Emergency evaluation of syncope in children and adolescents

INTRODUCTION — This topic will review the evaluation and diagnostic approach for syncope in pediatric patients.

The causes of syncope in children and the evaluation of adults with syncope are discussed separately. (See "Causes of syncope in children and adolescents" and "Approach to the adult patient with syncope in the emergency department".)

DEFINITION AND CAUSES — Syncope is a sudden, brief loss of consciousness associated with loss of postural tone from which recovery is spontaneous [1]. Approximately 15 percent of children experience a syncopal episode prior to the end of adolescence [2].

Syncope is a symptom that can be classified according to the underlying cause: autonomic (eg, vasovagal [neurocardiogenic], situational, and orthostatic syndromes), cardiac, metabolic, or a condition that mimics syncope (table 1). Based upon case series of pediatric patients evaluated in the emergency department setting, autonomic forms comprise up to 80 percent of cases [3-6]. Neurologic etiologies, such as seizures or migraine headaches, are present in up to 20 percent of patients. Life-threatening conditions such as hypoglycemia, heat illness, anaphylaxis, cardiac arrhythmia, or structural cardiac disease are relatively rare but occur frequently enough (1 to 2 percent of children) to warrant diagnostic consideration.

Causes of syncope and paroxysmal conditions that mimic syncope are discussed in more detail separately. (See "Causes of syncope in children and adolescents" and "Nonepileptic paroxysmal disorders in infancy" and "Nonepileptic paroxysmal disorders in children".)

EVALUATION — The goal of the evaluation of a child with syncope is to identify life-threatening conditions, as well as conditions that are associated with the risk of significant injury. A cardiac etiology for syncope is particularly important to identify. In most children, cardiac syncope is suggested by a careful history (including a detailed family history), physical examination, and electrocardiogram (ECG) and is a rare etiology for pediatric syncope (table 2) [7-10]:

●In a prospective, multicenter observational study of over 1200 patients undergoing a standardized ambulatory evaluation by a pediatric cardiologist, 85 percent of patients were diagnosed with typical syncope based upon history, physical examination, and electrocardiogram (ECG) [11]. One patient was identified with cardiac syncope caused by hypertrophic cardiomyopathy. This patient also had exercise-induced syncope and abnormal findings on ECG.

●In one retrospective series describing 480 children with a chief complaint of syncope, 21 of 22 patients with a cardiac cause were identified by a pediatric cardiologist using a combination of history, physical examination, and ECG [12]. Echocardiography was not diagnostic in any of these patients.

History — A careful history is often the most useful tool for identifying an etiology and directing further evaluation of a syncopal event [6,9,10,13].

Preceding events or precipitating factors — The circumstances immediately preceding the event should be identified. These include the child's position and the activity in which the child was engaged.

The following findings are of particular importance (table 2):

●Exercise – Syncope that occurs during physical exertion is concerning for a cardiac etiology and warrants evaluation. However, vasovagal syncope remains a common etiology in these patients [5,8,14-17]. (See "Suspected heart disease in infants and children: Criteria for referral", section on 'Timing of referral'.)

●Acute arousal or loud noise – Some triggers are associated with specific primary electrical disturbances. As an example, for patients with long QT syndrome, the triggers for the most common genotypes are acute arousal (or startle) and auditory stimuli (ie, a fire alarm) [18].

●Postural changes – Children with a vasovagal cause of syncope typically have been upright (prolonged standing or taking a hot shower) or changed position (eg, went quickly from lying or sitting to standing) just prior to the event [5].

●Pain, or emotional stress – A trigger (such as pain [eg, blood draw or intramuscular injection] or emotional stress) may be the precipitant in some cases of vasovagal syncope [5]. However, rarely, children with familial catecholaminergic polymorphic ventricular tachycardia can also develop arrhythmias in association with emotional or physical stress. (See "Causes of syncope in children and adolescents", section on 'Arrhythmias (primary electrical disturbances)' and "Catecholaminergic polymorphic ventricular tachycardia".)

