SYNCOPE IN CHILDREN

SELECTED TOPICS IN EMERGENCY CARDIAC CARE

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SYNCOPE IN CHILDREN Robert J. Prodinger, DO, and Earl J. Reisdorff, MD, FACEP

The sudden loss of consciousness in a child is concerning to both the patient and their parents. Between 15% and 50% of adolescents have at least one episode of syncope.17,19, 32, 34, 37, 38 Although most causes are benign (e.g., vasovagal), an adequate evaluation is required to exclude life-threatening disorders. The history and physical examination may be sufficient to define the cause of syncope in 25% to 77% of pediatric cases (Table 1).l6, The events and setting preceding the syncopal episode provide clues in defining the nature of the event. For example, recently missing meals may cause hypoglycemia that is accompanied by sweating, weakness, and tachycardia. Dieting, diuretic use, and exertional activity can lead to orthostatic hypotension. The activity and position of the child at the time of the event are also important. If the child were crying, urinating, defecating, or coughing at the time, a vagally mediated syncopal event is probable. Changing positions just prior to syncope indicates orthostatic hypotension. The child who has a syncopal episode while sitting needs a close evaluation because this is more common with arrhythmias. Typical vagal-mediated episodes are preceded by nausea, syncope, lightheadedness, sensation of warmth, and a slow visual loss. Scintillating scotomatas may precede a migraine headache, which eventually results in syncope. Witnesses can indicate the length of the event and if there were seizure activity (e.g., abnormal eye movement or incontinence). A slow recovery or confusion following the event suggests a seizure disorder,l4 whereas severe pallor or cyanosis suggests a cardiac origin for the event. The risk of pregnancy is assessed, and a menstrual history should be

From the Michigan State University Emergency Medicine Residency, Ingham Regional Medical Center and Sparrow Hospital, Lansing, Michigan

EMERGENCY MEDICINE CLINICS OF NORTH AMERICA

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VOLUME 16 NUMBER 3 * AUGUST 1998

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Table 1. CONSIDERATIONS IN THE CHILD WITH SYNCOPE Description of Event Preceding Events Length of event Missed meals Tonic or clonic movement Heavy exercise or physical exertion Posturing Environmental or Precipitating Factors Pallor or cyanosis Environment Incontinence Hypodermic injections Tongue biting Sudden fear Postictal drowsiness or Prolonged standing confusion Extreme heat Eye movement Constitutional Symptoms Medical History Nausea, vomiting Syncope Diarrhea Headache Myalgias Epilepsy Arthralgias Trauma Fever Diabetes Rash Congenital heart disease Anxiety Palpitations Cold hands or feet Recent viral illness Activity and Position of Child at Time of Event Toxins Sitting or standing Antihistamines Changing positions Macrolides Crying Antifungal agents Tantrum Antihypertensives Breath holding Antiarrhythmics Urinating Alcohol Exercising Illicit agents (including inhalants) Defecation Antipsychotics Coughing Carbon monoxide Premonitory Symptoms Family History Sweating Sudden death Dizziness Heart disease Lightheadedness Hypercholesterolemia Nausea Diabetes mellitus Palpitations Epilepsy Hunger Syncope Blurred vision or scotomatas Perioral paresthesias

taken when considering an ectopic pregnancy in the adolescent. One should inquire about any over-the-counter (OTC) or prescription drugs that the patient may have taken. Any illicit drug, volatile substance, or ethanol misuse should be determined. One should note if there is a history of sudden death, heart disease, hypercholesterolemia, diabetes, epilepsy, or recurrent syncope in the family. PHYSICAL EXAMINATION

Following a general assessment, one should evaluate the airway, the respiratory effort, and hernodynamic stability. The temperature, pulse,

