Evaluation and Management in an Urgent Care Setting

Syncope Evaluation and Management in an Urgent Care Setting Urgent message: When a patient 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 consciousness with a loss of postural tone (typically, falling). It results from an abrupt, transient, and diffuse cerebral Smalfunction and is quickly followed by sponta- neous recovery. The term syncope excludes seizures, coma, shock, or other states of altered consciousness. Many patients 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 diagnostic 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 www.jucm.com The Journal of Urgent Care Medicine | October 2006 13 SYNCOPE: EVALUATION AND MANAGEMENT IN AN URGENT CARE SETTING coronary artery and the sight of blood, and myocardial disease, arr- Table 1. Presyncopal Signs and Symptoms 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 Nausea 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 syncopal event was vasovagal cope and death.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- Orthostatic hypotension is a clinical syndrome ery of a vital substrate (usually oxygen) to both cerebral indicating diminished intravascular volume. A com- hemispheres or to the brainstem’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 dehydration reduction (35% or more) in blood flow to these areas. (often secondary to acute gastroenteritis), and is also Since brain 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 diabetes). rhythmias may arise from any focus (supraventricular, Patients who experience vasovagal reactions have sub- nodal, or ventricular) and be bradycardic, tachycardic, or normal vagal baroreflex 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 cardiac output. 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 alcoholism, hypothyroidism) or rapidly (e.g., hypo- number of factors, such as the bradycardia often seen in glycemia, hypoxia). 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, hyperventilation, or a drug or something more sinister (Table 2). effect. However, it is dangerous to ascribe a syncopal If the patient experiences typical pre-seizure 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 Chest pain, 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 prodrome, 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 monitoring 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/alcohol 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 heart failure, 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 headache 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, dysarthria, diplopia, and ataxia. diaphoresis, graying of vision) These may suggest a stroke 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

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