- In which patients with syncope do you get a NCHCT?
Syncope is defined as a transient loss of consciousness and postural tone. It has a rapid onset, short duration, spontaneous recovery and is due to transient global cerebral hypoperfusion. It may have a prodromal phase. In the Emergency Room, about 3% of patients present with a chief complaint of syncope. As part of the work-up, a non-contrast Head CT-scan (NCHCT) is often ordered. The question is whether such a test is necessary and who should get it?
A 2007 prospective observational study looked at 293 adult ED patients with syncope, of which 113 (39%) underwent head CT and of those, 5 patients (5%) had an abnormal head CT (Grossman 2007). These abnormal findings included 2 subarachnoid hemorrhages, 2 intracranial hemorrhages, and 1 stroke. Each of these patients either had a focal neurologic finding, headache, or signs of trauma. Of the patients who did not have a head CT, none were found to have a new neurologic disease during hospitalization or 30-day follow-up. The results from this study suggested that limiting head CT to patients with neurologic signs or symptoms, trauma above the clavicle, or use of warfarin would potentially reduce scans by over 50%.
Several other small retrospective studies have shown a low yield for obtaining a head CT in syncope patients. In a 2005 study in Emergency Radiology, 128 patients presented to a community hospital with syncope of which 44 received a head CT scan (Giglio 2005). Only 1 CT (2%) showed acute evidence of a posterior circulation infarction. In another retrospective review of patients who got a head CT for syncope alone, none of the 117 patients had CT findings that were clinically related to the syncopal event (Goyal 2006). The authors concluded that a head CT in the absence of focal neurologic findings may not be necessary. It is important to note that the reason for obtaining head CTs in these retrospective studies is unclear. Additionally, syncope patients who did not get a head CT were not analyzed.
A more recent prospective study looked at 254 head CT patients (out of 292 with syncope) and classified them into four groups: 1) normal CT / normal neuro exam; 2) abnormal CT / abnormal neuro exam; 3) abnormal CT not related to their syncope presentation; 4) abnormal CT / normal neuro exam. The last group (abnormal head CT with normal neuro exam) which we are interested in capturing in the ED only included 2 patients (0.7%) (Al-Nsoor 2010).
Bottom Line: For patients presenting to the Emergency Department with a chief complaint of syncope, a NCHCT is of low yield and should only be considered in patients with focal neurologic deficits, complaints of headache, or signs of head trauma. This is consistent with the ACEP clinical policy for syncope, which states that no test should be routinely used in the absence of specific findings on physical exam or history (ACEP 2007).
- In which patients with syncope do you get a troponin?
Cardiovascular etiologies are at the top of the differential for dangerous causes of syncope. Identifying those at risk for adverse cardiac outcome after syncope is challenging. Cardiac markers such as troponins are often sent on patients with syncope as part of a standard work up, presumably as a general screen for cardiac etiology such as acute myocardial infarction (AMI). As with any test, its results are only relevant if interpreted correctly. To that end, the diagnostic and prognostic utility of troponin in syncope patients is examined here.
AMI is a relatively rare cause of syncope, accounting for approximately 1.4-3.5% of cases (Link 2001, Grossman 2003, Hing 2005). The diagnosis of AMI in patients without EKG changes on presentation is even less common, likely due to the significant infarct required to induce either a non-perfusing dysrrhythmia or severely impaired cardiac output, which manifests in syncope. The utility of ED troponins for diagnosis of AMI is quite limited, especially in the patient without EKG changes. One prospective cohort study evaluating troponin-I at 12 hours post-syncope for diagnosis of AMI diagnosed four AMIs, 1.5% of their 289 patients (Reed 2010). Of these four patients, all had ischemic changes on their presenting EKG.
A larger prospective cohort study of 1474 patients found a 3.1% incidence of AMI within 30 days of a syncopal event (McDermott 2009). Of these patients, 80% had abnormal EKGs on presentation (any change from baseline or any abnormality-overtly ischemic or not- if no comparison). A normal EKG showed a negative predictive value of 99%. Of these AMI patients, only 50% had positive troponins obtained in the ED. Along with an abnormal EKG, being male gender, having history of coronary artery disease (CAD) were both significantly more sensitive than a positive troponin in detecting AMI.
Although the utility of troponins in patients with syncope and normal EKGs looking for AMI is limited, a troponin may be useful in risk stratification of patients with alternate causes of syncope. Pulmonary embolism, type A dissection, and intracranial hemorrhage can all cause syncope and can cause type II ischemia (e.g. supply/demand ischemia). Additionally, an elevated troponin in the setting of syncope has been associated with worse outcomes. In one study, 50% of patients with a positive troponin (at 12 hours post-syncope) had a serious outcome (not including AMI) or all-cause death at 1 month, as opposed to only 6% of patients without the positive biomarker (Reed 2010).
