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EMERGENCY MEDICINE PRACTICE . EMPRACTICE NET A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E January 2004 Syncope: An ED Approach To Risk Stratification Volume 6, Number 1 Authors It’s Sunday morning. You’ve just discharged the last Saturday night warrior from the ED when you get a call that the local EMS crew is bringing in a woman who has had a syncopal episode at church. When the crew arrives, you get a typical story from the paramedic. “She’s a 44-year-old woman who was sitting during a 20-minute sermon. When the congregation stood, she stood and then fell to the ground. She awoke seconds after falling, no serious injuries noted. She takes a heart pill of some kind, and a water pill. She says she has high blood pressure. Heart rate on our monitor was 60 and normal sinus. BP in the left arm was 110/64. Sats 99% on two liters. No other complaints. Her husband is on the way.” You introduce yourself to the patient, who tells you that her heart doctor recently increased the dose of her heart pill. The patient thinks this might be the problem. She denies any serious symptoms now or before the event. You’re thinking, “Too much betablocker—case solved.” Just then, the patient’s anxious husband arrives. He corroborates the EMS story. Then he adds, “I sure hope this isn’t that bleed on her brain like the last time she passed out in church. Her heart doctor also said we should watch out for the main blood vessel in her chest. It was big on the last scan they took.” So much for the slam-dunk case. S YNCOPE is a common and challenging symptom that brings patients to the ED. It is estimated that 12%-40% of adults younger than 40 years will experience at least one episode of syncope, with up to 20% experiencing syncope before the end of adolescence.1-3 Patients older than 75 years have a reported 6% annual incidence of syncope.2 Syncope accounts for 3% of all ED visits and up to 6% of all hospital admissions.1,4-6 The overall cost per hospital admission was estimated to be about $5300 in 1996.2 According to data from the year 2000 collected by the Healthcare Cost and Utilization Project, syncope ranked 58 in a list of the top 100 diagnoses for U.S. hospital stays. Syncope accounted for 229,867 hospital discharges and an aggregate charge of $2,122,072,519.7 Syncope has many causes, which range from benign, self-limited problems to immediately life-threatening events. The etiology of syncope can be difficult to diagnose. Syncope is a transient event, and not a specific disease entity; furthermore, the patient often is completely asymptomatic at the time of the Guest Editor Keith A. Marill, MD, Emergency Medicine Attending, Massachusetts General Hospital; Faculty, Harvard Medical School, Boston, MA. Associate Editor Andy Jagoda, MD, FACEP, ViceChair of Academic Affairs, Department of Emergency Medicine; Residency Program Director; Director, International Studies Program, Mount Sinai School of Medicine, New York, NY. Editorial Board Judith C. Brillman, MD, Associate Professor, Department of Emergency Medicine, The University of New Mexico Health Sciences Center School of Medicine, Albuquerque, NM. W. Richard Bukata, MD, Clinical Professor, Emergency Medicine, Los Angeles County/USC Medical Center, Los Angeles, CA; Medical Director, Emergency Department, San Gabriel Valley Medical Center, San Gabriel, CA. Francis M. Fesmire, MD, FACEP, Director, Heart-Stroke Center, Erlanger Medical Center; Assistant Professor of Medicine, UT College of Medicine, Chattanooga, TN. Valerio Gai, MD, Professor and Chair, Department of Emergency Medicine, University of Turin, Italy. Michael J. Gerardi, MD, FAAP, FACEP, Clinical Assistant Professor, Medicine, University of Medicine and Dentistry of New Jersey; Director, Pediatric Emergency Medicine, Children’s Medical Center, Atlantic Health System; Department of Emergency Medicine, Morristown Memorial Hospital. Michael A. Gibbs, MD, FACEP, Chief, Department of Emergency Medicine, Maine Medical Center, Portland, ME. Gregory L. Henry, MD, FACEP, CEO, Medical Practice Risk Assessment, Inc., Ann Arbor, MI; Clinical Professor, Department of Emergency Medicine, University of Michigan Medical School, Ann Arbor, MI; Past President, ACEP. Jerome R. Hoffman, MA, MD, FACEP, Professor of Medicine/Emergency Medicine, UCLA School of Medicine; Attending Physician, UCLA Emergency Medicine Center; Co-Director, The Doctoring Program, UCLA School of Medicine, Donald J. Kosiak, Jr., MD Emergency Medicine Chief Resident, Department of Emergency Medicine, Mayo Clinic and Mayo Graduate School of Medicine, Rochester, MN. Wyatt W. Decker, MD, FACEP Chair, Department of Emergency Medicine, Mayo Clinic and Mayo Medical School, Rochester, MN. Peer Reviewers David C. Pigott, MD, FACEP Assistant Professor of Emergency Medicine, Department of Emergency Medicine, The University of Alabama at Birmingham, Birmingham, AL. Sid M. Shah, MD Assistant Clinical Professor, Michigan State University, Sparrow/MSU Emergency Medicine Residency Program, Lansing, MI. CME Objectives Upon completing this article, you should be able to: 1. describe cardiac, central nervous system, vasovagal, and metabolic/drug-related causes of syncope; 2. describe ways that the history and physical examination can be used to identify potentially lethal causes of syncope; 3. discuss factors that indicate the need for diagnostic tests such as the ECG; and 4. describe an evidence-based process for the ED encounter that can risk stratify patients to determine who should be admitted vs. who can safely be discharged. Date of original release: January 1, 2004. Date of most recent review: December 5, 2003. See “Physician CME Information” on back page. Los Angeles, CA. Francis P. Kohrs, MD, MSPH, Lifelong Medical Care, Berkeley, CA. Michael S. Radeos, MD, MPH, Attending Physician, Department of Emergency Medicine, Lincoln Medical and Mental Health Center, Bronx, NY; Assistant Professor in Emergency Medicine, Weill College of Medicine, Cornell University, New York, NY. Steven G. Rothrock, MD, FACEP, FAAP, Associate Professor of Emergency Medicine, University of Florida; Orlando Regional Medical Center; Medical Director of Orange County Emergency Medical Service, Orlando, FL. Alfred Sacchetti, MD, FACEP, Research Director, Our Lady of Lourdes Medical Center, Camden, NJ; Assistant Clinical Professor of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA. Corey M. Slovis, MD, FACP, FACEP, Professor of Emergency Medicine and Chairman, Department of Emergency Medicine, Vanderbilt University Medical Center; Medical Director, Metro Nashville EMS, Nashville, TN. Mark Smith, MD, Chairman, Department of Emergency Medicine, Washington Hospital Center and Georgetown University School of Medicine, Washington, DC. Charles Stewart, MD, FACEP, Colorado Springs, CO. Thomas E. Terndrup, MD, Professor and Chair, Department of Emergency Medicine, University of Alabama at Birmingham, Birmingham, AL. COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC prolonged confusion. When defined broadly, syncope may be due to any condition that temporarily decreases the availability of critical nutrients such as oxygen or glucose to the brain, or that disrupts or poisons brain function. The brain requires an adequate supply of glucose and oxygen to work properly. When the minimum threshold is not met, syncope will occur within 10 seconds.9 Syncope can also be defined more narrowly as being due to any condition that causes a sudden decrease in, or brief cessation of, cerebral blood flow to the brainstem and, specifically, the reticular activating system. Thus, any condition that decreases cerebral blood flow below a critical level would be a potential etiologic agent. It has been suggested that the cause of syncope can be broken into five broad categories: 1) cardiac; 2) central nervous system; 3) vasovagal/psychogenic; 4) metabolic and drug-related; and 5) unknown.1,2,16,18-20 Because of the mortality associated with cardiac-related syncope, many elect to view the fundamental branch on the decisionmaking pathway as that separating the cardiogenic causes of syncope from the non-cardiogenic causes.5,16,20 Cardiogenic causes can be further separated into primarily obstructive or dysrhythmia-related. Table 1 summarizes the causes of syncope. evaluation. Also, the cause can be multifactorial, which makes a final diagnosis complicated. In as many as 50% of ED patients, no readily apparent diagnosis is available on ED discharge.1,4-6,8 The principal task of the ED practitioner is to identify those patients at risk for an adverse outcome. However, even with extensive and costly testing such as echocardiograms and electrophysiology studies, it is often difficult to be sure that the exact cause of syncope has been determined, or that potentially lethal causes have been ruled out. This issue of Emergency Medicine Practice is designed to help clinicians maximize the ED work-up of syncope as well as differentiate those patients who are at high risk for an adverse outcome from those who can safely be discharged home. Critical Appraisal Of The Literature Syncope has been studied throughout the history of medicine.9,10 However, the literature that discusses syncope mainly consists of small, retrospective evaluations, cohort studies, and many case reports. Clinical guidelines regarding the evaluation and diagnosis of syncope have been published by organizations such as the American College of Emergency Physicians (ACEP), the American College of Physicians (ACP), and the European Society of Cardiology.11-14 A few prospective trials have been done, but most are small in scale. More recently, a larger emphasis has been placed in this area, and several large, quality studies have been completed or are currently under investigation.15-17 Cardiogenic Syncope There are many cardiac-related causes of syncope, but they can all generally be placed into one of two categories. The cause of syncope can be due to a primary dysrhythmia or related to obstruction of blood flow. The obstruction-to-flow category can be further subdivided into obstructive and vascular causes. (Review Table 1 for a list of common causes under each category.) Inadequate cardiac output is the underlying premise in all of these patients with cardiogenic syncope. Pathophysiology Syncope is defined as a sudden and transient loss of consciousness associated with a loss of postural tone, with a spontaneous and full recovery. There is also an absence of Table 1. Etiology Of Syncope. Cardiac Causes Obstruction to flow • Subaortic stenosis • Aortic valve stenosis • Mitral valve stenosis • Atrial myxoma (rare) • Pulmonic valve stenosis • Hypertrophic cardiomyopathy • Dilated cardiomyopathy • Restrictive cardiomyopathy • Pericardial tamponade • Severe congestive heart failure Vascular disease • Pulmonary emboli • Pulmonary hypertension • Acute myocardial infarction • Air embolism • Aortic dissection/leaking Emergency Medicine Practice Noncardiac Causes aortic aneurysm • Subclavian steal syndrome • Subarachnoid hemorrhage • Subdural/epidural hemorrhage Vasodepressor (vasovagal, neurocardiogenic) • Situational • Micturition • Post-tussive • Swallow • Defecation • Valsalva (weightlifters) • Carotid sinus sensitivity Dysrhythmias Tachydysrhythmias • Supraventricular tachycardia • Ventricular tachycardia • Ventricular fibrillation • Atrial fibrillation with fast conduction • Wolff-Parkinson-White syndrome • Prolonged QT syndrome • Brugada syndrome Orthostatic • Anemia/GI bleed • Dehydration Central nervous system / neurologic • Seizure (excluded by most syncope studies) • Neuralgias (trigeminal, glossopharyngeal) • Neurologic (TIA, strokes, migraines [rare]) Bradydysrhythmias • Atrioventricular block • Atrial fibrillation with slow conduction • Sick sinus syndrome • Pacemaker malfunction 2 Metabolic / toxic • Hypoglycemia • Hypoxia • Drug-induced • Carbon monoxide poisoning • Chemical / toxic gas exposure • Carotid sinus sensitivity • Infectious agent Psychogenic • Somatization disorder • Anxiety disorder • Conversion disorder • Panic disorder • Hyperventilation • Breath-holding spells www.empractice.net • January 2004 Congenital long QT syndrome refers to a collection of heritable defects of the myocardial Na+ and K+ channel proteins that cause prolongation of the QT interval on the resting ECG and predispose the patient to a specific malignant ventricular dysrhythmia—torsades de pointes. The condition may be either autosomal recessive (Jervell and Lang-Nielson syndromes) or autosomal dominant (Romano-Ward syndrome).28 Torsades de pointes is defined as polymorphic ventricular tachycardia that occurs in the setting of a prolonged QT interval. The ECG is of critical importance in the evaluation of these patients. The QT interval is measured from the onset of the Q wave to the end of the T wave. The QT interval normally varies with heart rate, so several formulas, such as Bazzet’s, are available to derive the heart rate-corrected (QTc) interval. The QTc is considered abnormally long when it is greater than 0.45 in men, 0.46 in children, and 0.47 in women in units of seconds.29 The ECG may also demonstrate a notched or bifid T wave in leads V2 to V4. Syncope in patients with long QT syndrome is usually due to self-limited episodes of torsades de pointes. Torsades de pointes may also be persistent and deteriorate into ventricular fibrillation and resultant sudden cardiac death. The risk of sudden death increases in proportion to the duration of the QTc.29,30 A prolonged QT interval and the associated risk of torsades de pointes can also be acquired. Medicines that prolong the QT interval by blocking the K+ repolarization channels or via other mechanisms, or exacerbate the problem by altering drug metabolism, are potential causes. Drugs associated with acquired long QT syndrome include type IA antidysrhythmics such as procainamide and quinidine as well as type III antidysrhythmics such as sotalol, phenothiazines, haloperidol, tricyclic antidepressants, erythromycin, pentamidine, and the nonsedating antihistamines astemizole (Hismanal) and terfenadine (Seldane). Drugs implicated in prolonging the hepatic metabolism of these agents include erythromycin, ketoconazole, cimetidine, and cisapride. Other etiologies of an acquired prolonged QT interval include electrolyte disturbances such as hypokalemia and hypomagnesemia, a low protein diet, severe bradycardia, and an acute cerebrovascular accident.31,32 Brugada syndrome is another autosomal dominant cardiac dysrhythmia disease.33,34 Brugada syndrome is recognized throughout the world, and it has been estimated that this syndrome may be responsible for 4%-12% of all cases of unexplained sudden cardiac death.35 It is characterized by syncopal episodes in patients with structurally normal hearts who demonstrate characteristic ECG patterns that define the syndrome. The disease is caused by a defect in the Na+ myocardial membrane channel protein, which leads to abnormalities of depolarization. The ECG manifestations include a pseudo-right bundle branch block and persistent downsloping ST segment elevation in leads V1 to V3.33-37 The presence of these ECG findings is not always constant and can confuse the diagnosis. As with prolonged QT syndrome, patients with Brugada syndrome are predisposed to ventricular dysrhythmias that can deteriorate into ventricular