Background
Syncope is defined as a transient, self-limited loss of consciousness with an inability to maintain postural tone that is followed by spontaneous recovery. The term syncope excludes seizures, coma, shock, or other states of altered consciousness.
Syncope is a prevalent disorder, accounting for 1-3% of emergency department (ED) visits and as many as 6% of hospital admissions each year in the United States. As much as 50% of the population may experience a syncopal event during their lifetime. Although many etiologies for syncope are recognized, categorization into reflex (neurally mediated), orthostatic, and cardiac (cardiovascular) may be helpful during the initial evaluation. Cardiac syncope is associated with increased mortality, whereas noncardiac syncope is not. Syncope may result in significant morbidity due to falls or accidents that occur as a result. In the United States alone, an estimated $2 billion annually is spent on patients hospitalized with syncope.
Although most causes of syncope are benign, this symptom presages a life-threatening event in a small subset of patients. It is unclear whether hospital inpatient admission of asymptomatic patients after syncope affects outcomes. No current criterion standard exists for diagnosing undifferentiated syncope. Many physicians continue to admit patients because of perceived risk. Recent reviews of the 2001 American College of Emergency Physician (ACEP) clinical policy suggest that evidence-based criteria may decrease admission rates by nearly half by identifying cardiac causes of syncope. Inpatient admission should be reserved for patients in whom identification of specific immediate risk, such as those with structural heart disease or history of ventricular arrhythmia, is needed. Outpatient management can be used for patients who are low risk for a cardiac etiology in order to define a precise cause in order to effect mechanism-specific treatment.
Pathophysiology
Syncope occurs due to global cerebral hypoperfusion. Brain parenchyma depends on adequate blood flow to provide a constant supply of glucose, the primary metabolic substrate. Brain tissue cannot store energy in the form of high-energy phosphates found elsewhere in the body; therefore, a cessation of cerebral perfusion lasting only 3-5 seconds can result in syncope.
Cerebral perfusion is maintained relatively constant by an intricate and complex feedback system involving cardiac output, systemic vascular resistance, arterial pressure, intravascular volume status, cerebrovascular resistance with intrinsic autoregulation, and metabolic regulation. A clinically significant defect in any one of these or subclinical defects in several of these systems may cause syncope.
Cardiac output (CO) can be diminished secondary to mechanical outflow obstruction, pump failure, hemodynamically significant arrhythmias, or conduction defects. Systemic vascular resistance (SVR) can drop secondary to vasomotor instability, autonomic failure, or vasodepressor/vasovagal response. Mean arterial pressure (MAP) decreases with all causes of hypovolemia. Medications can affect CO, SVR, or MAP.
Other conditions can mimic syncope. A CNS event, such as a hemorrhage or an unwitnessed seizure, can present as syncope. Syncope can occur without reduction in cerebral blood flow in patients who have severe metabolic derangements (eg, hypoglycemia, hyponatremia, hypoxemia, hypercarbia).
Epidemiology
Frequency
United States
Framingham data demonstrate a first occurrence rate of 6.2 cases per 1000 patient-years.[1, 2] Syncope reoccurs in 3% of affected individuals, and approximately 10% of affected individuals have a cardiac etiology.
International
Data from Europe and Japan suggest a similar occurrence rate to the United States, accounting for 1-3.5% of ED visits.
Mortality/Morbidity
Data suggest that patients with cardiac syncope are more likely to experience a poor outcome. Patients who have a significant cardiac history and those who seem to have a cardiac syncope (because of associated chest pain, dyspnea, cardiac murmur, signs of congestive heart failure [CHF], or ECG abnormalities) should be considered to be at increased risk. Most published methods of risk stratification take into account cardiac symptoms and risk factors.
Morbidity from syncope includes recurrent syncope, which occurs in 20% of patients within one year of the initial episode. Lacerations, extremity fractures, head injuries, and motor vehicle accidents can occur secondary to syncope.