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respiratory rate, orthostatic blood pressure, and pulse oximetry are measured. In adolescents, a standing blood pressure of less than 80 mm Hg is abnormal, and a decrease in the systolic blood pressure of 30 mm Hg or greater on standing is diagnostic of orthostatic hypotension, especially when accompanied by a feeling of lightheadedne~s.~~ Orthostatic testing may further identify children who have abnormal reflex mechanisms. The pulses are checked for quality and regularity to quickly exclude a persistent tachyarrhythmia or bradyarrhythmia. The cardiovascular system should be closely examined, including cardiac auscultation for murmurs, gallop rhythms, regularity, and for any extra cardiac sounds suggesting valvular disease or left ventricular dysfunction. A midsystolic click suggests mitral valve prolapse. Palpation for heaves or thrills is performed and may indicate valvular disease or a cardiomyopathy. Auscultation over the carotid arteries (primarily for translated cardiac murmurs) must be performed. A thorough neurologic examination must be performed, beginning with the evaluation of the patient’s mental status. Persistent or focal neurologic findings suggests a cerebral vascular event or seizure. The value of carotid sinus massage as a diagnostic maneuver in children is limited.5 Although rarely performed in the ED, the oculocardiac reflex is tested by compressing the eyeball for approximately 10 seconds while continuously recording the cardiac rhythm. Only an experienced person should perform this maneuver. The test result is ”positive” if there is asystole for greater than 2 seconds. Bradycardia alone is not considered to be positive.” Other physical features associated with cardiac disease (e.g., abnormal facies, Marfan habitus, deafness, ataxia) or neurologic disease (e.g., ashleaf spots, cafe-au-lait spots, cleft palate) should be sought. DIAGNOSTIC EVALUATION

Children with new-onset or unexplained syncope require minimal laboratory evaluation, including a complete blood count and a serum glucose level, and, in a menstruating female, a pregnancy test (Table 2). Standard serum electrolytes as well as magnesium, calcium, and phosphate levels are measured if the history indicates a cause for electrolyte disturbances such as endocrine abnormalities or malnutrition. A urinalysis (e.g., for specific gravity, ketones) assesses for dehydration. Ketonuria suggests malnutrition, or poorly controlled or new-onset diabetes. Toxicologic screens and arterial blood gases are performed if indicated by the history and physical examination. Twelve-lead electrocardiography (ECG) and cardiac rhythm monitoring are perhaps the most important diagnostic studies. These two modalities define the heart rate, rhythm, and conduction intervals, as well as provide indirect indications of heart chamber size and structural heart disease. Advanced outpatient studies may include echocardiography, angiography, electroencephalography, and tilt testing. Heart rate and blood pressure responses to tilt testing can often define the physiologic causes of syncope.27,31 In summary,

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Table 2. DIAGNOSTIC EVALUATION Primary Studies Serum glucose Oximetry Postural vital signs 12-Lead electrocardiogram Rhythm monitor Hemoglobinlhematocrit Pregnancy test

Secondary Studies Urinalysis Serum electrolytes (Na, K, CI, HCO,) Magnesium, calcium, phosphorus Drug toxin screen Carboxyhemoglobin level Arterial blood gas Electroencephalogram Chest radiograph BUN, creatinine Echocardiogram Tilt test Coronary angiography

children with syncope generally require a complete blood count, glucose level, an ECG, and continuous cardiac rhythm monitoring. CAUSESOFSYNCOPE Cardiovascular Causes Cardiac-related syncope, although uncommon in children, is potentially life-threatening. Syncope from a cardiac etiology can be due to anatomic abnormalities (e.g., congenital malformations, valvular disease), or electrical abnormalities (e.g., tachyarrhythmias, bradyarrhythmias, asystole). Vasodepressor and Vasovagal Events Episodes of vasodepressor or vasovagal syncope are usually in response to a sudden emotional stress. There is a sudden drop in the peripheral vascular resistance, resulting in a decreased venous return and a lowered cardiac output. Hypotension and bradycardia ensue, leading to syncope. In contrast to pallid breath holding (seen only in infants), vasodepressor syncope occurs at all ages. Vasovagal phenomena account for 32% to 50% of cases of syncope.26,28 A pallid breath-holding spell occurs when an infant or young child is startled, as by sudden unexpected injury. This is followed by a few seconds later by the infant’s (or child’s) becoming limp or falling to the ground. Tonic-clonic activity can even occur. Cerebral anoxia is the ultimate precipitate for losing consciousness from pallid breath holding6, Vasodepressor episodes can occur during micturition, defecation, painful stimuli, prolonged standing, or overwhelming fear. Carotid sinus syndrome acts similarly and is triggered by pressure exerted from tight