fibrillation and sudden cardiac death. Dysrhythmias are responsible for many episodes of syncope. In fact, cardiac dysrhythmias are the most common cause of syncope in patients with underlying heart disease, including coronary artery disease, congestive heart failure, and structural heart disease.19,21,22 Dysrhythmias can be due to the heart beating too fast, too slow, or in an abnormal manner. Tachycardic Dysrhythmias Tachycardic dysrhythmias cause decreased cardiac output by not allowing sufficient time for the heart to properly and completely fill during diastole. Examples include ventricular tachycardia and supraventricular tachycardias such as atrioventricular reentrant and atrioventricular nodal reentrant tachycardia as well as atrial fibrillation or atrial flutter. The atrial tachydysrhythmias may occur in the setting of Wolff-Parkinson-White syndrome, where there is an unconcealed bypass tract between the atrial and ventricular myocardial tissue. Ventricular fibrillation can also be considered a tachydysrhythmia, but in this case loss of cardiac output may be primarily due to unsynchronized and ineffective myocardial contraction. Patients with tachydysrhythmias have a spectrum of presentations from completely asymptomatic to full cardiac arrest.23 Bradycardic Dysrhythmias Bradycardic dysrhythmias can also cause syncope. Bradycardia may have an intrinsic cardiologic etiology, such as dysfunction of the specialized cardiac conduction system at the level of the sinoatrial or atrioventricular nodes, or within the His-Purkinje bundle branch fibers. It may also be due to extrinsic factors, such as excessive cholinergic stimulation or negative chronotropic poisoning, such as from excessive beta- or calcium-channel-blocking agents. Sick sinus syndrome is commonly seen in our aging population.24,25 This is a dysrhythmia that presents with periods of normal cardiac rhythm, mixed with sinus bradycardia, asystolic pauses, and/or sinoatrial block. It can be a sign of other underlying heart disease. A pacemaker is generally warranted for treatment of this condition.25 Other bradycardic rhythms that can cause syncope are the heart blocks. Specifically, second-degree type II heart block and third degree or complete heart block are common causes of syncope. If the ventricular escape rhythm is unable to maintain cerebral perfusion, a syncopal event known as a Stokes-Adams attack will occur.19,26 Pacemaker malfunction may cause syncope. Possible etiologies include device malfunction or battery exhaustion, failure to sense, failure to capture, or disruption of communication such as damage to the leads.27 Careful interrogation of pacemaker function should be performed by the cardiologist for all patients who present with syncope who have a pacemaker. The Rare But Deadly Dysrhythmias Two dysrhythmia syndromes deserve special attention. They are long QT syndrome and Brugada syndrome. They occur infrequently in the general population, but to miss a case could be deadly to the patient. January 2004 • www.empractice.net 3 Emergency Medicine Practice COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC Dysrhythmic Causes Of Cardiac Syncope COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC Obstructive Causes Of Cardiac Syncope Generalized seizures include atonic seizures, where there is a sudden transient loss of postural tone, and absence seizures, where there is a brief loss of consciousness without loss of postural tone. Cerebrovascular accidents and transient ischemic attacks are common neurologic events that are sometimes confused with syncope.39 (See also the October 2003 issue of Emergency Medicine Practice, “Transient Ischemic Attacks: Transient Trouble Or Action-Warranted Attacks?”) Mechanistically, it would seem that only a cerebrovascular event involving the vertebrobasilar system or both cerebral hemispheres should lead to depressed consciousness and syncope. Since occlusion of both carotid arteries simultaneously would be unlikely, compromise of both cerebral hemispheres would likely only occur due to a large hemorrhagic stroke and mass effect. Associated specific neurologic symptoms and signs often distinguish stroke syndromes from syncope. Disease involving both hemispheres would be expected to demonstrate widespread deficits, and patients with vertebrobasilar disease often demonstrate diplopia, ataxia, vertigo, and dysarthria.9 Like the other cardiac causes of syncope, this is also a large group. (Table 1 lists the causes of syncope due to obstruction.) These diseases of the heart valves, musculature, and pericardial lining can cause obstruction to forward flow of blood through the heart, and acute and chronic compromise in cardiac output. It is important to remember, however, that obstruction itself is sometimes not the acute cause of syncope and sudden death in affected patients. Many of these conditions are associated with primary disease of the myocardial tissue, such as with hypertrophic cardiomyopathy, or secondary myocardial abnormalities, such as left ventricular hypertrophy. The abnormal myocardial tissue or hypertrophy predisposes patients to ventricular dysrhythmias, which may often be the primary etiology of syncope and sudden death.38 Additional factors that may be causative or contribute to acute symptoms include myocardial ischemia exacerbated by hypertrophy, abnormal peripheral vascular and ventricular baroreflexes, and acute conduction block. Non-Cardiogenic Syncope Vasodepressor Syncope Metabolic Syncope Vasodepressor syncope (also termed neurocardiogenic, neurogenic, or vasovagal syncope) is the most common cause of syncope. The exact mechanism of vasodepressor syncope is poorly understood. In vasodepressor syncope, there is a failure in, or possibly an interruption of, the sympathetic excitation to the heart and peripheral vascular system.9,20 This is followed by excess parasympathetic excitation, which leads to severe vasodilation and bradycardia. This is termed the Bezold-Jarisch reflex. These autonomic alterations and the ensuing transient hypotension may cause the patient to experience dizziness, weakness, pallor, sweating, lightheadedness, and, ultimately, possible syncope.9 These episodes are often associated with an increase in emotional lability, such as in a patient under stress, in a crowded environment, or during prolonged standing. Situational syncope is related to vasodepressor syncope, except it is usually associated with a specific activity such as coughing, micturition, or defecation. The mechanism of situational syncope is thought to be similar to that of vasodepressor syncope, and it’s generally considered a variant. Orthostatic hypotension is also related to vasodepressor syncope. This condition has a variety of etiologies, including volume depletion, medications, advanced age, and certain illnesses. (Orthostatic hypotension will be discussed in more detail later in this review.) The critical substrates for brain metabolism include glucose and oxygen. Compromised delivery or utilization of either of these substances can lead to syncope or prolonged loss of consciousness. Many of the mechanisms described thus far address compromised blood flow to the brain. There may also be an inadequate blood concentration of these substrates. Hypoglycemia is a common cause of altered consciousness and syncope-like events in diabetic patients.40 The most common etiology is an imbalance between insulin or oral hypoglycemic administration and food intake. Other uncommon causes such as insulinomas have also been described in these patients.41 Hypoxemia can occur due to inadequate or ineffective ventilation, and loss or malfunction of red blood cell hemoglobin. Finally, the brain may be provided with an adequate supply of oxygen, but the cells may be unable to utilize it. There are a variety of drugs and poisons that can acutely affect each step of the oxygen delivery process. Hemorrhage and red cell lysis can contribute to syncope, but loss of blood volume and flow is often more important than loss of oxygen-carrying capacity with hemorrhage. Finally, other metabolic derangements can impair systems critical for brain function. Perhaps most importantly, hypo- or hyperkalemia can lead to cardiac dysfunction, dysrhythmias, and syncope. Neurologic Syncope Drugs and poisons can cause or exacerbate all of the mechanisms responsible for syncope. Syncope may occur due to toxic effects of appropriate therapeutic dosing or intentional or inadvertent overdosage. Accidental exposure at home or work is possible. Intentional environmental exposure to a wide variety of toxic and lethal agents must also be considered today. Terrorists have successfully disseminated sarin vapor, a cholinergic agent, in the Tokyo subway, and the Russian military has demonstrated the Drug-Related Syncope And Poisoning Neurologic conditions rarely cause, but often mimic, syncope. The most common neurologic condition that is confused with syncope is seizure. By definition, complex seizures are associated with an impairment in consciousness. These seizures may be partial and localized to one area of the brain, or generalized throughout both hemispheres. There may or may not be obvious associated automated or tonic-clonic activities suggesting epileptoform activity. Emergency Medicine Practice 4 www.empractice.net • January 2004 Differential Diagnosis Clearly, the differential diagnosis of syncope is wide. As always, the emergency clinician should consider the most lethal diagnoses first. Cardiovascular disease is associated with the highest long-term mortality, and patients are often at high risk for recurrent unstable events in the ED as well. Cardiogenic Syncope Beyond the usual benefits of a firm diagnosis, there are two important reasons to correctly identify cardiogenic syncope. First, syncope from cardiogenic causes has a one-year mortality rate ranging between 18% and 33%, compared to 0%-12% for non-cardiogenic causes and 6% for unexplained causes.1,4,5,14,44,45 Second, the treatment of many of the conditions responsible for cardiogenic syncope has advanced dramatically in the past decade. Many of the conditions can be successfully treated with medications and potentially cured with invasive procedures. One study conducted by Martin et al developed and validated a clinical prediction rule for risk stratification of patients with syncope. The authors first derived the prediction rule by reviewing the charts of 252 patients presenting to the ED with syncope. The study was validated using 374 patients. The study found four factors that were useful for risk stratification: 1) age greater than 45 years; 2) history of ventricular dysrhythmias; 3) history of congestive heart failure; and 4) an abnormal ECG. In the validation cohort, one-year mortality ranged from 1.1% with no risk factors to 27.3% with three or more risk factors.46 Another study done by Alboni et al found that the presence of suspected or certain heart disease on examination was an independent predictor of a cardiac cause of syncope, with a sensitivity of 95% and a specificity of 45%. The same study found that the absence of heart disease on history and physical examination ruled out a cardiac cause of syncope in 97% of subjects.47 Cardiac syncope can occur without exertion or while in a sitting or supine position. In fact, a complaint of syncope while sitting is highly suggestive of a cardiac origin. Obstructive Causes Of Cardiac Syncope Table 1 lists some of the causes of syncope due to obstructive cardiologic disease. Valvular disease, particularly of the left side of the heart, is associated with syncope. In fact, syncope, along with angina and congestive heart failure, is one of the three most common presenting complaints of patients with aortic stenosis.50 This disease, along with conditions such as hypertrophic cardiomyopathy and other causes of structural heart disease, is usually associated with exertional syncope. Hypertrophic cardiomyopathy is a complex cardiac disease with a large spectrum of clinical variance.51 Its diagnosis is generally based on a combination of physical examination findings and diagnostic testing such as echocardiography. Classic physical findings include a loud S-4 heart sound and a harsh and crescendo-decrescendo systolic murmur. The murmur is best heard between the apex and the left sternal border.52 During strain, such as a Valsalva maneuver, the murmur will increase in volume secondary to an increase in gradient. Squatting or an isometric handgrip can decrease the murmur’s intensity. Murmurs on examination are usually characteristic for each specific valvular disorder. For example, aortic stenosis has a characteristic diamond-shaped, midsystolic murmur most often radiating to the neck. It can also be associated with an S-4 heart sound.52 (Further discussion about evaluation of murmurs can be found under the cardiac examination section of this review.) One special group of valvular patients is the group that has undergone artificial valve replacement. The combination of mechanical heart valves and syncope is an ominous sign that could suggest a number of complications, includ- Dysrhythmic Causes Of Cardiac Syncope Sustained ventricular tachycardia is most commonly due to a reentrant electrical wavefront involving a scar from a prior myocardial infarction. The diagnosis must be entertained in any patient with a history of prior myocardial infarction. The patient may feel palpitations, chest discomfort, or lightheadedness prior to syncope. Ventricular tachycardia may also occur in patients with dilated or hypertrophic cardiomyopathies, valvular diseases, and other uncommon conditions such as right ventricular dysplasia. Supraventricular tachycardias and atrial fibrillation and atrial flutter are more common than ventricular tachycardia, but are less commonly associated with syncope. Syncope, however, is more likely to occur if the rate is very rapid or if there is an abnormal vasomotor response.48 Patients with Wolff-Parkinson-White syndrome have a bypass tract January 2004 • www.empractice.net 5 Emergency Medicine Practice COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC between the atria and ventricles, allowing rapid conduction with a relatively short refractory period. These patients are at particular risk for atrial fibrillation and atrial flutter with rapid, aberrant conduction to the ventricles via the bypass tract as well as cardiovascular instability. Symptomatic sinus bradycardia should be suspected particularly in elderly patients with evidence of a slow or varying sinus heart rate in the ED. The emergency physician should check for current use of oral or ophthalmologic beta-blocking agents, calcium-channel blockers, and other agents or conditions that may increase vagal tone. Evidence of second degree type II or type III heart block or a paced rhythm on the ECG should raise the suspicion for a symptomatic bradycardic dysrhythmia. In one prospective cohort, patients with atrioventricular block had minimal prodromal symptoms (mean duration of warning, < 2 seconds) and a shorter duration of residual/ recovery symptoms as compared to patients with ventricular tachycardia.49 Evidence of a long QT interval and/or abnormal notched T wave on the ECG suggests possible congenital or acquired long QT syndrome. A family history of sudden death or the use of medicines associated with this