© Springer International Publishing Switzerland 2018Christian Nickel, Abdelouahab Bellou and Simon Conroy (eds.)Geriatric Emergency Medicinedoi.org/10.1007/978-3-319-19318-2_10
10. Syncope in Older People in the Emergency Department
Department of Emergency Medicine, Mount Auburn Hospital and Harvard Medical School, Cambridge, MA, USA
Department of Emergency Medicine, Tufts Medical Center and Tufts University School of Medicine, Boston, MA, USA
Department of Geriatrics, CHRU-Nancy, Nancy, F-54000, France
Department of Emergency Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA
Department of Emergency Medicine, Shaare Zedek Medical Center and Hebrew University, Jerusalem, Israel
KeywordsOlder adultsSyncopePre-syncopeEmergency medicineCardiovascular
Although syncope is one of the most common symptoms of older patients presenting to the ED, the underlying etiology of geriatric syncope is frequently difficult to discern [1–4]. It is estimated that cardiac causes may claim up to 40% of syncopal episodes in patients aged 65 or more, whereas non-cardiac causes involve only 20% . However, the diagnosis of syncope is particularly challenging in older patients as the causes are complex and often multifactorial . Older people commonly have multiple medical conditions requiring numerous medications, many of which can contribute to syncope due to drug side effects and potential lack of compliance. Unfortunately, syncope is also associated with a higher level of morbidity and mortality in older patients as they are more likely to have associated comorbidities and are more prone to trauma associated with falls following syncope events [7–10]. The differential diagnosis is broad and complex in older individuals. A multidimensional geriatric assessment can be performed in these cases in order to provide a synthesis of the problems, leading to a specific care plan. Thus, it is important to recognize treatable etiologies not only to care for the event at hand but to prevent recurrent syncope in older adults as well.
10.2 Background and Epidemiology
Syncope, by definition, is a transient loss of consciousness, which is caused by a brief loss in generalized cerebral blood flow. Syncope produces a temporary period of unresponsiveness and a loss of postural tone, ultimately resulting in spontaneous recovery requiring no resuscitation measures . It occurs in the absence of clinical features specific for other forms of transient loss of consciousness. Syncope is very common in older patients as well as in the general population, accounting for nearly 3% of all ED visits and 1–6% of all hospital admissions [8, 12, 13]. Syncope is more frequently found in older patients than in any other age group . Age-related degeneration causing impairment of the heart rate, blood pressure, baroreflex sensitivity, and cerebral blood flow, combined with the higher prevalence of comorbidities and utilization of multiple medications, likely accounts for this increased incidence of syncope . Furthermore, as one grows physiologically older, there may be a decrease in the body’s ability to respond to hypotensive challenges, causing syncope . Atypical presentations of conditions are also more likely in older patients than in the younger population .
Older patients frequently experience amnesia of the syncopal event. One study demonstrates amnesia after vasovagal syncope to be particularly common in older people, although not unique to older age groups, with findings of amnesia following tilt testing in 42% of people >60 years and 20% in <60 years . Due to the amnesia, it is hypothesized that unexplained falls might be related to syncope or near syncope in older patients . Thirty to forty percent of non-institutionalized older adults over the age of 65 years fall each year, with an estimated 20% of these falls as unexplained . Of the unexplained falls, it has been suggested that 20% are due to a modifiable cardiac dysrhythmia causing syncope .
Despite extensive medical evaluation, 30–50% of all cases of syncope in older patients are not given a definable etiology [4, 5, 18–20]. Furthermore, most diagnoses are presumptive, cannot be confirmed by standard criterion, and may not be able to exclude a dysrhythmic cause of syncope . Many of the conditions that may be responsible for producing syncope in older patients, such as cardiac conduction system disease and myocardial ischemia, may go undiscovered and have potentially life-threatening consequences as patients with cardiac syncope are at increased risk of death . One study found 6.1% of patients suffered serious outcomes within 10 days of syncope, with 10% occurring within 48 h of the sentinel event. Nine percent of syncope patients have long-term severe outcomes, particularly those with the following risk factors: of age over 65, neoplasms, cerebrovascular disease, structural heart disease, and ventricular dysrhythmias .
Women over the age of 65, despite being less likely to have concomitant coronary artery disease or diabetes, have been shown to be significantly more likely to present to an ED with syncope, yet less likely to be discharged with a defined etiology . Syncope is included as a manifestation of somatization, generalized anxiety, and substance abuse disorder . Furthermore, psychiatric diagnoses were demonstrated in 22% of patients >65 and are more common in patients with syncope of unknown etiology . This has prompted thought that to improve the quality of care for syncope in older patients, and for older women in particular, clinicians need to pursue a broader differential in evaluation of such patients to include sociodemographic and psychosocial contributors as well as organic causes .
