Syncope Evaluation and Management in an Urgent Care Setting

Urgent message: When a presents to urgent care after a syncopal event, the clinician’s charge is to determine whether the episode was of benign or potentially life-threatening etiology and whether the patient should be transferred for further evaluation.

Kenneth V. Iserson, MD, MBA, FACEP, FAAEM, Professor of Emergency Medicine, The University of Arizona, Tucson, AZ

Introduction yncope is a sudden, transient loss of with a loss of postural tone (typically, ). It results from an abrupt, transient, and diffuse cerebral Smalfunction and is quickly followed by sponta- neous recovery. The term excludes , coma, , or other states of altered consciousness. Many will ascribe their syncopal episode to a sit- uationally mediated vasovagal episode. Despite this, the goals in the urgent care setting include the following: Ⅲ Determining whether the patient’s episode was actually a syncopal or presyncopal event, and if it could have a life-threatening etiology Ⅲ Stabilizing the patient Ⅲ Transferring those patients who need further diag- nostic studies or therapeutic interventions © John Bolesky, Artville © John Bolesky, Epidemiology Syncope accounts for up to 3% of emergency depart- common in young adults, while cardiac syncope ment (ED) visits and up to 6% of hospital admissions becomes increasingly more frequent with advancing each year in the United States.1,2 At some time in their age.4 The chance of having at least one syncopal episode lives, up to about half the population (12% to 48%) of in childhood is between 15% and 50%.5 Though a people may experience syncope.3 benign cause is usually found, syncope in children war- Syncope occurs in all age groups, but it is most com- rants prompt detailed evaluation.6 mon in adults. Non-cardiac causes tend to be more With advancing age comes an increased frequency of

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coronary artery and the sight of blood, and myocardial disease, arr- Table 1. Presyncopal pain may often precipitate hythmia, vasomotor insta- these events. Diabetics and bility, autonomic failure, Ⅲ Pallor Ⅲ Epigastric discomfort the elderly often have dis- polyneuropathy, and the Ⅲ Diaphoresis Ⅲ ruption of their autonomic use of polypharmacy—all Ⅲ Palpitations Ⅲ Blurred or faded vision systems leading to syn- of which can contribute to Ⅲ Vertigo Ⅲ Parasthesias cope. In all these cases, a syncope. Therefore, ad- Ⅲ Weakness good history may help vanced age is an independ- determine whether a syn- ent risk factor for both syn- copal event was vasovagal cope and .7 or due to a more serious cause. (While tilt-testing may eventually suggest that a syncopal event from unknown Pathophysiology cause was vasovagal, no real “gold standard” for vasova- Regardless of specific cause, on the most basic level gal syncope exists.)9 syncope results from the sudden reduction in the deliv- is a clinical syndrome ery of a vital substrate (usually oxygen) to both cerebral indicating diminished intravascular volume. A com- hemispheres or to the ’s reticular activating sys- monly encountered cause of syncope that often tem. Most often, this is due to a localized or systemic requires treatment, it is often caused by reduction (35% or more) in blood flow to these areas. (often secondary to acute gastroenteritis), and is also Since tissue cannot store energy, cessation of cere- seen with excess intake of medication and acute ane- bral perfusion lasting only three to five seconds will mia from hemorrhage. result in syncope. This is most frequently caused by a Dysrhythmias may have multiple causes but, if they transiently diminished vagal tone or autonomic nervous cause syncope, are usually of acute onset. Such dys- system disorders (such as in patients with ). rhythmias may arise from any focus (supraventricular, Patients who experience vasovagal reactions have sub- nodal, or ventricular) and be bradycardic, tachycardic, or normal vagal responses with a disappearance unorganized (e.g., ventricular fibrillation). Pacemaker fail- of muscle sympathetic nerve activity.8 ure results in syncope when the underlying rhythm Syncope can, however, also be due to transient hypo- cannot sustain a sufficient . Severe brady- glycemia, toxins, metabolic abnormalities, failure of cardia, caused by minimal pressure on the carotid, caus- autoregulation, and primary neurological derangements. es carotid sinus syncope. It can be exacerbated by carotid The causes of syncope may be categorized into three lesions or digitalis toxicity. broad groups: cardiovascular, non-cardiovascular, and Obstructive lesions result from a diminished effective unknown. This categorization stratifies the patient’s cardiac output due to structural abnormalities. Most future risk for serious associated illnesses and death; commonly, these are in or around the heart—either generally, cardiovascular syncope is associated with acquired or congenital lesion—but can also occur with higher mortality than syncope due to non-cardiovascu- outflow obstruction due to a pulmonary embolus or aor- lar or unknown causes. tic dissection.