syndrome should raise suspicion further. Brugada syndrome appears to be most common in males from Southeast Asia and is suggested by characteristic ECG findings. effectiveness of an aerosolized fentanyl derivative to transiently incapacitate and inadvertently kill both terrorists and hostages in a Moscow auditorium.42,43 COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC syncope. Medical conditions may cause occult gastrointestinal or vaginal bleeding, or internal hemorrhage from a vascular catastrophe such as a ruptured abdominal aortic aneurysm. The vasodepressor syncopal syndromes are common but generally suggest low morbidity and mortality. The key may be to keep a healthy suspicion for other, more serious conditions while making this diagnosis in patients with a suggestive history who appear well. Features of the history that suggested vasodepressor as opposed to dysrhythmic syncope in one study included palpitations, blurred vision, nausea, warmth, diaphoresis, or lightheadedness prior to syncope, and the presence of nausea, warmth, diaphoresis, or fatigue following syncope. Vasodepressor syncope was associated with more than five seconds of warning symptoms and more prolonged recovery symptoms.49 The emergency physician should also be wary for significant trauma that may have occurred during the syncopal event. Carotid sinus sensitivity can also cause syncope. A bradycardic response can be elicited when the carotid sinus is stimulated. This is more common in the elderly population. This can be seen in patients who are wearing neck ties or who have tight collars, or even during simple activities such as shaving. Carotid sinus massage is a useful test in patients with suspected carotid sinus sensitivity.61 A positive test is defined as one that causes at least a three-second pause during massage of the carotid sinus. This test can be difficult to master and should be reserved for those who have been trained in its proper use. It should be avoided in patients with known or suspected carotid artery disease. ing valvular thrombosis, structural failure, paravalvular regurgitation, or ventricular dysrhythmia. Careful evaluation must be undertaken, and hospital admission of these patients is recommended.53,54 There are other, less obvious types of obstructive cardiologic conditions. Cardiac tamponade can present as syncope. This can be difficult to diagnose in the ED. The classic findings of Beck’s triad (distant/muffled heart sounds, pulsus paradoxus, and hypotension) are only present in about one-third of the patients who present with cardiac tamponade. If signs and symptoms are suggestive, a bedside echocardiogram may rapidly clarify the diagnosis. The treatment remains needle decompression of the pericardial fluid, either in the cardiac catheterization lab or the ED, if emergent. Congestive heart failure is another cause of obstruction to flow. Although newer modalities such as the use of B-type natriuretic peptide have been investigated to aid in the diagnosis of congestive heart failure, it remains largely a clinical diagnosis. Vascular Causes Of Cardiac Syncope Other types of heart disease that can present as syncope include those that primarily affect the vascular system. They include aortic dissection, a large pulmonary embolus, pulmonary hypertension, and myocardial infarction.55-60 Enough case reports exist regarding the vascular causes of syncope to make even the most seasoned emergency practitioner sweat. For instance, syncope has been observed in 13% of patients with pulmonary embolism, and up to 20% of patients with a massive pulmonary embolism will complain of syncope.55-58 Each of these conditions is associated with its own classic signs and symptoms and will not be reviewed in detail in this article. Neurologic Syncope One of the most difficult mimickers of syncope is seizure, as it can be difficult to be sure whether a “spell” was syncope or a seizure. (See also the October 2000 issue of Emergency Medicine Practice, ”Seizures: Accurate Diagnosis And Vascular Syncope External or internal hemorrhage due to medical conditions or trauma may serve as an obvious or occult cause of Cost- And Time-Effective Strategies For Patients With Syncope be 100% sensitive and 46% specific for cardiac problems. Following this rule led to an 18% reduction in the admission rate.15 It appears that using a simple, systematic approach to the evaluation of patients who present with syncope can be very beneficial. 1. Limit testing. Let the history and physical examination dictate the need for diagnostic tests. Obtaining routine tests like CBCs, electrolyte studies, CT scans, and echocardiograms has not been proven beneficial in the literature. While no formal cost-benefit analyses of limited evaluation of syncope in the ED exist, it stands to reason that routine tests that do not impact management will add unnecessary costs. 3. Use observation units. It’s not surprising that most patients admitted to the hospital for further evaluation for a potential cardiac cause of their syncope turn out not to have a cardiac cause. Even if no further diagnostic studies are performed during the hospital stay, this still adds considerable cost to the patient and the healthcare system. In the subset of patients who are at higher risk for morbidity or mortality from their syncopal episode— but who do not clearly need to be admitted to the hospital—it is possible that an observation unit stay can risk stratify patients with greater accuracy than a much shorter ED visit. Several prospective studies using observation protocols are under way. One article detailed a possible algorithm for the use of an observation unit in the ED setting.108 ▲ 2. Limit admissions. Syncope leads over 225,000 hospital admissions per year in the United States. Elesber et al studied the application of the ACEP level A and B recommendations for admission in 201 patients presenting with syncope.16 These recommendations proved to be 100% sensitive for finding cardiac-related causes of syncope. They also cut down the admission rate by 29%.16 Quinn et al derived a rule for admitting patients that included: 1) age greater than 75; 2) an abnormal ECG; 3) shortness of breath on presentation; 4) a respiratory rate greater than 24; or 5) a history of congestive heart failure.15 They found this rule to Emergency Medicine Practice 6 www.empractice.net • January 2004 from peripheral vertigo generally do not have a feeling of faintness or alteration in their level of consciousness. Central vertigo may be due to a tumor such as an acoustic neuroma, multiple sclerosis, or neurovascular disease such as vertebrobasilar insufficiency. Patients with the latter condition may experience syncope as well as vertigo. Features that distinguish vertigo syndromes from syncope include associated auditory complaints, evidence of nystagmus on ocular examination, or inducible nystagmus with the Hall-Pike maneuver.66,67 The Hall-Pike maneuver may only reproduce vertigo and nystagmus from cupulolithiasis, but not other peripheral causes of vertigo such as neuronitis. A subarachnoid, subdural, or epidural bleed can also present as a syncopal episode, and obtaining a careful history is key. A history of a severe headache with acute “thunderclap” onset may help point to a subarachnoid bleed, while a recent or distant history of head trauma may help to diagnose a subdural or epidural hematoma as the cause of syncope. Drop attacks are also sometimes included as a neurologic cause of syncope. However, they are most often not associated with a loss of consciousness. They are generally believed to be caused by a transient ischemic attack involving the posterior circulation to the brain. (See also the October 2003 issue of Emergency Medicine Practice, “Transient Ischemic Attacks: Transient Trouble Or Action-Warranted Attacks?”) Therefore, most authors consider drop attacks a mimic of syncope. Another neurologic cause sometimes considered in the differential diagnosis is narcolepsy. Migraine headaches can cause bizarre symptoms, including transient neurologic deficits and syncope. Keep this option in the differential diagnosis, especially in patients with a history of atypical migraines. Table 2. Diagnostic Questions To Determine Whether Loss Of Consciousness Is Due To Seizure Or Syncope. Question Points (if yes) At times do you wake with a cut tongue after your spells? At times do you have a sense of déjà vu or jamais vu before your spells? At times is emotional stress associated with losing consciousness? Has anyone ever noted your head turning during a spell? Has anyone ever noted that you are unresponsive, have unusual posturing or jerking limbs during your spells, or have no memory of your spells afterwards? (score as yes for any positive response) Has anyone ever noted that you are confused after a spell? Have you ever had lightheaded spells? At times do you sweat before your spells? Is prolonged sitting or standing associated with your spells? 2 Metabolic Syncope Hypoglycemia should be considered in any known diabetic patient presenting with a syncope-like syndrome. Many case reports exist in the literature associating syncope and hypoglycemia.40,41 However, it is difficult to imagine that hypoglycemia can correct itself without intervention in order to fit with the standard definition of syncope that includes spontaneous and full resolution. Hypoxia can also lead to syncope. Any condition that leads to a decrease in oxygenation or ventilation can lead to hypoxia, and ultimately a syncopal episode. This includes a wide variety of pulmonary and other acute and chronic disease processes. Keep this diagnosis in mind, particularly in young children who may play a high-risk game of inducing syncope by breath-holding, choking each other, or placing bags over their head until syncope occurs.68 1 1 1 1 1 -2 -2 -2 Syncope Due To Toxins And Poisons There are a variety of agents, including narcotics, benzodiazepines, and barbiturates, that can cause both central nervous system and respiratory depression. Exposure to variants with a rapid onset and short half-life may simulate syncope. Decreased oxygen delivery to the central nervous system can also be caused by alterations in hemoglobin function. Carbon monoxide poisoning and methemoglobin- The patient has seizures if the point score is ≥ 1, and syncope if the point score is <1. Source: Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish syncope from seizures. J Am Coll Cardiol 2002 Jul 3;40(1):142-148. January 2004 • www.empractice.net 7 Emergency Medicine Practice COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC Effective Treatment.”) Another study examined just the presence of tongue biting. That study found that tongue biting was found only in the seizure patients, but its absence did not exclude the possibility of a seizure.63 While a lateral tongue laceration appeared specific in this study, it has been observed in patients with psychogenic seizures. Finally, a recent study of patients with syncope or seizures found a simple set of questions (outlined in Table 2) useful in distinguishing a syncopal episode from a seizure.64 (This diagnostic approach has yet to be validated independently.) In general, unconsciousness lasting more than five minutes, a slow return to full alertness, and disorientation or an aura prior to the event are suggestive of a seizure.8,62,64,65 Sweating and nausea prior to the episode, a brief loss of consciousness, a quick return to baseline mental status, and a lack of tongue biting are more indicative of a primary syncopal event.8,62,64,65 Vertigo is a symptom that refers to an abnormal sensation of movement or rotation of the patient or his or her environment. (See also the March 2001 issue of Emergency Medicine Practice, “The Dizzy Patient: An EvidenceBased Diagnosis And Treatment Strategy.”) Vertigo can cause diaphoresis, pallor, nausea, vomiting, and difficulty with ambulation—similar to syncope. This disequilibrium can range from a simple spinning sensation to full veering, staggering, and/or imbalance. Vertigo can be divided into centrally or peripherally mediated causes. Peripheral vertigo is much more common, and patients who suffer COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC emia can present with acute loss of consciousness. Methemoglobinemia is caused by a variety of agents, including nitrates, local anesthetics, and sulfonamides. Pulse oximetry is unreliable in the setting of both of these poisonings, and the diagnosis should be made by direct measurement of a blood sample with a multiple wave-length co-oximeter. In the setting of smoke inhalation from a residential or industrial fire and mental status changes, the diagnosis of cyanide toxicity must also be entertained. In the petroleum, rubber, and mining industries, exposure to hydrogen sulfide can cause altered mental status and syncope. Both cyanide and hydrogen sulfide arrest cellular respiration by interfering with mitochondrial cytochrome function. Cholinergic and anticholinergic toxidromes may include syncope among a variety of characteristic symptoms. Toxic exposures should be in the differential diagnosis of syncope when several members of the same family or from the same location present to the ED simultaneously for evaluation. Emergency Department Evaluation Infection-Related Syncope Just as the list of the potential causes of syncope is quite Infection can be the primary cause of a syncopal episode or a secondary cause by leading to dehydration, sepsis, and hypotension.26 The history and physical examination will often identify the primary site of infection and the mechanism leading to syncope. Table 3. Important Historical Facts. Patients presenting to the ED with syncope should be treated as a possible emergency; avoid prolonged wait times. Whenever possible, they should be taken immediately to an area in the ED that provides for close cardiac monitoring, intravenous access, oxygen therapy, and invasive procedures if they become necessary. The initial evaluation in the ED begins as all encounters should, with stabilization of the patient (i.e., ABCs, IV, O2, monitor). History The cause of syncope is revealed by a careful history and physical examination in approximately 40%-50% of patients.1,2,4-6,47,71 A detailed account of the syncopal episode from any bystanders or family members can be very helpful in the diagnosis. Table 3 is a list of important historical features that should be asked of syncopal patients.14 Is It Really Syncope? Questions about just prior to the event • Activity (exertional vs. rest, during or after, changing position) • Precipitating events (warm room, stress, fear, intense pain) • Other factors (crowded area, prolonged standing, postprandial) Psychiatric Syncope Psychiatric conditions can mimic syncope. They can range from fully conscious actions for secondary gain purposes to dissociative states where the patient has no conscious control over the activity. While psychiatric conditions that mimic syncope exist, they must remain a diagnosis of exclusion. A study by Kapoor et al of syncope patients found that up to 20% of the population studied met diagnostic criteria for at least one major psychiatric disorder or substance abuse problem. Up to one-half of these patients with a psychiatric disorder did not have their disorder identified by the attending physician. This study found