Note: This article is our CME Now offering for the January 2023 issue. After you read it, visit ACEP’s Online Learning Center to earn CME credit.

The last two decades have seen ever-increasing utilization of diagnostic testing in emergency departments (EDs) across the United States.¹ When it comes to the assessment and workup of patients who present to the ED with syncope, advanced imaging, such as head CT, has very low diagnostic yield.^2,3,4 One of the problems with indiscriminate ordering of tests for patients who present with syncope is that it may diminish our efforts in taking a thorough history and performing a thoughtful physical examination—the very areas that we should be concentrating our energies. The most recent ACEP Clinical Policy on Syncope state that history, physical examination, and ECG are the only level A recommendations for the evaluation of syncope.⁵

Step 1: Distinguish Syncope from Seizure

The first step in the evaluation of syncope is to distinguish it from seizure. There are several clinical findings with impressive specificities and likelihood ratios (LR) to help distinguish syncope from seizure. If one can accumulate enough accurate clinical findings of seizure, syncope can essentially be ruled out. Witnessed head turning during the event has a specificity of 97 percent and +LR of 14 for seizure, while unusual posturing during the event has a specificity of 97 percent and a +LR of 13.⁶ The absence of presyncope has a specificity of 86 percent and +LR of 5.6 while postictal state is present in 96 percent of patients with seizures.⁶

One common clinical pitfall is assuming the presence of seizure when urinary incontinence occurs during the event. Even though one review found that the specificity of urinary incontinence is 96 percent with a +LR 6.7 for seizure, urinary incontinence has subsequently been found unreliable in distinguishing syncope from seizure.^6,7 On physical examination, evidence of a tongue laceration has a specificity of 97 percent and +LR of 17, and even better, evidence of a lateral tongue laceration has a specificity of 100 percent for tonic-clonic seizure, essentially clinching the diagnosis.^6,8 One explanation for this is that the tongue often deviates laterally during a tonic-clonic seizure. Hence, one can ostensibly rule out syncope by ruling in seizure using these clinical features.

On the flip side, several clinical findings make syncope much more likely than seizure for the patient who has lost consciousness. Loss of consciousness with prolonged sitting or standing has a specificity of 98 percent and +LR 20 for syncope, while dyspnea and palpitations before loss of consciousness have a specificity of 98 percent and 96 percent and +LR of 13 and 8.3 respectively.⁶ Increased muscle tone during the event suggests seizure while decreased muscle tone during the event suggests syncope.

Another common pitfall is to assume seizure when there are any number of limb-jerking movements witnessed. A few limb jerks during a syncopal event are present in approximately 90 percent of witnessed syncopal episodes, as lack of blood perfusion to the brain causes anoxic neuronal irritation.⁷ One rule of thumb and clinical pearl to help

distinguish seizure from syncope is the 10:20 Rule. It states that patients with less than 10 witnessed myoclonic jerks after sudden loss of consciousness are more likely to have syncope as the cause, versus more than 20 myoclonic jerks witnessed makes the cause more likely to be seizure.⁹

Step 2: Consider Vascular Catastrophes Leading the Syncope

Acute vascular catastrophes such as subarachnoid hemorrhage, massive gastrointestinal bleeding, pulmonary embolism, and ruptured ectopic pregnancy may present as syncope, however additional clinical features make these diagnoses more apparent compared to syncope that presents in isolation.

Step 3: Distinguish Cardiac Syncope from Non-Cardiac Syncope

After considering syncope caused by vascular catastrophes, the priority in the ED should be distinguishing cardiac syncope from noncardiac syncope, as cardiac syncope carries significant morbidity and mortality and usually requires hospital admission. All other categories of syncope (such as reflex syncope and orthostatic syncope) are generally more benign. One exception is Eagle’s Syndrome, a rare cause of reflex syncope that involves a calcified, elongated stylohyoid ligament that presses on the carotid during neck extension that can lead to syncope. In patients who present with recurrent syncope after activities that involve neck extension (e.g., car mechanic, yoga, stargazing, etc.) with associated tinnitus or throat pain, consider a CT of the neck to rule out this rare syndrome.¹⁰