Cardiovascular Syncope Non-Cardiovascular Syncope Cardiovascular syncope may be due to autonomic dys- Non-cardiovascular syncope may be due to metabolic function, orthostatic hypotension, obstructive lesions, derangements, neurologic abnormalities, or psychiatric and dysrhythmias. Each of these has its own etiology. disease. Again, establishing the root of the suspected At all ages, the most common cause of syncope is cause of the syncope may help clarify management autonomic dysfunction, which results from a slowing of options. the heart and decreased cardiac output due to increased Metabolic derangements can develop slowly (e.g., vagal tone. This is often described as “fainting.” Any , ) or rapidly (e.g., hypo- number of factors, such as the bradycardia often seen in glycemia, ). Syncope is the sudden, final com- athletes, may cause increased vagal tone, and some mon pathway for these disorders. On occasion, they may individuals seem more prone to these episodes than lead to seizures or coma, rather than syncope. others. Emotional stress, hot or crowded conditions, Neurologic abnormalities are a relatively rare cause of

14 The Journal of Urgent Care Medicine | October 2006 www.jucm.com 1 7 syncope. Instead, atypical seizures may initially be events they can last about 2 ⁄2 minutes. described as syncope. Without extensive testing, the A group at the University of Calgary, Canada, devel- two may be difficult to differentiate. oped a set of historical questions that can help determine Psychiatric disease or medications may cause syn- if the patient’s syncope was due to a vasovagal episode cope due to a vagal effect, , or a drug or something more sinister (Table 2). effect. However, it is dangerous to ascribe a syncopal If the patient experiences typical pre- aura, episode to a psychiatric cause without some investiga- this suggests a seizure rather than syncope. tion, including a good history and physical examination. Red Flags Diagnostic Evaluation Some specific symptoms or activities associated with the History and physical examination are the most specific syncopal event should raise concern about life-threaten- and sensitive ways to evaluate syncope. Cursory review ing causes. of the literature shows that diagnosis can be made with Ⅲ , with or without palpitations or dysp- a thorough history and physical examination in 50% to nea, may accompany myocardial ischemia or infarc- 85% of patients.7 No single laboratory test has greater tions, aortic dissections, or dysrhythmias. These diagnostic efficacy. symptoms may be present as a presyncopal pro- drome, following syncope, or both. Ventricular History and supraventricular dysrhythmias may not be Proper diagnosis, or at least correct patient disposition, present on an initial ECG; prolonged requires combining patient and bystander history with may be necessary. Bradyarrhythmias and pacemak- risk factors (age, cardiac history, and significant other er malfunctions can usually be seen immediately. medical history—including medication/drug/ Ⅲ Dyspnea may accompany cardiac-related syncope, use) and the limited information that can be gained or may be a symptom of pulmonary embolus or from the physical examination and diagnostic tests. congestive , both of which may cause Witnesses to the syncopal event can often describe its syncope. character and time course far better than the patient Ⅲ Severe or new neurological deficits may (who, by definition, was unconscious). Key historical indicate a neurological cause for the syncope or a clues include: serious consequence of the syncopal event. Neuro- Ⅲ Setting (activities preceding syncope) logical syncope may have prodromal symptoms Ⅲ Prodrome (aura, chest pain, dyspnea, vertigo, such as vertigo, , diplopia, and . diaphoresis, graying of vision) These may suggest a or transient ischemic Ⅲ Abruptness of onset (gradual or sudden) attack. If symptoms appeared following a fall asso- Ⅲ Position when it occurred (standing, sitting, supine) ciated with syncope, trauma should be considered. Ⅲ Movement during/after syncope (tonic-clonic or Ⅲ Abdominal or back pain may suggest a source of myoclonic movements) acute , such as from a ruptured abdominal Ⅲ Duration (seconds, few minutes, longer) aortic aneurism, or in the pregnant patient, an Ⅲ Rate of recovery (rapid, slow, incomplete/prolonged) ectopic pregnancy or placental abruption. Presyncope, where there is no loss of consciousness, Ⅲ Strenuous exertion just before syncope, especially in requires the same evaluation as syncope. While patients young athletes with a cardiac murmur, suggests with syncope do not remember actually hitting the syncope due to cardiac outflow obstruction. In ground, those experiencing presyncope have the same any group, syncope can be very worrisome if it is symptoms, but the event terminates prior to loss of due to aortic stenosis, hypertrophic obstructive consciousness. Presyncope can still cause the patient to cardiomyopathy, mitral stenosis, pulmonary steno- lose postural tone, however. sis, pulmonary embolus, left atrial myxoma, or Prior faintness, , or light-headedness occurs pericardial tamponade. in 70% of patients experiencing syncope; other pre- Certain predisposing events may suggest more benign syncopal signs and symptoms may also occur, alone causes of syncope. Even here, however, care should be or in combination (Table 1), whether syncope actual- taken to avoid missing serious underlying disease. A ly follows or not. In dysrythmia-related syncope, presyn- variety of events can increase vagal tone and cause syn- copal symptoms last only seconds, though in vasovagal cope. In these cases, syncope occurs from decreased

