Syncope

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CHAPTER 27 Syncope

James M. Callahan, MD, FAAP, FACEP

1 What is syncope?

Syncope is a sudden, brief, and transient loss of consciousness and muscle tone due to a reversible impairment in cerebral perfusion or substrate delivery (oxygen or glucose). Unconsciousness usually lasts no longer than 1–2 minutes. Patients or their families may say they fainted, passed out, or blacked out.

2 How common is syncope in the pediatric age group?

Syncope is relatively common. The overall incidence is 0.5–1.0% in children and adolescents. In younger children, incidence does not differ by sex. Syncope is more common in adolescents, with 15–50% of all adolescents experiencing at least one episode of syncope by adulthood (not all of these patients will present to medical care). In adolescence, twice as many females as males have syncope. In one series, syncope accounted for about 0.1% of all visits to an urban pediatric emergency department (ED), with a presenting age range of 21 months to 21 years (mean age, 12.7 years).

Pratt JL, Fleisher GR: Syncope in children and adolescents. Pediatr Emerg Care 5:80–82, 1989.

Weitlin W, Ganzeboom KS, Saul JP: Reflex syncope in children and adolescents. Heart 90:1094–1100, 2004.

3 Is syncope serious in children?

Most cases of syncope in children are due to benign etiologies. One-third to as many as 80% of cases are simple neurocardiogenic or vasodepressor (vasovagal) episodes. In the adult population, only 5% of episodes are vasodepressor events, and one-quarter are due to a cardiac etiology. Even so, syncope may be due to a life-threatening condition in children and adolescents. Up to 25% of pediatric and adolescent patients with sudden death have had at least one prior episode of syncope.

Massin MM, Bourguignont A, Coremans C, et al: Syncope in pediatric patients presenting to an emergency department. J Pediatr 145:223–228, 2004.

Pratt JL, Fleisher GR: Syncope in children and adolescents. Pediatr Emerg Care 5:80–82, 1989.

4 What are the common causes of syncope in children and adolescents?

Up to half of patients have experienced a simple vasodepressor episode. Other disorders of autonomic control, including orthostatic hypotension (20% of cases in one series), breath-holding spells, situational syncope (e.g., tussive syncope, micturition syncope), and hyperventilation, are also common. Hysterical faints (pseudosyncope) are common in adolescents.

5 Name the potentially life-threatening causes of syncope in children and adolescents.

image Cardiac arrhythmias

image Structural heart disease

image Seizures

image Subarachnoid hemorrhage

image Carbon monoxide poisoning

image Medications and ingestions

KEY POINTS: POTENTIALLY FATAL CAUSES OF SYNCOPE IN CHILDREN AND ADOLESCENTS

1 Cardiac arrhythmias (especially long QT causing ventricular tachycardia)

2 Structural heart disease (e.g., hypertrophic cardiomyopathy and aberrant coronary arteries)

3 Seizures

4 Subarachnoid hemorrhage

5 Carbon monoxide poisoning

6 Medications and ingestions

6 How is the etiology of a syncopal event usually determined?

The history and physical examination are enough to suggest the most likely cause of syncope in the vast majority of patients. Even so, remember that tachyarrhythmias often present in much the same way as vasodepressor syncope. All patients presenting with syncope should have electrocardiography.

7 What historical factors help to separate benign from serious causes of syncope?

Patients with vasodepressor syncope usually experience a prodrome and often faint after a precipitating event (e.g., pain, fright, startle). The patient can usually describe dizziness or lightheadedness, nausea, warmth, and a visual gray-out, often with tunnel vision, before fainting. They often have time to lower themselves slowly or brace themselves against something, and associated injuries such as lacerations or large hematomas are rare. Vasodepressor syncope usually occurs in a standing position.

Syncope that occurs with associated injuries, with exertion, when the patient is supine, or in infancy, or syncope that recurs is more likely due to a serious, underlying disorder.

Strieper MJ: Distinguishing benign syncope from life-threatening cardiac causes of syncope. Semin Pediatr Neurol 12:32–38, 2005.

