Syncope and Dizziness
Syncope is a transient loss of consciousnessand postural tone usually produced by impaired cerebral blood flow.Generally, a syncopal episode in childhood is a benign isolatedevent; however, some causes can be life threatening. Because dizzinessoften precedes syncope, it is also discussed in this chapter.
Principal Causes of Syncope and Dizziness
- Cardiovascularsyncope
- Neurocardiogenicsyncope
- Cardiac syncope
- Congenitaland acquired heart disease
- Hypercyanotic episodes
- Arrhythmias in structurally normalheart
- Arrhythmias in structurally abnormalheart
- Vascular syncope
- Orthostaticsyncope
- Cerebrovascular syncope
- Carotid sinus syncope
- Noncardiovascular syncope
- Breath-holding
- Hyperventilation
- Migraine
- Metabolic
- Hypoxia including anemia
- Hypoglycemia
- Psychologic
Clinical Features and Diagnosis
Cardiovascular Syncope
Neurocardiogenic Syncope (Common Faint)
Most commontype of syncope in childhood and adolescence.Often a response to anxiety, fear,pain, or other emotional stress.Also may occur after extreme fatigue,prolonged standing, or fasting.Pathogenesis involves vasodilatationof skeletal muscle vasculature and failure of heart rate and strokevolume to maintain cardiac output for adequate cerebral blood flow.Dizziness, nausea, sweating, and abdominaldiscomfort may precede syncope. Interruption of cerebral perfusionfor 2–3 secs produces dizziness, but lying down duringpresyncopal phase may prevent syncopal episode.If cerebral perfusion is interruptedfor >10 secs, syncope occurs.Onset is sudden with hypotension (vasodepressorresponse), and BP decreases to ≤60 mm Hg. Bradycardia usuallyoccurs, and often junctional rhythm or period of asystole (cardioinhibitory response)may follow.Most episodes are associated with uprightposition, and child becomes limp and falls to ground. Loss of consciousnessusually lasts <1 min.Seizures are unusual but may occurwith prolonged syncope.Once individual is horizontal, BP,heart rate, and color return toward normal.History and physical exam are usuallydiagnostic. Individuals with this form of syncope do not need furthertesting unless syncope is recurrent, when tilt table testing mayconfirm its presence.Both tussive and micturition syncopeare now considered forms of neurocardiogenic syncope.Tussive syncopehas been attributed to large increase in intrathoracic pressure,which decreases venous return to the heart. It may occur after significantcoughing of any cause, but especially after severe paroxysmal coughingwith pertussis.Micturition syncope is most commonin elderly men, but it can occur in older adolescents. Syncope usuallyoccurs at the end of micturition. The mechanism is unclear, buta full bladder causes peripheral vasoconstriction, and with emptying,peripheral vasodilatation occurs, which in the erect posture mayproduce syncope. Cardiac Syncope
Congenital and Acquired Heart Disease
Syncopemay occur with outflow obstruction of left ventricle (LV) (valvar,subvalvar, or supravalvar aortic stenosis; hypertrophic cardiomyopathy),outflow obstruction of right ventricle (RV) (pulmonic stenosis,primary pulmonary artery hypertension, pulmonary vascular disease),inflow obstruction of LV (mitral stenosis, atrial myxoma), and inflowobstruction of RV (cardiac tamponade). More likely to occur duringor just after physical exertion, when cardiac output cannot increaseenough to meet demands of oxygen delivery to brain.Syncope also may occur with cardiomyopathy,myocarditis, and endocarditis as a result of decreased cardiac output.Another cause is myocardial ischemia,which may occur with coronary artery anomalies, especially anomalousorigin of left coronary artery from pulmonary artery and abnormalcourse of left coronary artery between aortic and pulmonary trunkswith compression of artery during exercise. Coronary artery aneurysmsand thrombosis found in Kawasaki disease also may produce myocardialischemia and syncope.In most cases, history, physical exam,chest radiograph, ECG, and 2-D echocardiogram are diagnostic.Diagnosis of primary pulmonary hypertensionusually requires lung biopsy to exclude pulmonary venoocclusivedisease. Although pulmonary vascular disease may be diagnosed clinicallywith support of echocardiography, cardiac catheterization and angiographycan confirm these findings. Hypercyanotic Episodes
