ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Causes of syncope in children and adolescents

Causes of syncope in children and adolescents
Literature review current through: Jan 2024.
This topic last updated: Oct 21, 2022.

INTRODUCTION — This topic will review the serious and benign causes of syncope. A discussion of the emergent evaluation and algorithmic approach to children and adolescents with syncope is presented separately (algorithm 1). The evaluation of adults with syncope is also discussed elsewhere. (See "Emergency evaluation of syncope in children and adolescents" and "Syncope in adults: Clinical manifestations and initial diagnostic evaluation".)

BACKGROUND — Syncope is a sudden, brief loss of consciousness associated with loss of postural tone from which recovery is spontaneous [1-3]. Up to 15 percent of children experience a syncopal episode prior to the end of adolescence [4,5].

Although the etiology of syncopal events in children is most often benign, syncope can also occur as the result of more serious (usually cardiac) disease with the potential for sudden death. The vast majority of cases of syncope in the pediatric age group represent benign alterations in vasomotor tone [2,6-8]. Life-threatening causes of syncope generally have a cardiac etiology (table 1).

LIFE-THREATENING CONDITIONS — Life-threatening conditions that may present with syncope include cardiac causes and other medical causes:

Cardiac causes – Although rare, cardiac causes of syncope can be life-threatening. A review of the literature describing sudden death in children noted the following mortality risks for comparison [9]:

Unselected population 1 to 18 years of age: 0.00001 cases per patient-year

Long QT syndrome (LQTS): 0.001 cases per patient-year

High-risk tetralogy of Fallot and congenital heart disease patients: 0.03 cases per patient-year

Infant/pediatric dilated cardiomyopathy: 0.14 to 0.3 cases per patient-year

Life-threatening cardiac conditions cause syncope as the result of an abrupt decrease in cardiac output, either from an arrhythmia or related to structural heart disease [10]. Arrhythmias are typically tachyarrhythmias. In children, syncope caused by isolated bradycardia (ie, complete atrioventricular block) is uncommon [11]. (See "Bradycardia in children", section on 'Clinical presentation'.)

Other medical causes – Other medical causes of life-threatening syncope in children include hypoglycemia, poisoning, heat illness, and anaphylaxis.

Arrhythmias (primary electrical disturbances) — Syncope caused by ventricular arrhythmias may develop in patients without structural heart disease who have acquired disturbances (eg, electrolyte disorders [eg, hypo- or hyperkalemia, hypomagnesemia, or hypocalcemia] or poisoning) or inherited primary electrical disturbances. These conditions are much less common causes of syncope than structural lesions [9]. (See "Approach to sudden cardiac arrest in the absence of apparent structural heart disease".)

Long QT syndrome — LQTS is a disorder of myocardial repolarization characterized by prolongation of QT interval on the electrocardiogram (ECG) and an increased risk of sudden death due to the potential to degenerate into polymorphic ventricular tachycardia (waveform 1). LQTS may be acquired or congenital [12].

Acquired LQTS usually results from adverse effects of therapeutic medication use or electrolyte disturbances (table 2) (see "Acquired long QT syndrome: Definitions, pathophysiology, and causes"). Patients with eating disorders may have prolongation of the QT interval, as well as other ECG abnormalities. These changes typically normalize during nutritional rehabilitation.

Two clinical phenotypes of congenital LQTS have been described. The more common autosomal dominant form, the Romano-Ward syndrome, has a purely cardiac phenotype. The autosomal recessive form, the Jervell and Lange-Nielsen syndrome, is associated with LQTS and sensorineural deafness and a more malignant clinical course. The complex genetic underpinning of LQTS is important in risk stratification, prognosis, and management after initial diagnosis (see "Congenital long QT syndrome: Epidemiology and clinical manifestations"). Causes of acquired LQTS (eg, medications, selected toxins, hypokalemia, and hypomagnesemia) can also precipitate ventricular arrhythmia in patients with congenital LQTS.

