ce:para><ce:para view="all" id="para.0115">The congenital form of the long Q-T syndrome may present during the newborn period. These patients, who are often the most symptomatic and have the longest measured Q-T intervals, are at highest risk for sudden death. Presentation later in childhood has a slightly more favorable prognosis and is usually recognized during the evaluation of a syncopal event. Syncope is due to the development of a polymorphic ventricular tachycardia, Torsades de pointes <ce:cross-ref refid="f4">(Fig. 4)</ce:cross-ref><ce:float-anchor refid="f4"></ce:float-anchor>, classically occurring at times of sudden stress or excitement. Torsades de pointes is episodic and usually self-terminating, but the risk of sudden death occurs when sustained episodes degenerate to ventricular fibrillation.</ce:para><ce:para view="all" id="para.0120">There is currently no single diagnostic test to confirm the diagnosis of the long Q-T syndrome, so that identification of patients requires a clinical suspicion. Some ECGs are unmistakable, but often the diagnosis is subtle. Scoring systems <ce:cross-ref refid="cetable2">(Table 2)</ce:cross-ref><ce:float-anchor refid="cetable2"></ce:float-anchor> are used as a guide to stratify patients into high, moderate, and low probability of having the disorder based on symptoms, electrocardiographic findings, and family history. Gene mapping techniques will potentially result in a more rapid and definitive diagnostic test as well as the development of therapy specific to the ion channel defect.</ce:para><ce:para view="all" id="para.0125">Treatment for patients with the long Q-T syndrome depends on the severity of symptoms. Initial therapy for young patients with syncope and no documentation of arrhythmia is usually beta-blockade alone. The more severely affected infants who present during the neonatal period have been traditionally treated with beta-blockade plus pacing. Older children and adolescents who survive infancy with significant symptoms and episodic ventricular tachycardia are good candidates for implantable cardioversion-defibrillators as therapy for this complex high-risk form of the disease.<ce:cross-ref refid="bib25"><ce:sup loc="post">25</ce:sup></ce:cross-ref></ce:para></ce:section><ce:section id="cesec13" view="all"><ce:section-title>Sinus Node Dysfunction.</ce:section-title><ce:para view="all" id="para.0130">Isolated sinus node dysfunction rarely, if ever, causes syncope in children. In patients who have undergone complex cardiac surgery, however, it may be seen in conjunction with recurrent atrial reentry tachycardia as the <ce:italic>tachycardia-bradycardia syndrome.</ce:italic> The two most common surgical procedures that result in sinus node dysfunction are the atrial switch (Mustard or Senning) procedure for transposition of the great arteries and the Fontan operation for palliation of single ventricle cardiac physiology. The electrophysiologic abnormalities <ce:cross-ref refid="f5">(Fig. 5)</ce:cross-ref><ce:float-anchor refid="f5"></ce:float-anchor> include sinus bradycardia, sinus pauses or arrest, intraatrial conduction delays, prolonged atrial refractoriness, and atrial tachyarrhythmias.</ce:para><ce:para view="all" id="para.0135">Patients with tachycardia-bradycardia syndrome can become syncopal as a result of low cardiac output during either sinus bradycardia and sinus pauses or an atrial tachyarrhythmia with rapid ventricular conduction. The latter scenario is much more likely to occur, particularly when the hemodynamic status is compromised, owing to residual structural disease. The incidence of symptomatic atrial arrhythmias among patients who have had the atrial switch or Fontan operation may be as high as 50%.<ce:cross-refs refid="bib49 bib70"><ce:sup loc="post">49,70</ce:sup></ce:cross-refs> Syncope in a young postoperative patient is an indication for aggressive diagnostic evaluation, usually including cardiac catheterization and electrophysiologic study.</ce:para><ce:para view="all" id="para.0140">Some data suggest that medical therapy and permanent cardiac pacing has not affected the risk of sudden death, and failure of therapy may even be a predictor of sudden death.<ce:cross-ref refid="bib73"><ce:sup loc="post">73</ce:sup></ce:cross-ref> Current approaches to therapy include antibradycardia pacing, optimally with atrioventricular synchrony. Antitachycardia pacemakers have allowed an additional option for some patients with longer cycle length atrial tachycardias that are amenable to overdrive pacing for cardioversion. Another therapeutic option for atrial arrhythmias that are sustained and hemodynamically tolerated is radiofrequency catheter ablation, which has a 77% acute success rate in the authors' institutional experience.<ce:cross-ref refid="bib89"><ce:sup loc="post">89</ce:sup></ce:cross-ref> These patients use fewer antiarrhythmic medications and have fewer arrhythmia-related clinical events during 2-year follow-up.<ce:cross-ref refid="bib88"><ce:sup loc="post">88</ce:sup></ce:cross-ref> Finally, the development of low-energy atrial implantable cardioversion-defibrillators in the future may be a useful device for patients with more medically refractory atrial tachycardias.</ce:para></ce:section><ce:section id="cesec14" view="all"><ce:section-title>Atrioventricular Block.</ce:section-title><ce:para view="all" id="para.0145">In pediatric patients, atrioventricular block occurs most frequently as a complication of intracardiac surgery for congenital heart disease, particularly after procedures performed around the region of the atrioventricular node and His bundle. In addition, heart block can occur as a congenital condition with or without structural heart disease <ce:cross-ref refid="f6">(Fig. 6)</ce:cross-ref><ce:float-anchor refid="f6"></ce:float-anchor>. Isolated congenital heart block occurs at a rate of 1/15,000 to 1/20,000 live births.