8 What is the goal of the evaluation of syncope in the ED?

It has been said that “Syncope and death are the same—except that in one you wake up.” The goal of the ED evaluation is to identify the rare pediatric patient with a serious underlying disorder, while realizing that the majority of patients have probably suffered a vasodepressor episode (a diagnosis of exclusion). Extensive workups are rarely required, usually nondiagnostic, and often expensive.

Steinberg LA, Knilans TK: Syncope in children: Diagnostic tests have a high cost and low yield. J Pediatr 146:355–358, 2005.

9 Are there diagnostic tests that every patient with syncope should undergo in the ED?

A thorough history (including family history and social history) and physical examination are the most important parts of the ED evaluation. Measure orthostatic blood pressures and complete cardiac and neurologic examinations on every patient. Screen all patients with electrocardiography (ECG), looking for signs of hypertrophy or abnormal conduction times (e.g., long QT syndrome). Other diagnostic testing is guided by the results of the history, physical examination, and ECG (see question 17). When there are diagnostic questions after this initial workup, or when syncope recurs, referrals for specialized testing (echocardiography, tilt-table testing, Holter or event-recorder monitoring, or stress testing) may be made.

KEY POINTS: INITIAL WORKUP FOR ALL PEDIATRIC PATIENTS WITH SYNCOPE

1 Complete history, including family history of syncope, sudden death, cardiac diseases, and sensorineural hearing loss

2 Thorough physical examination, including complete cardiac examination with orthostatic vital signs and complete neurologic examination

3 Electrocardiography

10 How are episodes of vasodepressor syncope and seizures different?

The description of the syncopal event and surrounding circumstances may help distinguish between the two. With vasodepressor syncope, the patient is usually unconscious for only a matter of seconds, and incontinence is rare. Once awake, there may be some mild fatigue, but a true postictal period with decreased responsiveness and marked confusion is absent. Tonic-clonic movements usually occur near the end of a syncopal episode and last for only a few seconds, while they often are more persistent and last for at least a few minutes in patients with seizures. If the nature of the event is uncertain, electroencephalography may be helpful. It will be normal in patients with vasodepressor syncope and frequently abnormal—even in an interictal period—in patients with seizures.

11 What is the proposed pathophysiology of vasodepressor syncope?

It is thought that a prolonged upright position leads to venous pooling in the lower extremities, causing a decreased left ventricular volume. In response to this and possibly a precipitating event, there is a catecholamine surge that causes increased contractility and a strong contraction against a relatively empty ventricle. Cardiac vagal fibers in the ventricular wall are activated and stimulate the medulla oblongata, causing a sympathetic withdrawal with or without vagal stimulation. This sequence is known as the Bezold-Jarisch reflex. These events produce bradycardia as well as a profound loss in systemic vascular resistance, decreased cerebral perfusion, and syncope. The term vasodepressor syncope is more accurate than vasovagal syncope because it has been shown that vagal activity may contribute to these events but is not necessary for them to occur.

Batra AS, Hohn AR: Palpitations, syncope and sudden cardiac death in children: Who’s at risk? Pediatr Rev 24:269–275, 2003.

Wieling W, Ganzeboom KS, Saul JP: Reflex syncope in children and adolescents. Heart 90:1094–1100, 2004.

12 What are breath-holding spells?

Breath-holding spells are a common cause of syncope in infants and toddlers, probably related to developmental differences in autonomic control. Classically, two types are described. In cyanotic breath-holding spells, some provocation produces crying. The child develops a sustained expiration and becomes silent. Deepening cyanosis, a loss of muscle tone, and, often, opisthotonus occur. There may be a brief period of tonic-clonic movement at the event’s conclusion. The child then makes an inspiratory gasp, normal respirations resume, and the child slowly awakens.

With pallid breath-holding spells, there is usually the abrupt onset of pallor and loss of consciousness after one to two cries. Opisthotonus is followed by relaxation and gradual awakening. In one series, 17% of children with pallid breath-holding spells went on to have vasodepressor syncope in later life.