Prolongation of the QT interval is an essential component of the diagnosis of LQTS. However, the QTc varies in response to a number of factors, such as autonomic state, electrolyte imbalance, drugs, and diurnal changes. The hand calculated QTc interval, in combination with clinical and historical features, can be used to establish the diagnosis of congenital LQTS in some cases. The approach to diagnosis of LQTS is discussed in greater detail separately. (See "Congenital long QT syndrome: Diagnosis", section on 'Our approach' and "Congenital long QT syndrome: Diagnosis", section on 'Diagnosis'.)

Congenital short QT syndrome — The association of sudden cardiac death, syncope, or atrial fibrillation and short QT interval has been noted in multiple case reports, including several children [13]. Three genetic mutations have been described. The QT interval in this syndrome is ≤0.36 seconds. Congenital short QT syndrome is considerably less common than LQTS. (See "Short QT syndrome".)

Brugada syndrome — Patients with Brugada syndrome (BS) have a characteristic pattern on ECG and an increased risk of sudden death. Sudden cardiac death may be the first and only clinical event in BS. Arrhythmic events generally occur between ages 22 and 65, although cases in children as young as three years of age have been reported [14-16]. Arrhythmic events in children with BS are uncommon but may be more likely during febrile episodes [14,17].

Typical ECG findings include pseudo-right bundle branch block and persistent ST segment elevation in leads V1 to V3 (waveform 2). ECG changes may be transient in some patients.

A number of antiarrhythmic, antianginal, and psychotropic drugs can induce a Brugada-like ECG pattern (table 3). BS is discussed in detail elsewhere. (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".)

Catecholaminergic polymorphic ventricular tachycardia — Children with catecholaminergic polymorphic ventricular tachycardia (VT) may present during childhood or adolescence with syncope as the result of VT or ventricular fibrillation (VF) induced by emotional or physical stress. Familial and sporadic cases occur, and several genetic patterns have been described. Arrhythmias typically cannot be induced at electrophysiologic study but can be provoked by exercise testing or intravenous (IV) catecholamine infusion. A detailed discussion of catecholaminergic polymorphic ventricular tachycardia can be found separately. (See "Catecholaminergic polymorphic ventricular tachycardia".)

Preexcitation syndrome — Among children and young adults who suffer sudden death, a preexcitation syndrome (such as Wolff-Parkinson-White) may be the underlying cause (waveform 3). This association was described in a prospective series of 273 children or young adults who died suddenly and had a prior ECG [18]. A preexcitation syndrome was noted in 10 subjects (3.6 percent). (See "Clinical features and diagnosis of supraventricular tachycardia (SVT) in children", section on 'Ventricular fibrillation and sudden death'.)

Electrolyte disturbance — Several acquired electrolyte disturbances can cause arrhythmias in children:

Hyperkalemia – Severe hyperkalemia (potassium level >7 mEq/L [7 mmol/L]) is associated with significant and potentially life-threatening disturbances in cardiac conduction. ECG changes reflect the impact of increasing levels of serum and plasma potassium on the electrical activity of the heart including aberrant ventricular depolarization (QRS), and abnormal repolarization (T wave). A rapid overview provides guidance on the emergency assessment and management of these patients (table 4). (See "Management of hyperkalemia in children".)

Hypokalemia – Severe hypokalemia (potassium level <2.5 mEq/L [2.5 mmol/L]) is associated with muscle weakness and arrhythmias, including paroxysmal atrial or junctional tachycardia, atrioventricular block, and polymorphic ventricular tachycardia (torsades de pointes) or fibrillation. Treatment requires rapid potassium supplementation as discussed separately. (See "Hypokalemia in children", section on 'Potassium supplementation'.)

Hypomagnesemia – Hypomagnesemia may be solitary or occur in association with hypokalemia and result in polymorphic ventricular tachycardia. Treatment consists of magnesium infusion. (See "Hypomagnesemia: Evaluation and treatment".)

Hypocalcemia – Hypocalcemia in children can prolong the QT interval and predispose to polymorphic ventricular tachycardia, although less commonly than hypokalemia or hypomagnesium. Treatment requires IV infusion of calcium. (See "Clinical manifestations of hypocalcemia", section on 'Cardiovascular' and "Primary drugs in pediatric resuscitation", section on 'Calcium'.)