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clothing around the neck, hyperextension or turning of the head, orthodontic appliances, and wrestling.*Any process resulting in significant vascular volume loss (e.g., hemorrhage or dehydration), venous pooling (pregnancy), or prolonged standing may cause orthostatic syncope. Structural Cardiac Abnormalities

Physical examination findings are usually subtle, with hypertrophic cardiomyopathy, especially idiopathic hypertrophic subaortic stenosis (IHSS).A fourth heart sound is usually audible and even palpable. There is a murmur of turbulence or obstruction from the left ventricular outflow track, which increases with intensity during maneuvers that decrease venous return (standing) and diminishes with maneuvers that increase venous return (squatting). Atrial fibrillation results from atrial enlargement, further decreasing ventricular filling. Hypertrophic cardiomyopathy is the most common cause of sudden cardiac death in young athletes.24Syncope from HCM is due to low-input-low-output failure induced by tachycardia in the presence of a low filling volume.25In familial right ventricular dysplasia, the myocardium is replaced with abnormal fatty cells and degenerated myocardial cells. Right ventricular dysplasia causes ventricular dy~rhythmias.~ Mitral valve prolapse rarely produces syncope1s;however, some patients with mitral valve prolapse have an elevated adrenergic tone that may contribute to arrhythmogenesis.3 Severe aortic stenosis causes syncope from decreased cardiac outflow obstruction. The murmur of aortic stenosis is a systolic murmur at the middle and upper sternum associated with a palpable thrill at the base of the heart or the suprasternal notch. Pulses can be diminished (pulsus parvus et tavdus). With coarctation of the aorta, infants can present with a syncope, a high systolic and diastolic blood pressure, and decreased or absent femoral pulses. Anomalous coronary arteries cause syncope, dysrhythmias, and sudden cardiac death during exercise. Ischemia presumably results from decompression or kinking of the aberrantly coursing vessel. Subclavian steal syndrome causes syncope by diverting blood from the basilar circulation.1° Congenital heart disease raises concerns about life-threatening ventricular arrhythmias. There is an increased incidence of ventricular tachycardia following repair of tetralogy of Fallot, presumably because of elevated right ventricular pressures from persistent obstruction in the right ventricular outflow track. Adolescents with primary pulmonary hypertension usually experience dyspnea on exertion. Syncope results from an inadequate cardiac output through a progressively narrowing and constricting pulmonary vascular bed. There is no murmur until pulmonary hypertension becomes extremely advanced.I3 Cardiac Rhythm Abnormalities Cardiac rhythm and conduction disturbances can decrease cardiac output and reduce cerebral perfusion, resulting in syncope. Bradyar-

