Syncope

Syncope & Vertigo: Introduction

Syncope and vertigo are relatively common symptoms. They are often described by patients using the term ‘dizziness’; however, it is essential to differentiate between the two. Syncope and vertigo both represent a significant diagnostic challenge and it is important to risk-stratify patients accurately to distinguish between potentially life-threatening and benign causes. We adapt this study to address syncope. Vertigo, however, is addressed here Opens in new window.

Syncope as a presenting symptom represents about 1–1.5% of all emergency department (ED) attendances. It is a symptom, not a diagnosis.

Syncope is a transient loss of consciousness induced by the temporarily insufficient flow of blood to the brain, leading to interruption of awareness of one's surroundings and falls with risk of injury.

Patients recover spontaneously, without therapeutic intervention or prolonged confusion. There is no simple test to distinguish between the benign and the potentially life-threatening causes of syncope, but a careful history, examination and bedside investigations can help determine appropriate disposition.

The causes of syncope are summarized in Table X. The most common cause in all age groups is neutrally mediated syncope, also known as neurocardiogenic or vasovagal syncope Opens in new window. Orthostatic hypotension and cardiac causes are the next most common.

Clinical Features

Patients with syncope are often completely asymptomatic by the time they arrive at hospital. A thorough history and physical examination is the key to fining the correct cause for the syncope. The history should focus on the patient’s recollection of the preceding and subsequent events, including environmental conditions, physical activity, prodromal symptoms and any intercurrent medical problems.

Accounts from eyewitnesses or first responders are also vital. Medications that may impair autonomic reflexes need to be scrutinized and a postural blood pressure measurement performed. Physical examination should concentrate on finding signs of structural heart disease, as well as assessing any subsequent injuries.

Neurally mediated syncope causes a typical prodrome: patients complain of feeling lightheaded and faint, and often describe a blurring or ‘tunneling’ of their vision. This may be accompanied by other vagally mediated symptoms such as nausea or sweating. More pronounced vagal symptoms include an urge to open their bowels. If patients are unable or unwilling to follow their body’s natural instincts to lie flat, they may collapse to the ground as they lose consciousness.

This reflex brings the head level with the heart, resulting in an improvement in cerebral perfusion and a return to consciousness. During this time the patient may exhibit brief myoclonic movements, which can be mistaken for seizure activity, but in contrast to true epileptic seizures, there are no prolonged post-ictal symptoms. Fatigue is common following syncope.

Orthostatic hypotension occurs when the patient moves from a lying position to a sitting or standing position. If the required autonomic changes fail to compensate adequately, even healthy individuals will experience lightheadedness or bluring of their vision, and possibly a loss of consciousness. The most vulnerable people are those with blunted or impaired autonomic reflexes, such as the elderly, those on certain medications (particularly vasodilators, antihypertensive agents and β-blockers) and those who are relatively volume depleted due to heat, excessive fluid losses or inadequate oral intake.

Cardiac syncope is more likely to present with an absent or brief prodrome. Sudden unexplained loss of consciousness should raise suspicion in the high-risk patient. Both tachycardia and bradycardia can be responsible. A syncopal event while supine is of particular concern, and a predictor for a cardiac cause. Those that occur during exertion should prompt a search for structural heart disease, in particular aortic stenosis.

Risk Stratification

Most of the published literature on assessment of patients presenting to EDs with syncope has focused on identifying risk factors for mortality or adverse cardiac outcome.

Colivicchi et al. developed the OESIL score, based on four high-risk factors identified in a multicentre Italian study aimed at predicting mortality at a year. These were age 65 years, a history of cardiovascular disease (which encompasses ischaemic heart disease, congestive cardiac failure, cerebrovascular disease and peripheral vascular disease), an abnormal ECG (including signs of ischaemia, arrhythmias, prolonged QT interval, AV block or bundle branch block) and absence of the typical prodrome.