Poisoning (agents with direct cardiac effects) — Poisoning due to selected medications or other toxins may alter cardiac conduction (table 5) and cause arrhythmias in children. Prolongation of the QRS or QT intervals or atrioventricular blockade can help identify the presence of these agents when an accurate history is not available. Emergency stabilization of these patients is discussed separately. (See "Approach to the child with occult toxic exposure", section on 'Supportive care'.)

Structural heart disease — Structural heart disease, either repaired or unrepaired, can result in syncope due to arrhythmia and/or reduced cardiac output, particularly during exercise. Among young athletes with sudden death, the majority have unrecognized structural heart lesions (eg, hypertrophic cardiomyopathy [HCM]) [19]. (See "Athletes: Overview of sudden cardiac death risk and sport participation", section on 'Structural abnormalities associated with SCD'.)

Congenital heart disease — Children with congenital heart disease, including those who have undergone surgical palliation or correction, are also at risk for malignant arrhythmias. In particular, repaired defects such as tetralogy of Fallot and, especially for children who underwent Rastelli and atrial switch procedures, transposition of the great arteries have been associated with sudden cardiac death [9,20-23]. (See "D-transposition of the great arteries (D-TGA): Management and outcome", section on 'Complications after Rastelli procedure' and "D-transposition of the great arteries (D-TGA): Management and outcome", section on 'Complications after Mustard and Senning procedures' and "Tetralogy of Fallot (TOF): Long-term complications and follow-up after repair", section on 'Management of VT and prevention of SCD'.)

Although the majority of children with aortic stenosis are asymptomatic, sudden death can occur, mostly in patients older than 10 years who have significant obstruction and/or aortic regurgitation (AR). (See "Valvar aortic stenosis in children", section on 'Clinical course'.)

Hypertrophic cardiomyopathy — HCM is a relatively common autosomal dominant disorder (incidence of 1 in 500 in the general population) that is characterized by asymmetric hypertrophy of the left ventricle. Patients may experience exertional syncope. HCM is the most common cause of sudden death during exercise. Mechanisms that lead to inadequate cardiac output include left ventricular outflow obstruction, ischemia during exertion, and arrhythmia. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation".)

Coronary artery anomalies — Congenital abnormalities in the origin of the coronary arteries may present as syncope or sudden death in teenagers and young adults. An abnormally located coronary artery (as an example, between the aorta and pulmonary artery) may become compressed during exercise, resulting in myocardial ischemia and syncope or sudden death. (See "Congenital and pediatric coronary artery abnormalities", section on 'Variations of coronary artery origin from the aorta'.)

Arrhythmogenic right ventricular cardiomyopathy — Patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) may present with an arrhythmia of right ventricular (RV) origin and/or sudden death. Presentation is most common between the ages of 10 and 50, with a mean age at diagnosis of approximately 30 years. (See "Arrhythmogenic right ventricular cardiomyopathy: Anatomy, histology, and clinical manifestations".)

Dilated cardiomyopathy — Dilated cardiomyopathy may develop in association with a variety of conditions, the majority of which are idiopathic. Other causes include sequelae of myocarditis, severe anemia, and muscular dystrophy. Patients with cardiomyopathy who develop syncope as the result of ventricular arrhythmias also typically have severe heart failure. (See "Causes of dilated cardiomyopathy".)

Pulmonary hypertension — Children with pulmonary hypertension, either idiopathic or related to a congenital heart defect with a systemic to pulmonary shunt (Eisenmenger syndrome), may experience syncope. However, most patients initially develop exertional dyspnea. Syncope is an indication of more severe pulmonary hypertension and impaired right heart function. (See "Treatment and prognosis of pulmonary arterial hypertension in adults (group 1)" and "Pulmonary hypertension with congenital heart disease: Clinical manifestations and diagnosis".)

Acute myocarditis — Syncope may occur in patients with acute myocarditis as the result of ventricular dysfunction or arrhythmia. Common viruses include Coxsackie A and B and adenovirus. However, these conditions rarely present as an isolated syncopal event. (See "Clinical manifestations and diagnosis of myocarditis in children", section on 'Clinical manifestations'.)