Breath-holding spells associated with unconsciousness are seen in up to 5% of all children. Onset of spells is usually in the first year of life and almost always by age 2. These are benign events that resolve spontaneously, and the spells cease occurring in 50% of children by age 4, 90% by age 6, and > 99% by age 8.

13 What types of syncope are associated with orthostatic changes?

Orthostatic hypotension may be due to dehydration or anemia. Micturition syncope, syncope with defecation, and syncope occurring during menses are all related to orthostatic changes. A variety of medications (prescribed; accidentally or intentionally ingested) may cause orthostasis, including antihypertensives, antidepressants, phenothiazines, sedatives, and diuretics. Tussive syncope (seen in patients with pertussis and severe asthma) results when coughing, respiratory spasm, and the Valsalva maneuver cause increased intrapleural pressure, decreased venous return, and decreased left ventricular filling.

14 What arrhythmias may produce syncope in children and adolescents?

Ventricular tachycardia, although rare, is a potentially life-threatening cause of syncope. Supraventricular tachycardia may cause presyncopal symptoms, but rarely true syncope. Congenital complete heart block may not become symptomatic until later childhood or adolescence. Complete heart block may also be acquired (e.g., in patients with untreated Lyme disease). Patients with structural heart disease and those who have had previous surgery to repair congenital heart disease are at increased risk of arrhythmias. Paroxysmal episodes of ventricular tachycardia may occur in the setting of a long QT interval.

15 How is the diagnosis of long QT syndrome made?

Long QT syndrome is diagnosed by finding a long QT interval on the patient’s ECG. The QT interval must be corrected (QTc) for the patient’s heart rate by using Bazett’s formula:

image

The QTc should be <0.45 seconds in infants under 6 months of age, <0.44 seconds in children, and <0.425 seconds in adolescents. Occasionally, a patient’s QTc may only become long with exertion, and exercise testing may be required to make the diagnosis.

16 What are the familial forms of long QT syndrome?

Long QT syndrome is associated with sensorineural hearing loss and autosomal recessive inheritance in the Jervell and Lange-Nielsen syndrome, and with autosomal dominant inheritance and normal hearing in the Romano-Ward syndrome. Family history of recurrent syncope, tachyarrhythmias, seizures, sudden death, and hearing loss should be ascertained.

Friedman MJ, Mull CC, Sharieff GQ, Tsarouhas NT: Prolonged QT syndrome in children: An uncommon but potentially fatal entity. J Emerg Med 24:173–179, 2003.

17 If a diagnosis of long QT syndrome is made, what should be done?

Patients with long QT have a mortality rate of up to 70% if not treated. Immediate cardiology consultation is required. β-blockers are the usual medical treatment for this disease. Disposition often includes admission for further monitoring. Advise family members to have ECGs to investigate for the familial forms of this syndrome. A long QT interval may be acquired in the setting of electrolyte abnormalities (e.g., hypocalcemia) and may be due to certain medications.

18 Name the medications and other drugs that may be associated with tachyarrhythmias.

image Nonsedating antihistamines (terfenadine and astemizole)*

image Cisapride

image Tricyclic antidepressants

image Cocaine (including crack)

image Carbamazepine (usually in overdose only)

image Amphetamines

image Inhalants (especially Freon)

19 Are there other causes of syncope that are cardiac in nature?

Structural heart disease may cause episodes of syncope or sudden death. Hypertrophic cardiomyopathy (idiopathic hypertrophic subaortic stenosis) is associated with a thickened left ventricular wall, especially along the septum in the subaortic outflow tract. With exertion and increased contractility, outflow tract obstruction and syncope occur. Hypertrophic cardiomyopathy is the most common autopsy-proven cause of death in young athletes.

An aberrant coronary artery that courses between the aorta and pulmonary artery also can be associated with exertional syncope, due to ischemia resulting in arrhythmias. Other rare causes that result in ventricular outflow obstruction include valvular aortic stenosis, atrial myxoma, and primary pulmonary hypertension. Dilated cardiomyopathies can be associated with arrhythmias or pump failure.