Clinical clues that should heighten one’s suspicion of cardiac syncope include the presence of multiple cardiovascular risk factors, history of structural heart disease, such as aortic stenosis or hypertrophic cardiomyopathy, pacemaker, syncope in the supine position, absence of prodrome prior to the syncopal event or prodrome that includes chest pain, shortness of breath, or palpitations, and syncope during exertion.^11,12,13,14

One lesser-known clinical clue for cardiac syncope is associated facial injury (including dental injury, eyeglasses damage, or tip of tongue bite), which is less likely to occur with reflex or orthostatic syncope.^15,16 While many emergency physicians appropriately ask about a family history of unexplained sudden death as a risk factor for cardiac syncope, the astute clinician will ask specifically about unexplained drowning and single motor vehicle crash in young first-degree relatives, which may uncover a positive family history of unexplained sudden cardiac death and prompt a referral to a cardiac electrophysiologist to rule out a hereditary life-threatening cardiac dysrhythmia as the cause of syncope.¹⁷ One physical examination finding suggestive of cardiac syncope is a new aortic stenosis murmur. Uncovering critical aortic stenosis in a patient with syncope may be lifesaving, as this combination portends a high short-term mortality rate that can be prevented if they undergo timely aortic valve replacement.¹⁸

Two further common clinical pitfalls are worth noting. One is assuming that the cause of syncope in older patients is orthostatic syncope in those that have an orthostatic drop.¹⁹ This may lead to failure to search further for cardiac causes. Orthostatic vital signs do not predict 30-day serious outcomes in older emergency department patients with syncope.²⁰ Many older patients will have an orthostatic drop at baseline, and some patients with orthostatic symptoms will not have an orthostatic drop; orthostatic vitals are non-specific and may lead to premature closure. The other common pitfall is assuming that presyncope alone is less morbid than syncope. The differentials for patients with presyncope and syncope are similar.²¹ Older patients with syncope or pre-syncope have comparable one-month risk of major adverse cardiac events.^22,23

Clinical factors that are more often associated with a noncardiac cause of syncope include syncope only following position change from sitting or lying to standing position, presence of a prodrome of nausea, vomiting or feeling warm, presence of a specific trigger such as pain, stressful stimulus or blood draw, and presence of a situational trigger such as coughing, laughing, micturition, defecation, or deglutition.^19,24

Do Clinical Decision Tools Perform Better Than Physician Gestalt for Determining Low Risk Syncope for Safe Discharge?

Decision tools, despite their varying levels of external validation, can be used to reassure clinicians and assist in shared decision-making when considering safe discharge of patients who have presented to the ED after a syncopal episode. The problem with these decision tools is that they include laboratory tests that are generally not useful in the evaluation of isolated syncope.⁵ For example, the San Francisco Syncope Rule (SFSR) requires a hematocrit. The SFSR’s sensitivity for adverse events was poor in external validation studies and a meta-analysis (86 percent and 87 percent, respectively).^25,26

The Canadian Syncope Risk Score (CSRS) requires a troponin level which, alone, has questionable value in the evaluation of syncope. The CSRS has shown excellent sensitivities in internal validation studies. Scores of negative two or higher were found to have a sensitivity of 99 percent and on secondary internal validation in Canada, patients with “very low” and “low” risk scores had 0.3 percent and 0.7 percent risks of a serious outcome, respectively.^27,28 However, a 2021 external validation in Italy demonstrated that the CSRS is no better than physician gestalt at predicting outcomes for patients with syncope. Additionally, physician gestalt had a lower rate of adverse events compared to low-risk patients on the CSRS.²⁹ Physician gestalt is incorporated into the score, which may limit its usefulness.

Physician gestalt garnered from the three-step approach outlined here should be used to identify low-risk patients who are safe for discharge from the ED. A thorough history and thoughtful but directed physical examination, rather than laboratory tests and imaging, should guide management. Syncope decision tools, laboratory testing, and imaging still have a role—lab tests and imaging should be used in patients suspected of a secondary vascular catastrophe as the cause of syncope and decision tools can be used to reassure physicians and patients.

A special thanks to Dr. David Carr, the guest expert on the EM Cases podcast from which this column was inspired.

Dr. Helman is an emergency physician at North York General Hospital in Toronto. He is an assistant professor at the University of Toronto, Division of Emergency Medicine, and the education innovation lead at the Schwartz/Reisman Emergency Medicine Institute. He is the founder and host of Emergency Medicine Cases podcast and website.

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