Approach

The initial steps when assessing a patient with suspected syncope are to differentiate syncope from non-syncopal conditions, such as seizures, falls, psychogenic pseudosyncope, drop attacks, and transient ischaemic attacks, and to try to identify the cause (mechanism) so that appropriate treatment may be offered.[11] Data from several studies have shown that history and physical examination can identify a potential cause of syncope in many patients whose primary disorder can be diagnosed.[11][22]

The next step is to assess the specific risk to the patient.[9][11] For instance, the presence of structural heart disease or abnormal ECG findings indicates that an individual may be at higher risk of death.[16]

History

Syncope and non-syncopal conditions, with real or apparent loss of consciousness, can be differentiated in most cases with a detailed clinical history, but this may sometimes be extremely difficult.[23][24]

When a patient presents to the accident and emergency (A&E) department, it is important to correctly differentiate benign from potentially life-threatening causes of syncope. Red flag symptoms indicating the latter include: chest pain, palpitations, back pain, haematemesis, melena before the syncopal episode, and syncope with exercise.[10][25] Palpitations before loss of consciousness are a significant predictor of a cardiac cause of syncope.[26]

A detailed account of the event is taken from the patient or bystander. Precipitating factors, prodrome of symptoms, patient's position at the time of event, duration of syncope, recovery time, and family history are all important points to be considered. The history helps to narrow the differential diagnosis, and aims to identify risk for conditions linked with a poor prognosis.[9]

Specific triggers

Situational syncope with activities, including coughing, swallowing, micturition, and defecation, suggests that the cause is neurally mediated or vasovagal. Neurally mediated syncope is frequently recurrent and precipitated by fatigue, hot environment, severe pain, starvation, alcohol consumption, emotional or stressful situations, and prolonged standing. The patient is usually in the standing position and complains of prodromal symptoms of feeling weak, and may have nausea, diaphoresis, palpitations, blurring of vision, and becomes noticeably pale. Fatigue is common after regaining consciousness.

Syncope while shaving or turning the head to one side may be related to carotid sinus hypersensitivity, affecting mainly men aged ≥50 years.

Differentiating between syncope and epileptic seizure

Differentiating between syncope and epileptic seizure can sometimes be challenging. Information obtained from onlookers can help narrow the diagnosis. Seizures are typically associated with longer duration of loss of consciousness, loss of bowel and bladder control, rhythmic clonic movements, and disorientation after the episode. While tongue biting can occur in patients with syncope, it greatly increases the chance that the patient has had an epileptic seizure.[27]

Twitching and jerking are often seen with vasovagal or cardiac syncope, but these can be differentiated from rhythmic jerking of all the limbs in tonic-clonic seizures. Further testing is required when the diagnosis remains uncertain.[12]

Past medical history

Taking a past medical history is important, particularly noting any known cardiovascular conditions.[9]

Patients with advanced congestive heart failure, with low mean ejection fraction (<20%) and syncope, have increased risk of ventricular arrhythmia and 1-year mortality of 45%.[28] Some patients with pulmonary arterial hypertension have a history of syncope at the time of presentation, which is an independent predictor of a poor prognosis.[29]

Symptomatic patients with Brugada syndrome have a higher risk of sudden death than do asymptomatic patients.[30][31] Patients with hypertrophic cardiomyopathy who have had an episode of syncope also have a high risk of sudden death.[32]

People with psychogenic pseudosyncope often have a history of frequent, recurrent episodes. The duration of apparent loss of consciousness is often long. It is more common in young women and there is a higher prevalence in people with a history of physical or sexual abuse.[9][33]

Family history

A family history of syncope is important. Patients with exertional syncope and positive family history of syncope or sudden cardiac death are at increased risk of sudden death, and need further evaluation to rule out cardiac causes of syncope such as prolonged QT syndrome.

Medication history

A detailed medication history should be obtained and may provide useful information that suggests a possible cause of the syncopal episode. Drug classes that have been implicated in syncopal episodes include: diuretics, vasodilators, venodilators, negative chronotropes, and sedatives.[9]

Vasoactive medications, including anti-hypertensive agents, anti-anginal medications, and medications used to treat erectile dysfunction, may lead to syncope because of their vasodilatory effects.

Medication interactions may prolong the QT interval and lead to potentially life-threatening dysrhythmias.

Elderly patients in particular are more susceptible to medication effects that may cause syncope, and close attention should be directed to potential medication interactions in these individuals.

Physical examination and ECG

Vital sign abnormalities, including persistent tachycardia or hypotension, are concerning and must prompt a search for an underlying cause.