<ce:cross-ref refid="bib57"><ce:sup loc="post">57</ce:sup></ce:cross-ref> The most common condition is that of an infant of a mother with connective tissue disease, first recognized in 1957<ce:cross-ref refid="bib29"><ce:sup loc="post">29</ce:sup></ce:cross-ref> and later proposed as a causative association<ce:cross-ref refid="bib9"><ce:sup loc="post">9</ce:sup></ce:cross-ref> among mothers diagnosed with systemic lupus erythematosus. The pathogenesis involves transplacental anti-Ro and anti-La antibodies, which presumably cross-react with fetal cardiac tissue at a critical point in development.<ce:cross-ref refid="bib79"><ce:sup loc="post">79</ce:sup></ce:cross-ref> When heart block is associated with congenital heart disease, the most common structural lesions are ventricular inversion and defects of the atrioventricular septum. Finally, acquired heart block may occur in pediatric patients in association with several systemic infections and conditions. They include Lyme disease, Rocky Mountain spotted fever, diphtheria, bacterial endocarditis, viral myocarditis, acute rheumatic fever, some muscular dystrophies, Kearns-Sayre disease, and myotonic dystrophy.</ce:para><ce:para view="all" id="para.0150">Syncope associated with atrioventricular block may result from either bradycardia or ventricular tachycardia of the Torsades de pointes variety that is conditioned by the slow rate.<ce:cross-ref refid="bib59"><ce:sup loc="post">59</ce:sup></ce:cross-ref> Patients with congenital atrioventricular block essentially never recover conduction, whereas postoperative patients and children with Lyme disease and myocarditis sometimes do. At Children's Hospital, Boston, recovery from postoperative complete heart block occurs in up to 65% of patients and normal sinus rhythm usually returns by the eighth postoperative day.<ce:cross-ref refid="bib92"><ce:sup loc="post">92</ce:sup></ce:cross-ref> Symptomatic patients with any form of persistent atrioventricular block are treated with permanent cardiac pacing.</ce:para></ce:section><ce:section id="cesec15" view="all"><ce:section-title>Arrhythmogenic Right Ventricular Dysplasia.</ce:section-title><ce:para view="all" id="para.0155">Arrhythmogenic right ventricular dysplasia is a rare primary myocardial disorder in which fibrous or adipose tissue replaces the right ventricular myocardium. The cause and pathogenesis are not well understood. The clinical diagnosis is made by recognition of ventricular arrhythmias with a left bundle-branch pattern and sinus rhythm with abnormal anterior precordial lead (V<ce:inf loc="post">1</ce:inf>–V<ce:inf loc="post">4</ce:inf>) T-wave inversion, decreased right ventricular voltages, tall P waves in lead II, ventricular postexcitation (epsilon waves), increased right ventricular volume, and idiopathic right ventricular dynamic akinesis or dyskinesis.<ce:cross-ref refid="bib60"><ce:sup loc="post">60</ce:sup></ce:cross-ref> Cardiac magnetic resonance imaging may be a useful diagnostic test in pediatric patients.<ce:cross-refs refid="bib58 bib74"><ce:sup loc="post">58,74</ce:sup></ce:cross-refs></ce:para><ce:para view="all" id="para.0160">The clinical presentation is usually in adulthood, but recognition of this illness in children has identified a familial pattern with probable genetic transmission.<ce:cross-refs refid="bib42 bib63"><ce:sup loc="post">42,63</ce:sup></ce:cross-refs> Patients may present with cardiomegaly, congestive heart failure, or syncope and sudden death as a result of ventricular arrhythmias originating from the aneurysmal and dyskinetic right ventricular outflow tract. The diagnosis may be difficult because some patients reportedly have a normal echocardiogram as a result of localization of the pathologic abnormality. The disease may be an underrecognized cause of sudden death in young patients.</ce:para><ce:para view="all" id="para.0165">The clinical prognosis and extent of right ventricular dysplasia are quite variable among affected patients. Some patients have frequent recurrences of ventricular tachycardia, whereas others have few symptoms before sudden death. Antiarrhythmic drug therapy has generally been unsuccessful, and catheter ablation and surgical techniques have not had good long-term outcomes. An automatic implantable cardioverter-defibrillator may be needed for the treatment of this condition.</ce:para></ce:section><ce:section id="cesec16" view="all"><ce:section-title>Postoperative Ventricular Arrhythmias.</ce:section-title><ce:para view="all" id="para.0170">Ventricular arrhythmias occurring after repair of a congenital cardiac defect are not uncommon, and postoperative patients who develop arrhythmias are frequently quite symptomatic. Garson<ce:cross-ref refid="bib20"><ce:sup loc="post">20</ce:sup></ce:cross-ref> reported a 36% incidence of prior cardiac surgery in pediatric patients with sudden cardiac death. Postoperative tetralogy of Fallot is the most common clinical setting for ventricular arrhythmias to cause syncope and sudden death, occurring in as many as 6% of patients.<ce:cross-refs refid="bib21 bib62"><ce:sup loc="post">21,62</ce:sup></ce:cross-refs> These arrhythmias are most likely to originate from the right ventricular outflow tract incision site. Patients who may be at higher risk of syncope and sudden death are those with residual hemodynamic lesions, older age at repair, longer QRS duration on ECG, and history of a prior large palliative shunt.<ce:cross-refs refid="bib21 bib23 bib36"><ce:sup loc="post">21,23,36</ce:sup></ce:cross-refs> Syncope in patients after cardiac surgery for tetralogy of Fallot and ventricular septal defect is an indication for thorough evaluation with 24-hour ambulatory Holter monitoring, exercise tolerance testing, and intracardiac electrophysiologic testing.</ce:para><ce:para view="all" id="para.0175">Repair of residual hemodynamic lesions in the cardiac catheterization laboratory or operating room is of primary importance. Mapping and radiofrequency catheter ablation of sustained and more hemodynamically stable rhythms have been successfully achieved. Finally, implantable cardioversion-defibrillators have an important role for patients with life-threatening symptoms who are not good candidates for catheter-directed therapy.