Syncope, also described as “fainting” or “blackouts,” is defined as a transient period of unconsciousness that is brief and abrupt in onset and resolves spontaneously to a restored level of function. It is a symptom rather than a diagnosis and does not necessarily indicate disease. The causes of syncope in children are heterogeneous and are most often benign in nature. Nevertheless, syncopal events can cause significant distress among patients, families, school personnel, and physicians. Since it is a relatively common occurrence in childhood, hospitalists should have a practical approach to the evaluation of pediatric syncope, focusing on identification of those rare individuals who are at risk for serious underlying disease.

PATHOPHYSIOLOGY

Patients experience syncope when inadequate cerebral perfusion results in a transient loss of consciousness and postural tone. Presyncope describes a similar event without full loss of consciousness. Girls present more commonly for the evaluation of syncope than boys, with a peak incidence between 13 and 19 years of age.¹ Most syncope in pediatric patients is autonomic in origin, isolated, and benign. In fact, the risk of sudden death among pediatric patients with prior syncopal events has been found to be equivalent to the risk of sudden death in the general population.²

History and physical examination can provide valuable clues to the probable cause of a syncopal episode and may curtail or circumvent the need for further diagnostic evaluation. Important historical features of a patient presenting with syncope are included in Table 37-1. Recent circumstances and those immediately preceding the syncopal event should be thoroughly explored. Because patients are often unable to provide details of an episode, witnesses to the event are important. Past medical history, especially with regard to previous syncopal episodes, cardiac or neurologic conditions, and medications, should always be obtained. Specific inquiries about family history should include sudden death, syncope, sudden infant death syndrome, congenital heart disease, seizures, and congenital deafness (associated with a genetic disorder that includes Long-QT). A patient’s baseline level of health should also be ascertained, including any overall changes in energy level, exercise tolerance, nutritional status, or the development of new respiratory symptoms, chest pain, or tightness and any emotional stressors.

Although the findings are often normal, a thorough physical examination should be performed. Global mental status should be evaluated and compared to the patient’s baseline level of function. Blood pressure measurements and evaluation of distal pulses in both the supine and upright positions and from both upper extremities and a lower extremity should be obtained. Cardiac examination may reveal a gallop, murmur, or click and there may be hepatomegaly or crackles on lung examination. Any of these examination findings raises the concern for cardiac disease. In addition, a complete neurologic examination is indicated. In young children and infants, a thorough skin and musculoskeletal examination should be performed to assess for any signs of trauma.

The differential diagnosis of pediatric syncope is listed in Table 37-2. The etiologies of childhood syncope can be divided into three major categories: (1) autonomic, (2) cardiac, and (3) metabolic. Regardless of the cause, syncope is the end result of inadequate cerebral perfusion, oxygen, or glucose delivery to the brain.

AUTONOMIC SYNCOPE

Autonomic syncope is the most common cause of syncope in pediatrics and can be further described as either reflex or dysautonomic. Of these two types, reflex syncope is more common. Many triggers are known to precipitate autonomic syncope. Although their exact mechanisms of action are not clearly understood, physical stressors such as anemia, dehydration, hunger, illness, heat, and physical exhaustion can predispose patients to autonomic syncopal episodes. Orthostatic hypotensive syncope occurs during an excessive or prolonged decrease in blood pressure when an individual suddenly assumes an upright position or after prolonged standing. Patients with high basal vagal tone are at higher risk for autonomic syncope.

Neurocardiogenic syncope (often referred to as vasovagal or vasodepressor syncope) is the most common type of reflex syncope and can usually be diagnosed by gathering a careful and complete history, performing a thorough physical examination, and with minimal use of diagnostic testing. Postural changes and variation in cardiac output or blood volume are triggers for pressure sensors that send signals to the medulla by vagal C fibers. This signaling causes compensatory changes in heart rate, ventricular contractility, and blood vessel compliance by neurohormonal transmitters as a way to maintain cerebral perfusion. A common clinical presentation begins with a prodrome lasting seconds to minutes, followed by a brief period of unconsciousness, after which the patient returns to a previous level of alertness. The premonitory symptoms may include lightheadedness, dizziness, nausea, pallor, shortness of breath, diaphoresis, and visual changes. Figure 37-1 depicts one hypothesized mechanism for neurocardiogenic syncope, called the hypotensive cardioinhibitory response (Figure 37-2).