The need for prompt risk stratification and concern for cardiac etiology may be a factor influencing ED physicians to pursue extensive evaluations and hospital admission for many older patients who present to the ED with syncope. There have been multiple scoring systems developed to guide the rationale for inpatient versus outpatient management of syncope [26–29]. However, the value and success of such evaluations has been incompletely studied, and the rationale for inpatient versus outpatient evaluation of older patients with syncope remains unproven [21, 30–32].
There is also limited information related to near syncope in older patients. It has been shown that older patients with near syncope are as likely as those with syncope to have adverse outcomes or critical interventions . However, near syncope patients are less likely to be admitted [34, 35]. Although further studies on near syncope in older patients are warranted, a workup similar to that of syncope should be considered.
The causes of syncope in older people are diverse, ranging from the benign to the life threatening. Syncope in older patients may be grouped into cardiac and non-cardiac etiologies. In those younger than 65 years of age, 10% may be attributed to cardiac abnormalities, whereas non-cardiac causes make up approximately 40% of the remaining syncope cases in which an etiology can be defined [20, 36]. In contrast, cardiac etiologies may cause up to 40% of cases in patients aged 65 or more, and non-cardiac causes involve only 20% .
Cardiac syncope is commonly characterized by an absent or brief prodrome, palpitations, and a transient loss of consciousness. It is important to gather collateral or bystander history to obtain relevant information that may suggest a cardiac cause . Syncope that occurs while in a sitting/supine position or during effort/exercise is also concerning for a cardiac etiology [27, 28]. Cardiac etiologies can be classified into mechanical/structural causes and dysrhythmic causes. Dysrhythmias , which induce hemodynamic impairment that can cause a critical decrease in cardiac output and cerebral blood flow, are the most common cardiac cause [27, 38]. Bradycardias are the most frequent dysrhythmias in the older population and are often caused by sinus node dysfunction, atrioventricular conduction disease, or implanted device malfunction [2, 38]. Tachycardias include supraventricular and ventricular dysrhythmias. Structural cardiovascular disease produces syncope when circulatory demands are greater than the heart’s ability to increase output . Structural causes may include valvular disease, obstruction of the left outflow tract, cardiac masses, tamponade, pulmonary embolism or dissection, acute coronary syndrome, and ischemic cardiopathy.
As noted, older patients often take multiple medications and, thus, are especially at risk for medication-induced syncope . Nitrates and antihypertensives such as beta-blockers are often implicated, particularly if multiple medications for supine hypertension are prescribed, which is common in older adults . Additional common medications to consider in older patients include but are not limited to vasodilators (alpha blockers, calcium channel blockers, ACE inhibitors), diuretics, antidysrhythmics, L-Dopa, antidepressants, and antipsychotics [5, 38]. Medications, including antidysrhythmics, which can prolong the QTc interval over 500 ms, increase the probability of dangerous dysrhythmias such as torsades de pointes. Medication side effects and patient compliance must be considered in assessing the etiology of geriatric syncope and in risk/benefit analysis when considering adding new medications to an older patient’s regimen. The drug side effects may be confounded due to the pharmacokinetic and pharmacodynamic changes that occur with aging, which in turn may cause a delay in elimination and increased bioavailability of these drugs in the older population . To help avoid these effects, the numerous electronic medical record systems that include specific tools for safe medication prescribing including the risk of drug interactions and potential side effects have been developed.
The most commonly identified etiology of syncope in all patients is vasovagal or sometimes called neurocardiogenic syncope. Vasovagal syncope history differs from cardiac syncope in that it is characterized by a prodrome and is commonly associated with precipitating events or stresses [41–43]. Typical prodromes include nausea, flushing, sweating, blurred vision, and light-headedness. Patients may also report provoking causes such as prolonged standing, a warm environment, a stressful event, or change in posture. Therefore, it is extremely important to obtain a detailed history by both the patient and witnesses of events prior to the syncopal event to help determine the etiology. Unfortunately, an older patient may be less likely to have the usual prodromes or provoking causes that one may expect in a younger patient with a vasovagal mechanism . In addition, in younger individuals, syncope is most often associated with a single, isolated disease process . Neurally mediated hypotension is often the lone culprit in this patient population . In contrast, it is often difficult to find a single etiology of syncope in the older population. Lastly, a carefully obtained history is often the only way to differentiate a seizure from a syncopal event.