20 Other than seizures, are there other central nervous system events that may precipitate syncope?

Syncope may be a presenting symptom of atypical migraines. Often there is a history of an aura and headaches. Nausea and vomiting are common. Pain is frequently unilateral and may be throbbing in nature. Basilar artery migraines may affect equilibrium and the patient’s vision. A family history of migraines can help make the diagnosis.

Spontaneous subarachnoid hemorrhage is rare in children but may present with severe, thunderclap headache (worst of the patient’s life) and a period of syncope.

21 What metabolic derangements can cause syncope?

Hypoglycemia can cause syncope. This is rare in children after infancy, except those receiving insulin. A decreased level of consciousness due to hypoglycemia usually does not resolve spontaneously. Fasting, which leads to increased counter-regulatory hormones (including catecholamines), may play a role in vasodepressor syncope. Carbon monoxide poisoning, anemia, dehydration, and pregnancy may also be associated with syncope.

22 How does a patient with pseudosyncope (hysterical faints) present?

Hysterical faints are usually seen in adolescents. They typically occur in front of an audience, with an absence of physical findings. There is often eye fluttering behind half-closed eye lids. Self-protective behaviors are preserved (e.g., patients will not allow their own hand to fall and hit their face). Social history often reveals marked stress at home, in school, or in other social situations.

23 What is the treatment for the most common causes of syncope (vasodepressor and orthostatic)?

The most effective treatment for vasodepressor and orthostatic causes of syncope is to ensure adequate fluid intake. Older children and adolescents should drink at least 64 ounces of noncaffeinated fluids daily. The patient should drink enough so that their urine remains pale and clear. Small amounts of salty food may also help to maintain intravascular volume. Counsel patients to lie down when they have prodromal symptoms to prevent episodes of syncope. Patients who continue to have episodes of syncope should be referred for tilt-table testing and possible pharmacologic therapy.

24 Which patients with syncope require referral to a cardiologist or neurologist?

Patients who have syncope with exertion, syncope associated with chest pain, arrhythmias, or palpitations; syncope that recurs or does not respond to usual therapies; and syncope accompanied by an abnormal cardiac history, physical examination, or ECG should be referred to a cardiologist. Patients who have a family history of sudden death or who have atypical episodes of syncope should also be referred. Focal neurologic findings, other neurologic abnormalities, or a history that is consistent with the presentation of a seizure should be seen by a neurologist as soon as possible.

Delgado CA: Syncope. In Fleisher GR, Ludwig S, Henretig FM (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 649–655.

25 What findings in patients with syncope require admission?

Admit patients to the hospital who have cardiovascular disease or an abnormal cardiac examination, patients with serious ECG abnormalities (e.g., long QTc or complete heart block), patients with syncope and chest pain, and patients with cyanotic spells, apnea, or focal neurologic findings. Patients with toxic ingestions, focal neurologic findings, and orthostatic hypotension that doesn’t respond to IV fluids should also be admitted for observation, further diagnostic testing, and treatment.

Delgado CA: Syncope. In Fleisher GR, Ludwig S, Henretig FM (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 649–655.

* Especially when taken with macrolide antibiotics, metronidazole, or ketoconazole; of note, these medications are no longer available in the United States.

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CHAPTER 27 Syncope

James M. Callahan, MD, FAAP, FACEP

1 What is syncope?

Syncope is a sudden, brief, and transient loss of consciousness and muscle tone due to a reversible impairment in cerebral perfusion or substrate delivery (oxygen or glucose). Unconsciousness usually lasts no longer than 1–2 minutes. Patients or their families may say they fainted, passed out, or blacked out.