</ce:para></ce:section></ce:section></ce:section><ce:section id="cesec17" view="all"><ce:section-title>Noncardiac Syncope</ce:section-title><ce:section id="cesec18" view="all"><ce:section-title>Seizure Disorder</ce:section-title><ce:para view="all" id="para.0180">Despite the fact that seizures are not truly syncopal events, they are frequently included in the differential diagnosis during a clinical evaluation of syncope. Most seizures in children are easily distinguishable from syncope of other causes, but specific exceptions may be difficult to recognize clinically. For example, neonatal seizures and complex partial seizures may be especially subtle. Typical seizures are accompanied by a premonitory aura, generalized tonic-clonic activity, and a postictal period of confusion and lethargy. Other findings that may help the clinician to diagnose a seizure rather than syncope include (1) a supine rather than upright posture at onset; (2) convulsions before rather than after a loss of consciousness; and (3) a warm, flushed or cyanotic skin color rather than pallor and diaphoresis.</ce:para><ce:para view="all" id="para.0185">Myoclonic jerks of the extremities, tonic extension of the body, or generalized seizures sometimes follow syncopal events that are unusually prolonged and have been referred to as anoxic seizures, convulsive syncope, or syncope seizures. These seizures may be nearly clinically identical to primary seizures. Lempert and associates<ce:cross-ref refid="bib43"><ce:sup loc="post">43</ce:sup></ce:cross-ref> induced syncope in 59 healthy volunteers and noted 71% to have behaviors consistent with seizure activity. These findings are due to transient global hypoxia leading to cortical suppression and disinhibition of limbic and subcortical structures.<ce:cross-ref refid="bib43"><ce:sup loc="post">43</ce:sup></ce:cross-ref> Because of their similarities to other causes of syncope, seizures should generally be worked-up to exclude more life-threatening disorders. For example, it is the authors' institutional policy to obtain an ECG during the consultation of any seizure patient because the long Q-T syndrome has been diagnosed in patients who were initially diagnosed with seizures refractory to anticonvulsant therapy.</ce:para></ce:section><ce:section id="cesec19" view="all"><ce:section-title>Breath Holding</ce:section-title><ce:para view="all" id="para.0190">Breath-holding spells are provoked by a sudden, emotionally intense trigger that is followed by crying and loss of consciousness. These events typically occur in 6- to 18-month-old children. Clinically the child usually becomes cyanotic but may alternatively develop pallor.<ce:cross-ref refid="bib47"><ce:sup loc="post">47</ce:sup></ce:cross-ref> The pallid variety of breath-holding spells is believed to be related to a vasovagal reflex.<ce:cross-refs refid="bib72 bib81"><ce:sup loc="post">72,81</ce:sup></ce:cross-refs> Syncope and tonic-clonic activity are due to cerebral ischemia as a consequence of hypocapnia and cerebral vasoconstriction during crying or from asystole or pulmonary artery reactivity leading to reduced cardiac output.</ce:para><ce:para view="all" id="para.0195">Breath holding has a characteristic clinical presentation that begins with a loud cry associated with a physical or emotional insult, such as pain, fright, or anger. The child then holds his or her breath in expiration, may become either cyanotic or pale, and loses consciousness. Central cyanosis is associated with rigidity and opisthotonos, which is followed by limpness. The entire episode is rapid, usually lasting less than 1 minute. With longer episodes, the child may develop tonic-clonic activity. The spell ends with the child taking gasping breaths, which results in the return of normal color, activity, and consciousness. Patients with pallid breath holding have events in response to injury and pain (typically following head trauma) rather than fright or anger, sudden apnea without crying, and a greater frequency of associated rhythmic muscular contractions. Extreme bradycardia is more common during a pallid breath-holding spell. Both cyanotic and pallid breath holding require no specific therapy and essentially always spontaneously resolve.<ce:cross-ref refid="bib47"><ce:sup loc="post">47</ce:sup></ce:cross-ref> Rarely a child with severe and frequent episodes may require permanent cardiac pacing. Of children with breath holding, approximately 10% to 20% develop more typical neurocardiogenic syncope later in life.<ce:cross-refs refid="bib46 bib47"><ce:sup loc="post">46,47</ce:sup></ce:cross-refs></ce:para></ce:section><ce:section id="cesec20" view="all"><ce:section-title>Orthostatic Hypotension</ce:section-title><ce:para view="all" id="para.0200">Orthostatic hypotension refers to syncope related to the failure of compensatory mechanisms, which normally maintain adequate cardiac output when assuming an upright posture. These mechanisms are normally vasoconstriction, relative tachycardia, muscular contractions of the lower extremities, and venous valve competency and are mediated by increased sympathetic activity and parasympathetic inhibition. Typical symptoms include dizziness, lightheadedness, blurred or tunnel vision, weakness, and syncope and occur more frequently in the morning or after meals or exercise. Several conditions and medications can provoke orthostatic hypotension, including dehydration, blood loss, pregnancy, prolonged bed rest, calcium channel blockers, vasodilators, phenothiazines, and diuretics. Peripheral neuropathies and other neurogenic causes should be considered. The evaluating clinician should obtain blood pressures in both the supine and the standing positions. The standing blood pressure should be performed after several minutes because the development of hypotension and syncope may be delayed.</ce:para></ce:section><ce:section id="cesec21" view="all"><ce:section-title>Migraine</ce:section-title><ce:para view="all" id="para.0205">Migraine headache may be associated with syncope directly or as an atypical presentation. The more typical situation begins with a headache and premonitory aura and is followed by a loss of consciousness and arousal with a severe occipital headache.