Blood pressure should be checked in both arms in supine and standing positions, on immediate standing, and after 3 minutes of standing.[9] Orthostatic hypotension is defined, by consensus, as a fall in systolic blood pressure of at least 20 mmHg and/or a fall in diastolic blood pressure of at least 10 mmHg within 3 minutes of standing.[34] The European Cardiology Society has added a fall in systolic blood pressure to <90 mmHg after 3 minutes of standing to the criteria for diagnosis of orthostatic hypotension.[11]

Orthostatic hypotension may identify some patients with syncope related to volume depletion, autonomic insufficiency, or medications.[34] However, it is a common finding in asymptomatic patients. The diagnosis of orthostatic hypotension as the sole cause of syncope should probably represent a diagnosis of exclusion in high-risk patients, because many high-risk patients also have orthostasis.

Pulse rate and rhythm are useful in the diagnosis of arrhythmias and pulmonary embolism. Cardiac auscultation may reveal murmurs (e.g.,of aortic stenosis, atrial myxoma, and pulmonary arterial hypertension).

A basic neurological examination is required. The presence of sensory, motor, speech, or vision deficits suggests an underlying neurological problem requiring further investigation or referral. In patients with suspected carotid hypersensitivity, carotid sinus massage may reproduce the symptoms. Carotid sinus massage should not be performed in patients who have experienced transient ischaemic attack or stroke within the past 3 months or in patients with carotid bruits (unless carotid Doppler studies convincingly exclude significant carotid artery narrowing).[11]

A 12-lead ECG should be performed on every patient presenting with syncope.[9][35]

Risk assessment

The 2017 American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS) guideline for the evaluation and management of patients with syncope recommends assessing short-term (up to 30 days after syncope) and long-term (up to 12 months of follow-up) risk of morbidity and mortality in people presenting with syncope in the outpatient clinic or A&E department.[9]

Short-term risk factors

  • Male

  • No prodrome

  • Palpitations preceding loss of consciousness

  • Exertional syncope

  • Structural heart disease

  • Heart failure

  • Cerebrovascular disease

  • Family history of sudden cardiac death

  • Trauma

  • Evidence of bleeding

  • Persistent abnormal vital signs

  • Positive troponin.

Long-term risk factors

  • Male

  • Older age

  • Absence of nausea/vomiting preceding syncopal event

  • Ventricular arrhythmia

  • Cancer

  • Structural heart disease

  • Heart failure

  • Cerebrovascular disease

  • High CHADS-2 score

  • Abnormal ECG

  • Abnormal glomerular filtration rate.

The ACC/AHA/HRS guideline also considers factors associated with intermediate risk, where structured observation in the A&E department may be considered:[9]

  • 50 years of age or older

  • Prior history of cardiac disease

  • Cardiac device without evidence of dysfunction

  • Concerning ECG findings

  • Family history of early sudden cardiac death

  • Symptoms not consistent with reflex-mediated syncope.

When the cause of syncope is unclear and the patient falls into the intermediate risk group, the use of a structured A&E department observation protocol may be effective as a means of reducing hospital admission.[9]

Predictors of short-term adverse outcomes

Often, despite a thorough history and physical examination, no obvious cause of syncope is identified. In these cases, it is important to identify those patients at highest risk of serious short-term outcomes.

A number of studies have attempted to identify predictors of short-term adverse outcomes in patients presenting to the A&E department and whose initial workup did not reveal an obvious cause of syncope.[7][36][37]

Patients who are clinically considered to be at intermediate or high risk for dysrhythmia or sudden death should be admitted to an inpatient unit, observation unit, or other monitored area. Although the definition of high- and low-risk patients is not consistent across studies, certain clinical and diagnostic features confer a lower or higher risk of adverse outcomes, including dysrhythmia.[36][37]

Patients thought to be low risk are those with syncope at a younger age (<40 years), syncope that occurred while in a standing position, or when moving from a sitting/supine position to standing, syncope triggered by a painful or emotionally distressing situation, or by cough, micturition or defecation.[7][36]

Patients with near syncope (patients who feel like they are going to pass out, but do not) have similar risks for adverse outcome when compared with patients with transient loss of consciousness, and should be treated similarly.[38]

Patients presenting to A&E with syncope determined to be of benign aetiology (clearly vasovagal or dehydration related) with a negative A&E workup should be considered for discharge regardless of the presence of other risk factors.

Ancillary tests

Further investigations needs to be individualised so that the work-up is cost-effective and appropriate.[9]

The diagnosis of vasovagal syncope is based mostly on the history, physical examination, and eyewitness observation, if available, so further testing in this group may not be needed in healthy individuals. However, features may not be typical in older people, making the diagnosis less clear.[9]

Blood tests may be useful and need to be tailored for a particular patient.[9] In practice, it is common to measure cardiac enzymes (e.g., high-sensitivity troponin) in all patients presenting in hospital with syncope, although the 2017 ACC/AHA/HRS guideline recommends targeting people with signs suggestive of acute myocardial infarction, such as chest pain or dyspnoea.[9]

Full blood count (FBC) and blood glucose levels are useful routine tests. In an unselected group of patients presenting to the emergency department with syncope from any cause, a haematocrit <30% was an important predictor of adverse events.[39]

Uraemia and electrolyte abnormalities can cause seizures, and testing may help make the diagnosis in patients in whom seizure activity cannot be excluded. Elevated creatine kinase may also suggest seizures.