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Table 2. Questions to Determine if Syncope is Vasovagal in Nature9

Question Points (if answer to question is yes) Is there a history of at least one of bifascicular block, asystole, -5 supraventricular tachycardia, or diabetes? At times, have bystanders noted you to be blue during a faint? -4 Did your syncope start when you were )35 years old? -3 Do you remember anything about being unconscious? -2 Do you have lightheaded spells, or faint with prolonged sitting or standing? 1 Do you sweat or feel warm before a faint? 2 Do you have lightheaded spells or faint with pain or in medical settings? 3 Point total The patient has vasovagal syncope if the point score is *-2.

peripheral vascular resistance due to stimulation of mon precipitants of syncope, so this history should be efferent vasodepressor reflexes. Asking about the patient’s taken in detail. Medications that reduce activity prior to syncope may suggest the etiology. These (e.g., antihypertensive drugs, , nitrates), affect often self-limiting problems are the most common cardiac output (e.g., beta-blockers, digitalis, antiarrhyth- cause of syncope in young adults; behavioral changes mics), prolong the Q-T interval (e.g., tricyclic antidepres- may help to avoid a recurrence. sants, phenothiazines, quinidine, amiodarone), or alter In elderly patients, 45% of orthostatic syncope cases the sensorium (e.g., sedating analgesics, hypnotics, anx- are related to medications. Medications may increase iolytics) may all cause syncope, for example. vagal tone and incite these events. In those cases, the Clinicians should ask about any recent changes in dosage may need to be adjusted or the medication medication dosage, new medications, and anything changed. Dehydration and decreased intravascular vol- that may have changed the body’s level of the medica- ume can also lead to syncope, but consideration should tion, such as food, illness, or dieting. Illicit drug and alco- be given to underlying heat illness, blood loss, or other hol use may also cause syncope and, on occasion, may more serious causes for this condition. presage serious events (e.g., cocaine-induced myocardial infarction, delirium tremens). Syncope or Seizure? Finally, the clinicians must also inquire about other A common challenge for the clinician is distinguishing serious personal and family medical conditions, especial- syncope from seizures. While this may require extensive ly cardiovascular disease. Patients with a history of testing in some patients, there are some historical clues myocardial infarction, , structural cardiac that can help. If witnesses note convulsive activity or, defects, cardiomyopathy, or congestive heart failure fall especially, postictal confusion, this probably indicates a into a high-risk group for death and disability. Those seizure. Post-syncopal confusion occurs, but rarely lasts with a family history of sudden death or serious cardiac more than 30 seconds; confusion following a seizure disease should also be considered in this category. usually lasts much longer. In addition, patients should be asked if they remember being confused about their Physical Examination surroundings after the event and whether they have oral The physical examination supplements clinical opinions trauma, incontinence, or myalgias. Witnesses may also formed from the patient and bystander history. While it be confused by the myoclonic jerks that sometimes may confirm suspicions or add new information, it accompany syncope, although these usually last only a should only be considered a supplement to the clinical very short time. history. During the physical exam, it is important to rec- Medication, drug, and alcohol use are relatively com- ognize signs of trauma, since syncope from any cause