<ce:cross-ref refid="bib6"><ce:sup loc="post">6</ce:sup></ce:cross-ref> Syncope may also occur, however, in the absence of headache. Basilar artery migraine accounts for 24% of childhood migraines, most frequently in adolescent girls.<ce:cross-ref refid="bib28"><ce:sup loc="post">28</ce:sup></ce:cross-ref> Vasoconstriction or inflammation of the vertebrobasilar arterial supply results in occipital headache, vertigo, visual disturbances in the temporal and nasal fields, dysarthria, tinnitus, ataxia, and confusion or syncope.<ce:cross-ref refid="bib13"><ce:sup loc="post">13</ce:sup></ce:cross-ref> The diagnosis of basilar artery migraine may be elusive but should be considered in patients with severe paroxysmal headaches, a family history, symptoms referable to the brain supplied by the vertebrobasilar arteries, and normal heart rate and blood pressure.<ce:cross-ref refid="bib60"><ce:sup loc="post">60</ce:sup></ce:cross-ref></ce:para></ce:section><ce:section id="cesec22" view="all"><ce:section-title>Drug or Toxic Exposure</ce:section-title><ce:para view="all" id="para.0210">Drugs and toxins may cause an acute loss of consciousness or a gradual onset of lethargy leading to syncope. Drug exposure in pediatric patients may be accidental or intentional, and the responsible agent may be a prescribed medication or an illicit substance. Therefore, the clinician must take a thorough history to include the medications of relatives, environmental exposures, and participation in illicit drug use by older children and adolescents.</ce:para></ce:section><ce:section id="cesec23" view="all"><ce:section-title>Metabolic Abnormality</ce:section-title><ce:para view="all" id="para.0215">Serum metabolic abnormalities may result in syncope but are frequently associated with other symptoms or a syndrome of presyncope. Hypoglycemia, which can be a component of several childhood disorders, including diabetes mellitus, ketotic hypoglycemia, and hepatic enzyme deficiencies, is usually a gradual cause of syncope associated with symptoms of hunger, tachycardia, diaphoresis, and weakness. Unconsciousness because of hypoglycemia can be prolonged and usually requires the administration of glucose for recovery. Hypoglycemia, in addition to some other metabolic causes of syncope, such as hypoxia, results from a deficiency of the metabolic substrates used by the brain. Some metabolic abnormalities, such as hyperammonemia, can cause syncope by direct cytotoxic effects in the central nervous system.<ce:cross-ref refid="bib2"><ce:sup loc="post">2</ce:sup></ce:cross-ref></ce:para></ce:section><ce:section id="cesec24" view="all"><ce:section-title>Hyperventilation</ce:section-title><ce:para view="all" id="para.0220">Hyperventilation is frequently associated with highly emotional circumstances during which the patient complains of dyspnea, shortness of breath, and chest discomfort. Other nonrespiratory symptoms include lightheadedness, dizziness, paresthesias, and visual disturbances. Hyperventilation is more common in adolescents than younger children and is frequently associated with unrecognized anxiety. The proposed mechanism involves hypocapnia and cerebral vasoconstriction resulting in ischemia. The diagnosis of hyperventilation is usually not obvious to the patient, who is unaware of a change in respiratory rate and volume. The symptoms of hyperventilation, however, can frequently be reproduced during the office visit to avoid extensive diagnostic tests.</ce:para></ce:section><ce:section id="cesec25" view="all"><ce:section-title>Situational Syncope</ce:section-title><ce:para view="all" id="para.0225">Several specific circumstances have been associated with syncope and are not well defined: micturition, defecation, cough, and swallow. The most commonly affected pediatric patients are those with obstructive lung disease, specifically cystic fibrosis. Cough can result in high intrathoracic pressures and an exaggerated Valsalva response. In addition, the high intrathoracic pressure can be transmitted to the subarachnoid space, which is thought to reduce cerebral blood flow. Swallow syncope is probably due to a dysfunction of the afferent-efferent loop between the brain stem and the heart. Afferent input from the esophagus leads to reflex stimulation of the central nervous system through the glossopharyngeal nerves, and efferent output results in bradycardia, atrioventricular block, or asystole. Situational syncope is not uncommon in pediatric patients, but care must be taken not to overlook a more potentially lethal cause.</ce:para><ce:para view="all" id="para.0230">Another form of situational syncope specific to pediatric medicine is adolescent stretch syncope. This phenomenon has been reported to be due to a combination of the Valsalva maneuver and neck hyperextension in patients with a familial tendency to faint.<ce:cross-ref refid="bib67"><ce:sup loc="post">67</ce:sup></ce:cross-ref> Other reports have demonstrated reductions in blood flow velocities by transcranial Doppler monitoring of the posterior cerebral arteries during neck hyperextension.<ce:cross-ref refid="bib82"><ce:sup loc="post">82</ce:sup></ce:cross-ref> In addition, angiography has shown evidence of extracranial compression of the craniocervical arteries.<ce:cross-ref refid="bib82"><ce:sup loc="post">82</ce:sup></ce:cross-ref> This form of syncope is noted to be rare and distinct, described only in adolescents. There is no specific therapy other than the identification and avoidance of neck hyperextension.