Martin derived a similar group of risk factors in a cohort of syncope patients and then validated these prospectively. More recently, Quinn et al. devised and then validated the San Francisco Syncope Rule (SFSR), where five factors were used to predict serious short-term and longer-term outcomes. These factors are:

  • History of congestive cardiac failure.
  • Haematrocrit < 30%.
  • Abnormal ECG.
  • Patient complaining of shortness of breath.
  • Systolic blood pressure < 90 mmHg at triage.

Distilling these factors, patients with syncope can be divided into high– and low-risk groups. Low-risk patients can be safely discharged for outpatient follow-up, but controversy over high-risk patients remains. It is likely that there is a significant proportion of patients in the high-risk group who are actually intermediate risk, and given further evaluation in the ED or a short-stay unit could also be safely discharged; however, it is more difficult to identify this subset.

A number of projects have attempted to further define risk groups or assess risk stratification approaches. The Risk Stratification of Syncope in the Emergency department (ROSE pilot) compared the performance of the OESIL Score, SFSR and the Edinburgh Royal Infirmary ED Syncope Guidelines and found that although the SFSR showed the best sensitivity for detecting adverse events, this was at the expense of increased hospital admissions. Similarly, an Australian validation study found that the SFSR was fairly sensitive but that it would have increased admissions by 9% if all high risk patients were admitted.

The Syncope Evaluation in the Emergency Department Study (SEEDS) randomized patients deemed to be intermediate risk to either conventional assessment or assessment in a specialized syncope unit. It reported that a specialized unit increased the diagnostic yield and reduced the need for inpatient hospital admission.

Differential Diagnosis

Seizures Opens in new window are commonly listed as a cause for syncope. Although they do cause a transient loss of consciousness, the pathophysiology is very different. Post-ictal confusion often helps to differentiate the two; however, urinary incontinence may also occur in syncope. True tonic-clonic activity needs to be distinguished from the brief myoclonic jerks occasionally seen in syncope.

Transient ischaemic attacks (TIAs) are often attributed as potential causes for syncope, but this is rare. Only vertebrobasilar territory TIAs can affect the reticular activating system of the brain to cause a loss of consciousness.

Clinical investigations

The only two mandatory investigations are a 12-lead ECG and blood glucose. These should add enough information to the clinical findings to stratify the patient as high or low risk for an adverse outcome. Research has found that a serum troponin taken at least 4 hours after a syncopal event is not a sensitive predictor of an adverse cardiac outcome.

Syncope may also be the presenting symptom of a potentially life-threatening condition such as pulmonary embolus, subarachnoid haemorrhage, gastrointestinal bleed or aortic aneurysm. If these are suspected, appropriate investigations based on clinical suspicion should be initiated.

Treatment

Treatment depends on the presumptive diagnosis. Those with neutrally mediated syncope require explanation and reassurance only. After ensuring that the vital signs have returned to baseline, their blood and ECG are within normal limits, and that they have had something to eat and drink, these patients may be discharged without further investigations.

Patients with orthostatic hypotension often require intravenous fluids and an adequate oral intake to reverse their postural blood pressure changes. Any decision regarding potential changes to chronic medications should ideally include the patient’s primary care/treating doctor.

Patients who are deemed high risk for a cardiac cause need continuous cardiac monitoring for at least 24 hours and admission for further evaluation. This may include echocardiography to identify structural heart problems and to quantify structural heart problems and to quantify an ejection fraction, or electrophysiological studies.

Prognosis

Syncope in a patient with underlying heart disease implies a poor prognosis, with data suggesting that a third will die within a year of the episode. Overall, those with syncope on a background of congestive cardiac failure are at the highest risk for an adverse outcome. In the absence of underlying heart disease, syncope is not associated with excess mortality.

related literatures:
    Adapted from: Textbook of Adult Emergency Medicine E-Book. Authored By Peter Cameron, George Jelinek, Anne-Maree Kelly, Lindsay Murray, Anthony F. T. Brown. References as cited include:
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