In patients with anaemia, stool guaiac examination should be considered to evaluate for occult gastrointestinal (GI) blood loss as a possible cause of syncope. To assess for colorectal cancer, the US and UK guidelines report risk thresholds for testing symptomatic patients.[40][41][42]​ The UK’s National Institute for Health and Care Excellence (NICE) recommends certain quantitative faecal immunochemical tests (FITs) to recognise and guide referral of patients at risk of colorectal cancer.[41][42]​​​​​

Pregnancy testing is required for all sexually active women of childbearing age. Blood and urine toxicology screens are performed on patients with high clinical suspicion for alcohol misuse or illicit drug use, or in patients with no obvious cause for syncope on history and examination.

Chest x-ray may be useful as a baseline.[43]​ It is an important initial test in some clinical circumstances, such as myocardial infarction, aortic dissection, and perforated peptic ulcer. There is no evidence to suggest that routine screening of patients with advanced imaging (such as computed tomography [CT] scans), functional cardiac echocardiography, or electrophysiological testing is indicated.[44]

If a cardiovascular cause is suspected

If a cardiac cause is suspected on ECG, transthoracic echocardiography is done to evaluate for the presence of organic heart disease.​[43]​ One retrospective study of adults hospitalised with syncope found that 44% of patients with an abnormal physical exam or ECG had a significant echocardiographic finding, compared with 10% of patients who had a normal physical exam and normal ECG.[45]

Patients with organic heart disease as inpatients with, for example, electrophysiology studies, Holter monitors, and loop recorders for 24 to 48 hours. Various types of cardiac monitoring devices exist; choice is based on the frequency and nature of the syncopal events.[9] Electrophysiological studies may be considered in select patients where the aetiology is suspected to be an arrhythmia.

In some patients, exercise testing or cardiac catheterisation is necessary to confirm the presence of coronary artery disease. Exercise testing may also be used in select patients who have reported syncope or pre-syncopal symptoms associated with exercise. However, extreme caution is required and this test should only be performed in a suitable environment where advanced life support is available.[9]

In patients with suspected atrial myxoma, trans-oesophageal echocardiography and cardiac magnetic resonance imaging (MRI) are used to demonstrate the tumour. CT chest with contrast is indicated to visualise the abnormal aorta wall in patients with aortic dissection. Abdominal ultrasound (along with blood chemistries) is performed on people with suspected ruptured abdominal aortic aneurysm. Duplex ultrasonography is done in people with suspected subclavian steal syndrome.

CT or MRI may be used if a cardiac cause is suspected but initial evaluation is inconclusive. If arrhythmogenic right ventricular cardiomyopathy (ARVC) or cardiac sarcoidosis is suspected, MRI may be considered.[9] Right ventricular angiography may also be performed if ARVC is suspected. 18F-fluorodeoxyglucose positron emission tomography may be considered if cardiac sarcoidosis is suspected.

Chest x-ray, D-dimer, CT pulmonary angiography, ventilation/perfusion scan, or pulmonary angiography are indicated in suspected pulmonary embolism (PE). The choice of investigation depends on the likelihood of PE and the patient’s comorbidities.

If a neurological (including neurally mediated) cause is suspected

Tilt table test may be performed in apparently healthy young patients, or patients with recurrent syncope with a suspected neurally mediated (vasovagal) syncope. A positive tilt-table test suggests a tendency to vasovagal syncope, but does not provide a definitive diagnosis.

Haemodynamic testing and autonomic reflex testing are performed to evaluate dysautonomia.

Head CT scan is done in patients with neurological deficits or trauma to the head secondary to a fall from syncope.[46]

MRI, carotid Doppler ultrasonography, and magnetic resonance angiography are ordered to evaluate vertebrobasilar atherosclerosis in patients presenting with neurological deficits.

If seizure cannot be excluded, electroencephalography should be requested.

If obstetric, gastrointestinal, or endocrine cause is suspected

Transvaginal ultrasound is done in pregnant women to exclude ectopic pregnancy. A urine pregnancy test may also be followed up with serum human chorionic gonadotrophin.

FBC and blood chemistries are performed in all patients with (suspected) gastrointestinal (GI) bleeding. In upper GI bleeding, oesophagogastroduodenoscopy may demonstrate underlying oesophageal, gastric, or duodenal disease, whereas colonoscopy is performed in lower GI bleeding.

Additional laboratory testing for C-peptide and sulfonylurea levels is indicated in suspected hypoglycaemia. Patients with suspected Addison's disease require measurement of electrolytes and morning serum cortisol, adrenocorticotropic hormone (stimulation test), and a CT abdomen.

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