Consistof intense cyanosis and hyperpnea. Occur most commonly with tetralogyof Fallot but also can occur with tricuspid atresia, transpositionof great arteries with pulmonary stenosis, and pulmonary vasculardisease.Children who can walk may squat duringepisode, which increases systemic vascular resistance and decreasesright-to-left shunt.Occasionally episodes may be prolongedand associated with syncope and seizures. During episode, murmuris less intense or disappears.Several factors seem to play a role:prolonged crying with decreased venous return, constriction of RVinfundibulum, decreased systemic vascular resistance secondary toimmobilization or spontaneous vasomotor changes, relative anemia,and increased physical activity with higher oxygen requirement. Arrhythmias in Structurally Normal Heart
Syncopemay occur from sinus bradycardia, junctional bradycardia, second-and third-degree (atrioventricular) AV block with low ventricularrate, supraventricular tachycardia, atrial flutter, or ventriculartachycardia.Atrial fibrillation with rapid ventricularresponse over the accessory pathway may be associated with syncopeor near syncope in Wolff-Parkinson-White (WPW) syndrome. Diagnosisis usually confirmed by ECG, which shows short PR interval and deltawave.Syncope also may occur with prolongedQT interval, in which variable recovery time with reentry depolarizationmay cause torsade de pointes ventricular tachycardia.ProlongedQT interval has a number of genetic causes. Hypokalemia, hypocalcemia, andhypomagnesemia also may cause QT interval prolongation. Tricyclicantidepressants and phenothiazines have been associated with prolongedQT interval, and so have overdoses of quinidine, procainamide, anddisopyramide.Prolonged QT interval can be diagnosedby measuring this interval on routine ECG, but it must be correctedfor heart rate. 1 method for correction of QT interval is to measureQT interval (in secs) and divide by the square root of the RR interval(in secs). In 95% of individuals, the corrected QT interval is <0.45secs. Sympathomimetic drugs when taken inlarge doses or from idiosyncratic reaction may produce supraventricularor ventricular tachycardia. Cocaine also may produce ventriculartachycardia and syncope. Metabolic derangements (e.g., hyperkalemia,hypoglycemia, and hypercalcemia) also may result in syncope by producingarrhythmias, but this is rare.ECG may be diagnostic of these arrhythmias.If syncopal episodes are frequent, Holter monitoring may be useful;if they occur during exercise, maximal exercise testing may be diagnostic.Otherwise, event recorder or implanted loop recorder should be considered.If syncope still remains unexplained,electrophysiologic studies should be performed. Arrhythmias in Structurally Abnormal Heart