that patients who have suffered a syncopal event and carry a psychiatric diagnosis were more likely to report frequent episodes of syncope (four or more within one year), to be younger than control groups who did not have a psychiatric diagnosis, and to have multiple somatic complaints associated with the event.69 Questions about the onset of the attack • Associated symptoms (headache, nausea, vomiting, abdominal pain, sweating, visual aura, blurred vision, pain in back, neck, or shoulder) • Timing of symptoms / attack (prolonged vs. immediate) Questions about the attack (obtain information from bystanders) • Fall (sudden vs. gradual, slumping vs. fall without protection) • Duration of loss of consciousness (seconds vs. minutes) • Movements (jerking, tonic and/or clonic activity, none; duration) • Other associated findings (other injuries caused by fall) Questions about the period following the attack • Duration of confusion / postictal state • Associated symptoms (headache, nausea, vomiting, abdominal pain, sweating, visual aura, blurred vision, pain in back, neck, or shoulder) • Other associated findings (other injuries caused by fall, tongue biting, incontinence, mental status) Prehospital Care Prehospital care of patients with syncope and altered mental status should include a fundamental diagnostic and therapeutic protocol. Assessment for and/or treatment of hypoglycemia and hypoxia should be completed. Naloxone should be administered for depressed consciousness and possible opiate intoxication. Occult head trauma must be considered, and the neck should be immobilized if there is a suspicion of trauma or the patient suffered an injury to the head or neck from syncope. An IV catheter should be placed if the patient is hypotensive or tachycardic. Recall that in the setting of trauma, hypotension in the field is an independent predictor of morbidity and mortality, even if the patient is normotensive upon ED arrival.70 Emergency Medicine Practice Questions about past medical history / family history • Family history of sudden death, fainting, congenital heart problems • Significant metabolic problems (thyroid, diabetes) • Previous cardiac history • Medications (prescribed, over-the-counter, herbal, recreational) • Previous history of fainting (time since last event, associated symptoms, similar feelings, previous diagnosis) Source: Brignole M, Alboni P, Benditt D, et al; Task Force on Syncope, European Society of Cardiology. Guidelines on management (diagnosis and treatment) of syncope. Eur Heart J 2001 Aug;22(15):1256-1306. 8 www.empractice.net • January 2004 significantly less common in black than white high school blood donors.72 On the other hand, syncope due to vascular diseases may be more common in older blacks due to the higher prevalence of uncontrolled hypertension. The past medical, social, and family histories are all relevant to the evaluation. A past history of cardiovascular disease increases the likelihood of cardiac syncope and portends a higher 12-month mortality rate.72 A history of illicit substance use or the possibility of surreptitious poisoning should be assessed. The emergency physician should always inquire about a history of sudden death in the family. Sudden death in young adults suggests the possibility of long QT syndrome, familial cardiomyopathy, or other genetic illnesses. The Drug Did It! A review of the patient’s medications should not be overlooked. Medication use has been implicated as the cause of syncope in 3%-13% of patients.73-75 A careful review of medications the patient is taking, including over-thecounter preparations, should be performed. The patient should be asked which medications are new and/or if any recent changes have been made to the dosage or dosing interval. Some common drugs that are associated with druginduced syncope include beta-blockers, calcium-channel blockers, insulin, drugs of abuse (opiates, cocaine, etc.), diuretics, antidysrhythmics, digoxin, nitrates, sildenafil, ACE inhibitors, antidepressants, phenothiazines, alcohols, and central-acting antihypertensives. Finally, check for possible adverse drug interactions. One study of patients with syncope who take medicines found that 51% of patients were positive for a potential drug-drug interaction that may have explained their syncopal event.75 The Event Finding out exactly what happened is the goal of the initial evaluation. Taking the time to obtain a step-by-step history of the acute event may be the most important factor in ultimately making an accurate diagnosis. Interview the patient and, ideally, a witness to the event. Although the patient can be very helpful in discussing what may have happened just before the event, any past history of similar episodes, and current status, he or she may not recall the actual event. A witness (family member, friend, neighbor, EMS provider, or other bystander) can relate such information as duration of unconsciousness, evidence of movements suggesting a seizure, events just prior to the spell, duration of confusion following the spell, and/or other important details. A witness may also be able to predict other potential associated injuries. Certain clusters of historical information can help indicate the right direction when trying to determine the cause of the syncopal episode. For instance, a history of a stressful event or other obvious precipitating circumstances may suggest a vasodepressor cause of syncope. A syncopal episode that occurs only after standing may point to orthostasis or hypovolemia. A complaint of cough and dyspnea in association with syncope suggests possible pulmonary embolism or other obstructive cardiopulmonary disease. Any associated focal neurologic deficits suggest an underlying neurologic event. Rapid onset and offset with no warning before, or confusion after, the event suggests a transient dysrhythmia or other cardiac cause.4,46,49,71 One study found that most patients with otherwise typical vasovagal syncope had warning symptoms for minutes prior to the syncopal event. In fact, the study stated that in the absence of any warning signs or symptoms, the practitioner should be leery about making the diagnosis of vasovagal syncope.4 The Physical Examination Vital Signs As with any physical examination, the emergency physician should begin with the vital signs. Abnormalities in one or more may point to a specific cause of syncope. For instance, tachycardia and hypotension may represent hypovolemia as a cause of the syncopal episode. Taking the blood pressure in both arms and looking for concordance is helpful. A difference greater than 20 mmHg in blood pressure between both arms suggests thoracic aortic dissection. Tachypnea may point to pulmonary embolism or congestive heart failure as a cause of syncope. Orthostatic Changes In Syncope Many debates have centered on the significance of orthostatic hypotension. Orthostatic hypotension is usually defined as a decline of 20 mmHg or greater in systolic blood pressure on standing.76-78 Measurements are usually taken after lying supine for five minutes. The blood pressure is then repeated after standing for 1-3 minutes. A study done by Atkins et al found that most patients who have orthostatic changes would be discovered in the first few minutes of standing.76 However, the presence of orthostatic changes does not necessarily mean that they caused a particular episode of syncope. In this same study, 29% of those with a Demographics And Past History The patient’s demographic information is also important. Studies have consistently demonstrated that advancing age and male gender are associated with cardiovascular and neurologic causes of syncope.17,39,49 Vasovagal reactions were January 2004 • www.empractice.net Continued on page 11 9 Emergency Medicine Practice COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC long, there are many symptoms that can be confused with syncope. The emergency physician must first determine if the patient’s complaint is truly syncope. Vertigo, dizziness, faintness, lightheadedness, seizure, hypoglycemia, presyncope, and drop attacks can all be mistaken for syncope. It is important to determine whether there was a loss of consciousness and postural tone. Syncope is associated with a brief, transient loss of consciousness accompanied by a generalized weakness and loss of muscular tone. Drop attacks are defined as a loss of postural tone while remaining conscious. Lightheadedness usually refers to a feeling of faintness. It can be a precursor to syncope (pre-syncope). Dizziness, vertigo, and pre-syncopal episodes are generally not associated with a loss of consciousness. The distinction between these symptoms can be important. All can be associated with syncope, but they may have a different underlying mechanism, treatment, and prognosis.52 NO Patient with syncope? ➤ YES Consider seizure, drop attack, vertigo, or psychiatric disorder (Class III) ➤ • Assess ABCs (Class II) • History, physical examination, and ECG (Class II) ➤ Findings of life threat? NO ➤ ➤ • Elderly • Congestive heart failure • Abnormal ECG • Acute coronary syndrome / coronary artery disease • Over 45; otherwise healthy • No significant ECG findings • No clear inciting event • Young • Normal ECG • Prodrome suggesting vasodepressor or orthostatic etiology ➤ ➤ High risk Intermediate risk Low risk ➤ ➤ ➤ Work up and treat (Class III) Stable syncope patient ➤ YES ➤ ➤ Consider: • Pulmonary embolism • Subarachnoid hemorrhage • Aortic dissection/ aneurysm • Myocardial infarction • Gastrointestinal bleed • Ventricular dysrhythmia • Heart block • Carbon monoxide poisoning ➤ COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC Clinical Pathway: Risk Stratification In Patients With Syncope Admit to monitored hospital bed (Class II) • Consider admission (Class II) • Possible ED observation unit stay (Class III) • Outpatient workup if available promptly and patient is reliable (Class III) Discharge to home with primary care follow-up (Class II) The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended. Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable, possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research. This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care. Copyright ©2004 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Practice, LLC. Emergency Medicine Practice 10 www.empractice.net • January 2004 younger than 60 years of age have orthostatic blood pressure drops.2,76,77 What is most important is not the actual measurement of the change when standing, but the ability to reproduce the patient’s symptoms on standing.76 proven cardiac cause of syncope would have been missed if the work-up ended at just orthostatic pressures.76 Another study found that orthostatic changes were the cause of syncope in 24% of the patients who presented to the ED for the evaluation of syncope.77 In this same study, orthostatic changes were also found in patients with other diagnosed causes of syncope. Also complicating the picture is the fact that orthostatic hypotension is present in about 40% of patients over 70 years old and that up to 23% of patients Physical Findings Due to time constraints, ambient noise, and numerous distractions, it can be a challenge to perform a quality cardiac and neurologic examination in the ED. Several key features are important. For example, the presence of a new murmur may suggest a cardiac etiology of syncope. Ten Pitfalls To Avoid 1. Failure to obtain a detailed history of the acute event. Remember that the most important step in obtaining an accurate diagnosis is the history of present illness. Invest the time to tease out the facts from the patient, family, and bystanders. This investment will yield returns in a more efficient ED diagnostic workup, a more accurate diagnosis, and a higher quality of emergency care. Patients who suffer from syncope—specifically those at the extremes of age—should follow up with their primary care provider after discharge from the ED. If you do not explicitly instruct or arrange this for your patients, they will assume it is not important. They may also assume that if syncope happens again, they don’t need to see a practitioner because “it was nothing the last time.” Take time to explain why follow-up is important. Make sure they understand the importance of it, and document that the conversation took place. 2. Failure to consider and diagnose life-threatening causes of syncope. Syncope is generally a benign process. However, one must be proactive in trying to identify life-threatening causes, most of which are cardiac-related. Generally, other physical examination findings may help, but if you don’t keep your differential large, you will miss the rare lifethreatening conditions. 7. Failure to inform patients about the potential for recurrent syncope and the dangers associated with it. Again, if you don’t take the time to inform your patients about the possible dangers of syncope, they will assume that it’s benign. Patients should be warned about possible triggers of syncope, associated signs and symptoms, and the risk of a sudden attack. Particularly in the elderly, instructions should be provided for procedures to decrease the risk of falls, such as using a cane or walker, taking extra time to equilibrate when changing position, and paying attention to symptoms and “feelings” that may precede the syncopal attack. 3. Failure to treat life-threatening causes of syncope. It’s one thing to recognize the potential high-risk patient in front of you; it’s another to begin aggressive treatment in a patient who now appears stable. Don’t fall into this trap. If you identify a potentially life-threatening cause, you must act quickly to prevent possible disaster. 8. Failure to inform patients about the risk of returning to activities such as driving, sports, and operating heavy machinery. Some municipalities now have laws requiring physicians to report patients who have syncope.103,104 People with occupations that are at high risk for disastrous outcomes include truck drivers, bus drivers, airplane pilots, and heavy equipment operators, to name a few. The emergency physician could be held liable for a bad outcome if he or she did not provide and document counseling about the risks of driving after syncope. 4. Failure to admit patients who are clearly at high risk for morbidity and mortality. While some patients may not appear acutely ill in the ED, they are still at higher risk for morbidity and mortality. Factors associated with higher risk include male gender, advanced age, syncope without warning, and cardiovascular risk factors or a history of cardiac disease. Patients with these and other characteristics described in this article may require admission for observation and further evaluation. It may sometimes be difficult to convince consultants of this. Recall that in most situations, you are the only physician who has seen and examined the patient, and you are now their physician. Don’t settle for outpatient follow-up when the right thing to do is to admit the patient. Your patient is counting on you to be their advocate. Insist on the admission. 9. Failure to assess for a prolonged QTc. Remember to assess for both a long QTc (0.45 seconds in men, 0.46 in children, and 0.47 in women) and an abnormal notched T wave. If abnormalities are present, consider congenital or acquired prolonged QT syndrome. Also, when checking the patient’s medication list, be alert for medicines known to cause acquired prolonged QT syndrome. 