</ce:para><ce:para view="all" id="para.0235">Finally, one other unique report<ce:cross-ref refid="bib45"><ce:sup loc="post">45</ce:sup></ce:cross-ref> described 15 children who developed syncope and convulsions during hair grooming. These episodes were all similar, with presyncopal symptoms, loss of consciousness, and collapse into a convulsion. The mechanism of syncope was not identified, but possible explanations included pain from hair pulling, scalp stimulation of the trigeminal nerve or cervical roots, or neck extension or flexion causing compression of carotid baroreceptors or vertebrobasilar blood flow. An editorial response<ce:cross-ref refid="bib94"><ce:sup loc="post">94</ce:sup></ce:cross-ref> described a cluster of young girls who developed brief, generalized seizures while having their hair groomed with a hot iron and hair gels. The lack of scalp burns and the history of “smelling something burning” immediately before the loss of consciousness suggested a noxious trigger for a vagal response causing syncope.</ce:para></ce:section><ce:section id="cesec26" view="all"><ce:section-title>Dysautonomia</ce:section-title><ce:para view="all" id="para.0240">Variable degrees of autonomic disregulation may result in an abnormality of heart rate or blood pressure control as an isolated or familial disorder. The familial dysautonomia, Riley-Day syndrome, is inherited in an autosomal recessive pattern predominantly in children of Ashkenazi Jewish ancestry. The reduction of neurons in sensory and autonomic ganglia is thought to be due to a lack of nerve growth factor during embryogenesis. The typical manifestations are frequently present from birth and include failure to thrive because of a poor suck and swallow, corneal injury and vision loss because of alacrima, developmental delay, temperature instability, aspiration pneumonia, sleep apnea and breath-holding spells, and seizures. Syncope may occur as a result of decreased cardiac output from inappropriate heart rate and blood pressure responses.</ce:para></ce:section><ce:section id="cesec27" view="all"><ce:section-title>Hysteria</ce:section-title><ce:para view="all" id="para.0245">Syncope caused by hysteria is most common in the adolescent patient. There are no neurologic (seizures), autonomic (pallor, diaphoresis), or cardiovascular (heart rate, blood pressure) changes associated with the episode. Characteristics of the clinical event are helpful in differentiating hysteria from other organic causes of syncope. The event usually occurs in the presence of an audience, is not dependent on posture, may be prolonged (up to 1 hour) despite recumbency, and rarely results in injury. The patient describes the event in a calm and indifferent manner and sometimes has recall of the surrounding environment, suggesting a lack of complete loss of consciousness.</ce:para></ce:section><ce:section id="cesec28" view="all"><ce:section-title>Carotid Sinus Hypersensitivity</ce:section-title><ce:para view="all" id="para.0250">An exaggerated response of the baroreceptor of the carotid sinus may result in a cardioinhibitory response, a vasodepressor response, or a mixed response of both bradycardia and hypotension. Stimulation of the carotid body may occur by direct massage, turning of the head to one side, a tight collar, or other triggering postures. The syndrome is rare in pediatric patients but can occur in adolescents. Unusual reports in adolescent patients include a 17-year-old boy who lost consciousness during wrestling matches,<ce:cross-ref refid="bib4"><ce:sup loc="post">4</ce:sup></ce:cross-ref> a 14-year-old boy who developed syncope on application of a cervical extraoral orthodontic device,<ce:cross-ref refid="bib1"><ce:sup loc="post">1</ce:sup></ce:cross-ref> and another 14-year-old with a history of rheumatic fever and mitral stenosis who became bradycardic, dizzy, and pale when pressure was applied to the right carotid sinus.<ce:cross-ref refid="bib93"><ce:sup loc="post">93</ce:sup></ce:cross-ref> Pathologic conditions that are known to include carotid sinus hypersensitivity include glossopharyngeal and trigeminal neuralgias and tumors of the head and neck. There is usually a high rate of spontaneous remission of symptoms, but patients with persistent symptoms should avoid any triggering activities. Patients with the cardioinhibitory type of carotid sinus syndrome are candidates for cardiac pacing, whereas those with the vasodepressor type may benefit from mineralocorticoids or anticholinergic agents.</ce:para></ce:section></ce:section><ce:section id="cesec29" view="all"><ce:section-title>Neurocardiogenic Syncope</ce:section-title><ce:para view="all" id="para.0255">Neurocardiogenic syncope, also referred to as neurally mediated syncope and vasovagal syncope, is the most common cause for syncope in children.<ce:cross-ref refid="bib71"><ce:sup loc="post">71</ce:sup></ce:cross-ref> It is a constellation of signs and symptoms beginning with a prodrome lasting several seconds to minutes, progressing to a brief period of unconsciousness, and ending with arousal to a previous level of alertness. The episode may be initiated by one of many provocative events that is usually an emotional stress, such as fear, anxiety, pain, phlebotomy, and the sight of blood. In addition, several physical states are known precipitators, including anemia, dehydration, hunger, recent illness, physical exhaustion, and crowded and poorly ventilated confines.<ce:cross-ref refid="bib71"><ce:sup loc="post">71</ce:sup></ce:cross-ref> The premonitory symptoms, which are frequently due to autonomic activity, may include lightheadedness, dizziness, nausea, shortness of breath, pallor, diaphoresis, and visual changes (decreased acuity, tunnel vision, or double vision). Neurocardiogenic syncope is likely to occur when two conditions hold: (1) a physical injury or threat that is unfamiliar or one that previously caused syncope and (2) an injury or threat that occurs under circumstances requiring equanimity or courage.