Description of the event — A description of the event should include the child's report of symptoms prior to the onset of syncope, as well as witnesses' description of the syncopal event itself. Vital signs should be noted during and immediately after the event if possible.

Important features to elicit include (table 2) [6]:

●Palpitations or chest pain prior to or during a syncopal event are concerning for a cardiac etiology [8]. These symptoms occasionally occur with vasovagal syncope as well.

●Loss of consciousness followed by abnormal motor activity (ie, tonic clonic movement or posturing) can occur at the end of a syncopal event, and most often correlates with neurocardiac syncope [13] although arrhythmia should also be suspected [19]. The duration of such activity is usually brief, and recovery is rapid.

●Motor activity that starts at the beginning of the event and is followed by a prolonged recovery time is more consistent with a seizure [20]. By contrast, "convulsive syncope" is characterized by brief (usually less than 20 seconds) motor activity, including tonic extension of the trunk and limbs or several clonic jerks, followed by quick recovery of consciousness, and is nonepileptic. (See "Nonepileptic paroxysmal disorders in adolescents and adults", section on 'Syncope'.)

●Patients with orthostatic hypotension or vasovagal syncope may report that symptoms recurred when they tried to sit up immediately after the initial syncopal event.

●Children with vasovagal (neurocardiogenic) syncope frequently report prodromal symptoms that include dizziness, lightheadedness, sweating, nausea, weakness, and visual changes (blurred vision, tunnel vision, slow visual loss).

●Children with vasovagal syncope may experience fatigue for hours after the event.

●Loss of bowel and/or bladder function is more commonly seen with seizures

Past medical history — A past medical history of congenital heart disease (corrected or uncorrected), acquired heart disease with residual cardiac dysfunction (eg, Kawasaki disease, rheumatic heart disease, or myocarditis) or arrhythmia should immediately focus attention on a potentially serious cardiac etiology (table 2) [6].

Previous syncopal events suggest a vasovagal, psychogenic cause, or (less commonly) a cardiac etiology [5].

Other elements of the history that suggest a specific etiology include the following:

●Significant medical problems associated with hypoglycemia (ie, diabetes mellitus)

●A menstrual history (pregnancy or anemia in the menstruating female)

●Access to medications or illicit drugs (substance abuse)

Family history — A family history in parents, siblings, grandparents or other first or second degree relatives of any of the following increases the concern for a cardiac etiology (table 2) [6,14]:

●Early cardiac death (<50 years of age)

●Sudden deaths including unexplained accidents involving a single motor vehicle or drowning

●Known arrhythmia (eg, long or short QT syndromes or Brugada syndrome)

●Familial cardiomyopathy

A family history of vasovagal syncope may be present in up to 90 percent of children with this condition and can be reassuring if no other red flag clinical findings are present [20].

Physical examination — A complete physical examination should be performed, including vital signs (with orthostatic pulse and blood pressure measurements) and cardiac and neurologic examinations [9,10].

Measurements of blood pressure and heart rate to identify orthostatic hypotension should be taken while the patient is sitting, then after standing for three minutes. Abnormal values include a decrease in systolic blood pressure by 10 mmHg or an increase in heart rate by 20 beats per minute from sitting to standing. A marked increased in heart rate (40 beats per minute or greater) is consistent with postural orthostatic tachycardia syndrome. However, the recurrence of symptoms, such as light-headedness or even syncope on standing, is more significant than any numeric change in blood pressure. The presence of orthostatic hypotension does not rule out other causes of syncope, particularly long QT syndrome [21].

Cardiac auscultation should assess the quality of heart sounds, evidence of gallops, rubs, and presence of murmurs, especially those that suggest an outflow obstruction.

Findings specific for a structural lesion include the following (table 2):

●The characteristic findings of aortic stenosis include a systolic ejection murmur and ejection click. (See "Valvar aortic stenosis in children".)

●In patients with coarctation, a difference in upper and lower extremity systolic blood pressures 20 mmHg or more (arm >leg) may be present and may also be suggested by a difference in pulse intensity between radial or brachial and femoral pulses. Thus, in patients with systemic hypertension or with findings suggesting aortic stenosis (sometimes associated with coarctation), four extremity blood pressures should be measured. (See "Clinical manifestations and diagnosis of coarctation of the aorta", section on 'Blood pressure and pulses'.)