5. Failure to consider multiple causes of syncope. In many cases, there are multiple causes of a syncopal episode. Your job is to think of the causes that make a patient too high a risk to send home for outpatient management. Just because a patient had an obvious stressor prior to the syncopal episode, or you find orthostatic hypotension, this does not mean that cardiac causes have been ruled out. 10. Failure to obtain continuous ECG monitoring while in the ED in addition to the static ECG. Continuous ECG monitoring increases the sensitivity for acute ischemia and increases the likelihood of capturing an intermittent dysrhythmia. The automated alarm may help to alert the ED staff to patients with recurrent syncope in the ED. All patients with a possible cardiac cause of syncope should be placed on continuous ECG monitoring in the ED. ▲ 6. Failure to arrange outpatient follow-up for patients with syncope. January 2004 • www.empractice.net 11 Emergency Medicine Practice COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC Continued from page 9 COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC altered mental status suggests a metabolic or pharmacologic etiology, and poor cognitive function increases the possibility of a qualitative or quantitative medication error. Findings consistent with congestive heart failure are indicators of high risk of early mortality, including sudden death.11 These and other key features can be used to help risk stratify syncope patients. Although they may not identify the exact cause, important physical findings can help to determine if the patient can be discharged home or should be admitted for further evaluation. Other Examination Findings Consider the possibility of trauma due to a fall in all syncope patients. The greatest concern is for occult trauma to the head and neck. The neck should be immobilized until the extent of trauma, if any, can be fully evaluated. The scalp and neck should be inspected and palpated for hematomas and tenderness. A careful abdominal examination should be undertaken to feel for tenderness, masses, or distention. An abdominal aortic aneurysm can present as syncope associated with abdominal or back pain. Other abdominal findings such as those of an acute abdomen should be searched for and treated if found. A rectal examination with stool guaiac to examine for an occult gastrointestinal bleed should be considered in all adult patients presenting with syncope. The Cardiac Examination The cardiovascular examination should not only focus on the auscultation of the chest, but also the non-auscultory findings as well. Subtle abnormalities and changes can help sort out difficult cases in a loud ED. Neck veins provide information regarding the patient’s volume status and can give an idea of right heart function. Neck vein distention can suggest right-sided heart failure, constrictive pericarditis, tricuspid stenosis, superior vena cava obstruction, and a variety of other cardiopulmonary diseases. Venous distention measured as greater than 4 cm above the sternal angle, most commonly with the head of the bed at a 45º angle, is considered elevated.52 Characteristics of the carotid pulse waveforms can also be helpful. Large, bounding pulses may indicate volume excess or high stroke volume conditions such as obstructive causes or a complete heart block. Small, weak pulses may indicate such conditions as hypovolemia, congestive heart failure, or severe aortic stenosis.59,79,80 When auscultating the heart, it can be very difficult to determine a benign murmur from a life-threatening one. Some characteristics to listen for are diastolic vs. systolic timing, the response of the murmur to changes in position, and whether there is any response to a Valsalva maneuver. Also, abnormalities in the heart sounds themselves can be helpful. For instance, an S-3 heart sound can be indicative of congestive heart failure. A midsystolic click suggests mitral valve prolapse. As mentioned, the peripheral vascular examination should include monitoring the blood pressure in both arms. Check for capillary refill, edema, or cyanosis. Pulses should be palpated at several locations and compared for strength and character. Auscultation of the central pulses should be undertaken looking for the presence of bruits. Diagnostic Testing Electrocardiography An ECG should be performed on most patients with syncope. Although the chance of finding the cause of syncope is 2%-12% with the ECG alone,4,12 the cardiac causes can be extremely dangerous and potentially lethal. An ECG is easy to obtain, is relatively inexpensive, and can lead to immediate treatment of life-threatening problems. The ECG yields information beyond the rate and rhythm. Examples include ischemic changes, a short PR interval and delta wave suggestive of Wolff-Parkinson-White syndrome, a prolonged QT interval, evidence of right heart strain, and/ or evidence of Brugada syndrome. A completely normal ECG can also be used to risk stratify patients. Georgeson et al searched for evidence of acute cardiac ischemia in patients who presented with syncope without chest pain and found that 18 of 251 patients were ultimately diagnosed with acute cardiac ischemia, all of whom had ischemic abnormalities on their presenting ECGs.81 Thus, a patient with no chest pain or cardiac risk factors and a normal ECG is unlikely to have an ischemic cause for syncope. A normal ECG also lowers the likelihood of a primary dysrhythmic cause for syncope. The ECG can be supplemented with continuous ECG monitoring in the ED, and outpatient ambulatory cardiac event recording. Continuous ECG monitoring in the ED with periodic physician inspection of the 12-lead tracing increases the diagnostic yield for ongoing ischemia.82 Cardiac event recorders with continuous automatic dysrhythmia detection increase the sensitivity for relevant dysrhythmia detection when worn for 2-4 days after a syncopal event.83 The latest innovation in this field is the subcutaneously implantable loop recorder. Recording can be activated automatically or manually, and the device can be implanted for one year or more.84,85 The Neurologic Examination Neurologic examination findings can help point to certain etiologies such as central nervous system thrombotic or hemorrhagic disorders as the cause of syncope. At a minimum, the examination should include an assessment of cranial nerve function, motor and sensory function in the extremities, reflexes, and orientation. Nystagmus, diplopia, and dysarthria may all suggest disease of the vertebrobasilar system, including thrombosis or dissection. Vertebrobasilar disease can also affect the long motor and sensory tracts traveling through the brainstem, resulting in focal weakness or numbness in the extremities. Cerebellar involvement may be suggested by ataxia or veering to one side with ambulation. Assess for physical findings, as they may relate to neurovascular causes of syncope. For example, evidence of atrial fibrillation or a carotid bruit would suggest an embolic source of disease. Isolated ongoing Emergency Medicine Practice Chest X-Ray The chest x-ray is a commonly ordered test in patients presenting with syncope. Its value is less well-established 12 www.empractice.net • January 2004 history and physical examination, routine blood work is not recommended. The following is a look at each test individually, and a summary of what the literature tells us. Complete Blood Count In one prospective study, 134 complete blood counts (CBCs) were performed, and no cases of occult bleeding were found.4 Four cases of suspected gastrointestinal bleeding were confirmed by low hemoglobin. These results are similar to those found in several retrospective reviews.1,4,12,18 One study stated that the CBC did confirm the need for admission of the patient, but it did not help in the diagnosis of the cause of syncope. This study stated that two patients out of 33 had elevations of the white blood cell count that led to their admission.18 From this information, we can conclude that the routine use of a CBC does not add to the work-up of syncope if it is not already clinically indicated. This conclusion is supported by ACEP, ACP, and European Society of Cardiology guidelines.11,12,14 Head Computed Tomography Obtaining a routine head CT on all patients with syncope is also not supported by the current literature. Day et al found that a head CT demonstrated important new abnormalities in seven of 20 patients who had either a focal seizure or a focal deficit on physical examination, but in zero of 17 patients who did not have focal findings.1 In a pooled case series presented by Linzer et al of 195 patients who were studied with head imaging, the average yield of CT was 4%. All patients who had positive scans had a focal abnormality on neurologic examination or a witnessed seizure.12 In general, the routine use of a head CT for the diagnosis of the cause of syncope is not supported by current literature. Electrolytes/Glucose Electrolytes are defined as sodium, potassium, chloride, bicarbonate, blood urea nitrogen, and creatinine. In one prospective study, only one non-suspected abnormality was detected in 134 electrolyte and/or glucose panels. This was a case of a serum sodium level of 101 mEq/L in a patient with diuretic-induced orthostasis.4 In a retrospective review, five of 130 tests drawn proved helpful, although only one was an unexpected metabolic abnormality.1 Another retrospective study found that by dividing the electrolyte panel into individual components, two abnormalities that proved helpful were identified in 33 patients.18 In the same study, the blood urea nitrogen and creatinine values contributed to the decision to admit one of 33 cases by confirming the clinical impression of dehydration.18 In general, drawing routine electrolyte panels on patients with syncope is not supported by the literature; it should be guided by the medical history and medications of the patient. Electroencephalography As with obtaining a head CT, an electroencephalogram (EEG) is only indicated if there is a suggestive finding in the history and physical examination. Several studies have been performed regarding the use of EEG as a diagnostic tool.12,86 Little evidence exists of its benefit in a syncope patient with no history of seizure activity. This test is unlikely to uncover the cause of syncope if it was not already suggested by the history and physical examination. Therefore, the routine use of an EEG is not recommended. Echocardiography The literature regarding the use of echocardiography as a screening tool for syncope is mixed. Some case reports have shown a benefit to the use of echocardiography, but larger studies have found this not to be the case. Unsuspected causes of syncope found on echocardiography are reported in 5%-10% of patients.13,71,85,87,88 The European Task Force Guidelines on the management of syncope gives echocardiography a Class I recommendation for use in patients with syncope when cardiac disease is suspected.14 The problem is that echocardiography is not readily available in most EDs. Although the diagnostic benefit may be similar to that of the ECG, the fact that a formal study is up to seven times the cost and that it is not readily available makes it difficult to recommend this test for routine use in the ED.13 Echocardiography should be performed when cardiac disease is suspected, but in patients with no underlying cardiac history, no cardiac symptoms, and a normal physical examination, echocardiography is likely to add little to the diagnostic evaluation. Cardiac Laboratory Tests Cardiac serum markers are of little value unless indicated by the history and physical examination. In one study of patients with syncope and no chest pain, 18 of 251 patients (7%) were diagnosed with cardiac ischemia as the cause of their syncope. However, all 18 patients had ischemic abnormalities (ST-segment elevation or depression, pathologic Q waves, or T wave abnormalities) identified on their initial ECG.81 In syncope patients who deny chest pain or discomfort on examination, have no cardiac history, and have a normal ECG, the chance of cardiac ischemia being the cause of syncope is highly unlikely. Routine use of cardiac markers to search for the cause of syncope is unnecessary.89 The evaluation of cardiac ischemia should be reserved for patients who have suggestive history or physical examination findings. Serum/Urine Pregnancy Test Laboratory Testing Although there is no prospective study that shows an absolute benefit of obtaining a pregnancy test in women of childbearing age, common sense guides us to do this. This is In general, unless one has a specific reason to suspect an abnormality in the laboratory evaluation based on the January 2004 • www.empractice.net 13 Emergency Medicine Practice COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC than that of the ECG. The chest x-ray can be helpful in a select number of causes of syncope. For instance, one might find a widened mediastinum in case of aortic dissection, or an enlarged heart or other evidence of congestive heart failure. Another possible finding is the classic x-ray findings of pulmonary embolism, including Hampton’s hump or Westermark’s sign. However, the absence of these x-ray findings does not rule out these etiologies as the cause of syncope. Again, unless guided by the history and physical examination findings, it is unlikely that a routine chest x-ray will uncover the cause of syncope. COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC 2) syncope during exercise; 3) syncope while supine; 4) a family history of sudden death in a person less than 30 years old; and 5) syncope with an “odd” history.3 The first warning bell in the list could suggest one of the variants of the long QT syndrome. Pediatric patients should have a careful cardiac examination. Other physical features associated with cardiac disease (e.g., deafness, ataxia, abnormal facies, congenital syndromes, and Marfan habitus) or neurologic disease (e.g., ash-leaf spots, café-au-lait spots, and cleft palate) should be sought.94 Based on the preceding data and case reports of sudden death,96 the following recommendations about children presenting with syncope can be made. First, obtain a detailed family history for all patients who seek medical attention for syncope. Ask specifically about a family history of cardiac dysrhythmias or sudden, unexplained death. Second, all children should undergo a thorough physical examination to assess for cardiac pathology. This includes an ECG and, possibly, cardiac monitoring while in the ED. a relatively inexpensive test that can be performed in a noninvasive way. Pregnancy is associated with a risk of internal hemorrhage from ectopic implantation as well as external vaginal hemorrhage. Furthermore, the propensity for supraventricular tachydysrhythmias in patients with and without preexcitation, and for premature ventricular contractions, seems higher during pregnancy.90,91 Other Studies No studies currently support the routine ED use of liver enzymes, arterial blood gasses, toxicology screens, coagulation studies, or urine dipsticks for screening purposes. Abnormalities have been found in all of these test groups; however, random screening