A similar study design performed by the same research group used a lower cutoff for a diagnostically positive troponin-I and examined the outcomes in patients with any detectable troponin level (Reed 2012). They found the majority of syncope patients (77%) to have detectable values and 20% to have troponin levels above the new diagnostic threshold (although only 2.9% diagnosed with AMI). At both one month and one year, patients with any detectable troponin level were at higher risk of adverse outcomes and mortality. This risk increased with higher troponin values.
Another prospective study similarly showed a positive troponin-T (taken at least 4 hours post-syncope) to strongly predict adverse cardiac outcome (Hing 2005). However, a positive troponin proved to have no added value in predicting adverse cardiac outcomes over the OESIL* score (Colivicci 2003). The study also reports troponin to have a sensitivity of only 13% and a low negative predictive value.
*The OESIL score is a risk stratification score to predict recurrent syncope or adverse outcome and includes the following risk factors:
- Age >65years old
- History of cardiovascular disease (CAD, CHF, cerebrovascular or peripheral vascular disease)
- Syncope without prodrome
- Abnormal EKG
The benefit of a troponin’s prognostic ability in syncope patients has not been clearly determined. A recent study reports on the significantly improved clinical outcomes associated with using troponin-I at a lower threshold to detect positive values in patients with suspected acute coronary syndrome (Mills 2011). While this is a different subset of patients with a clearly defined disease, the results raise the question of whether the test’s prognostic value may translate into improved outcomes in syncope patients.
As a diagnostic screening test for AMI in syncope patients without chest pain or EKG changes, a single troponin is inadequate and does not appear to be helpful in risk stratification. Admitting syncope patients for serial troponins, or ‘rule-out AMI,’ is also low-yield and should be considered only in conjunction with patients’ symptoms and significant risk factors such as known CAD or CHF, older age, syncope preceded by palpitations or without prodrome. However, the value of a positive troponin is not limited to diagnosis of AMI. The value of a troponin as a predictor of adverse outcome may have utility for an inpatient team and potentially in the ED as high sensitivity troponins become more ubiquitous. Whether obtaining this prognostic data significantly improves outcomes is not clear.
- Do you get orthostatic measurements in patients with syncope and how do you use them?
Volume depletion (i.e. dehydration) and blood loss are two of the myriad reasons for patients to present with syncope in the Emergency Department. While it isn’t difficult for us to determine whether the patient with an active upper gastrointestinal bleed has significant volume loss, this determination can be more challenging in other patients (i.e. the elderly patient with a urinary tract infection). Thus, clinicians would benefit from having an easy bedside test that assesses volume status, particularly, one that improves our ability to pick up patients with moderate volume depletion or blood loss.
Orthostatic blood pressure measurements have historically been taught to be useful in determination of volume status. It is defined as either:
- A drop in systolic blood pressure (SBP) > 20 mm Hg OR
- Increase in heart rate (HR) by > 30 beats per minute (bpm)
when a patient stands from a supine position (McGee 1999). It is unclear from the available literature how these numbers were originally derived, but they are likely based on consensus rather than empirical data. Even available consensus statements differentiate the entities of symptomatic and asymptomatic orthostatic hypotension, bringing the overall utility of the test in to question. (Kaufmann 1996).
Despite the traditional teaching, orthostatic measurements have little if any proven utility. There are two major criticisms:
- Many patients without signs or symptoms of intravascular volume depletion will demonstrate orthostatic vital signs when measured
- Many patients with clear evidence of intravascular volume depletion will not exhibit orthostatic vital signs.
How prevalent are orthostatic vital sign measurements among asymptomatic patients? A number of studies investigated elderly patients living in nursing facilities. Results of these studies are inconsistent. Mader et al and Aronow et al found relatively low prevalence (6.4% and 8% respectively) of orthostatic vital signs in absence of symptoms (Mader 1987, Aronow 1988). These studies, however, were small and excluded elderly patients on medications that may cause hypotension reducing generalizability to the general population of elderly patients. More recent larger studies on unselected elderly patients showed higher rates ranging from 28 – 50% (Raiha 1995, Ooi 1997). Studies in adolescents show similarly poor numbers with approximately 44% of patients exhibiting orthostatic changes (Stewart 2002).
Witting et al attempted to define vital sign thresholds that would decrease false positives. They performed tilt-table testing in healthy volunteers after blood donation (moderate blood loss). In patients < 65 years of age, a change in pulse > 20 bpm or a change in SBP > 20 mm Hg had a sensitivity/specificity of 47%/84% (Witting 1994). This yields a (+) LR = 2.94 and a (-) LR = 0.63. Sensitivity and specificity were similar in patients > 65 (41%/86%) with similarly poor (+) LR = 2.93 and (-) LR = 0.69. McGee et al performed a systematic review in 1999 showing similarly dismal sensitivity for moderate blood or fluid loss (McGee 1999)
|Blood Loss – Pulse Change (> 30 bpm)||22%||NA|
|Blood Loss – SBP Change (> 20 mm Hg)||7-27%||NA|
|Fluid Loss – Pulse Change (> 30 bpm)||43%||75%|
|Fluid Loss – SBP Change (> 20 mm Hg)||29%||81%|
Mendu et al performed a retrospective study that stands as one of the few studies supporting the use of orthostatic blood pressure management in patients with syncope (Mendu 2009). The researchers found that in 18% of patients, orthostatics affected the final diagnosis and affected management in 25% of patients. However, the study is deeply flawed. The utility of the measurements was determined by the clinician with no gold standard for diagnosis with which to compare. Additionally, 55% of patients in whom orthostatics were measured were found to have abnormal results but far less of these findings were thought to be relevant. Finally, the average age in this study was near 80 years of age, the exact population in which prior studies (previously discussed) have shown poor sensitivity and specificity of these measurements (Raiha 1995, Ooi 1997).