18 The Journal of Urgent Care Medicine | October 2006 www.jucm.com can result in with levels with renal function significant morbidity and Table 3. Post-Syncopal Event Physical Exam tests and the complete mortality, especially in the Elements blood count are of scant elderly10 (Table 3). utility in making a diagno- Examine Look for sis or determining disposi- Laboratory/Imaging Vital signs Pulse rate and rhythm tion, although one predic- Ancillary testing rarely pro- Respiratory rate and depth tive model, the San vides additional useful Temperature Francisco Syncope Rule, information. The exception Blood pressure, including does use the hematocrit as 11 is the ECG, which can be orthostatic measurements one factor. Fecal occult diagnostic for acute myocar- General Evidence of trauma blood testing and testing dial ischemia or infarction, Alertness and orientation for significant abdominal dysrhythmias, prolonged Skin Color pain during the physical Q-T intervals, bundle Diaphoresis exam is a far better way of branch blocks, pacemaker HEENT Evidence of mouth, head or facial identifying occult blood malfunction, and other car- trauma loss. Electrolyte testing may diac disease. Most patients Papilledema be needed only if seizure is presenting with syncope or Smell of acetone being seriously considered. presyncope should have an Neck Jugular venous distention If the patient is on anti- ECG. Patients should be Bruits (carotid sinus massage may epileptic medications, those referred if they require pro- precipitate sinus arrest and should levels may also need to be longed cardiac monitoring not be done in urgent care centers) drawn after consulting with to identify intermittent dys- Lungs Equal breath sounds the patient’s neurologist. rhythmias. Rales If the patient warrants Although diagnostic in Heart Systolic murmur having cardiac enzymes or less than 2% of syncopal Rub creatine kinase (for a pro- patients, the rapid and Dysrhythmias longed seizure or period of inexpensive fingerstick Abdomen Bruit ) drawn, blood always Pulsatile mass he or she should be sent should be checked. In Rectum Gross or occult blood to the emergency depart- those patients with hypo- Pelvis Vaginal bleeding ment, and probably admit- glycemia, rapid therapy Lower abdominal pain ted to the hospital. may immediately be insti- Urinary or fecal incontinence Those patients requiring tuted. If is Extremities Delayed capillary refill more intensive imaging found, a diabetic compli- Equal pulses in upper extremities (e.g., head CT scan, chest- cation may be considered Peripheral neuropathies abdomen scan, pelvic ultra- (ketoacidosis, neuropathy, Neurologic Newly altered mental status sound, MRI, echocardiogra- and autonomic dysfunc- Focal neurologic findings phy, EEG, or tilt testing) tion). For similar reasons, a should be referred to an dipstick urinalysis should HEENT=head, eyes, ears, nose, and throat ED or their personal physi- be performed, especially on cian, depending upon the all elderly patients, since a urgency of the situation. urinary tract may precipitate syncope and can be easily treated.7 Criteria to Transfer/Refer Patients Likewise, a chest radiograph should be considered Two decision rules have been published that help to in all patients, especially the elderly. It may demon- identify those at most risk after syncope. However, strate evidence of infectious or aspiration , patients not meeting these criteria still were at significant congestive heart failure, a pleural effusion, a lung mass risk for untoward events in the subsequent year. or a widened mediastinum.7 One model demonstrated that between 58% and Except in unique circumstances, serum electrolyte 80% of patients with at least three of the following risk

