Dizziness is a common but very nonspecific chief complaint about which some elaboration by the patient is generally required for the physician to understand exactly what the patient is experiencing. The description of the sensation is critical in distinguishing whether it is caused by vertigo, disequilibrium, lightheadedness, presyncope, or even ataxia ( Table 6.1 ). Although the differential diagnoses of these entities may overlap, there are conditions that are most specific to the individual symptom. All of the entities are conditions that may affect children at any age, but older children are more capable of articulating the abnormal sensation they feel. Children younger than 6 years of age may present with nausea, vomiting, ataxia, or frank syncope.
| Vertigo | Presyncope | Disequilibrium | Lightheadedness | |
|---|---|---|---|---|
| Patient complaint |
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| Associated features | Motion, swaying, spinning, nystagmus |
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| Anxiety, hyperventilation, paresthesias, respiratory alkalosis, panic attacks |
| Usual cause | Vestibular disorders | Impaired cerebral perfusion | Sensory and/or central neurologic dysfunction | Anxiety and/or depressive disorders |
| Key differential diagnoses |
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|
|
|
Syncope is the transient loss of consciousness and postural tone that results from inadequate cerebral perfusion. Syncope is a common phenomenon in children and adolescents that is usually benign. Between 20% and 35% of all young adults have had one episode of syncope.
Presyncope is the feeling that the person is “about to pass out.” The patient feels as if he or she is going to lose consciousness but does not. Presyncope may or may not reflect the same pathophysiologic process as true syncope. The diagnostic approach to presyncope is the same as for syncope.
Dizziness must be considered a change in mental status. It may potentially herald serious underlying central nervous system dysfunction. Dizziness must be better defined to distinguish vertigo from lightheadedness. The principal distinction with vertigo is the description of perceived motion: swaying, whirling, or spinning. Lightheadedness is frequently associated with psychological stress, including anxiety, hyperventilation, depression, and panic attacks. The history surrounding episodes of lightheadedness is vital for formulating the differential diagnosis.
Disequilibrium refers to “balance problems” without vertigo. The characteristic historical feature is difficulty ambulating. A rare complaint among children, disequilibrium in the young is most often caused by vestibular or cerebellar dysfunction and manifests as ataxia. Ataxia is an impairment of coordination, movement, and balance; this impairment is generally associated with dysfunction of the cerebellum or of the sensory and/or motor pathways connecting to the cerebellum. There are transient forms and progressive degenerative conditions that produce ataxia.
Syncope
(See Nelson Textbook of Pediatrics , p. 514.)
Syncope is a common phenomenon among children and adolescents. As many as 25% of children experience a syncopal event between the ages of 8 and 18 years. Before age 6 years, syncope is very unusual except in the setting of seizure disorders, breath-holding spells, and primary cardiac dysrhythmias. Syncopal episodes cause a large number of health care visits and a surprising number of admissions to hospitals. The differential diagnosis of syncope is noted in Tables 6.2 and 6.3 ; distinguishing features are noted in Tables 6.4 and 6.5 .