Childrenwho have congenital or acquired heart disease are at risk for arrhythmias thatmay produce syncope. These include sinus bradycardia, sick sinussyndrome, supraventricular tachycardia, atrial fibrillation, atrialflutter, ventricular tachycardia, ventricular fibrillation, andcomplete heart block.WPW syndrome and supraventricular tachycardiaare occasionally associated with Ebstein anomaly.Complete heart block may be associatedwith ventricular inversion and transposition of great arteries.Ventricular tachycardia may occur fromarrhythmogenic RV dysplasia, although echocardiography may not bediagnostic because a heavily trabeculated RV may be indistinguishablefrom dysplasia. Recurrent ventricular tachycardia, especially exercise-induced,and left bundle branch pattern suggest this diagnosis, which canbe confirmed by MRI.Children who have had surgical repairof a cardiac defect are also at risk for development of arrhythmias.An incision in the ventricle is a risk factor for ventricular tachycardia.Supraventricular tachycardia, atrial fibrillation, atrial flutter,sick sinus syndrome, and ventricular tachycardia may occur after Mustardor Senning procedure for repair of transposition of great arteries.Surgical manipulation in the area of sinus or AV nodes in repairof AV canal defects, posterior ventricular septal defects, or tunnelaortic stenosis may predispose to development of sinus bradycardiaand heart block.ECG may be diagnostic of these arrhythmias.Holter monitoring and maximal exercise testing also may be helpfulin diagnosis.If these tests are normal consideringhigher risk of life-threatening events in children with structurallyabnormal hearts, electrophysiologic studies should be considered. Vascular Syncope
Orthostatic Syncope
Occurs whenindividual assumes upright posture and systolic arterial BP decreasesby ≥15 mm Hg.Possible causes includeDecreasedblood volume (blood loss, GI fluid loss, excessive diuretic use)Failure of normal postural reflexes(suddenly standing up after prolonged bedrest, familial dysautonomia,spinal cord lesions)Drugs (vasodilators, tricyclic antidepressants,sedatives, opiates, cocaine) Supine and standing BPs should be measuredin any individual with unexplained syncope. Cerebrovascular Syncope
This typeof syncope may be due to excessive vagal stimulation, which causessevere bradycardia or AV block.Examples include intubation, placementof nasogastric tube or esophageal overdrive pacing catheter, removalof pleural or peritoneal fluid, and distention of viscera.Excessive vagal tone also may occurin normal adolescents or well-trained athletes, and a further increasein vagal tone may worsen bradycardia or AV block enough to causesyncope. Carotid Sinus Syncope
Pressure on baroreceptors in carotid sinusmay cause carotid sinus syncope. Uncommon in children but can occurwith excessive pressure on neck (e.g., wearing tight collar).
Noncardiovascular Syncope
Breath-Holding
Common inchildren 6 mos–6 yrs of age. Precipitating factors includepain, frustration, and anger.Pallid breath-holding, which is nowthought to be variation of neurocardiogenic syncope, usually followsacute pain or injury. The infant or child becomes pale and losesconsciousness. Complete recovery occurs in 1–2 mins.More common is cyanotic breath-holdingspell in which infant or child cries, holds breath during expiration,and turns dusky until breathing begins again. Loss of consciousnessand tonic-clonic movements may occur with prolonged episode. Hyperventilation
Frequentcause of dizziness but rare cause of syncope.Common in adolescent girls and usuallydue to emotional stress.Frequent complaints include lightheadedness,blurred vision, difficulty breathing, choking, smothering, chesttightness, and numbness or tingling of fingers, toes, and face.Individuals who are hyperventilating appear anxious and have fastand deep respirations.Rebreathing into paper bag and thoughtfulreassurance usually lessen hyperventilation, so that individualscan begin talking about what is upsetting them. Migraine
Severe migraine headache may cause syncopalepisode, especially if basilar arterial system is affected (see Chap. 25, Headache).
Metabolic
Hypoxia Including Anemia
Severe hypoxia or severe anemia of any causemay result in syncope. See Chap.45, Pallor (Anemia), and Chap. 56, Respiratory Distress and Apnea.