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rhythmias can result from excess vagal tone or sick sinus syndrome. Bradycardia or asystole is seen with neurally mediated (vagal) syncope. Congenital heart block presents as a marked bradycardia and complete heart block in a fetus or neonate. Congenital heart block can go undetected for years, however. Congenital heart block has also been associated with maternal antibodies to fetal cardiac tissuez2and neoplasms involving the atrioventricular (AV) node. Lyme disease can cause complete heart block that is transient and usually does not require a cardiac pacemaker.35 Supraventricular tachycardia and ventricular tachycardia can cause syncope or near ~yncope.~O In sick sinus syndrome, atrial tachycardia or atrial flutter spontaneously terminates without the prompt return of normal sinus rhythm or junctional escape rhythm. A period of asystole follows immediately after spontaneous termination of the tachycardia, resulting in syncope. Syncopal events after pacemaker insertion suggest that tachyarrhythmias are a contributing cause of syncope in these patients. Sick sinus syndrome is more common following corrective surgery for congenital heart disease but can also occur in an otherwise normal heart.29 Wolff-Parkinson-White (WPW) syndrome is associated with a shortened PR interval, an abnormal QRS complex that is often slurred in its initial portion (delta wave), and tachycardia owing to an accessory pathway (bundle of Kent) between the atria and the ventricles. The most common arrhythmia associated with WPW syndrome is a reciprocating or reentrant loop supraventricular tachycardia. Rarely is the tachycardia sufficient enough to cause syncope unless other comorbidities are associated.l, Atrial fibrillation with transmission of the impulses across both the AV node and accessory pathway result in ventricular rates as high as 300 to 400 beats per minute (bpm). This results in hemodynamic instability and syncope. Congenital prolonged QT syndrome is a rare inherited condition associated with delayed ventricular repolarization. There is an increased risk of fatal ventricular arrhythmias, most commonly, polymorphic ventricular tachycardia (torsades de pointes). Three risk factors associated with prolonged QT syndrome include congenital deafness, female gender, and prior episodes of syncope. ECG findings show QT interval prolongation (QTc > 440 msec), although this may be difficult to assess when the patient is in normal sinus rhythm. Abnormally shaped or giant T waves may be seen as well as TU waves. Alternating positive and negative T waves may also be seen. Because the QT interval varies with the heart rate, a corrected QT interval (QTc) must be used to determine prolongation. A single episode may result in sudden death, and the mortality rate may be as high as 70%. Patients with prolonged QT syndrome require referral to a cardiologist. Syncope often occurs with tachycardia (e.g., exertion, a sudden startle, emotional upset). In some children, exercise-induced tachycardia causes increased prolongation of the QTc interval.4l The patients with a familial dysautonomia can have a QTc that lengthens with postural changes.33Acquired QT prolongation

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is usually secondary to electrolyte imbalances, malnourishment, and drugs, such as antiarrhythmics, antidepressants, and phen~thiazines.~~ Catecholamine-induced polymorphic ventricular tachycardia is sought in the child with stress- or emotionally induced syncope.20The syndrome of idiopathic exercise-induced ventricular tachycardia in children and adolescents is another cause of ~yncope.~, 39 Neurologic Disorders Syncope may be confused with a seizure; in fact, seizures are the most common mimics for syncope-like events. Many seizures present with atypical findings, thus making definition of the episode more difficult. Likewise, syncopal episodes often appear to be similar to seizures. In fact, brief convulsions sometimes accompany or follow a vasodepressive episode. A further confounding factor is that cardiac dysrhythmias can accompany status epilepticus. One author recommends that any patient who presents with a first-time nonfebrile seizure should have an ECG, with the purpose of seeking QT prolongation.8Tilt testing may also help differentiate syncope with subsequent convulsions from a primary seizure disorder.I2 A prodromal aura is common with seizures but uncommon with syncope. Facial cyanosis, frothing at the mouth, tongue biting, postictal drowsiness, and prolonged mental status changes after the event suggest a seizure. When the cause of the patient’s symptoms are unclear, evaluation for both syncope and seizure is required. Electroencephalography may differentiate between syncope and seizure. Seizures may present with atypical findings; for example, temporal lobe epilepsy may demonstrate only simple motor activity, which often appears semipurposeful. An atypical migraine headache can mimic syncope. These patients usually have other symptoms atypical for syncope, including headache, visual changes, ataxia, or vertigo. Other neurologic causes of syncope include CNS trauma, tumors, and cerebral vascular accidents involving arteriovenous malformations. Toxic Disorders Many drugs can cause syncope, including both prescription and OTC medications, even when used as recommended. Antihistamines such as terfenadine (Seldane) and astemizole (Hismanal) can cause abnormal QT prolongation, with resultant torsades de p o i n t e ~Prolonga.~~ tion of the QTc is exacerbated with the concurrent use of macrolides (e.g., erythromycin)and ketoconazole. Antihypertensive agents, diuretics, beta blockers, and antiarrhythmics can cause syncope. Other drugs decreasing cardiac output are barbiturates, tricyclic antidepressants, and phenothiazines. Substances of abuse such as cocaine, alcohol, marijuana, inhalants, and opiates can all cause an acute loss of consciousness. Inhalant