<ce:cross-ref refid="bib15"><ce:sup loc="post">15</ce:sup></ce:cross-ref></ce:para><ce:para view="all" id="para.0260">There are three clinically recognized patterns of neurocardiogenic syncope: (1) vasodepressor type, primarily marked hypotension; (2) cardioinhibitory type, primarily marked bradycardia; and (3) mixed type, a combination of both vasodepressor and cardioinhibitory types. The mechanism of neurocardiogenic syncope is probably related to decreased systemic venous return commonly encountered on assuming an upright posture and an excessive stimulation of cardiac vagal fibers because of decreased ventricular filling. In patients with neurocardiogenic syncope, adaptive mechanisms are unsuccessful, the central venous pressure remains low, and sympathetic activation results in an increase in circulating catecholamines. This results in forceful myocardial contractions and mechanoreceptor stimulation in the setting of a diminished left ventricular end-diastolic volume. The mechanoreceptors respond to stretch and cause a paradoxic withdrawal of sympathetic activity, as would normally be expected during stretch receptor stimulation in hypertension or hypervolemia. This reflexive withdrawal of sympathetic vasoconstrictor activity results in hypotension, while simultaneously enhanced parasympathetic activity results in profound bradycardia. Immediately before syncope, there is evidence of increased sympathetic activity and decreased vagal activity demonstrated by an increased heart rate and blood pressure.</ce:para><ce:para view="all" id="para.0265">Vasodepressor syncope associated with exercise is well described in pediatric patients<ce:cross-refs refid="bib8 bib34"><ce:sup loc="post">8,34</ce:sup></ce:cross-refs> and occurs most commonly immediately after the termination of activity. Calkins and associates<ce:cross-ref refid="bib8"><ce:sup loc="post">8</ce:sup></ce:cross-ref> reported a series that included 12 adolescent patients who developed exercise-related syncope with typical prodromal symptoms and a positive head-upright tilt test alone or with isoproterenol. Treatment with atenolol, disopyramide, or a combination of the two medications was successful in preventing recurrent syncope or a response to repeat head-upright tilt testing in the six adolescent patients who received therapy. Therefore, athletes with exercise-related vasodepressor syncope can be treated to avoid recurrent events and may safely continue to participate in athletics.<ce:cross-ref refid="bib8"><ce:sup loc="post">8</ce:sup></ce:cross-ref></ce:para><ce:para view="all" id="para.0270">Prognostically, neurocardiogenic syncope is considered a benign illness. In most cases, a prophylactic approach is taken to prevent symptoms of presyncope or near-syncope. Frequently, patient education results in more rapid symptom recognition allowing the patient to assume a recumbent position and abort a potential syncopal event. Other simple prophylactic measures include the avoidance of dehydration, encouragement of a salt-enriched diet, and use of mineralocorticoids to induce salt and water retention. If these therapies are unsuccessful, medical management can be directed at breaking the cycle of events that results in syncope. Beta-adrenergic receptor blockade is a commonly used strategy, which attempts to decrease the mechanical stimulation of the cardiac mechanoreceptors. Some patients have had a favorable response to disopyramide, which acts as an anticholinergic, negative inotropic, and vasoconstrictive agent. Direct alpha-adrenergic receptor stimulation and stimulation of peripheral norepinephrine release by ephedrine and etilefrine have had some benefit. Finally, some reports cite the use of atrioventricular sequential pacing in reducing the magnitude of hypotension but not preventing the symptoms associated with neurocardiogenic syncope. Therefore, pacemaker implantation is reserved for refractory cases when aggressive pharmacologic trials have failed.</ce:para></ce:section></ce:section><ce:section id="cesec30" view="all"><ce:section-title>DIAGNOSTIC EVALUATION</ce:section-title><ce:para view="all" id="para.0275">Pediatric syncope is a common clinical problem that requires a thorough diagnostic investigation to ensure the detection of potentially life-threatening diagnoses and the provision of accurate prognostic information. A thorough history is frequently the most important part of the evaluation. The pediatric patient may often not be able to provide a complete or specific history. In those cases, however, parents, relatives, and teachers can frequently contribute important clues to the cause of the syncopal event. Many of the diagnoses mentioned previously can almost certainly be confirmed or excluded by the history. Breath-holding spells have a characteristic presentation during which a toddler begins crying in response to a sudden emotional insult, becomes apneic and cyanotic, and then has a short syncopal and limp period followed by arousal and a normal level of consciousness. The typical signs and symptoms experienced by the adolescent who has an episode of neurocardiogenic syncope include the setting of an acute illness, mild dehydration, or an emotional event, associated with a prodrome of nonspecific symptoms (headache, nausea, dizziness, diaphoresis, and chest discomfort). The absence of an injury following a fall with the syncopal event helps to support either hysteria or neurocar-diogenic syncope. Finally, the pediatric history is incomplete without the details of a family history, which should specifically include sudden death, syncope, sudden infant death syndrome (SIDS), congenital heart disease, seizures, and deafness.</ce:para><ce:para view="all" id="para.0280">The pediatric physical examination should include all of the components of the routine adult examination except they may occur in a different order or priority to accommodate the anxious or fearful child. Vital signs should include blood pressures recorded in both the supine and the standing positions from the right upper extremity and a lower extremity. Careful attention to the presence of pathologic cardiac clicks, gallops, or murmurs could identify a specific cardiac abnormality.