Hypoglycemia — Hypoglycemia is a life-threatening condition that is frequently cited as a cause of syncope. However, outside of the insulin-dependent diabetic, it is an uncommon cause of syncope [23,24]. Before the onset of syncope, patients with hypoglycemia frequently report feeling weak, hungry, and sweaty. As blood glucose continues to fall, they may exhibit agitation, confusion, and finally, altered mental status. (See "Causes of hypoglycemia in infants and children" and "Approach to hypoglycemia in infants and children", section on 'Clinical features'.)

Poisoning (agents with direct CNS effects) — Intoxication may present as syncope due to excessive sedation and coma (eg, ethanol, sedative-hypnotics [eg, benzodiazepines and barbiturates], cannabis [young children], or opioids) or impaired oxygen delivery to the brain (eg, carbon monoxide, inhalants, or asphyxiants [eg, cyanide, hydrogen sulfide]) (table 6). Evaluation of mental status, vital signs, and pupils along with assessment of skin and other findings (toxidrome recognition) may provide clues to the type of poisoning and help guide empiric and directed treatment (table 7). (See "Approach to the child with occult toxic exposure".)

Heat illness — Heat syncope (or exercise-associated collapse) occurs when an athlete is unable to stand or walk due to lightheadedness or syncope. This form of syncope usually occurs immediately after completing a race or workout and is commonly observed at distance running events. The mechanism for collapse is an abrupt decrease in venous return once that athlete completes the event. Given the typical degree of vasodilatation seen with prolonged exertion, the sudden loss of the pressure exerted by the skeletal muscles on the vasculature leads to a precipitous decline in venous return, as well as postural tone, causing the athlete to collapse. (See "Exertional heat illness in adolescents and adults: Epidemiology, thermoregulation, risk factors, and diagnosis", section on 'Heat syncope and exercise associated collapse'.)

Heat stroke may also cause collapse in association with progressive altered mental status, seizures, or coma. Heat stroke is differentiated from other causes of syncope by an elevated core temperature, tachypnea, tachycardia with hypotension, nausea, vomiting, and diarrhea (table 8). (See "Heat stroke in children", section on 'Clinical features' and "Heat stroke in children", section on 'Diagnostic evaluation'.)

Anaphylaxis — Anaphylaxis can occasionally involve syncope and loss of consciousness, and patients or caregivers sometimes overlook or forget the more subtle, earlier symptoms, such as flushing, itching, hives, cough and bronchospasm, vomiting, or abdominal cramping. In addition, these less dramatic symptoms may have resolved by the time the patient is evaluated. A rapid overview provides recognition and initial management of anaphylaxis (table 9). (See "Anaphylaxis: Acute diagnosis", section on 'Definition'.)

COMMON CONDITIONS

Vasovagal syncope — Vasovagal syncope (also known as neurocardiogenic, reflex, or situational syncope, and common fainting) is the most common cause of syncope among children, accounting for 50 percent or more of cases presenting to the emergency department [6,7].

Typical clinical features are a precipitating event and a prodrome.

Precipitating events include standing or stress (physical or emotional), although reflex precipitants (such as swallowing, hair grooming, and micturition) have been reported [25,26].

Patients often describe a prodrome, which may include lightheadedness, dizziness, visual changes (decrease acuity, tunnel vision, or double vision), nausea, pallor, and diaphoresis.

The underlying mechanism for the syncopal episode is an exaggeration of reflex-mediated alterations in vasomotor tone and heart rate normally responsible for maintaining blood pressure (figure 1). (See "Reflex syncope in adults and adolescents: Clinical presentation and diagnostic evaluation".)

Breath holding spells — Breath holding spells typically occur in children 6 months to 24 months of age and are triggered by an emotional insult, such as pain, anger, or fear. The spells may be cyanotic or pallid. They are associated with iron deficiency anemia and other types of anemia such as transient erythroblastopenia of childhood. The cyanotic variety begins with breath holding, followed by cyanosis and loss of consciousness. In a pallid spell, loss of consciousness occurs before breath holding. Brief posturing or tonic-clonic motor activity may occur with either cyanotic or pallid spells. (See "Nonepileptic paroxysmal disorders in infancy", section on 'Breath-holding spells'.)