●In patients with hypertrophic cardiomyopathy, maneuvers that affect the degree of obstruction cause a change in murmur intensity.

•An increase in intensity, due to enhancement of obstruction, is seen with the assumption of an upright posture from a squatting, sitting, or supine position, or with the Valsalva maneuver, during the more forceful contraction that follows the compensatory pause after a premature ventricular complex/contraction (PVC; also referred to as premature ventricular beats or premature ventricular depolarizations). (See "Physiologic and pharmacologic maneuvers in the differential diagnosis of heart murmurs and sounds".)

•A decrease in intensity, due to attenuation of obstruction, is heard after going from a standing to a sitting or squatting position, with sustained gripping of the hand, and following passive elevation of the legs.

•The classic murmur of hypertrophic cardiomyopathy is an outflow murmur that decreases in intensity with increased venous return to the heart (during a Valsalva maneuver or squatting).

●Signs of heart failure (ie, rales, a gallop, and/or hepatomegaly) are consistent with cardiac disease.

An age-appropriate neurologic exam should be performed to identify focal deficits. (See "Detailed neurologic assessment of infants and children", section on 'Neurologic examination'.)

Ancillary studies — History of the event and physical examination findings should be used to guide ancillary studies.

Electrocardiogram — The electrocardiogram (ECG) is widely considered an essential part of the syncope work up, despite its low diagnostic yield [9,10,22,23]. A patient with syncope not precipitated by exertion and a normal ECG has a low likelihood of arrhythmia as a cause of syncope [1].

However, ECG abnormalities may be variable and/or subtle [11,24]. Consequently, a cardiologist should be consulted whenever there are worrisome clinical features regardless of the ECG findings. If the ECG is normal at the initial evaluation, pediatric patients who may require a more extensive cardiac evaluation (ie, additional ECG monitoring, echocardiography, or a stress test) can generally be referred to a cardiologist for an outpatient evaluation. (See 'Indications for referral or admission' below.)

In patients with syncope, incidental findings occur in approximately 10 percent of ECGs and abnormal findings caused by important cardiac pathology are seen in <1 percent of cases [11].

ECG findings that should be noted include (table 2):

●Nonsinus rhythms, excessive bradycardia, atrioventricular block, and abnormal age-appropriate intervals of the cardiac cycle (hand calculated) (waveform 1) (see "ECG tutorial: Basic principles of ECG analysis")

●Signs of myocardial injury (see "Electrocardiogram in the diagnosis of myocardial ischemia and infarction")

●A corrected QT interval (hand calculated: QTc = QT interval ÷ √RR interval [in sec]), with attention to T wave morphology (calculator 1) (see "Congenital long QT syndrome: Diagnosis", section on 'General ECG principles')

●Findings suggestive of Brugada syndrome, including pseudo-right bundle branch block (RBBB) and persistent ST segment elevation in leads V1 to V3 (waveform 2)

●Delta wave or other findings suggestive of ventricular preexcitation (Wolff-Parkinson-White syndrome) (waveform 3) (see "ECG tutorial: Preexcitation syndromes")

●Several abnormalities, most notably epsilon waves, may be present in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) (waveform 4) (see "Arrhythmogenic right ventricular cardiomyopathy: Diagnostic evaluation and diagnosis")

●Findings indicative of hypertrophic cardiomyopathy including left axis deviation; prominent abnormal Q waves, especially inferior leads (II, III, aVF); left atrial or bilateral atrial enlargement, especially with left ventricular hypertrophy; and/or deeply inverted T waves (“giant negative T waves”) in the mid-precordial leads (V₂ through V₄) (see "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation", section on 'Electrocardiography')

●Ventricular hypertrophy and strain patterns suggesting heart failure (waveform 5 and waveform 6) (see "Left ventricular hypertrophy: Clinical findings and ECG diagnosis" and "ECG tutorial: Chamber enlargement and hypertrophy")