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Table 4. Differential Diagnosis*

Cardiovascular Causes Non-Cardiovascular Causes

Autonomic (most common cause in children) Metabolic Ⅲ Carotid sinus syncope Ⅲ Alcoholism Ⅲ Cough Ⅲ Carbon monoxide poisoning Ⅲ Defecation Ⅲ Drug-induced (insulin, oral hypoglycemics) Ⅲ Excessive vagal tone (athletes, adolescents) Ⅲ Hyperventilation Ⅲ Micturition Ⅲ Ⅲ Postprandial Ⅲ Hypothyroid Ⅲ Sneeze Ⅲ Hypoxia/asphyxiation Ⅲ Swallow Ⅲ Pheochromocytoma Ⅲ Valsalva

Orthostatic hypotension Neurologic Ⅲ Ⅲ Basilar artery migraine Ⅲ Autonomic insufficiency/dysfunction: alcoholic, Ⅲ Cerebrovascular insufficiency/Transient Ischemic degenerative CNS diseases, diabetic Attack (TIA) Ⅲ Dehydration Ⅲ Narcolepsy Ⅲ Drug-induced (beta blockers, central antihypertensives, Ⅲ Normal pressure diuretics, drugs/chemicals of abuse, narcotics, Ⅲ Peripheral polyneuropathy sympathetic blockers, vasodilators) Ⅲ Seizure Ⅲ Hemorrhage, acute Ⅲ Ⅲ Idiopathic Ⅲ Subclavian steal syndrome Ⅲ Vertebrobasilar insufficiency Ⅲ Increased intracranial pressure

Obstructive lesions Psychiatric Ⅲ Aortic dissection Ⅲ Anxiety disorder Ⅲ Aortic, mitral or pulmonary stenosis Ⅲ Breath-holding spells Ⅲ Atrial myxoma Ⅲ Conversion reaction Ⅲ Cardiac tamponade Ⅲ Drug-induced (anticonvulsants, antihistamines, Ⅲ Congenital heart disease antiparkinsonians, bromocriptine, cholinesterase Ⅲ Hypertrophic cardiomyopathy inhibitors, CNS , MAO inhibitors, Ⅲ Left ventricular dysfunction tricyclic antidepressants) Ⅲ Pulmonary embolism Ⅲ Panic disorder Ⅲ Pulmonary hypertension Ⅲ Hysteria Ⅲ Pulmonary stenosis Ⅲ Major depression

Dysrhythmias Ⅲ Bradyarrhythmias Ⅲ Cardiomyopathy Ⅲ Drug-induced (anticonvulsants, antihistamines, beta blockers, digitalis, diuretics, drugs/chemicals of abuse, tricyclic antidepressants, Q-T prolonging) Ⅲ Implanted defibrillator malfunction Ⅲ Myocardial infarction Ⅲ Sick sinus syndrome Ⅲ Long Q-T syndrome Ⅲ Pacemaker failure Ⅲ 2o & 3o blocks Ⅲ Supraventricular and ventricular tachyarrhythmias Ⅲ Torsades de pointes

*The cause of syncope cannot be determined in 38% to 47% of cases.