</ce:para><ce:para view="all" id="para.0285">An ECG should be included with all initial evaluations for syncope in children. Items that require special attention include (1) the Q-T interval and T-wave morphology for evidence of congenital long Q-T syndrome, (2) voltage criteria consistent with ventricular hypertrophy for evaluation of obstructive outflow lesions, (3) manifest preexcitation of the Wolff-Parkinson-White syndrome, and (4) ectopy and conduction disturbances. The patient with a normal ECG but a history suspicious for an arrhythmia is a good candidate for a 24-hour ambulatory Holter monitor. This test is indicated for detection of frequently episodic paroxysmal supraventricular or ventricular tachycardia, intermittent preexcitation of Wolff-Parkinson-White syndrome, overall rate trends for patients with automatic tachyarrhythmias or sinus node dysfunction, and atrioventricular block. For the patient with less frequent episodic symptoms, an event monitor is a more appropriate test in which the patient can initiate a recording at the time of recognizable symptoms.</ce:para><ce:para view="all" id="para.0290">Additional diagnostic tests depend on the history and physical examination, the certainty of the clinical diagnosis, and occasionally the level of anxiety of the patient and parents. Sometimes, few, if any, diagnostic tests are necessary. The child or adolescent who faints, however, does require a more significant cardiovascular workup if any of the following conditions exist: (1) exercise-induced syncope that occurs during exertion, (2) chest pain that precedes the faint, (3) seizure activity, (4) atypical faint (nonvasodepressor), (5) recurrent syncope (more than two or three times), or (6) abnormal cardiac examination.<ce:cross-ref refid="bib66"><ce:sup loc="post">66</ce:sup></ce:cross-ref> Each diagnostic test should be requested with a specific question in mind. Unfortunately, sometimes the clinician is not directed in any particular direction because of either a vague or nonspecific history and physical examination, and a more extensive workup is required.</ce:para><ce:para view="all" id="para.0295">Phlebotomy for determination of serum laboratory values is easily obtained and relatively inexpensive. The most routine tests include a blood glucose and hemoglobin. A patient suspected of an ingestion or participation in illicit drug use should have serum and urine toxicology screens performed. An echocardiogram may be a helpful diagnostic test for the recognition of aortic stenosis, hypertrophic cardiomyopathy, dilated myopathy, Ebstein's anomaly in patients with Wolff-Parkinson-White syndrome, mitral valve prolapse, anomalous coronary artery, right ventricular dysplasia, cardiac tumors, or residual obstructive disease following cardiac surgery.</ce:para><ce:para view="all" id="para.0300">The utility of tilt-table testing in pediatric patients remains controversial for the diagnosis of neurocardiogenic syncope. The head-upright tilt-table test came into clinical use during the last decade as a method for evaluating patients with syncope of an unknown cause. Although pediatric studies have different outcomes than those of adult studies, concern persists regarding the sensitivity and specificity of the test. The head-upright tilt-table test appears to be more specific but less sensitive in young patients. Several groups<ce:cross-refs refid="bib17 bib44 bib77"><ce:sup loc="post">17,44,77</ce:sup></ce:cross-refs> have demonstrated sensitivities from 43% to 57% and specificities from 83% to 100% in children and adolescents. Responses of symptomatic patients to the head-upright tilt test were compared to similar healthy control subjects during protocols using tilt angles of 60 to 90 degrees and durations from 12 to 60 minutes. The addition of an isoproterenol infusion appears to enhance the rate of positive outcomes during tilt-table studies to 70% to 80%.<ce:cross-refs refid="bib26 bib68 bib86"><ce:sup loc="post">26,68,86</ce:sup></ce:cross-refs> One study that addressed the effect of isoproterenol reported an increase in sensitivity to 77% and no change in specificity from baseline.<ce:cross-ref refid="bib5"><ce:sup loc="post">5</ce:sup></ce:cross-ref> The poor specificity (48%) at baseline in this study, however, may not truly assess the effect of isoproterenol. The same study also suggested that the duration of the head-upright tilt may help differentiate between false-positive and true-positive responses. An additional concern was proposed by de Jong and colleagues,<ce:cross-ref refid="bib12"><ce:sup loc="post">12</ce:sup></ce:cross-ref> who reported a high incidence of near-fainting after simple intravenous line placement in pediatric patients. Overall, head-upright tilt testing may be of some value in pediatric patients, but caution must be used in interpreting results with isoproterenol because intravascular instrumentation and provocative agents may decrease specificity.</ce:para><ce:para view="all" id="para.0305">Because hypotension, bradycardia, and symptoms can be provoked by upright tilt testing in people without a history of syncope, the authors have adopted a cautious institutional use of the upright tilt test by first excluding other more life-threatening diagnoses and then using the head-upright tilt-table study only as supportive data in making the diagnosis of neurocardiogenic syncope. This is a particularly important issue in patients with exercise-induced syncope because a missed diagnosis of myocarditis, long Q-T syndrome, or hypertrophic cardiomyopathy may have fatal consequences. Exercise-related neurocardiogenic syncope usually occurs immediately after an activity, so that patients who lose consciousness during exercise should be carefully evaluated for specific cardiac pathology.</ce:para><ce:para view="all" id="para.0310">In light of the rising cost of health care and the need to contain costs, the clinician must be mindful of the utility and expense of diagnostic studies that are used to evaluate syncope. Health care cost containment should emphasize the importance of a detailed history and complete physical examination. One study<ce:cross-ref refid="bib24"><ce:sup loc="post">24</ce:sup></ce:cross-ref> that reported the expenses related to a syncope workup in pediatric patients in 1987 found an average cost per patient of $1060. Among the 73 pediatric patients, 443 tests were ordered, and 18 (4%) showed abnormal results. This appears directly related to the fact that 44 (60%) of the patients were diagnosed with <ce:italic>unknown etiology</ce:italic> or <ce:italic>vasovagal reaction,</ce:italic> neither of which has a good, specific diagnostic test available. This and other studies<ce:cross-refs refid="bib24 bib35"><ce:sup loc="post">24,35</ce:sup></ce:cross-refs> support the notion that when the case is not obvious from the initial history and physical examination, detailed, expensive tests are often performed that frequently afford little additional diagnostic information.