2 How common is syncope in the pediatric age group?

Syncope is relatively common. The overall incidence is 0.5–1.0% in children and adolescents. In younger children, incidence does not differ by sex. Syncope is more common in adolescents, with 15–50% of all adolescents experiencing at least one episode of syncope by adulthood (not all of these patients will present to medical care). In adolescence, twice as many females as males have syncope. In one series, syncope accounted for about 0.1% of all visits to an urban pediatric emergency department (ED), with a presenting age range of 21 months to 21 years (mean age, 12.7 years).

Pratt JL, Fleisher GR: Syncope in children and adolescents. Pediatr Emerg Care 5:80–82, 1989.

Weitlin W, Ganzeboom KS, Saul JP: Reflex syncope in children and adolescents. Heart 90:1094–1100, 2004.

3 Is syncope serious in children?

Most cases of syncope in children are due to benign etiologies. One-third to as many as 80% of cases are simple neurocardiogenic or vasodepressor (vasovagal) episodes. In the adult population, only 5% of episodes are vasodepressor events, and one-quarter are due to a cardiac etiology. Even so, syncope may be due to a life-threatening condition in children and adolescents. Up to 25% of pediatric and adolescent patients with sudden death have had at least one prior episode of syncope.

Massin MM, Bourguignont A, Coremans C, et al: Syncope in pediatric patients presenting to an emergency department. J Pediatr 145:223–228, 2004.

Pratt JL, Fleisher GR: Syncope in children and adolescents. Pediatr Emerg Care 5:80–82, 1989.

4 What are the common causes of syncope in children and adolescents?

Up to half of patients have experienced a simple vasodepressor episode. Other disorders of autonomic control, including orthostatic hypotension (20% of cases in one series), breath-holding spells, situational syncope (e.g., tussive syncope, micturition syncope), and hyperventilation, are also common. Hysterical faints (pseudosyncope) are common in adolescents.

5 Name the potentially life-threatening causes of syncope in children and adolescents.

image Cardiac arrhythmias

image Structural heart disease

image Seizures

image Subarachnoid hemorrhage

image Carbon monoxide poisoning

image Medications and ingestions

KEY POINTS: POTENTIALLY FATAL CAUSES OF SYNCOPE IN CHILDREN AND ADOLESCENTS

1 Cardiac arrhythmias (especially long QT causing ventricular tachycardia)

2 Structural heart disease (e.g., hypertrophic cardiomyopathy and aberrant coronary arteries)

3 Seizures

4 Subarachnoid hemorrhage

5 Carbon monoxide poisoning

6 Medications and ingestions

6 How is the etiology of a syncopal event usually determined?

The history and physical examination are enough to suggest the most likely cause of syncope in the vast majority of patients. Even so, remember that tachyarrhythmias often present in much the same way as vasodepressor syncope. All patients presenting with syncope should have electrocardiography.

7 What historical factors help to separate benign from serious causes of syncope?

Patients with vasodepressor syncope usually experience a prodrome and often faint after a precipitating event (e.g., pain, fright, startle). The patient can usually describe dizziness or lightheadedness, nausea, warmth, and a visual gray-out, often with tunnel vision, before fainting. They often have time to lower themselves slowly or brace themselves against something, and associated injuries such as lacerations or large hematomas are rare. Vasodepressor syncope usually occurs in a standing position.

Syncope that occurs with associated injuries, with exertion, when the patient is supine, or in infancy, or syncope that recurs is more likely due to a serious, underlying disorder.

Strieper MJ: Distinguishing benign syncope from life-threatening cardiac causes of syncope. Semin Pediatr Neurol 12:32–38, 2005.

8 What is the goal of the evaluation of syncope in the ED?

It has been said that “Syncope and death are the same—except that in one you wake up.” The goal of the ED evaluation is to identify the rare pediatric patient with a serious underlying disorder, while realizing that the majority of patients have probably suffered a vasodepressor episode (a diagnosis of exclusion). Extensive workups are rarely required, usually nondiagnostic, and often expensive.

Steinberg LA, Knilans TK: Syncope in children: Diagnostic tests have a high cost and low yield. J Pediatr 146:355–358, 2005.

9 Are there diagnostic tests that every patient with syncope should undergo in the ED?

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