is not justified unless clinically indicated by the history and physical examination. Management The wide range of causes of syncope results in an even wider range of possible treatment strategies. The goal in the ED is to identify life threats and treat them accordingly. When no immediate life threat is identified, the goal shifts to risk stratifying the patient for likelihood of an adverse outcome. However, in about one-third to one-half of cases, it may also be possible to identify the cause of syncope. Table 4 lists the common causes of syncope and the potential treatments for each cause. At this time, there are no largescale, randomized, controlled trials studying the advantages and disadvantages of inpatient vs. outpatient management of patients with syncope. (See the disposition section later in this article.) Table 4. Medical Care Of Syncope. I. Vasodepressor syncope / Metabolic / Psychiatric Patients with specific triggers (stress, drawing blood) need no specific treatment Specific treatments • Nonpharmacologic measures • Hypovolemia: Fluid resuscitation • Vasodepressor: Avoidance of triggering situations • Orthostatic hypotension: Dangling the legs over the side of the bed prior to standing; Slowly changing positions; Support stockings • Pharmacologic measures • Discontinuation of potential pharmacological causes that are not necessary • Orthostatic hypotension: Midodrine, phenylephrine; Caffeine, theophylline; Fludrocortisone • Vasodepressor: Beta-blockers; Selective serotonin reuptake inhibitors; Scopolamine • Permanent pacemakers: Useful in patients with carotid sinus hypersensitivity Special Circumstances Pediatric Syncope Syncope in children is generally a benign event. As stated earlier, up to 20% of patients experience syncope before the end of adolescence.2,3,92 There are a few serious, but rare, causes of syncope in children. Little research is done in this population. The only population-based study of syncope in children to date was done by Driscoll et al.93 The study examined 151 patients between the ages of 1 and 22 years presenting between 1987 and 1991 with symptoms consistent with syncope. The authors estimated that the incidence of syncopal episodes in children coming to medical attention per 100,000 population was 125.8. For both male and female patients, the rate of syncopal episodes peaked in the 15- to 19-year-old age groups, but the peak for female patients was much greater than that in males. Only one patient was ultimately found to have a long QT syndrome. The majority of children were thought by the evaluating physician to have had vasodepressor syncope. Recurrence of syncopal episodes occurred in 9% of the 151 patients. No deaths related to syncope were reported in this group of children at follow-up.93 Just as in their adult counterparts, a detailed history and physical examination may be sufficient to define the cause of syncope in many cases.3,93-95 In a recent review by McLeod, several anecdotal but useful “warning bells” in the history are defined. They include: 1) syncope in response to loud noise, fright, or extreme emotional stress; Emergency Medicine Practice II. Structural heart disease Treatment is directed at the underlying problem; admission is often warranted III. Dysrhythmias Bradycardia • Discontinue / decrease medications if can be done safely • A permanent pacemaker is generally indicated for symptomatic bradycardia and high-grade AV block Tachycardia • Ventricular tachycardia—ACLS guidelines for immediate treatment, electrophysiologic testing may be warranted; possible automatic implantable cardioverter/defibrillator placement, antidysrhythmic therapy, or radio frequency catheter ablation as needed • Supraventricular tachycardia—ACLS guidelines for immediate treatment, ED studies with radiofrequency catheter ablation may be warranted 14 www.empractice.net • January 2004 Elderly Patients Disposition Syncope is a common presenting complaint of the elderly. It has an annual incidence of 6% and a recurrence rate of about 30%.97 As most emergency physicians have found in practice, syncope in the elderly can often lead to a timeconsuming and challenging evaluation. Syncope from any cause in the elderly patient population is usually associated with a poor prognosis. First, from a primary event standpoint, syncope is responsible for 2%15% of falls in geriatric subjects.98 Data have shown that injury is the sixth-leading cause of death in patients older than 65 years.97-100 Falls are directly or indirectly the cause of death in as many as 12% of people in the geriatric population.98,101 Second, the underlying cause of syncope in the elderly population is more likely to be of a cardiac nature. As stated earlier, syncope of cardiac etiology has a much worse prognosis. There are a number of specific cardiac etiologies that are much more common in the elderly population. These include dysrhythmias (such as bradycardia or sick sinus syndrome), atrioventricular blocks (such as second-degree Mobitz II and third-degree block), and ventricular ectopy (such as ventricular tachycardia). Congestive heart failure is more prominent in the elderly. These patients may present with “reverse postural” January 2004 • www.empractice.net Disposition of syncope patients can fit into three main categories: 1) patients who clearly need to be admitted; 2) those who are safe to discharge home with follow-up; and 3) patients who have some higher-risk features but are not clearly at risk for morbidity and mortality from this event. Who Needs To Be Admitted? A patient should be admitted to the hospital for rapid workup and diagnostic procedures if the initial evaluation reveals concerns about the risk of sudden death. The ACEP clinical guidelines on syncope state criteria for patients that absolutely need to be admitted to the hospital for further evaluation and treatment.11 These criteria include all patients with: 1) a history of congestive heart failure or ventricular dysrhythmias; 2) associated chest pain or other symptoms compatible with acute coronary syndrome; 3) evidence of significant congestive heart failure or valvular heart disease on physical examination; and 4) ECG findings of ischemia, dysrhythmia, prolonged QT interval, or bundle branch block. The European Task Force Guidelines on the management of syncope also have recommendations as to which 15 Emergency Medicine Practice COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC syncope, which would occur with recumbency.97 The prevalence of valvular disorders also increases with age. Syncope is a common presenting complaint in patients with aortic stenosis. This is significant because once symptoms such as syncope begin in these patients, they are at high risk for mortality. In fact, left untreated, the life expectancy is three years or less. Finally, syncope in the elderly for all reasons is much more dangerous. In a study of syncope in patients 60 years or older, mortality rates were compared between the elderly and a younger control group of patients. The mortality rate from non-cardiac syncope was 22% and 5% in the two groups, respectively.102 This difference is likely due to the general decrease in reserve of older patients and the fact that they are more likely to have multiple comorbidities. Neurologic causes are much more common in the elderly population. A cerebrovascular event such as a stroke can often present with a syncopal-type episode. Another often-overlooked cause in the elderly is carotid sinus syndrome. Syncope related to orthostatic hypotension, gastrointestinal bleeding, and medications are more common in this age group. Orthostatic hypotension can be present in up to 40% of patients over the age of 70. Reproduction of the patient’s symptoms upon standing is just as helpful as a numerical change in the heart rate or blood pressure.2,76 Keep in mind that syncope can be multifactorial, especially in the elderly. A recent study found that up to 18% of all cases of syncope had multiple potential causes.80 This study also found that the presence of multiple potential causes of syncope was an independent predictor of increased mortality. Because of the higher risk of mortality from all causes of syncope in the elderly, maintain a very low threshold for admission of these patients either to the hospital ward or a dedicated observation unit. Third, special attention should be directed toward children who have a history or complaint of exercise-induced or exertional syncope. Extra time should be given to these children, and a cardiac cause must be aggressively ruled out. Fourth, just as in adults, the use of adjunctive diagnostic laboratory tests should be guided by the history and physical examination. While one review advocated for serum glucose, basic electrolytes, and a CBC in all children,94 this recommendation has not been independently validated. Finally, children who have negative findings in the personal and family history, a normal physical examination, and nonexertional syncope are unlikely to have a cardiac cause of syncope, and are at low risk for sudden death. These patients usually can be discharged home with outpatient follow-up. All children who have had a syncopal episode should be reexamined by a primary care physician and referred for more advanced studies as appropriate.3,94,95 Management of syncope in children is dependent on the underlying cause. As with all conditions in emergency medicine, start with the ABCs. If the primary cause is suspected to be neurally mediated syncope, the mainstay of therapy is reassurance.3 Advice to maximize fluid intake may be appropriate, and a warning to avoid precipitating events is warranted. For frequent, recurrent syncope, close primary care follow-up is recommended. If this cannot be arranged, then admitting the child for further testing and possible pharmacologic management with drugs such as fludrocortisone and/or a beta-blocker may be warranted.3 If the ED evaluation suggests a cardiac or neurologic cause, admission for further diagnostic testing and monitoring is required. If an underlying dysrhythmic cause is identified, the child should be admitted to a service with cardiac monitoring and advanced life support availability. COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC strategies on page 6. Also, be sure to consider the social situation of the patient, the ability to get a follow-up appointment in a particular institution or community, and the patient’s wishes. All of these factors may alter management. patients need to be hospitalized after a syncopal episode. Table 5 is a summary based on these recommendations. Other published guidelines on syncope support the criteria above.12,13,71 Patients with worrisome pulmonary findings such as a pulmonary embolism as well as patients with any signs of instability (such as severe orthostatic hypotension), functional bleeding (such as a gastrointestinal bleed), or sustained tachycardia or bradycardia without a clear cause should also be admitted for further evaluation and possible treatment. Discharge Instructions Driving Recommendations Should people who suffer from syncope be limited from driving? Driving an automobile is not a guaranteed right— it is a privilege that may be restricted when it poses a threat to other people. The occurrence of a syncopal episode during driving could have serious consequences to the patient, his or her passengers, and others on the roads. Laws exist in many municipalities regarding what is required when a patient has a syncopal episode.103,104 Physicians should be aware of the laws in the state in which they practice. In 1996, the American Heart Association and the North American Society of Pacing and Electrophysiology issued statements regarding driving after syncope.107,108 A study by Akiyama et al found that 2% of syncopal patients reported losing consciousness while driving.105 Only a small number of patients reported having an accident while driving. They concluded that although it was common for their patients to have symptoms of possible dysrhythmia while driving, accidents were found to be uncommon; they actually occurred at a lower frequency than the annual accident rate of the general population.105 Another study by Maas et al examined patient compliance with “no driving” advice given by their doctor.106 They found that three of 104 patients instructed not to drive reported a syncopal episode while driving within the next year. This resulted in one car crash with minor injury. Nine patients had stopped driving prior to the initial evaluation by the investigative team. On follow-up, all 95 patients who had been driving prior to being told to stop had continued to drive irrespective of any recommendations.106 Who Can Safely Be Discharged? Most patients in whom the suspicion for a cardiac cause of syncope is low can be safely evaluated in the ED and discharged for outpatient follow-up. In general, patients younger than 40 years with an isolated syncopal event who also have a normal physical examination, a normal ECG, and no evidence of structural or ischemic heart disease can safely be sent home from the ED. Patients may be advised to minimize driving, playing sports, or operating heavy machinery pending follow-up evaluation. Patients should generally follow up with their primary care physician within the next week or return to the ED sooner if they have additional syncopal events. Everyone Else Finally, another group represents the “gray area.” The ACEP guidelines define this group of patients as having: 1) age greater than 60; 2) a history of congenital heart disease; 3) a history of coronary artery disease in the absence of chest pain or ischemia during the examination; 4) a family history of unexpected sudden death; or 5) exertional syncope in younger patients without an obvious benign etiology.11 This includes a large number of patients who present with syncope, and some clinical judgment is required. These patients may be good candidates for an observation unit. This is discussed in detail in the section on cost-effective Summary Table 5. When To Hospitalize A Patient With Syncope: A Summary Of The European Task Force On Syncope Recommendations. For diagnosis • Suspected or known heart disease • ECG patterns known to cause syncope • Syncope occurring during exertion • Syncope causing severe injury • Family history of sudden death For treatment • Cardiac dysrhythmias causing syncope • Syncope due to acute coronary syndrome • Syncope due to structural cardiac disease • Stroke or focal neurologic Emergency Medicine Practice In patients with syncope, the primary goal of the emergency medicine practitioner is to be able to identify those who are at high risk for morbidity and mortality. Identifying lowerrisk patients who can be safely discharged from the ED with outpatient evaluation can result in significant savings. The inability of the emergency physician to establish the cause of each syncopal episode does not mean that the patient has not been appropriately treated. Indeed, up to 50% of the cases will never have a cause identified after a detailed evaluation.1,4-6,8 Even so, analyzing the information obtained through a thorough history, physical examination, baseline ECG, and other indicated studies allows emergency physicians to safely risk stratify patients and make appropriate disposition decisions. ▲ disorders • Patients with repeat vasodepressor syncope for which pacemaker implantation is planned Other categories that occasionally may need to be admitted • Patients without heart problems, but sudden onset of palpitations • Patients with syncope in supine position • Patients with frequent recurrent syncope • Patients with minimal or mild heart disease when there is high suspicion for cardiac-related syncope References Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial 16 www.empractice.net • January 2004 1.