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abuse (especially freons) can result in ventricular tachycardia and death. There is an increased frequency of sudden death in preadolescent boys taking tricyclic and antidepressants for attention deficit hyperactivity disorder.30Although the cause is unclear, children with syncopal episodes who are taking tricyclic agents should be evaluated for arrhythmias.

Respiratory Disorders Breath holding is a common cause of syncope in infants, toddlers, and preschool children. During these episodes children do become hypoxic and sustain a loss of consciousness. Tussive syncope or post-tussive syncope is provoked by severe coughing paroxysms. These episodes can be associated with respiratory illnesses, including bronchospasm from an acute infection, asthma, pertussis, or cystic fibrosis. Presumably, severe paroxysms of coughing result in a reduced cardiac output owing to the high intrathoracic pressures.

Psychological Disorders Conversion syncope may occur when the patient is in a supine position and is often accompanied by eyes fluttering behind partially closed eyelids; this often occurs in the presence of others. Psychogenic hyperventilation can also cause syncope. Severe hypocapnea produces a loss of consciousness. The syncope usually resolves and the patient awakens with no significant mental status changes and resolution of the hyperventilation. TREATMENT

When treating the child with syncope, assessing the airway, breathing, and circulation is axiomatic. Concurrently, one should obtain an appropriate history and physical examination. This guides the practitioner through the diagnostic work-up. A rapid bedside glucose measurement is obtained and pulse oximetry is performed. Orthostatic vital signs are taken. An electrocardiogram is obtained in all patients presenting with syncope. If the patient has no significant neurologic or cardiac history, and there is no family history consistent with cardiac or neurologic abnormalities, and clinical presentation is consistent with vasodepressor syncope, then the evaluation outlined above is sufficient. Children with persistent alterations in mental status or focal neurologic deficits require CT evaluation, electrolyte measurements, and toxicologic screens (including carbon monoxide). Unstable tachyarrhythmias are treated by standard advanced cardiac life support and pediatric advanced life support guidelines. If a tachycardia is toxin induced, then

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therapy should be focused on treating the underlying cause. For example, sodium bicarbonate is used for cocaine- and tricyclic-induced widecomplex tachycardia. Likewise, diazepam or lorazepam may slow a cocaine-induced narrow-complex tachycardia. The patient presenting with hypertension should be treated initially with a bolus of isotonic fluid (20 mL/kg). If this is ineffective, inotropic agents are required. If all diagnostic study results are normal and the child does not require immediate therapeutic intervention in the ED, the child should be sent home under the care of a responsible adult who can observe the child for the next 12 hours. All children who have had a syncopal episode should be reexamined by a primary care physician. The need for more advanced studies or referral to a cardiologist or electrophysiologist should then determined by the clinical circumstances.