Laboratory tests — The following laboratory tests may be helpful in some patients as follows [2,25,26]:

●Rapid blood glucose determination for children who present immediately after the episode

●Hematocrit for children who are at risk for anemia, including menstruating females

●Urine pregnancy tests in post menarcheal females

●Urine toxicology screens for drugs of abuse in patients with altered metal status

In the asymptomatic patient who presents hours to days after the event, extensive laboratory blood work such as serum glucose, electrolytes, and complete blood counts are rarely helpful. As an example, among 55 children who received 192 blood tests during evaluation for syncope in a pediatric neurology clinic, studies were helpful in only three individuals (5 percent); specifically glucose and thyroid function tests [13].

Other studies — Other studies are primarily indicated in patients with red flag findings for a cardiac etiology (table 2) or in whom neurologic findings raise concern for a space-occupying brain lesion, intracranial injury, or a seizure disorder.

●Cardiac studies – The following studies may be useful in selected patients but should be ordered by or in consultation with a pediatric cardiologist:

•Echocardiography – Emergency echocardiography should be reserved for those patients with a strongly suspected cardiac etiology due to the presence of red flag findings on history, physical examination, or ECG (table 2) [9]. In patients with a normal initial evaluation, a cardiac etiology is very unlikely and echocardiography is not indicated [6,11,12,27]. (See 'Evaluation' above.)

•Ambulatory ECG monitoring – Limited evidence suggests that ambulatory ECG monitoring has a low yield for children and adolescents with isolated syncope but may be useful in syncopal pediatric patients with palpitations, frequent syncopal episodes, or exertional syncope [6,11,28]. Among 75 children with isolated chest pain, presyncope, or syncope in one series, none had an identified arrhythmia compared with 8 percent of 420 patients with palpitations [28]. In a multicenter prospective observational study, none of the 124 patients who underwent ambulatory monitoring had results that explained the syncope [11].

•Exercise ECG or stress testing – Exercise ECG or exercise stress testing is potentially helpful to elicit characteristic changes in QT intervals in patients with long QT syndrome or arrhythmias in those with catecholaminergic polymorphic ventricular tachycardia (isolated preventricular contractions at a heart rate of about 130 beats per minute progressing to couplets and then polymorphic ventricular tachycardia as the heart rate increases) [6]. (See "Congenital long QT syndrome: Diagnosis", section on 'Exercise testing'.)

•Tilt table testing – Tilt table testing has low sensitivity (65 to 75 percent) but reasonable specificity (90 percent) for vasovagal syncope in children and adolescents [29]. Reproducibility within the same patient also varies. Thus, tilt testing is discouraged for patients with findings that suggest typical syncope [11]. However, tilt-testing is sometimes performed in those patients with frequent recurrent syncope or atypical syncope with otherwise negative cardiac evaluation and testing [9]. Although head up tilt testing is sometimes used to support the diagnosis of postural tachycardia syndrome (POTS), findings of excessive tachycardia (eg, ≥40 beats/min) before fainting does not always distinguish POTS from vasovagal syncope in children. POTS is a constellation of clinical findings and requires more than a heart rate change to make the diagnosis [30,31]. (See "Postural tachycardia syndrome", section on 'Diagnostic approach'.)

●Neuroimaging – For most pediatric patients with syncope, neuroimaging is not necessary [6,13] with the exception of the unusual child or adolescent with syncope and focal neurologic deficits, persistently altered mental status, or a significant head injury as the result of the syncopal episode. (See "Seizures and epilepsy in children: Clinical and laboratory diagnosis" and "Minor blunt head trauma in infants and young children (<2 years): Clinical features and evaluation", section on 'Approach'.)

●Electroencephalogram (EEG) – An elective outpatient EEG is appropriate for patients with syncope accompanied by prolonged loss of consciousness, seizure activity, and a postictal phase. However, epilepsy is a rare cause of syncope [13].

DIAGNOSTIC APPROACH — A systematic approach to the emergency evaluation of syncope (including a focused history, careful cardiac and neurologic evaluations, and selected ancillary studies) can identify a cause for most children (table 1 and algorithm 1 and table 2) [32].