Orthostatic hypotension (OH) is commonly seen in older patients presenting with recurrent episodes of syncope or light-headedness. Guidelines define OH as a decrease in systolic blood pressure (SBP) ≥ 20 mm Hg or a diastolic blood pressure (DBP) ≥10 mm Hg within 3 min of standing . Postural homeostasis is predominantly mediated by the autonomic nervous system . The prevalence of OH increases with age, thought to be associated with reduced baroreflex responsiveness, decreased cardiac compliance, and attenuation of the vestibulosympathetic reflex in older adults [47, 48]. One study demonstrates impaired blood pressure stabilization increases from 15.6% in people >50 to 41.2% in those >80 years . Studies have also suggested that the presence of OH increases the risk of mortality and cardiovascular events [46, 49]. Another type of OH, acute OH, can be observed as a consequence of fluid or blood loss or adrenal insufficiency . However, OH has been shown to be present in up to 40% of asymptomatic patients older than 70 years and 6–23% of patients who are younger than 60 years, limiting its use in sorting out a diagnosis in the ED following a syncopal event in older patients [46, 51]. Novel beat-to-beat measurements show an even higher incidence, with one study demonstrating an OH prevalence of 72% in fallers and 50% in non-fallers at an older patient day center . Since OH is common but not always symptomatic, it is important to correlate the finding with a patient’s syncope history, examination, and laboratory findings.
Common causes of OH in older adults include medications and primary/secondary autonomic disorders such as neurodegenerative diseases (i.e., Parkinson’s disease, multi-system atrophy, Lewy body dementia, pure autonomic failure) . Parkinson’s disease is particularly challenging as the disease itself can cause OH as well as treatment with levodopa . Overtreatment of supine hypertension with beta-blockers and other antihypertensive medications may also lead to OH in older patients. One study shows beta-blocker monotherapy was associated with more than twofold increase in initial OH and more than threefold increase in sustained OH in older adults as compared to untreated grade one hypertension . Older patients on bed rest are particularly susceptible to OH and appropriate precautions should be taken with any recently hospitalized patient.
Carotid sinus syndrome (CSS) should be considered in older patients who present with recurrent syncope after a negative diagnostic evaluation [5, 55]. Infrequently, patients may report a trigger such as neck turning, a tight collar, or a neck tumor; however, patients often report little or no warning prior to the event . CSS is defined as syncope with reproduction of symptoms during carotid sinus massage (CSM) of 10 s . One study showed the average duration of asystole to cause symptoms is 7.6 s and a decrease in systolic blood pressure of 65 mm Hg due to vasodepressive effects . CSS typically presents in the older adult with a mean age of 75 years, with a male dominance and is thought to be a pathological reflex from cardioinhibition via the vagus nerve and sympathetic withdrawal. Conversely, carotid sinus hypersensitivity (CSH) is more common in younger patients and is defined as a positive response to CSM without symptoms .
Atypical causes of syncope should be considered more closely in older patients than in younger populations. Pulmonary embolism (PE) may present with syncope or other atypical symptoms in older patients and should be considered in populations with risk factors, unexplained hypoxia or dyspnea . Less common causes of syncope, such as mesenteric steal, abdominal aortic aneurysm, and aortic dissection, are also important to consider in older patients. Syncope secondary to diffuse coronary vasospasms has been discussed in a case report as the cause of unexplained syncope . The patient’s risk factors, presenting history, medications, past medical history, and prior events must be taken into account when determining how aggressively to pursue these causes. Yet, once more, older patients may not present with the typical pain or dyspnea that is seen in younger groups. One retrospective study with a mean age of 66 years finds that 17% of patients with an aortic dissection have no pain on presentation, but 25% of these patients present with syncope . Another retrospective study with a mean age of 73.5 years shows 23% of patients admitted with a ruptured abdominal aortic aneurysm have syncope as a symptom .
Sepsis is another life-threatening illness that may manifest as syncope. Realizing that older adults may be less likely to mount a fever or express a leukocytosis, syncope may also be one of the few signs of impending sepsis or severe infection developing in an older patient.
As delineated above, determining the etiology of a syncopal event, particularly in older adults, can be challenging. Syncope is often transient and can resolve independently, without recurrence. Often the event is not witnessed and not remembered by the patient, making it difficult to find the specific circumstances that led up to and occurred during the syncopal episode . In determining whether the patient experienced a seizure, stroke, or a syncopal episode, several factors should be considered and a careful history taken. Unresponsiveness during syncope is brief, whereas generalized seizures will often have postictal confusion, and loss of consciousness from a stroke is generally not transient.
Therefore, one must first determine whether the patient had a syncopal event. Second, one must determine if this syncopal event is dangerous. If the syncopal event potentially had a worrisome cardiac etiology, one must decide what evaluation and what immediate therapy are appropriate. Lastly, if this event does not appear to be dangerous, one must determine whether the patient can be discharged home and define the appropriate follow-up.
The history, physical examination, and ECG have the greatest utility in evaluating syncope in older patients [62, 63]. To sort out the etiology, the physician must obtain the best history from the greatest number of witnesses. Similarly, all syncope patients need a thorough physical examination. The patient’s medication list should be reviewed for drugs that increase the risk for syncope, including antihypertensive, cardiovascular agents, and antipsychotics, as well as recent changes to these medications that may have influenced the event.