The clinical course for children with breath holding spells is generally benign. Spells typically stop by five years of age. Some children go on to develop vasovagal syncope [27]. Breath holding spells may represent a variation of vasovagal (neurocardiogenic) syncope. Autonomic dysfunction appears to play a role in both cyanotic and pallid breath holding spells [28,29].

Orthostatic hypotension — Syncope that occurs with postural change may be related to an abrupt drop in blood pressure. Orthostatic hypotension can result from volume depletion (hemorrhage or dehydration), pregnancy (venous pooling), anemia, anorexia nervosa, and medications that alter vasomotor tone and heart rate such as calcium channel blockers, vasodilators, phenothiazines, and diuretics.

OTHER CONDITIONS

Arrhythmias (not life-threatening) — Rhythm disturbances that are not ventricular in origin may cause syncope:

Supraventricular tachycardia – Syncope is an unusual presentation of supraventricular tachycardia. Accessory pathway mediated tachycardia and atrioventricular nodal reentry tachycardia are relatively common arrhythmias, but rarely present with syncope. (See "Clinical features and diagnosis of supraventricular tachycardia (SVT) in children", section on 'Syncope and atrial fibrillation'.)

Bradycardia – In children, syncope caused by isolated bradycardia is unusual [11]. Causes of symptomatic bradycardia in children are corrective surgery for congenital heart disease, hypervagotonia, hypothyroidism, and medications (such as beta-adrenergic blockers). (See "Bradycardia in children".)

Postural tachycardia syndrome — Postural tachycardia syndrome (POTS) is defined as a form of orthostatic intolerance characterized by an excessive increase in heart rate (>40 beats per minute [bpm] over baseline in children and adolescents and >30 bpm or to >120 bpm in adults) that occurs on standing without arterial hypotension. POTS is a common disorder among teenage girls that typically manifests as palpitations, anxiety, dizziness, and tremulousness. However, syncope may occur in up to 40 percent of patients. (See "Postural tachycardia syndrome".)

CONDITIONS THAT MIMIC SYNCOPE — Conditions that may mimic syncope include the following:

Seizures – A seizure typically includes loss of consciousness and postural tone. However, seizures usually last longer than syncopal episodes and include features such as an aura, prolonged tonic-clonic activity, and/or the presence of a postictal phase.

Migraine syndromes – Migraine syndromes, particularly basilar migraines, may present with symptoms that are similar to syncope such as loss of conscious, ataxia, or vertigo. Loss of consciousness is usually longer than several seconds. In addition, patients generally have other neurologic symptoms, as well as headache and nausea. (See "Migraine with brainstem aura", section on 'Clinical manifestations'.)

Somatization or conversion disorder – Somatization or conversion disorder is most common in adolescent patients. These events typically occur in the presence of an audience, lack hemodynamic (heart rate, blood pressure) or autonomic (sweating, pallor) changes, may be prolonged, and rarely result in injury. Patients typically describe the event in a calm indifferent manner. They may disclose details of the event that indicate no loss of consciousness.

Hyperventilation – Hyperventilation is usually associated with emotional stress. It occurs more commonly in adolescent patients. The patient may complain of chest pain, chest tightness, and shortness of breath. In addition, symptoms may include lightheadedness, paresthesias, and visual disturbances.

Intentional strangulation activities (eg, the "choking game") – The choking game is defined as self-strangulation or 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".)

Narcolepsy – Patients with narcolepsy may have cataplexy, emotionally-triggered muscle weakness with collapse that may mimic syncope. However, they also have other features that indicate a disorder of sleep-wake control such as chronic daytime sleepiness, hypnagogic hallucinations (vivid, often frightening visual, tactile, or auditory hallucinations occurring as the patient falls asleep), or sleep paralysis (inability to move for one or two minutes immediately after awakening). (See "Clinical features and diagnosis of narcolepsy in adults", section on 'Clinical features'.)

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 [1]. Although the etiology of syncopal events in children is most often benign and typically due to vasovagal syncope, it can also occur as the result of more serious (usually cardiac) disease with the potential for sudden death (table 1 and algorithm 1). (See "Emergency evaluation of syncope in children and adolescents", section on 'Definition and causes'.)