Prolonged loss of consciousness — Patients who were unconscious for more than several seconds should be evaluated for a neurologic disorder, such as a seizure or migraine syndrome. (See "Causes of syncope in children and adolescents", section on 'Conditions that mimic syncope'.)

Transient loss of consciousness — Syncope with transient loss of consciousness may be caused by a variety of conditions. Careful history, physical examination, and limited ancillary studies are typically sufficient to identify the underlying etiology.

Abnormal cardiac evaluation — Most children with a cardiac cause of syncope can be identified by a combination of historical features, cardiac examination, and ECG findings (table 2) [12,33].

Abnormal ECG — Abnormal findings on ECG, that can sometimes be subtle, may identify conditions that can cause ventricular arrhythmias (table 2). (See 'Ancillary studies' above.)

These include the following:

●A prolonged QT interval is consistent with the diagnosis of acquired or congenital long QT syndrome (waveform 7) (calculator 1). (See "Congenital long QT syndrome: Epidemiology and clinical manifestations" and "Acquired long QT syndrome: Definitions, pathophysiology, and causes".)

●A short QT interval (QTc ≤0.30 sec) suggests congenital short QT syndrome. (See "Congenital long QT syndrome: Diagnosis", section on 'General ECG principles'.)

●Findings suggestive of Brugada syndrome, including pseudo-RBBB and persistent ST segment elevation in leads V1 to V3 (waveform 2). (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".)

●Findings suggestive of preexcitation syndrome indicate the diagnosis of Wolff-Parkinson-White syndrome (waveform 3). (See "Clinical features and diagnosis of supraventricular tachycardia (SVT) in children".)

●Several abnormalities, most notably epsilon waves, may be present in patients with ARVC (waveform 4). ARVC is a progressive disorder, however, and these findings may not be present in young patients. (See "Arrhythmogenic right ventricular cardiomyopathy: Diagnostic evaluation and diagnosis".)

Other diagnoses that may be suggested by ECG findings include the following:

●Signs of left ventricular hypertrophy or strain are consistent with hypertrophic cardiomyopathy (waveform 5). (See "Left ventricular hypertrophy: Clinical findings and ECG diagnosis" and "ECG tutorial: Chamber enlargement and hypertrophy".)

●Right ventricular hypertrophy can occur with tetralogy of Fallot or primary pulmonary hypertension (waveform 6). (See "Treatment and prognosis of pulmonary arterial hypertension in adults (group 1)" and "Pulmonary hypertension with congenital heart disease: Clinical manifestations and diagnosis".)

●A pattern of myocardial injury may be seen with congenital coronary artery abnormalities. (See "Congenital and pediatric coronary artery abnormalities".)

●Bradyarrhythmias such as complete AV block can be identified on ECG (waveform 1). (See "Bradycardia in children".)

Abnormal cardiac examination — Children with known congenital heart disease may have abnormalities consistent with their diagnosis and/or surgical repair. Findings such as a systolic ejection murmur with ejection click (valvar aortic stenosis) or an outflow murmur that decreases in intensity with increased venous return to the heart during squatting or a Valsalva maneuver (hypertrophic cardiomyopathy) may indicate undiagnosed structural heart disease. (See 'Physical examination' above.)

Normal cardiac examination — Patients with a normal ECG and cardiac examination are unlikely to have a cardiac etiology for their syncopal episode. However, children with worrisome historical features still warrant further evaluation by a pediatric cardiologist (table 2). (See 'History' above.)

Features that help to further distinguish noncardiac causes of syncope include the duration of the episode, orthostatic changes in heart rate or blood pressure, abnormalities in laboratory studies, an abnormal respiratory pattern prior to the syncopal event, and inconsistencies between the history and physical examination.

Loss of consciousness for less than several seconds in a child with a normal ECG and cardiac examination likely represents noncardiac syncope. Clinical features and laboratory studies identify some specific causes for the syncopal event.