Based on the available literature, orthostatic vital signs do not appear to be either sensitive for screening patients for moderate blood or fluid loss or specific.
Bottom Line: Many asymptomatic patients will have positive orthostatic vital signs and many patients with moderate volume loss won’t have orthostatic vital signs. This makes checking orthostatic vital signs of questionable utility. More important is to see what the patient’s symptoms are. If the patient feels lightheaded or dizzy when they go from lying supine to sitting or from sitting to standing, they are orthostatic and this should be addressed.
- Do you manage patients with near-syncope differently than those with syncope?
Pre-syncope is a chief complaint commonly evaluated in the Emergency Department (ED). Defined as the sense of impending loss of consciousness, its symptoms can include lightheadedness, weakness, visual disturbances, “feeling faint”, and other nonspecific complaints. While there have been several attempts to develop and derive clinical prediction tools for syncope, most have been unsuccessful due to poor sensitivity and specificity and large performance variability (Constantino 2014, Birnbaum 2008, Serrano 2010). As one can imagine, if validation of prediction rules for the objective finding of syncope is fraught with difficulty, prediction rules for the more subjective and vague symptoms of pre-syncope would be an arduous task. As such, there is a lack of guidance when it comes to management and disposition decisions for patients who present to the ED with pre-syncope.
Though classically pre-syncope was thought to be benign with many of these patients being discharged from the ED, this may not be the case. In a study of approximately 200 patients presenting to the ED with nonspecific complaints (including weakness, dizziness, and feeling unwell) and Emergency Severity Index (ESI) scores of 2 or 3 with normal vital signs, 59% had a serious condition diagnosed within 30 days, and 30-day mortality was 6% (Nemec 2010). The median age of the study’s cohort was 82 years, and most had co-morbidities. While this study did not specifically assess patients with pre-syncope, given the overlap of the included symptoms with the symptoms seen in pre-syncope, it suggests that pre-syncope may similarly be a harbinger of serious disease.
Early syncope studies often excluded pre-syncope since its definition is poorly defined. However, recent literature corroborates the potential severity of pre-syncope. Some experts purport that the pathophysiologic mechanism for pre-syncope is the same as that for syncope except that the global cerebral hypoperfusion is not significant enough to cause complete loss of consciousness (Quinn 2014). A prospective observational pilot study of 244 patients with pre-syncope and 293 patients with syncope found similar ED hospitalization and 30-day adverse outcome rates in the two groups- 23% and 20% respectively (Grossman 2012). One of the reasons that the rates were so high may have been the broad and inclusive definition of adverse outcome (which included, amongst other conditions, cortical stroke, carotid stenosis and endarterectomy, and alterations in antidysrhythmics medications).
A larger prospective cohort study in 2014 found a significant number of adverse outcomes in pre-syncope patients. Of 881 adult patients with pre-syncope (which constituted 0.5% of total ED visits), 5.1% had serious outcomes at 30-day follow-up (Thiruganasambandamoorthy 2014). Furthermore, physicians were not accurate in predicting which patients were high risk for serious outcomes after their ED visit, with an area under the receiver operating characteristic (ROC) curve of 0.58-slightly better than a coin flip.
Should we be managing patients with pre-syncope similarly to those with syncope? Despite the paucity of literature on outcomes for ED patients presenting with pre-syncope, it appears as though the potential severity of pre-syncope has been under-appreciated. Once thought to be low-risk, recent literature challenges this dogma and suggests that a significant proportion of patients with pre-syncope suffer adverse outcomes similar to those who present with syncope. Intuitively it makes sense that true pre-syncope, syncope, and cardiac arrest exist on the same spectrum, differentiated by severity and duration of hypoperfusion, and thus should be risk stratified and managed similarly. However, to date no evidence exists on whether managing pre-syncope patients the same as syncope patients improves outcomes. As such, future studies are needed to further explore which patients with pre-syncope are at higher risk for adverse outcomes, with the ultimate goal to derive and validate a clinical decision rule for this patient population.
Previously thought to be a benign diagnosis, recent literature suggests that, like syncope, a non-insignificant proportion of patients with pre-syncope suffer serious adverse outcomes. Further studies are needed to determine which patients with pre-syncope are at higher risk for adverse outcomes, as we currently do not have clinical decision rules to guide our management for this patient population.
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