| Reflex Vasodepressor Syncope |
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| Miscellaneous Situational Reflex |
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| Systemic Illness |
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| Central Nervous System |
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| Dysautonomia |
| Basilar Artery Migraine |
| Drug Effects |
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| Other Etiologies |
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| Diagnostic Consideration |
| Neurocardiogenic |
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| Organic Heart Disease (e.g., Coronary Artery Disease, Aortic Stenosis, Primary Arrhythmia, Obstructive Hypertrophic Cardiomyopathy, Pulmonary Hypertension) |
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| Neurologic |
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| Other Vascular |
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| Drug Induced |
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| Psychiatric Illness |
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| Features | Syncope | Seizures |
|---|---|---|
| Relation to posture | Common | No |
| Time of day | Diurnal | Diurnal or nocturnal |
| Precipitating factors | Emotion, injury, pain, crowds, heat, exercise, fear, dehydration, coughing, micturition | Sleep loss, drug/alcohol withdrawal |
| Skin color | Pallor | Cyanosis or normal |
| Diaphoresis | Common | Rare |
| Aura or premonitory symptoms | Long | Brief |
| Convulsion | Rare, brief | Common |
| Other abnormal movements | Minor twitching | Rhythmic jerks |
| Injury | Rare | Common (with convulsive seizures) |
| Urinary incontinence | Rare | Common |
| Tongue biting | No | Can occur with convulsive seizures |
| Postictal confusion | Rare | Common |
| Postictal headache | No | Common |
| Focal neurologic signs | No | Occasional |
| Cardiovascular signs | Common (cardiac syncope) | No |
| Abnormal findings on EEG | Rare (generalized slowing may occur during the event) | Common |
The pathophysiologic mechanism of syncope follows a common pathway with many inciting stimuli. Cerebral perfusion is compromised by a transient decrease in cardiac output as a result of vasomotor changes, decreasing venous return, primary dysrhythmia, or impairment of cerebral vascular tone. Adolescents with syncope subjected to a head-up tilt-table test report blurred vision and constriction of visual fields before losing consciousness, as well as nausea, pallor, sweating, and dizziness, which are accompanied by hypotension (systolic blood pressure <60 mm Hg) and by bradycardia (heart rate <40 beats/min) with an occasional junctional rhythm and even asystole. Symptoms are relieved by returning to the supine position. Several situational factors can exacerbate this response, including warm temperature, a confined space such as being in a crowded room, anxiety or fear, sudden surprise, the sight of blood, pain, such as needle sticks or shots. Other situational factors include urination, swallowing, coughing, defecation, and hair combing.
This response is caused by an imbalance of parasympathetic and sympathetic tone, which results in peripheral vasodilatation, including venodilation, but in no augmentation of venous return, because there is no accompanying increase in large skeletal muscle activity to augment systemic venous return and maintain cardiac filling. Subsequent vagal output results in inappropriate bradycardia and further compromises cardiac output. The child faints and becomes supine, which restores systemic venous return. Awakening is accompanied by increased sympathetic output, which restores the heart rate. The episode tends to be brief but may recur if the patient is “helped up” too quickly.
In obtaining the history of a syncopal episode, attention should be paid to the time of day, time of last meal, activities leading up to the event, and associated symptoms (e.g., palpitations, racing heartbeat, chest pain, headache, shortness of breath, nausea, diaphoresis, visual changes, and hearing changes). Cataplexy may be confused with syncope and is characterized by partial or complete paralysis of skeletal muscles resulting in a rapid progression of weakness of the face and neck followed by the muscles of the trunk and extremities. The patient loses tone and may fall to the floor but remains awake and immobile for 1-2 minutes. Triggers include intense positive or negative emotions, such as laughing, frustration, fright, or anger. Details of the syncopal event, such as the patient’s position (syncope while supine suggests a cardiac arrhythmia) when symptoms appeared, duration of the episode, and characterization of the patient’s appearance during and immediately after the episode are also important. Almost without exception, by the time the patient presents to the office or emergency room, the physical examination findings are normal. Therefore, the history becomes the most important piece of information for developing the differential diagnosis, diagnostic evaluation, and management plan.
Neurocardiogenic Syncope
There are several causes of neurocardiogenic syncope . Excessive vagal tone may be primary or secondary to breath-holding, cough, (deglutition syncope), micturition or defecation, carotid sinus pressure sensitivity, and orthostasis. Neurocardiogenic syncope has been described in association with hair brushing, swallowing, stretching, orthodontic maneuvers, anomalies of the cervical spine, and dental trauma. Many of these episodes may actually be forms of carotid sinus sensitivity. Cough syncope probably is related to prolongation of high intrathoracic pressure that results in decreased venous return and subsequent decreased cardiac output.
The prodromal history is very important in evaluating neurocardiogenic syncope. In contrast, syncope without warning, while the patient is supine or during exercise implies a primary cardiac and usually more serious etiology; it is associated with greater morbidity and potential mortality (see Table 6.3 ).
Neurocardiogenic syncope is a type of autonomic dysfunction that is also referred to as vasodepressor syncope , vasovagal syncope , and reflex syncope . Potential mechanisms include:
- 1.
The first response is primary bradycardia, sometimes to the extreme of sinus arrest or even brief asystole, with subsequent hypotension. This is known as the cardioinhibitory response.