Vasovagal (neurogenic cardiac) syncope is usually diagnosed by the presence of consistent clinical features and the exclusion of other causes including:

●Abnormalities identified by laboratory tests that may explain syncope include hypoglycemia, pregnancy, and anemia. (See 'Laboratory tests' above.)

●Orthostatic hypotension is the likely etiology for syncope in patients with postural changes in heart rate and blood pressure and a normal ECG. The underlying cause of these changes (such as volume depletion or medications) must be identified and treated. (See "Causes of syncope in children and adolescents", section on 'Orthostatic hypotension'.)

Although orthostatic hypotension has also been associated with long QT syndrome, the ECG is abnormal in the vast majority of cases [21].

●A toxic exposure may be suggested by history (such as symptoms among other household members with carbon monoxide poisoning), blood or exhaled ethanol level, or a rapid urine toxicologic screen for drugs of abuse. (See "Causes of syncope in children and adolescents", section on 'Poisoning (agents with direct CNS effects)'.)

●A history of an abnormal respiratory pattern prior to the syncopal episode suggests hyperventilation or breath holding as the etiology. (See "Causes of syncope in children and adolescents", section on 'Conditions that mimic syncope' and "Causes of syncope in children and adolescents", section on 'Breath holding spells'.)

•Patients with hyperventilation are frequently adolescents experiencing some type of emotional stress. They may describe additional symptoms such as chest pain, lightheadedness, paresthesias, and visual disturbances.

•Breath holding spells occur in younger children (typically 6 to 24 months of age). Loss of consciousness develops in association with breath holding. A cardiac evaluation is indicated for children with a family history of syncope or sudden death or with episodes that are prolonged, frequent, or precipitated by startle or other nontraumatic stimuli.

●Patients with syncope related somatization or a conversion disorder are commonly seen in adolescents. Expected physiologic signs (such as sweating, pallor, or changes in heart rate and blood pressure) are often absent. In addition, patients may disclose details of the event that indicate no loss of consciousness and generally suffer no injury during collapse. (See "Causes of syncope in children and adolescents", section on 'Conditions that mimic syncope'.)

●Patients who engage in the choking game purposely attempt self-strangulation or allow strangulation by another person with the hands or a ligature to produce a euphoric state caused by cerebral hypoxia. The plan is to release the pressure just before loss of consciousness, but failure to do so can result in death, particularly when the game is played alone using ligatures. (See "The "choking game" and other strangulation activities in children and adolescents".)

●In the emergency evaluation of a child with syncope, a diagnosis of vasovagal (neurocardiogenic) syncope is typically a diagnosis of exclusion for patients with consistent clinical features (such as precipitating events and a prodrome). Children with concerning manifestations such as absence of a significant prodrome, associated palpitations or chest pain, or a family history of syncope or sudden death may require further cardiac evaluation.

INDICATIONS FOR REFERRAL OR ADMISSION — The overwhelming majority of children who have had a syncopal event from which they have completely recovered and have no red flags for cardiac syncope (table 2) can be followed as outpatients. Patients with recurrent vasovagal (neurocardiac) syncope that does not respond to empiric treatment with increased fluid and salt intake may warrant an elective pediatric cardiology consultation [6]. (See 'Treatment' below.)

Patients with a suspicion for cardiac syncope based upon history, physical examination, or electrocardiogram should undergo urgent consultation or referral to a pediatric cardiologist.

Consultation with a neurologist is warranted for children with findings suggestive of seizure by history or outpatient electroencephalogram, prolonged loss of consciousness and/or a history of focal neurologic abnormalities that have resolved.

Admission to the hospital for further evaluation and observation is rarely needed but may be warranted for patients with the following findings:

●Evidence of cardiovascular disease (ie, heart failure, arrhythmia or heart block)

●Persistent abnormal neurologic findings

●Orthostatic hypotension with continued postural syncope that does not resolve with fluid therapy

TREATMENT — The proper management of pediatric syncope requires appropriate recognition and treatment of the underlying cause (table 1).