20 The Journal of Urgent Care Medicine | October 2006 www.jucm.com factors suffered identifiable dysrhythmias or death with- ty rate of 20% to 30% and a 33% incidence of sudden in one year: death over five years.2,3,14,15 Risk is higher in older patients Ⅲ Abnormal ECG findings and those with serious comorbidities, with mortality Ⅲ History of ventricular arrhythmia rates significantly increased within both four weeks Ⅲ History of congestive heart failure and one year after presentation.1 Elderly patients have a Ⅲ Age >45 years 30% incidence of a recurrent syncopal episode.13 Incidence of dysrhythmias or death was 4%-7% Syncope of any etiology in a cardiac patient (to be dif- among patients with no risk factors, and was 58%-80% ferentiated from cardiac syncope) has also been shown for patients with three or four risk factors.12 to imply a poor prognosis. Patients with NYHA function- Another model identified patients who are at imme- al class III or IV who have any type of syncope have a diate risk for serious outcomes within seven days, with mortality rate as high as 25% within one year.7 a 96% sensitivity. Its criteria was the presence of abnor- mal ECG findings, a history of congestive heart fail- Summary ure, dyspnea, a hematocrit less than 30%, and a blood Syncope has a long differential diagnosis that includes pressure less than 90 mm Hg.11 many life-threatening conditions. History, from the The question is, will a 4% short-term serious out- patient and bystanders, is the key diagnostic tool in come rate be acceptable? urgent care to determine whether a patient needs further evaluation and treatment. Physical examination plays an Prognosis important, but lesser, role. Except for the ECG, finger- The differential diagnosis (Table 4) includes many stick glucose, dipstick urinalysis, and chest radiograph, life-threatening conditions. The clinician’s primary goal laboratory and imaging do not play an important role in is to distinguish life-threatening etiologies—mainly due urgent care decisions about patient disposition or treat- to cardiovascular causes—from those that are more ment after syncope. Any abnormal cardiac findings or benign. The most common serious causes of syncope are potentially serious suspected cause of the syncopal dysrhythmias and myocardial ischemia. Less common event warrants transfer to an ED. If a life-threatening serious causes include cerebrovascular events, toxic- condition is suspected, patients should be transported metabolic abnormalities, and critical aortic stenosis. immediately via the EMS system. ■ Rarely seen, but life-threatening, causes are thoracic aortic dissections, massive pulmonary emboli, and sub- REFERENCES 1. Colivicchi F, Ammirati F, Melina D. Development and prospective validation of a risk strat- arachnoid hemorrhages. ification system for patients with syncope in the emergency department: the OESIL risk Young, healthy patients with a clearly benign cause of score. Eur Heart J. 2003;24:811-819. 2. Hayes OW. Evaluation of syncope in the emergency department. Emerg Med Clin the syncopal episode are the only ones that can be dis- North Am. 1998;16: 601-615, viii. charged safely without a more intense evaluation or 3. Kapoor WN. Evaluation and management of the patient with syncope. JAMA. 1992:268:2553-2560. additional treatment. 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Vagal and sympathetic mechanisms in and orthostatic syncope do not increase mortality, patients with orthostatic vasovagal syncope. Circulation. 1997;96:2509-2513. 9. Sheldon R, Rose S, Connolly S, et al. Diagnostic criteria for vasovagal syncope based on though orthostatic syncope often recurs. a quantitative history. Eur Heart J. 2006;27:344-50. Typically, syncope of unknown etiology has a favor- 10. Rubenstein LZ, Josephson KR. The epidemiology of falls and syncope. Clin Geriatr Med. 2002;18:141-158. able prognosis, with one-year follow-up data showing a 11. Quinn JV, Stiell IG, McDermott DA, et al. Derivation of the San Francisco Syncope Rule low incidence of sudden death (2%), a 20% chance of to predict patients with short-term serious outcomes. Ann Emerg Med. 2004;43:224-232. 12. Martin TP, Hanusa BH, Kapoor WN. Risk stratification of patients with syncope. Ann recurrent syncope, and a 78% remission rate.7 Emerg Med. 1997;29:459-466. 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