The initial task in an older patient with syncope is to obtain vital signs and determine the need for immediate stabilization. Most syncope patients who are otherwise asymptomatic should have normal or near normal vital signs within minutes following resolution of their syncopal event. While the utility of orthostatic vital signs is controversial, orthostatics may be helpful in older adults if the syncopal event directly follows standing or in any patient thought to be volume depleted [51, 64]. To obtain orthostatics correctly, measure the blood pressure in the supine position and after 3–5 min of standing. Again, review of the patient’s medication list for causative drugs and careful physical examination may help determine risk of volume depletion. Consider comparing the patient’s current blood pressure to the baseline blood pressure, as older patients who appear normotensive may actually be relatively hypotensive if there is a history of hypertension. However, relative hypotension may be a false positive given the burden of vascular disease in older patients. Once more, OH findings should be linked to a patient’s symptoms and syncope history to help determine relevancy.
Physical examination should include careful auscultation of the heart and lungs and palpation of the peripheral arteries. A neurological examination should be performed if there is concern for neurological symptoms or head trauma secondary to a fall. There is no clear evidence to support routine stool sampling in syncope. However, if there is concern for gastrointestinal bleeding based on history, vital signs, or a low hemoglobin/hematocrit, then further testing might be required, potentially as an inpatient, if there are signs of an acute bleed. It is also important to look at all skin areas to evaluate for trauma or skin infections that may be easily missed, particularly if considering a source for sepsis.
Evidence of trauma such as contusions, tenderness, or lacerations from tongue biting should be meticulously noted.
There is no gold standard against which the results of diagnostic tests can be measured in syncope [62, 63]. All patients should have basic tests such as an ECG and a finger stick glucose test. ECG findings that may suggest a dysrhythmic or concerning cause of syncope include intraventricular conduction abnormalities, Mobitz II second-degree or third-degree block, non-sustained VT, prolonged QT intervals, bifascicular blocks, sinus pause ≥3 s, or evidence of myocardial infarction. Other concerning ECG findings that may be more common in younger patients with syncope include Brugada syndrome, Wolff-Parkinson-White syndrome, hypertrophic cardiomyopathy pattern, or epsilon waves. However, studies have shown that an ECG will determine the cause of syncope in only 5% of patients .
Blood tests such as cardiac enzymes, electrolytes, complete blood count, lactate, blood cultures, and imaging modalities such as head CT, echocardiography, and carotid ultrasonography should be guided by history and physical examination . Routine blood tests typically only confirm clinical suspicion in syncope as they only uncover an etiology in 2% of patients . Specifically, cardiac enzymes are of little value if drawn routinely on older patients who are admitted with syncope. Cardiac enzymes should only be drawn if the patient has other signs or symptoms suggestive of myocardial ischemia by history such as chest pain, dyspnea, a concerning ECG, or an ECG that is uninterpretable for ischemia . Similarly, it’s suggested that lactate only be sent if there’s concern for sepsis or mesenteric ischemia based on the history and physical examination. Urine and blood cultures should be sent if there’s concern for sepsis. Additional studies such as electroencephalography and cardiac stress testing have a low diagnostic use and should not be routinely performed .
Studies have shown that telemetry may help determine the etiology of syncope in 3–5% of patients and most commonly from causes such as atrial fibrillation or bradycardia [67, 68]. There is neither evidence nor consensus on the duration of monitoring in the ED for intermediate-risk patients, but many experts suggest at least 3 h . If a new murmur is heard on examination, then an echocardiogram may be obtained either in the ED or as an inpatient. However, if a patient doesn’t have a history of a murmur or an audible murmur on examination, they are unlikely to have a valvular etiology of their syncope . An echocardiogram may give a diagnosis 2–22% of the time and most often in older patients from aortic stenosis [67, 68].
Head CT scans should be limited in older adults to those presenting to the ED with syncope and concomitant signs of head trauma, neurologic deficit, or neurologic complaints [32, 69]. It is unlikely that a cerebral vascular event alone will cause syncope. However, neurological complaints may be due to head trauma that occurred during the syncopal event. All other patients presenting with syncope have a low likelihood of having abnormal findings on head CT and do not require a scan . In one pilot study, limiting CT scans to patients with neurological signs or symptoms, including headache and trauma above the clavicles, or medicating with warfarin, would have reduced scans by 56% . Additional studies should be used sparingly and based on the initial data, as many tests for syncope in older patients have a low diagnostic yield. Choosing tests based on history and examination and prioritizing less expensive and higher yield tests may enable a more informed and cost-effective approach to evaluating syncope in older patients .