For children and adolescents with vasovagal (neurocardiogenic) syncope, we suggest the following approach [6,29,32]:

●Increase oral intake of water to approximately 30 to 50 mL/kg per day (eg, 1.5 to 2.4 L in a 50 kg adolescent)

●Add salty snacks (eg, pretzels, pickles, or crackers)

●Avoid caffeinated beverages

●Perform techniques to prevent venous pooling, including keeping knees slightly bent when standing for a long time, isometric contraction of extremity muscles, toe raises, folding of the arms, and crossing of the legs

A large percentage of pediatric patients with vasovagal (neurocardiogenic) syncope may improve with this nonpharmacologic treatment. As an example, in a series of 58 patients, including children, adolescents, and young adults with neurocardiogenic syncope and a positive tilt test, oral fluids alone was associated with no further episodes in 90 percent of patients [34]. Thus, empiric initiation of this regimen in these children and adolescents at the initial evaluation and without referral to a pediatric cardiologist is a reasonable option [6].

Patients who continue to experience syncope despite adherence to increased fluid and salt intake warrant referral to a pediatric cardiologist for additional evaluation. (See 'Indications for referral or admission' above.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Syncope".)

SUMMARY AND RECOMMENDATIONS

●Definition – Syncope is a sudden, brief loss of consciousness associated with loss of postural tone from which recovery is spontaneous. (See 'Definition and causes' above.)

●Causes – Although the etiology of syncopal events in children and adolescents is most often benign, syncope can also occur as the result of more serious (usually cardiac) disease with the potential for sudden death (table 1). (See 'Definition and causes' above and "Causes of syncope in children and adolescents".)

●Diagnostic approach – An algorithmic approach to the emergency evaluation of the child with syncope is provided (algorithm 1). (See 'Diagnostic approach' above.)

A combination of historical features, physical examination, and ECG findings typically identifies children and adolescents with a life-threatening cardiac cause of syncope (table 2). These patients warrant urgent consultation with or referral to a pediatric cardiologist. (See 'Evaluation' above and 'Indications for referral or admission' above.)

●Ancillary studies – Ancillary studies are based upon physical findings and results of the ECG:

•ECG – An ECG is widely considered an essential part of the emergency evaluation of syncope despite its low diagnostic yield; a patient with syncope not precipitated by exertion and a normal ECG has a low likelihood of arrhythmia as a cause of syncope.

•ECHO – Emergency echocardiography should be reserved for those patients with a strongly suspected cardiac etiology due to the presence of red flag findings on history, physical examination, or ECG (table 2). In the absence of these findings, echocardiography is rarely useful. (See 'Other studies' above.)

If the ECG is normal at the initial evaluation, pediatric patients who may require a more extensive cardiac evaluation because of recurrent syncope or atypical features other than red flag findings can be referred to a pediatric cardiologist for an outpatient evaluation and determination of whether testing is needed. (See 'Other studies' above.)

•Laboratory testing – Laboratory studies that may be helpful in selected patients include (see 'Laboratory tests' above):

-Rapid blood glucose

-Hematocrit

-Urine pregnancy test (postmenarcheal females)

-Urine screen for drugs of abuse (patients with prolonged altered mental status or signs of intoxication)

•EEG – Electroencephalogram is rarely needed but is appropriate for the uncommon patient with syncope accompanied by prolonged loss of consciousness, seizure activity, and a postictal phase. (See 'Other studies' above.)

For most pediatric patients with syncope, neuroimaging is not necessary.

●The proper management of pediatric syncope requires appropriate recognition and treatment of the underlying cause (table 1). For children and adolescents with vasovagal (neurocardiogenic) syncope, we suggest the following approach (Grade 2C) (see 'Treatment' above):

•Increase oral intake to approximately 30 to 50 mL/kg per day (eg, 1.5 to 2.4 L in a 50 kg adolescent)

•Add salty snacks (eg, pretzels, pickles, or crackers)

•Avoid caffeinated beverages

•Teach techniques to prevent venous pooling, including keeping knees slightly bent when standing for a long time, isometric contraction of extremity muscles, toe raises, folding of the arms, and crossing of the legs

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Brian Coleman, MD, who contributed to earlier versions of this topic review.