Syncope in a patient with poor baseline cardiac function portends a poor prognosis irrespective of etiology. Middlekauff et al studied 491 patients with New York Heart Association (NYHA) functional class III or IV disease and noted that, regardless of the cause, 45% of those with syncope died within 1 year, whereas 12% of those without syncope died during the same interval.[3]
Patients with cardiac syncope appear to do worse than patients with noncardiac syncope. Soteriades et al followed 7814 patients with syncope for 17 years and found a higher mortality rate for patients with cardiac syncope compared with noncardiac syncope.[4] Suzuki et al studied 912 patients with syncope for an average of 3 years and found the same result.[5]
Decision rules may assist in identifying patients who are at risk. Martin et al describes a risk stratification system that predicts an increased incidence of death at 1 year based on the presence of abnormal ECG findings, a history of ventricular arrhythmia, a history of CHF, and age older than 45 years.[6]
Sarasin et al demonstrates a risk of arrhythmia that is proportional to the number of cardiac risk factors, including abnormal ECG findings, history of CHF, and age older than 65 years.[7]
The San Francisco Syncope Rule identifies patients who are at immediate risk for serious outcomes within 7 days, with a 96% sensitivity based on the presence of abnormal ECG findings, a history of CHF, dyspnea, a hematocrit level of less than 30, and hypotension.[8] The presence of these findings should prompt serious consideration for hospital admission. In an external retrospective review, validation of the San Francisco Syncope Rule in a Canadian emergency department was undertaken. The rule performed with a sensitivity of 90% (44/49 outcomes; 95% confidence interval [CI] 79-96%) and a specificity of 33%, which was much lower than previously reported. Based on results of this study, implementation of this rule would have significantly increased admission rates. These authors concluded further study is needed.[9] Another study was also unable to validate the rule, with sensitivity of 74% and specificity of 57% reported.[10]
The Risk stratification Of Syncope in the Emergency department, or ROSE, criteria suggest that an elevated B-type natriuretic peptide (BNP), Hemoccult positive stool, anemia, low oxygen saturation, and presence of Q waves on ECG predict serious outcomes at 30 days.[11] These rules had a 87% sensitivity and a 98.5% negative predictive value to help risk stratify patients. In this study, the isolated finding of BNP greater than 300 pg/mL was a major predictor of serious outcomes and was present in 89% of patients who died within 30 days.
Constantino et al discovered that 6.1% of patients had severe outcomes within 10 days of syncope evaluation.[12] The mortality rate was 0.7%, and 5.4% of patients were readmitted or experienced major therapeutic intervention. Risk factors associated with severe short-term outcomes included abnormal ECG, history of CHF, age older than 65 years, male gender, history of chronic obstructive pulmonary disease (COPD), structural heart disease, presence of trauma, and lack of prodromal symptoms.
The Evaluation of Guidelines in SYncope Study 2 (EGSYS 2) prospectively followed nearly 400 patients at 1 month and 2 years. The death rate was 2% at 1 month and 9% at 2 years. Patients with advancing age, presence of structural heart disease, and/or abnormal ECG had higher risk.[13]
Clinical judgement, Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL) score, and San Francisco Syncope Rule all have relatively low sensitivities individually for predicting severe short-term outcomes. Some evidence suggests that combining various risk stratification tools may increase sensitivity and reduce unnecessary admissions.[14] A review and meta-analysis by Serrano et al assessed the methodological quality and prognostic accuracy of the San Francisco Syncope Rule and the OESIL risk score.[15] The analysis of 18 eligible studies determined that the quality and accuracy of both sets of clinical decision rules are limited.
Race
No significant differences regarding race are observed with respect to syncope risk.
Sex
Larger prospective studies fail to show clinically significant differences between men and women.
Age
National Hospital Ambulatory Medical Care Survey (NHAMCS) data show that syncope occurs in all age groups but is most common in adult populations. Noncardiac causes tend to be more common in young adults, whereas cardiac syncope becomes increasingly more frequent with advancing age.
Syncope is relatively uncommon in pediatric populations. One small retrospective study by Pratt and Fleisher reported a prevalence of less than 0.1% in children.[16] Pediatric syncope warrants prompt detailed evaluation.
Advancing age is an independent risk factor for both syncope and death. Various studies suggest categorizing patients older than 45 years, 65 years, and 80 years as "higher risk." Advancing age correlates with increasing frequency of coronary artery and myocardial disease, arrhythmia, vasomotor instability, autonomic failure, polyneuropathy, and use of polypharmacy.
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