* Day SC, Cook EF, Funkenstein H, et al. Evaluation and outcome of emergency room patients with transient loss of consciousness. Am J Med 1982 Jul;73(1):15-23. (Retrospective; 198 patients) 2. Decker W. Down for the count! The evaluation of syncope. 2002. (Lecture practice guidelines) 3. McLeod KA. Syncope in childhood. Arch Dis Child 2003 Apr;88(4):350353. (Review) 4.* Martin GJ, Adams SL, Martin HG, et al. Prospective evaluation of syncope. Ann Emerg Med 1984 Jul;13(7):499-504. (Prospective; 170 patients) 5. Kapoor WN. Evaluation and outcome of patients with syncope. Medicine (Baltimore) 1990 May;69(3):160-175. (Retrospective; 433 patients) 6.* Kapoor WN. Evaluation and management of the patient with syncope. JAMA 1992 Nov 11;268(18):2553-2560. (Review) 7. HCUPnet, Healthcare Cost and Utilization Project. Agency for Healthcare Research and Quality, Rockville, MD. http://www.ahrq.gov/data/ hcup/hcupnet.htm. (National database) 8. Kapoor WN. Syncope. N Engl J Med 2000 Dec 21;343(25):1856-1862. (Review) 9. Abboud FM. Neurocardiogenic syncope. N Engl J Med 1993 Apr 15;328(15):1117-1120. (Editorial) 10. Lewis T. A lecture on vasovagal syncope. BMJ 1932;1:873-876. (Historical reference) 11.* American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of patients presenting with syncope. Ann Emerg Med 2001 Jun;37(6):771-776. (Practice guideline) 12. Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med 1997 Jun 15;126(12):989-996. (Practice guideline) 13. Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope. Part 2: Unexplained syncope. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med 1997 Jul 1;127(1):7686. (Practice guideline) 14.* Brignole M, Alboni P, Benditt D, et al; Task Force on Syncope, European Society of Cardiology. Guidelines on management (diagnosis and treatment) of syncope. Eur Heart J 2001 Aug;22(15):1256-1306. (Practice guideline) 15. Quinn J, McDermott D, Stiell I, et al. Physician judgment in evaluating patients with syncope. Acad Emerg Med 2002;9:452-453. (Abstract, retrospective; 559 patients) 16. Elesber A, Decker W, Smars P, et al. Evaluation of the safety and costeffectiveness of the ACEP clinical policy in regards to admission of the syncopal patient. Acad Emerg Med 2002;9:370-371. (Abstract, retrospective; 201 patients) 17. Colivicchi F, Ammirati F, Melina D, et al; OESIL (Osservatorio Epidemiologico sulla Sincope nel Lazio) Study Investigators. Development and prospective validation of a risk stratification system for patients with syncope in the emergency department: the OESIL risk score. Eur Heart J 2003 May;24(9):811-819. (Prospective cohort; 270 patients) 18. Junaid A, Dubinsky IL. Establishing an approach to syncope in the emergency department. J Emerg Med 1997 Sep-Oct;15(5):593-599. (Retrospective chart review; 33 patients) 19. Turnbull C, Bono M. Evaluating syncope in the acute setting. Emergency Medicine 2002;11:14-20. (Review) 20. Chen L, Jahangir A, Decker W, et al. Predictors for bradycardia and tachycardia in patients with syncope. A clinical score index for diagnosis. Circulation 2001;104 (17 Suppl II):346. (Abstract) 21. Hayes OW. Evaluation of syncope in the emergency department. Emerg Med Clin North Am 1998 Aug;16(3):601-615, viii. (Review) 22. Benditt DG, Lurie KG, Fabian WH. Clinical approach to diagnosis of syncope. An overview. Cardiol Clin 1997 May;15(2):165-176. (Review) 23. Olshansky B, Hahn EA, Hartz VL, et al. Clinical significance of January 2004 • www.empractice.net 17 Emergency Medicine Practice COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC syncope in the electrophysiologic study versus electrocardiographic monitoring (ESVEM) trial. The ESVEM Investigators. Am Heart J 1999 May;137(5):878-886. (Multicenter, randomized, controlled trial; 486 patients) 24. Brignole M. Sick sinus syndrome. Clin Geriatr Med 2002 May;18(2):211227. (Review) 25. Gold MR. Permanent pacing: new indications. Heart 2001 Sep;86(3):355-360. (Review) 26. Rosenfeld ME, Beckerman B, Ward MF, et al. Lyme carditis: complete AV dissociation with episodic asystole presenting as syncope in the emergency department. J Emerg Med 1999 Jul-Aug;17(4):661-664. (Case report) 27. Leung FW, Oill PA. Ticket for admission: unexplained syncopal attacks in patients with cardiac pacemaker. Ann Emerg Med 1980 Oct;9(10):527528. (Case report) 28. Moss AJ. Long QT Syndrome. JAMA 2003 Apr 23-30;289(16):2041-2044. (Review) 29. Moss AJ. Measurement of the QT interval and the risk associated with QTc interval prolongation: a review. Am J Cardiol 1993 Aug 26;72(6):23B-25B. (Review) 30. Nemec J, Hejlik JB, Shen WK, et al. Catecholamine-induced T-wave lability in congenital long QT syndrome: a novel phenomenon associated with syncope and cardiac arrest. Mayo Clin Proc 2003 Jan;78(1):40-50. (Prospective; 42 patients) 31. Viskin S. Long QT syndromes and torsades de pointes. Lancet 1999 Nov 6;354(9190):1625-1633. (Review) 32. Al-Khatib SM, LaPointe NM, Kramer JM, et al. What clinicians should know about the QT interval. JAMA 2003 Apr 23-30;289(16):2120-2127. (Review) 33. Brugada J, Brugada R, Brugada P. Right bundle-branch block and STsegment elevation in leads V1 through V3: a marker for sudden death in patients without demonstrable structural heart disease. Circulation 1998 Feb 10;97(5):457-460. (Cohort; 63 patients) 34. Wilde AA, Antzelevitch C, Borggrefe M, et al; Study Group on the Molecular Basis of Arrhythmias of the European Society of Cardiology. Proposed diagnostic criteria for the Brugada syndrome. Eur Heart J 2002 Nov;23(21):1648-1654. (Consensus development conference, review) 35. Antzelevitch C, Brugada P, Brugada J, et al. Brugada syndrome: a decade of progress. Circ Res 2002 Dec 13;91(12):1114-1118. (Review) 36. Jones R, Gage A. Brugada syndrome as the cause of syncope in a 49year-old man. Ann Emerg Med 2000 Aug;36(2):156-159. (Case report) 37. Vanpee D, Blommaert D, Gillet JB, et al. A young man with recurrent syncopes, right bundle branch block and ST segment elevation. Am J Emerg Med 1999 Oct;17(6):601-603. (Case report) 38. Sorgato A, Faggiano P, Aurigemma GP, et al. Ventricular arrhythmias in adult aortic stenosis: prevalence, mechanisms, and clinical relevance. Chest 1998 Feb;113(2):482-491. (Review) 39. Davidson E, Rotenbeg Z, Fuchs J, et al. Transient ischemic attackrelated syncope. Clin Cardiol 1991 Feb;14(2):141-144. (Retrospective cohort; 37 patients) 40. Pavlovic SU, Kocovic D, Djordjevic M, et al. The etiology of syncope in pacemaker patients. Pacing Clin Electrophysiol 1991 Dec;14(12):20862091. (Retrospective review; 46 patients) 41. Tavintharan S, Mukherjee JJ. A rare cause of syncope in a patient with diabetes mellitus—a case report. Ann Acad Med Singapore 2001 Jul;30(4):436-439. (Case report) 42. Lee EC. Clinical manifestations of sarin nerve gas exposure. JAMA 2003 Aug 6;290(5):659-662. (Review) 43. Wax PM, Becker CE, Curry SC. Unexpected “gas” casualties in Moscow: a medical toxicology perspective. Ann Emerg Med 2003 May;41(5):700-705. (Review) 44.* Kapoor WN, Hanusa BH. Is syncope a risk factor for poor outcomes? Comparison of patients with and without syncope. Am J Med 1996 Jun;100(6):646-655. (Prospective; 470 patients) 45. Oh JH, Hanusa BH, Kapoor WN. Do symptoms predict cardiac arrhythmias and mortality in patients with syncope? Arch Intern Med 1999 Feb 22;159(4):375-380. (Prospective cohort; 497 patients) 46.* Martin TP, Hanusa BH, Kapoor WN. Risk stratification of patients with syncope. Ann Emerg Med 1997 Apr;29(4):459-466. (Prospective cohort; 252 patients in first and 375 patients in second) 47. Alboni P, Brignole M, Menozzi C, et al. Diagnostic value of history in patients with syncope with or without heart disease. J Am Coll Cardiol 2001 Jun 1;37(7):1921-1928. (Prospective; 341 patients) 48. Doi A, Miyamoto K, Uno K, et al. Studies on hemodynamic instability in paroxysmal supraventricular tachycardia: noninvasive evaluations by head-up tilt testing and power spectrum analysis on electrocardiographic RR variation. Pacing Clin Electrophysiol 2000 Nov;23(11 Pt should carry more weight than a case report. To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study, will be included in bold type following the reference, where available. In addition, the most informative references cited in the paper, as determined by the authors, will be noted by an asterisk (*) next to the number of the reference. COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC associated with probable adverse drug reactions. Arch Intern Med 1990 Nov;150(11):2309-2312. (Retrospective; 70 patients) 75. Gaeta TJ, Fiorini M, Ender K, et al. Potential drug-drug interactions in elderly patients presenting with syncope. J Emerg Med 2002 Feb;22(2):159-162. (Retrospective; 263 patients) 76. Atkins D, Hanusa B, Sefcik T, et al. Syncope and orthostatic hypotension. Am J Med 1991 Aug;91(2):179-185. (Prospective; 223 patients) 77. Sarasin FP, Louis-Simonet M, Carballo D, et al. Prevalence of orthostatic hypotension among patients presenting with syncope in the ED. Am J Emerg Med 2002 Oct;20(6):497-501. (Prospective; 650 patients) 78. Goldschlager N, Epstein AE, Grubb BP, et al; Practice Guidelines Subcommittee, North American Society of Pacing and Electrophysiology. Etiologic considerations in the patient with syncope and an apparently normal heart. Arch Intern Med 2003 Jan 27;163(2):151-162. (Review) 79. Meyer MD, Handler J. Evaluation of the patient with syncope: an evidence based approach. Emerg Med Clin North Am 1999 Feb;17(1):189-201, ix. (Review) 80. Chen LY, Gersh BJ, Hodge DO, et al. Prevalence and clinical outcomes of patients with multiple potential causes of syncope. Mayo Clin Proc 2003 Apr;78(4):414-420. (Retrospective cohort; 987 patients) 81. Georgeson S, Linzer M, Griffith JL, et al. Acute cardiac ischemia in patients with syncope: importance of the initial electrocardiogram. J Gen Intern Med 1992 Jul-Aug;7(4):379-386. (Prospective, multicenter; 251 patients) 82. Fesmire FM, Percy RF, Bardoner JB, et al. Usefulness of automated serial 12-lead ECG monitoring during the initial emergency department evaluation of patients with chest pain. Ann Emerg Med 1998 Jan;31(1):3-11. (Prospective, observational; 1000 patients) 83. Balmelli N, Naegeli B, Bertel O. Diagnostic yield of automatic and patient-triggered ambulatory cardiac event recording in the evaluation of patients with palpitations, dizziness, or syncope. Clin Cardiol 2003 Apr;26(4):173-176. (Prospective cohort; 101 patients) 84. Seidl K, Rameken M, Breunung S, et al; Reveal-Investigators. Diagnostic assessment of recurrent unexplained syncope with a new subcutaneously implantable loop recorder. Europace 2000 Jul;2(3):256262. (Prospective cohort; 133 patients) 85. Arthur W, Kaye GC. Current investigations used to assess syncope. Postgrad Med J 2001 Jan;77(903):20-23. (Review) 86. Davis TL, Freemon FR. Electroencephalography should not be routine in the evaluation of syncope in adults. Arch Intern Med 1990 Oct;150(10):2027-2029. (Retrospective; 73 patients) 87. Recchia D, Barzilai B. Echocardiography in the evaluation of patients with syncope. J Gen Intern Med 1995 Dec;10(12):649-655. (Retrospective; 128 patients) 88. Sarasin FP, Junod AF, Carballo D, et al. Role of echocardiography in the evaluation of syncope: a prospective study. Heart 2002 Oct;88(4):363367. (Prospective cohort; 650 patients) 89. Morag R, Brenner B. Syncope. http://www.emedicine.com/. Accessed September 27, 2002. (Review) 90. Widerhorn J, Widerhorn AL, Rahimtoola SH, et al. WPW syndrome during pregnancy: increased incidence of supraventricular arrhythmias. Am Heart J 1992 Mar;123(3):796-798. (Case series; 3 patients) 91. Shotan A, Ostrzega E, Mehra A, et al. Incidence of arrhythmias in normal pregnancy and relation to palpitations, dizziness, and syncope. Am J Cardiol 1997 Apr 15;79(8):1061-1064. (Comparative; 162 patients) 92. Lewis DA, Dhala A. Syncope in the pediatric patient. The cardiologist’s perspective. Pediatr Clin North Am 1999 Apr;46(2):205219. (Review) 93.* Driscoll DJ, Jacobsen SJ, Porter CJ, et al. Syncope in children and adolescents. J Am Coll Cardiol 1997 Apr;29(5):1039-1045. (Retrospective; 151 patients) 94. Prodinger RJ, Reisdorff EJ. Syncope in children. Emerg Med Clin North Am 1998 Aug;16(3):617-626, ix. (Review) 95. Johnsrude CL. Current approach to pediatric syncope. Pediatr Cardiol 2000 Nov-Dec;21(6):522-531. (Review) 96. Driscoll DJ, Edwards WD. Sudden unexpected death in children and adolescents. J Am Coll Cardiol 1985 Jun;5(6 Suppl):118B-121B. (Retrospective; 515 patients) 97. Olsky M, Murray J. Dizziness and fainting in the elderly. Emerg Med Clin North Am 1990 May;8(2):295-307. (Review) 98. Baraff LJ, Della Penna R, Williams N, et al. Practice guideline for the ED management of falls in community-dwelling elderly persons. Kaiser Permanente Medical Group. Ann Emerg Med 1997 Oct;30(4):480492. (Practice guideline, review) 99. Sorock GS. Falls among the elderly: epidemiology and prevention. Am 1):1623-1631. (Prospective; 36 patients) Calkins H, Shyr Y, Frumin H, et al. The value of the clinical history in the differentiation of syncope due to ventricular tachycardia, atrioventricular block, and neurocardiogenic syncope. Am J Med 1995 Apr;98(4):365-373. (Prospective cohort; 80 patients) 50. Gilman JK. Syncope in the emergency department. A cardiologist’s perspective. Emerg Med Clin North Am 1995 Nov;13(4):955-971. (Review) 51. Kofflard MJ, Ten Cate FJ, van der Lee C, et al. Hypertrophic cardiomyopathy in a large community-based population: clinical outcome and identification of risk factors for sudden cardiac death and clinical deterioration. J Am Coll Cardiol 2003 Mar 19;41(6):987-993. (Comparative; 225 patients) 52. Braunwald E. Valvular heart disease. In: Heart Disease: A Textbook of Cardiovascular Medicine. 6th ed. St. Louis, MO: W.B. Saunders Company; 2001:1643-1722. (Textbook chapter) 53. Harrison EC, Rashtian MY, Allen DT, et al. An emergency physician’s guide to prosthetic heart valves: valve-related complications. Ann Emerg Med 1988 Jul;17(7):704-710. (Review) 54. Vongpatanasin W, Hillis LD, Lange RA. Prosthetic heart valves. N Engl J Med 1996 Aug 8;335(6):407-416. (Review) 55. Varon J, Fromm RE Jr. Syncope: the forgotten sign of pulmonary embolism. J Emerg Med 1998 Jan-Feb;16(1):117-118. (Editorial) 56. Wolfe TR, Allen TL. Syncope as an emergency department presentation of pulmonary embolism. J Emerg Med 1998 Jan-Feb;16(1):27-31. (Case report) 57. Bell WR, Simon TL, DeMets DL. The clinical features of submassive and massive pulmonary emboli. Am J Med 1977 Mar;62(3):355-360. (Cohort; 327 patients) 58. Stein PD, Willis PW 3rd, DeMets DL. History and physical examination in acute pulmonary embolism in patients without preexisting cardiac or pulmonary disease. Am J Cardiol 1981 Feb;47(2):218-223. (Prospective cohort; 215 patients) 59. Kuhlmann TP, Powers RD. Painless aortic dissection: an unusual cause of syncope. Ann Emerg Med 1984 Jul;13(7):549-551. (Case report) 60. Young J, Herd AM. Painless acute aortic dissection and rupture presenting as syncope. J Emerg Med 2002 Feb;22(2):171-174. (Case report) 61. Schweitzer P, Teichholz LE. Carotid sinus massage. Its diagnostic and therapeutic value in arrhythmias. Am J Med 1985 Apr;78(4):645-654. (Review) 62. Hoefnagels WA, Padberg GW, Overweg J, et al. Syncope or seizure? The diagnostic value of the EEG and hyperventilation test in transient loss of consciousness. J Neurol Neurosurg Psychiatry 1991 Nov;54(11):953-956. (Prospective; 119 patients) 63. Benbadis SR, Wolgamuth BR, Goren H, et al. Value of tongue biting in the diagnosis of seizures. Arch Intern Med 1995 Nov 27;155(21):23462349. (Prospective; 106 patients) 64.* Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish syncope from seizures. J Am Coll Cardiol 2002 Jul 3;40(1):142-148. 65. Bergfeldt L. Differential diagnosis of cardiogenic syncope and seizure disorders. Heart 2003 Mar;89(3):353-358. (Review) 66. Lanska DJ, Remler B. Benign paroxysmal positioning vertigo: classic descriptions, origins of the provocative positioning technique, and conceptual developments. Neurology 1997 May;48(5):1167-1177. (Review) 67. Froehling DA, Silverstein MD, Mohr DN, et al. The rational clinical examination. Does this dizzy patient have a serious form of vertigo? JAMA 1994 Feb 2;271(5):385-388. (Review) 68. Shlamovitz GZ, Assia A, Ben-Sira L, et al. “Suffocation roulette”: a case of recurrent syncope in an adolescent boy. Ann Emerg Med 2003 Feb;41(2):223-226. (Case report) 69. Kapoor WN, Fortunato M, Hanusa BH, et al. Psychiatric illnesses in patients with syncope. Am J Med 1995 Nov;99(5):505-512. (Prospective cohort; 414 patients) 70. Shapiro NI, Kociszewski C, Harrison T, et al. Isolated prehospital hypotension after traumatic injuries: a predictor of mortality? J Emerg Med 2003 Aug;25(2):175-179. (Retrospective cohort; 490 patients) 71. Pancioli A, McNeil P. The clinical challenge of syncope: a costconscious and outcome-driven approach to patient evaluation and disposition. Emerg Med Rep 1998 Sep 14;19. (Review) 72. Newman BH. Vasovagal reactions in high school students: findings relative to race, risk factor synergism, female sex, and non-high school participants. Transfusion 2002 Dec;42(12):1557-1560. (Retrospective cohort; 1302 subjects) 73. Kapoor WN. Current evaluation and management of syncope. Circulation 2002 Sep 24;106(13):1606-1609. (Review). 74. Hanlon JT, Linzer M, MacMillan JP, et al. Syncope and presyncope 49. Emergency Medicine Practice 18 www.empractice.net • January 2004 Physician CME Questions 1. 2. 3. 4. 5. Which of the following does not suggest a high-risk cause of syncope? a. Age greater than 45 years b. Prodrome suggesting vasodepressor or orthostatic etiology c. History of ventricular dysrhythmias or CHF d. An abnormal ECG 7. The highest mortality rates are generally associated with which of the following categories of syncope? a. Cardiac b. Central nervous system c. Vasovagal/psychogenic d. Metabolic/drug-related 8. A complaint of syncope while sitting most likely suggests which of the following causes? a. Cardiac b. Central nervous system c. Vasovagal/psychogenic d. Metabolic/drug-related 9. ECG findings of a pseudo-right bundle branch block and persistent downsloping ST segment elevation in leads V1 to V3 characterize: a. torsades de pointes. b. Wolff-Parkinson-White syndrome. c. Brugada syndrome. d. sick sinus syndrome. 10. Which of the following suggests a seizure rather than syncope? a. Waking with a cut tongue after the episode b. Lightheadedness c. Sweating before the episode d. An episode associated with prolonged sitting or standing All of the following regarding syncope in the ED are true except: a. Its cost to the healthcare system in the United States exceeds $2 billion per year. b. The ED practitioner must reach a specific diagnosis before discharging a patient with syncope. c. Syncope is common in young and elderly patients. d. ECGs can help risk stratify patients with syncope. 11. Questioning witnesses is a high-yield way to reveal duration of unconsciousness, events just prior to the spell, and duration of confusion following the spell. a. True b. False A brief, transient loss of consciousness plus generalized weakness and loss of muscular tone characterize: a. seizures. b. syncope. c. vertigo. d. drop attacks. 12. A finding of orthostatic hypotension: a. is generally defined as a decline of 20 mmHg or greater in systolic blood pressure on standing. b. rules out life-threatening causes of syncope. c. is present in less than 5% of patients over 70 years. d. all of the above. Unconsciousness lasting more than five minutes, a slow return to full alertness, and disorientation or an aura prior to the event suggest syncope, not seizure. a. True b. False 13. A chest x-ray should be ordered in all patients with syncope in order to rule out potentially lethal causes such as aortic dissection and pulmonary embolism. a. True b. False Which of the following can cause syncope? a. Bradycardic dysrhythmias b. Tachycardic dysrhythmias c. Long QT syndrome d. Brugada syndrome e. All of the above 14. Which of the following is/are “red flag(s)” in the history of pediatric patients with syncope? a. Syncope in response to loud noise or stress b. Syncope during exercise c. Syncope while supine d. A history of sudden death in a family member less than 30 years old e. Any of the above Which of the following is the most common? a. Vasodepressor syncope b. Cardiogenic syncope c. Neurologic syncope d. Metabolic/drug-related syncope January 2004 • www.empractice.net 6. 19 Emergency Medicine Practice COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC J Prev Med 1988 Sep-Oct;4(5):282-288. (Review) 100. Sattin RW, Lambert Huber DA, DeVito CA, et al. The incidence of fall injury events among the elderly in a defined population. Am J Epidemiol 1990 Jun;131(6):1028-1037. (Population-based surveillance data) 101. Nelson RC, Amin MA. Falls in the elderly. Emerg Med Clin North Am 1990 May;8(2):309-324. (Review) 102.* Kapoor W, Snustad D, Peterson J, et al. Syncope in the elderly. Am J Med 1986 Mar;80(3):419-428. (Prospective; 400 patients) 103. Simpson CS, Klein GJ, Brennan FJ, et al. Impact of a mandatory physician reporting system for cardiac patients potentially unfit to drive. Can J Cardiol 2000 Oct;16(10):1257-1263. (Retrospective, epidemiologic; 994 patients) 104. Strickberger SA, Cantillon CO, Friedman PL. When should patients with lethal ventricular arrhythmia resume driving? An analysis of state regulations and physician practices. Ann Intern Med 1991 Oct 1;115(7):560-563. (Survey) 105. Akiyama T, Powell JL, Mitchell LB, et al; Antiarrhythmics versus Implantable Defibrillators Investigators. Resumption of driving after life-threatening ventricular tachyarrhythmia. N Engl J Med 2001 Aug 9;345(6):391-397. (Prospective, randomized, controlled trial; 909 patients) 106. Maas R, Ventura R, Kretzschmar C, et al. Syncope, driving recommendations, and clinical reality: survey of patients. BMJ 2003 Jan 4;326(7379):21. (Prospective; 104 patients) 107. Epstein AE, Miles WM, Benditt DG, et al. Personal and public safety issues related to arrhythmias that may affect consciousness: implications for regulation and physician recommendations. A medical/scientific statement from the American Heart Association and the North American Society of Pacing and Electrophysiology. Circulation 1996 Sep 1;94(5):1147-1166. (Consensus statement) 108. Hauer KE. Discovering the cause of syncope. A guide to the focused evaluation. Postgrad Med 2003 Jan;113(1):31-38, 95; quiz 2. (Review) COPYRIGHTED MATERIAL—DO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC Physician CME Information 15. An ECG: a. can identify extremely dangerous and potentially lethal causes of syncope. b. is easy, inexpensive, and can facilitate rapid treatment of life-threatening problems. c. can be used to risk stratify patients with syncope. d. all of the above. This CME enduring material is sponsored by Mount Sinai School of Medicine and has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education. Credit may be obtained by reading each issue and completing the printed post-tests administered in December and June or online single-issue post-tests administered at www.empractice.net. Target Audience: This enduring material is designed for emergency medicine physicians. 16. Which of the following patients may be safely discharged from the ED for outpatient follow-up? a. A patient with a history of congestive heart failure or ventricular dysrhythmias b. A patient with chest pain or other symptoms compatible with acute coronary syndrome c. A patient younger than 40 with an isolated syncopal event and normal physical findings, a normal ECG, and no evidence of heart disease d. A patient with ECG findings of dysrhythmia, prolonged QT interval, or bundle branch block Needs Assessment: The need for this educational activity was determined by a survey of medical staff, including the editorial board of this publication; review of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation of prior activities for emergency physicians. Date of Original Release: This issue of Emergency Medicine Practice was published January 1, 2004. This activity is eligible for CME credit through January 1, 2007. The latest review of this material was December 5, 2003. Discussion of Investigational Information: As part of the newsletter, faculty may be presenting investigational information about pharmaceutical products that is outside Food and Drug Administration approved labeling. Information presented as part of this activity is intended solely as continuing medical education and is not intended to promote off-label use of any pharmaceutical product. Disclosure of Off-Label Usage: This issue of Emergency Medicine Practice discusses no off-label use of any pharmaceutical product. Faculty Disclosure: In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty for this CME activity were asked to complete a full disclosure statement. The information received is as follows: Dr. Marill, Dr. Kosiak, Dr. Decker, Dr. Pigott, and Dr. Shah report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational presentation. Class Of Evidence Definitions Each action in the clinical pathways section of Emergency Medicine Practice receives an alpha-numerical score based on the following definitions. Class I • Always acceptable, safe • Definitely useful • Proven in both efficacy and effectiveness Level of Evidence: • One or more large prospective studies are present (with rare exceptions) • High-quality meta-analyses • Study results consistently positive and compelling Class II • Safe, acceptable • Probably useful Level of Evidence: • Generally higher levels of evidence • Non-randomized or retrospective studies: historic, cohort, or case-control studies • Less robust RCTs • Results consistently positive Class III • May be acceptable • Possibly useful • Considered optional or alternative treatments Level of Evidence: • Generally lower or intermediate levels of evidence • Case series, animal studies, consensus panels • Occasionally positive results Accreditation: Mount Sinai School of Medicine is accredited by the Accreditation Council for Continuing Medical Education to sponsor continuing medical education for physicians. Indeterminate • Continuing area of research • No recommendations until further research Credit Designation: Mount Sinai School of Medicine designates this educational activity for up to 4 hours of Category 1 credit toward the AMA Physician’s Recognition Award. Each physician should claim only those hours of credit actually spent in the educational activity. Emergency Medicine Practice is approved by the American College of Emergency Physicians for 48 hours of ACEP Category 1 credit (per annual subscription). Emergency Medicine Practice has been reviewed and is acceptable for up to 48 Prescribed credit hours by the American Academy of Family Physicians. Emergency Medicine Practice has been approved for 48 Category 2-B credit hours by the American Osteopathic Association. Level of Evidence: • Evidence not available • Higher studies in progress • Results inconsistent, contradictory • Results not compelling Earning Credit: Two Convenient Methods Significantly modified from: The Emergency Cardiovascular Care Committees of the American Heart Association and representatives from the resuscitation councils of ILCOR: How to Develop EvidenceBased Guidelines for Emergency Cardiac Care: Quality of Evidence and Classes of Recommendations; also: Anonymous. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. Emergency Cardiac Care Committee and Subcommittees, American Heart Association. Part IX. Ensuring effectiveness of community-wide emergency cardiac care. JAMA 1992;268(16):2289-2295. • Print Subscription Semester Program: Paid subscribers with current and valid licenses in the United States who read all CME articles during each Emergency Medicine Practice six-month testing period, complete the posttest and the CME Evaluation Form distributed with the December and June issues, and return it according to the published instructions are eligible for up to 4 hours of Category 1 credit toward the AMA Physician’s Recognition Award (PRA) for each issue. You must complete both the post-test and CME Evaluation Form to receive credit. Results will be kept confidential. CME certificates will be delivered to each participant scoring higher than 70%. • Online Single-Issue Program: Paid subscribers with current and valid licenses in the United States who read this Emergency Medicine Practice CME article and complete the online post-test and CME Evaluation Form at www.empractice.net are eligible for up to 4 hours of Category 1 credit toward the AMA Physician’s Recognition Award (PRA). You must complete both the post-test and CME Evaluation Form to receive credit. Results will be kept confidential. CME certificates may be printed directly from the Web site to each participant scoring higher than 70%. Emergency Medicine Practice is not affiliated with any pharmaceutical firm or medical device manufacturer. President and CEO: Robert Williford. Publisher: Heidi Frost. Research Editors: Ben Abella, MD, University of Chicago; Richard Kwun, MD, Mount Sinai School of Medicine. Direct all editorial or subscription-related questions to EB Practice, LLC: 1-800-249-5770 • Fax: 1-770-500-1316 • Non-U.S. subscribers, call: 1-678-366-7933 EB Practice, LLC • 305 Windlake Court • Alpharetta, GA 30022 E-mail: [email protected] • Web Site: http://www.empractice.net Emergency Medicine Practice (ISSN 1524-1971) is published monthly (12 times per year) by EB Practice, LLC, 305 Windlake Court, Alpharetta, GA 30022. Opinions expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as a general guide and is intended to supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions. The materials contained herein are not intended to establish policy, procedure, or standard of care. Emergency Medicine Practice is a trademark of EB Practice, LLC. Copyright 2004 EB Practice, LLC. All rights reserved. No part of this publication may be reproduced in any format without written consent of EB Practice, LLC. Subscription price: $299, U.S. funds. (Call for international shipping prices.) Emergency Medicine Practice 20 www.empractice.net • January 2004