Hypoglycemia
Often causesfaintness and dizziness, but syncope is exceedingly rare. Othermanifestations of hypoglycemia include headache, hunger, sweating,and jitteriness, which may progress to confusion, seizures, andcoma.Low blood glucose level confirms presenceof hypoglycemia.With administration of oral or intravenousglucose, symptoms resolve.See further discussion of hypoglycemiain Chap. 59, Seizures. Psychologic
Acute stressmay produce anxiety and syncope with or without hyperventilation. Commonstresses are witnessing a tragic event or hearing news of the deathof close friend or relative.Hysteria is common cause of recurrentfainting in adolescents, especially in those with hysterical personalities.In this typeof episode, which almost always occurs in presence of other people,hysterical person falls or slumps in dramatic way but avoids injury.Fainting also may occur while lying or sitting down. There is noprodrome or change in heart rate, BP, or skin color. Diagnosis of psychologic causes ismade from history, physical exam, and clinical observation. Diagnostic Approach
Neurocardiogenicsyncope, vascular syncope, breath-holding, hyperventilation, and psychologicdisturbances can usually be distinguished by history and physicalexam.If syncopal episode occurs on assumingupright posture, BP should be measured in supine and upright positions.Postural difference in systolic pressure of >15 mm Hg confirmsdiagnosis of orthostatic syncope.Individuals with recurrent syncope,family history of sudden death, or syncope occurring during intensiveexercise need further evaluation.If recurrent syncope occurs, tilt testingmay determine whether syncope is neurocardiogenic.Family history of syncope and suddendeath suggests hypertrophic cardiomyopathy or long QT interval syndrome.Syncope during intense exercise mayoccur with hypertrophic cardiomyopathy, severe aortic stenosis,anomalous left coronary artery from pulmonary artery, primary pulmonaryhypertension, or exercise-induced atrial fibrillation associatedwith WPW syndrome. Diagnosis of cardiac disorders canbe made from history, physical exam, chest radiograph, ECG, and2-D echocardiogram. Cardiac catheterization and angiography maybe necessary to make definitive diagnosis and to determine severityof lesion. Arrhythmia may be suspected from history, and routine ECGwith rhythm strip may be diagnostic. Otherwise, further testingmay be needed (e.g., Holter monitoring, maximal exercise testing,event recorder or implanted loop recorder monitoring, and electrophysiologictesting).With syncopal episode of unknown cause,ECG should be initially performed searching for WPW syndrome, longQT interval syndrome, or LV hypertrophy with T-wave changes indicativeof cardiomyopathy. References
- Beder SD, et al. Occult arrhythmias asthe etiology of unexplained syncope in children with structurallynormal hearts. Am Heart J 1985;109:309–313.
- Delgado CA. Syncope. In: Fleisher GR, Ludwig S, eds.Textbook of pediatric emergency medicine, 4th ed. Philadelphia:Lippincott Williams & Wilkins, 2000:593–599.
- Feit LR. Syncope in the pediatric patient: diagnosis,pathophysiology, and treatment. Adv Pediatr 1996;43:469–495.
- Hannon DW, Knilans TK. Syncope in children and adolescents.Curr Probl Pediatr 1993;23:358–384.
- Kanter RJ. Syncope and sudden death. In: Garson A Jr,et al., eds. The science and practice of pediatric cardiology, 2nded. Baltimore: Williams & Wilkins, 1998:2169–2199.
- O'Laughlin MP, McNamara DG. Syncope. In: GarsonA Jr, et al., eds. The science and practice of pediatric cardiology.Philadelphia: Lea & Febiger, 1990:1929–1946.
- Rudolph AM, ed. Rudolph's pediatrics, 20thed. Stamford, CT: Appleton & Lange, 1996.
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Book Source Details
- Book Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics
- Author(s): Paul S. Bellet
- Year of Publication: 2006
- Copyright Details: The Diagnostic Approach to Symptoms and Signs in Pediatrics, Copyright © 2006 Lippincott Williams & Wilkins.
Other Book Chapters Related to Vertigo
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Medical Books Excerpts
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- "Algorithmic Diagnosis of Symptoms and Signs" (2003)
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- "Handbook of Signs & Symptoms (Third Edition)" (2006)
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- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
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- "The Diagnostic Approach to Symptoms and Signs in Pediatrics" (2006)
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- "Nursing: Interpreting Signs and Symptoms" (2007)
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- "Nursing: Interpreting Signs and Symptoms" (2007)
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- SYNCOPE
- "Differential Diagnosis in Primary Care" (2007)
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Copyright Details: The Diagnostic Approach to Symptoms and Signs in Pediatrics, Copyright © 2008 Williams & Wilkins.
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