Life-threatening conditions – Life-threatening conditions that cause syncope include (see 'Life-threatening conditions' above):

Arrhythmias (primary electrical disturbances) – Syncope caused by ventricular arrhythmias may develop in patients without structural heart disease who have acquired disturbances (eg, electrolyte disorders [eg, hypo- or hyperkalemia, hypomagnesemia, or hypocalcemia] or poisoning (table 5)) or inherited primary electrical disturbances. A rapid overview provides emergency management for hyperkalemia (table 4). (See 'Electrolyte disturbance' above and 'Poisoning (agents with direct cardiac effects)' above and 'Long QT syndrome' above.)

Structural heart disease – Arrhythmias may also develop as the result of structural heart disease or repaired congenital heart disease. In addition, syncope can occur in conditions such as aortic stenosis and hypertrophic cardiomyopathy (HCM) as the result of left ventricular outflow tract obstruction and compromised systemic blood flow, particularly during exercise. (See 'Structural heart disease' above.)

Acute myocarditis – Syncope may occur in patients with acute myocarditis as the result of ventricular dysfunction or arrhythmia. Common viruses include Coxsackie A and B and adenovirus. However, these conditions rarely present as an isolated syncopal event. (See "Clinical manifestations and diagnosis of myocarditis in children", section on 'Clinical manifestations'.)

Hypoglycemia – Before the onset of syncope, patients with hypoglycemia frequently report feeling weak, hungry, and sweaty. As blood glucose continues to fall, they may exhibit agitation, confusion, and finally, altered mental status. (See 'Hypoglycemia' above.)

Poisoning – In addition to syncope caused by arrhythmias, poisoning may also present as syncope due to excessive sedation and coma or impaired oxygen delivery to the brain (table 6). Evaluation of mental status, vital signs, and pupils, along with assessment of skin and other findings (toxidrome recognition) may provide clues to the type of poisoning and help guide empiric and directed treatment (table 7). (See 'Poisoning (agents with direct CNS effects)' above and "Approach to the child with occult toxic exposure".)

Heat illness – Heat syncope (or exercise-associated collapse) occurs when an athlete is unable to stand or walk due to lightheadedness or syncope. This form of syncope usually occurs immediately after completing a race or workout and is commonly observed at distance running events. Heat stroke may also cause collapse in association with progressive altered mental status, seizures, or coma. Heat stroke is differentiated from other causes of syncope by an elevated core temperature, tachypnea, tachycardia with hypotension, nausea, vomiting, and diarrhea (table 8). (See 'Heat illness' above.)

Anaphylaxis – Anaphylaxis can occasionally involve syncope and loss of consciousness, and patients or caregivers sometime overlook or forget the more subtle, earlier symptoms, such as flushing, itching, hives, cough and bronchospasm, or abdominal cramping. A rapid overview provides recognition and initial management of anaphylaxis (table 9). (See "Anaphylaxis: Acute diagnosis" and "Anaphylaxis: Emergency treatment".)

Common conditions – Common conditions that cause syncope include vasovagal syncope, breath holding spells, and orthostatic hypotension. The patient is stable on presentation and has a history, physical examination, and ECG that do not contain any red flags suggesting cardiac syncope (table 10). (See 'Common conditions' above and "Emergency evaluation of syncope in children and adolescents".)

Conditions that mimic syncope – Conditions that mimic syncope include seizures, migraine syndromes, somatization, conversion disorder, and hyperventilation. (See 'Conditions that mimic syncope' above.)