- 2.
The second is a primary vasodepressor response that is characterized by hypotension with the heart rate being relatively preserved.
- 3.
The third is mixed and is the most common response that features simultaneous hypotension and bradycardia.
The common pathway producing the heart rate and blood pressure responses and cerebral hypoperfusion is the Bezold-Jarisch reflex ( Fig. 6.1 ). For most children and adolescents, prodromal warning signs herald the impending syncopal episode and can, after the first episode, allow the child enough time to prevent fainting by sitting with the head between the knees or by lying supine.
FIGURE 6.1
Tilt-table testing: the Bezold-Jarisch reflex. BP, blood pressure; HR, heart rate; LVEDV, left ventricular end-diastolic volume.
The physiologic mechanisms of neurocardiogenic syncope have been demonstrated with head-up tilt-table testing. Tilt-table testing can be performed with or without invasive blood pressure monitoring. The goal is to reproduce the patient’s symptoms under close monitoring. Various tilt angles and durations have been described, as has the use of isoproterenol as a provocative stimulus.
If the history suggests the diagnosis of neurocardiogenic syncope with normal physical examination findings and a normal electrocardiogram (ECG), treatment may be empirically started ( Tables 6.6 and 6.7 ). The first line of treatment is education and counseling. Most patients will eventually outgrow neurocardiogenic syncope. Patients should maintain hydration and increase dietary salt if there are not any contraindications. Patients should be counseled to avoid situations that precipitate an event and taught to abort an event by lying down.
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| β-Adrenergic Antagonists |
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| α-Adrenergic Agonists |
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| Anticholinergics |
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| Selective Serotonin Receptor Reuptake Inhibitors |
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| Mineralocorticoids |
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If the patient fails conservative therapies, pharmacologic treatments may be tried. Physicians have used fludrocortisone with increased salt intake, β-adrenergic blockers, and midodrine which has had promising results. None of these medications has demonstrated consistent benefit to treat neurocardiogenic syncope.
Orthostatic Syncope
Conditions that produce hypotension (orthostatic or supine) frequently produce syncope or presyncope. Cardiac function and structure are usually normal before the episode; during the predisposing illness, cardiac filling pressures are often reduced because of reduced venous return from hypovolemia or decreased peripheral vascular resistance (peripheral pooling of blood). Dehydration from diarrhea and vomiting, hyperthermia, hyperpyrexia, heat exhaustion, polyuria (diabetes mellitus) or poor intake from anorexia, together with the systemic effects of the primary illness, may produce orthostatic or true hypotension and syncope. In these conditions, dizziness, hypotension, or syncope occurs rapidly when the patient assumes an upright position (seconds). Prolonged bed rest, combined with poor fluid intake during an illness, may also result in syncope or presyncope when the child arises to leave the bed. In most of these situations, fluid administration is sufficient to restore intravascular volume and venous return to alleviate postural or supine hypotension.
Postural Orthostatic Tachycardia Syndrome (Pots)
(See Nelson Textbook of Pediatrics , p. 516.)
Postural orthostatic tachycardia syndrome is characterized by recurrent and chronic symptoms of orthostatic intolerance, exercise intolerance, light headedness, fatigue, sweating, tremor, anxiety, and presyncope when upright. The syndrome may be secondary to autonomic dysfunction. Symptoms are improved with lying down. Criteria to diagnose POTS include symptoms that have lasted greater than 6 months, heart rate that increases by at least 40 beats/min, if <18 years or 30 beats/min if >18 years, after assuming a standing from supine position for at least 10 minutes, symptoms worsen with standing and improve with recumbence, and the absence of other overt causes of orthostatic intolerance.
A detailed history of orthostatic intolerance may identify symptoms of headache, fatigue, sleep disorder, weakness, hyperventilation, shaking, sweating, anxiety, dizziness, and presyncope. An evaluation for POTS may include a complete blood count, glucose, electrolytes, and thyroid function. Cardiac evaluation should include an ECG. A tilt-table test may be helpful to demonstrate the effects of orthostatic stress (increased heart rate).