</ce:para></ce:section><ce:section id="cesec31" view="all"><ce:section-title>CONCLUSION</ce:section-title><ce:para view="all" id="para.0315">Syncope is a common pediatric problem and usually has a benign, neurally mediated cause. 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contentType="CDATA"><title>SYNCOPE IN THE PEDIATRIC PATIENT</title></titleInfo><name type="personal"><namePart type="given">Ronn E.</namePart><namePart type="family">Tanel</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Cardiology, Children's Hospital; and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Edward P.</namePart><namePart type="family">Walsh</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Cardiology, Children's Hospital; and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1997</dateIssued><copyrightDate encoding="w3cdtf">1997</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Syncope during childhood is common. A variable incidence has been reported, from 1 of 2000 emergency department visits,71 to 47% of interviewed college students.61 Driscoll and colleagues14 reported an overall incidence of 125 of 100,000 (0.125%) for pediatric patients seeking medical attention. Girls were seen for evaluation more commonly than boys, with the peak incidence occurring between ages 15 and 19 years. Despite its frequency, syncope generates an extraordinary amount of anxiety among patients, families, teachers, coaches, and physicians.In children and adolescents, the list of causes is generally similar to that described for adults, although the relative frequency and prognosis for the individual diagnoses are somewhat unique. Fortunately, most syncopal events in young patients are isolated and benign in nature. Driscoll's data14 revealed an association of sudden death and prior syncopal events that was not different from that of sudden death in the general population. This article describes the causes, diagnosis, and treatment of syncope in infants, children, and adolescents, focusing on the differences that must be identified when caring for the pediatric versus adult patient. Recommendations are presented for an economically efficient diagnostic workup and practical approach to treatment.</abstract><note>Address reprint requests to Ronn E. Tanel, MD, Department of Cardiology, Children's Hospital, 300 Longwood Avenue, Boston, MA 02115</note><note>RET is currently supported by a research fellowship from the American Heart Association, Massachusetts Affiliate, Inc.</note><note type="content">Figure 1: A, A 12-lead ECG showing ventricular tachycardia at a rate of 226 beats per minute. This patient has Belhassen's tachycardia. Note the typical right bundle-branch pattern with a superior QRS axis. The ECG is recorded at half-standard amplitude. B, A 12-lead ECG showing sinus rhythm with salvos of slow ventricular tachycardia. The arrhythmia is due to an abnormal automatic focus in the right ventricular outflow tract. This is supported by the left bundle-branch pattern and inferior QRS axis.</note><note type="content">Figure 2: A, Supraventricular tachycardia in Wolff-Parkinson-White syndrome resulting from antegrade conduction over the atrioventricular node (AVN) and retrograde conduction over the accessory pathway (AP) yielding a normal narrow QRS complex. B, Supraventricular tachycardia in Wolff-Parkinson-White syndrome occurring in the reverse direction, antegrade over the AP and retrograde over the AVN. This results in a wide QRS complex. SAN = sinoatrial node.</note><note type="content">Figure 3: A 12-lead ECG from a newborn with congenital long Q-T syndrome. Note the sinus bradycardia and Q-Tc of 650 msec.</note><note type="content">Figure 4: Ambulatory Holter monitor recording from a patient with long Q-T syndrome. The recording shows sinus rhythm with ventricular premature beats followed by the induction of a polymorphic ventricular tachycardia (torsades de pointes).</note><note type="content">Figure 5: Ambulatory Holter monitor recording from a postoperative patient with electrocardiographic findings of sinus node dysfunction. The first beat is a conducted sinus beat followed by a sinus pause with a junctional escape beat. The fourth beat is an atrial premature beat followed by sinus arrest with another junctional escape beat.</note><note type="content">Figure 6: Ambulatory Holter monitor recording from a patient with congenital complete atrioventricular block. The ventricular rate is 45 beats per minute, and the sinus rate is 108 beats per minute. P = P wave; R = QRS complex.</note><note type="content">Table 1: CAUSES OF SYNCOPE</note><note type="content">Table 2: DIAGNOSTIC CRITERIA FOR LONG Q-T SYNDROME</note><relatedItem type="host"><titleInfo><title>Cardiology Clinics</title></titleInfo><titleInfo type="abbreviated"><title>CCL</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">19970501</dateIssued></originInfo><identifier type="ISSN">0733-8651</identifier><identifier type="PII">S0733-8651(05)X7022-9</identifier><part><date>19970501</date><detail type="volume"><number>15</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>165</start><end>339</end></extent><extent unit="pages"><start>277</start><end>294</end></extent></part></relatedItem><identifier type="istex">72B4D003078254DE56EB523B535252BFB6227AD3</identifier><identifier type="DOI">10.1016/S0733-8651(05)70336-2</identifier><identifier type="PII">S0733-8651(05)70336-2</identifier><identifier type="ArticleID">70336</identifier><accessCondition type="use and reproduction" contentType="">© 1997W. B. Saunders Company</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>W. B. 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