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

  1. Kapoor WN. Syncope. N Engl J Med 2000; 343:1856.
  2. Zavala R, Metais B, Tuckfield L, et al. Pediatric Syncope: A Systematic Review. Pediatr Emerg Care 2020; 36:442.
  3. van Dijk JG, Benditt DG, Fanciulli A, et al. Toward a Common Definition of Syncope in Children and Adults. Pediatr Emerg Care 2021; 37:e66.
  4. Friedman KG, Alexander ME. Chest pain and syncope in children: a practical approach to the diagnosis of cardiac disease. J Pediatr 2013; 163:896.
  5. Hu E, Liu X, Chen Q, Wang C. Investigation on the Incidence of Syncope in Children and Adolescents Aged 2-18 Years in Changsha. Front Pediatr 2021; 9:638394.
  6. Pratt JL, Fleisher GR. Syncope in children and adolescents. Pediatr Emerg Care 1989; 5:80.
  7. Massin MM, Bourguignont A, Coremans C, et al. Syncope in pediatric patients presenting to an emergency department. J Pediatr 2004; 145:223.
  8. Villafane J, Miller JR, Glickstein J, et al. Loss of Consciousness in the Young Child. Pediatr Cardiol 2021; 42:234.
  9. Alexander ME, Berul CI. Ventricular arrhythmias: when to worry. Pediatr Cardiol 2000; 21:532.
  10. Gillette PC, Garson A Jr. Sudden cardiac death in the pediatric population. Circulation 1992; 85:I64.
  11. Strickberger SA, Benson DW, Biaggioni I, et al. AHA/ACCF Scientific Statement on the evaluation of syncope: from the American Heart Association Councils on Clinical Cardiology, Cardiovascular Nursing, Cardiovascular Disease in the Young, and Stroke, and the Quality of Care and Outcomes Research Interdisciplinary Working Group; and the American College of Cardiology Foundation: in collaboration with the Heart Rhythm Society: endorsed by the American Autonomic Society. Circulation 2006; 113:316.
  12. Galić E, Bešlić P, Kilić P, et al. CONGENITAL LONG QT SYNDROME: A SYSTEMATIC REVIEW. Acta Clin Croat 2021; 60:739.
  13. Schimpf R, Wolpert C, Gaita F, et al. Short QT syndrome. Cardiovasc Res 2005; 67:357.
  14. Probst V, Denjoy I, Meregalli PG, et al. Clinical aspects and prognosis of Brugada syndrome in children. Circulation 2007; 115:2042.
  15. Righi D, Porco L, Calvieri C, et al. Clinical characteristics and risk of arrhythmic events in patients younger than 12 years diagnosed with Brugada syndrome. Heart Rhythm 2021; 18:1691.
  16. Bergamo D, Nelson C. Brugada pattern in adolescent with acute myocarditis due to SARS-CoV-2. J Am Coll Emerg Physicians Open 2022; 3:e12810.
  17. Skinner JR, Chung SK, Nel CA, et al. Brugada syndrome masquerading as febrile seizures. Pediatrics 2007; 119:e1206.
  18. Basso C, Corrado D, Rossi L, Thiene G. Ventricular preexcitation in children and young adults: atrial myocarditis as a possible trigger of sudden death. Circulation 2001; 103:269.
  19. Maron BJ. Sudden death in young athletes. N Engl J Med 2003; 349:1064.
  20. Garson A Jr, Smith RT, Moak JP, et al. Ventricular arrhythmias and sudden death in children. J Am Coll Cardiol 1985; 5:130B.
  21. Rocchini AP, Chun PO, Dick M. Ventricular tachycardia in children. Am J Cardiol 1981; 47:1091.
  22. Garson A Jr. Arrhythmias in pediatric patients. Med Clin North Am 1984; 68:1171.
  23. Driscoll DJ, Jacobsen SJ, Porter CJ, Wollan PC. Syncope in children and adolescents. J Am Coll Cardiol 1997; 29:1039.
  24. Scott WA. Evaluating the child with syncope. Pediatr Ann 1991; 20:350.
  25. Strieper MJ. Distinguishing benign syncope from life-threatening cardiac causes of syncope. Semin Pediatr Neurol 2005; 12:32.
  26. Igarashi M, Boehm RM Jr, May WN, Bornhofen JH. Syncope associated with hair-grooming. Brain Dev 1988; 10:249.
  27. DiMario FJ Jr. Prospective study of children with cyanotic and pallid breath-holding spells. Pediatrics 2001; 107:265.
  28. DiMario FJ Jr, Burleson JA. Autonomic nervous system function in severe breath-holding spells. Pediatr Neurol 1993; 9:268.
  29. DiMario FJ Jr, Bauer L, Baxter D. Respiratory sinus arrhythmia in children with severe cyanotic and pallid breath-holding spells. J Child Neurol 1998; 13:440.
Topic 6466 Version 24.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