There is no specific treatment for POTS. Medications that may aggravate symptoms of POTS should be avoided including antihypertensive agents, sedatives, and many other psychiatric medications. Patients should avoid aggravating factors, such as dehydration, extreme heat, and alcohol. Nonpharmacologic treatment includes aerobic exercise, compressive stockings, and increased fluid and salt intake. Pharmacologic treatment should be tailored to the variant the patient exhibits.
Cardiac Syncope/Sudden Cardiac Death
(See Nelson Textbook of Pediatrics , p. 2261.)
A variety of cardiac conditions can result in hypotension and syncope ( Tables 6.8 and 6.9 ; see Table 6.3 ). Dysrhythmias are common and are usually silent between episodes (see Table 6.8 ). Supraventricular tachycardia, ventricular tachycardia, and heart block are the most common types of dysrhythmia and may be primary or may result from medications or illicit drugs. Any form of acquired heart block carries a high mortality rate ( Fig. 6.2 ). A common cause of acquired heart block is Lyme disease. Heart block may necessitate temporary or permanent electronic pacing to maintain cardiac output.
| Primary Electrical Abnormalities | Features | ECG | Treatment |
|---|---|---|---|
| LQTS: Romano-Ward, Jervell–Lange-Nielsen, acquired |
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| Brugada syndrome |
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| Placement of ICD |
| Wolff-Parkinson White |
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| Undergo EPT and ablation |
| Dilated cardiomyopathy: ventricular tachycardia/fibrillation |
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| Permanent pacemaker and ICD placement |
| Catecholamine-exercise: ventricular tachycardia |
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| SIDS and SIDS “Mimics” |
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| Corrected or Unoperated Congenital Heart Disease |
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| Coronary Arterial Disease |
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| Myocardial Disease |
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| Conduction System Abnormality/Arrhythmia |
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| Miscellaneous |
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Primary cardiac conduction abnormalities that may result in syncope include Wolff-Parkinson-White syndrome, long QT syndromes, and catecholamine-sensitive ventricular tachycardia. Wolfe-Parkinson-White syndrome is characterized by a short PR interva l, preexcitation seen as a widened QRS duration and a delta wave on the proximal portion of the QRS. The delta wave represents the presence of accessory electrical tissue from atria to ventricle, with rapid antegrade conduction causing excitation of ventricular tissue before atrioventricular node–His bundle stimulation. If that pathway can conduct in the retrograde manner, a reentrant circuit is created, causing a narrow QRS complex tachycardia. This greatly shortens the diastolic ventricular filling time and results in diminished left ventricular end-diastolic volume, with subsequently decreased stroke volume and decreased cardiac output. Although the tachycardia is rarely sufficiently fast to result in syncope, some children have profound hypotension and a rapid loss of consciousness. In adults, a similar mechanism results from atrial flutter or fibrillation if the ventricular response rate is fast.
Long QT syndromes are inherited (usually autosomal dominant) abnormalities in the electrical recovery (repolarization) of the heart ( Fig. 6.3 ). Prolongation of the repolarization phase results in the risk of simultaneous depolarization, the “R-on-T” phenomenon, which causes disorganized ventricular electrical stimulation characterized by torsades de pointes (coarse ventricular tachycardia), a potentially lethal dysrhythmia ( Fig. 6.4 ). There may be a family history of sudden cardiac death. Family studies with the same mutation have demonstrated that affected patients may not always have a long QT interval on ECG as defined for the syndrome, but an increased QT interval may become evident with exercise or during catecholamine infusion. Long QT syndromes may be responsible for some of the incidents of sudden infant death syndrome and drowning. Although additional genetic forms have been described, most mutations for prolonged QT involve either a sodium channel or potassium channel ( Table 6.10 ). Genotype may predict the patient’s presentation with LQT1 events associated with stress, while LQT3 may be associated with sleep. Long QT syndromes may present as a syncopal episode, seizures, palpitations, or presyncope. Diagnosing long QT is based on clinical history and ECG findings of a prolonged rate-corrected QT interval. Genetic testing may identify approximately 75% of patients. Acquired prolongation of the QT interval may also be seen in electrolyte abnormalities (hyperkalemia) and with a variety of medications ( Table 6.11 ). A drug history and toxicology screen may be warranted if there is any question of QT prolongation.
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