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19. Kienzle MG: Syncope: Mechanisms and manifestations. Hosp Pract Dec:77-88, 1990 20. Kudenchuk PJ, McAnulty JH: Modem concepts of cardiovascular disease. J Am Heart 5125-29, 1985 21. Leenhardt A, Lucet V, Denjoy I, et a1 Catecholaminergic polymorphic ventricular tachycardia in children: A 7-year follow-up of 21 patients. Circulation 91:1512-1519,1995 22. Lerman-Sagie T, Lerman P, Mukamel M, et al: A prospective evaluation of pediatric patients with syncope. Clin Pediatr 33:66-70, 1994 23. Litsey SE, Noonan JA, OConnor WN, et al: Maternal connective tissue disease and congenital heart block. N Engl J Med 312:98-100, 1985 24. Lombroso CT, Lerman P: Breathholding spells (cyanotic and pallid infantile syncope). Pediatrics 39:563-581, 1967 25. Maron BJ, Epstein SE, Roberts WC: Causes of sudden death in competitive athletes. J Am Coll Cardiol 7204-214, 1986 26. Nienbaber CA, Hiller S, Spielmann RP, et al: Syncope in hypertrophic cardiomyopathy: Multivariant analysis of prognostic determinants. J Am Coll Cardiol 15:948-955, 1990 27. Ozme S, Alehan D, Yalaz K, et al: Causes of syncope in children: A prospective study. Int J Cardiol 40:111-114, 1993 28. Pongiglione G, Fish FA, Strasburger JF, et al: Heart rate and blood pressure response to upright tilt in young patients with unexplained syncope. J Am Coll Cardiology 16:165-170, 1990 29. Pratt J, Fleisher GR Syncope in children and adolescents. Pediatr Emerg Care 5:8082, 1989 30. Rasmussen V, Hams0 S, Skagen K: Cerebral attacks due to excessive vagal tone in heavily trained persons. Acta Med Scand 204:401405, 1978 31. Riddle MA, Nelson JC, Kleinman CS, et al: Sudden death in children receiving Norpramin: A review of three reported cases and commentary. J Am Child Adolesc Psychiatry 30:104-108, 1991 32. Ross BA, Hughes S, Anderson E, et al: Abnormal responses to orthostatic testing in children and adolescents with recurrent unexplained syncope. Am Heart J 122:748754, 1991 33. Ruckman RN: Cardiac causes of syncope. Pediatr Rev 9:lOl-108, 1987 34. Salim MA, DiSessa TG: QT interval response to exercise in children with syncope. Am J Cardiol 73:976-978, 1994 35. Scott WA: Evaluating the child with syncope. Pediatr Annals 20350-359, 1991 36. Steere AC, Batsford WP, Weinburg M, et al: Lyme carditis: Cardiac abnormalities of Lyme disease: I. Ann Intern Med 93:8-16, 1980 37. Stephenson JBP: Reflex anoxic seizures and ocular compression. Devel Med Child Neurol 22380-386, 1980 38. Strasberg B, Sagie A, Rechavia E, et a1 The noninvasive evaluation of syncope of suspected cardiovascular origin. Am Heart J 117160-163, 1989 39. Vacek JL: Diagnosing syncope with an emphasis on cardiac causes. Postgrad Med 90:175-184, 1991 40. von Bemuth G, Bemsau U, Gutheil H, et al: Tachyarrhythmic syncope in children with structurally normal hearts with and without QT-prolongation in the electrocardiogram. Eur L Pediatr 138:206-210, 1982 41. Wang Y, Scheinman MM, Chien WW, et al: Patients with supraventricular tachycardia presenting with aborted sudden death: Incidence, mechanism and long-term followup. J Am Coll Cardiol 18:1711-1719, 1991 42. Weintraub RG, Gow RM, Wilkinson JL: The congenital long QT syndromes in childhood. J Am Coll Cardiol 16:674-680, 1990 43. Wiley JF, Gelber ML, Henretig FM, et al: Cardiotoxic effects of astemizole overdose in children. J Pediatr 120:799-802, 1992

Address reprint requests to Earl J. Reisdorff, MD, FACEP Ingham Regional Medical Center Department of Emerging Medicine 401 West Greenlawn Avenue Lansing, MI 48910