Syncope is a common complaint in the emergency department (ED). Although most potential causes are benign and self-limited, others are associated with significant morbidity and mortality. the cause of syncope often remains unclear and management must focus on risk stratification to differentiate among patients safe for discharge and those who require emergent investigation and in-hospital management. Near syncope (ie, near loss of consciousness) and true syncope are considered a spectrum of the same symptom, and clinicians should approach them in similar fashion.
Life-threatening conditions — The primary responsibility of the emergency clinician is to assess whether a life-threatening cause of syncope is present, and to provide appropriate management and disposition. The most important causes to consider are: cardiac syncope, blood loss, pulmonary embolism, and subarachnoid hemorrhage. Other conditions, such as seizure, stroke, and head injury, do not meet the technical definition of syncope but should be considered during the initial assessment.
●Cardiac syncope – Cardiac causes are the most common life-threatening conditions associated with syncope. They include arrhythmia, ischemia, structural/valvular abnormalities (eg, aortic stenosis), cardiac tamponade, and pacemaker malfunction. Studies of short term and one year outcomes following syncope found patients with cardiac syncope to be at significant risk for sudden death [2,9]. Patients with syncope and a history of heart failure are at even greater risk .
●Hemorrhage – Large blood loss, particularly acute severe hemorrhage, can manifest as syncope. Important potential causes include: trauma, gastrointestinal bleeding, ruptured aortic aneurysm, ruptured ovarian cyst, ruptured ectopic pregnancy, and ruptured spleen.
●Pulmonary embolism – Hemodynamically significant pulmonary embolism is an uncommon but well documented cause of syncope [11].
●Subarachnoid hemorrhage – Patients presenting with syncope following a headache require evaluation for a possible subarachnoid hemorrhage.
Common conditions
●Neurocardiogenic syncope – Often referred to as vasovagal or vasodepressor syncope, neurocardiogenic syncope is the most common cause of syncope, accounting for 25 to 65 percent of cases [7]. Patients diagnosed with neurocardiogenic syncope have an excellent prognosis with no increase in mortality or morbidity [12].
Autonomic activation causes neurocardiogenic syncope. Three types of responses are seen: a cardioinhibitory response, a vasodepressor response, and a mixed response with features of both. Significant bradycardia and/or hypotension accompany the acute loss of consciousness. Potential triggers are numerous and often determination of the underlying cause is made in the outpatient setting. (See “Reflex syncope”.)
Most patients with neurocardiogenic syncope experience a prodrome, which may include dizziness or lightheadedness, a sense of warmth, pallor, nausea/vomiting, abdominal pain, and diaphoresis, prior to their loss of consciousness. Examples include micturition or defecation syncope, situational syncope (eg, while having blood drawn), or cough-mediated syncope.
●Carotid sinus hypersensitivity – Carotid sinus hypersensitivity is a variant of neurocardiogenic syncope, resulting from pressure at the carotid sinus. External pressure to the neck can induce this reflex response. Common causes include shaving, a tight collar, and turning of the head.
●Orthostasis – Orthostatic syncope comprises between 5 and 24 percent of syncope cases and can be defined by a drop in blood pressure of more than 20 mmHg, or a reflex tachycardia of more than 20 beats per minute. Orthostasis is most often caused by a loss of intravascular volume, from any number of causes, or by failure or instability of the autonomic nervous system. Nevertheless, clinicians should remain cautious because orthostasis can occur with cardiac syncope. Syncope from orthostatic hypotension is a diagnosis of exclusion in the emergency department, reserved for low risk patients who have symptoms consistent with the diagnosis.
Orthostatic vital signs are neither sensitive nor specific in assessing volume status or diagnosing syncope [13-15]. Many patients become symptomatic if their systolic blood pressure drops below 90 mmHg, but a large portion of the population who meets the definition of orthostasis do not have syncope. Elders, pregnant women, and patients taking drugs with vasodilating effects are predisposed to develop symptomatic orthostasis.
●Medications – The effects of medications account for 5 to 15 percent of syncopal events. The mechanism can be orthostasis or cardiotoxicity. Medications often implicated include calcium channel blockers, beta blockers, alpha blockers, nitrates, antiarrhythmics, diuretics (affecting volume status and electrolyte concentrations), and medications affecting the QTc interval (eg, antipsychotics and antiemetics).
Other conditions
●Neurologic syncope – True syncope is defined by an immediate, spontaneous return to baseline function following loss of consciousness, without new focal neurologic findings. Therefore, true neurologic causes, representing underlying neurovascular disease and not transient autonomic dysfunction, are rare.
Examples of neurologic syncope include: subarachnoid hemorrhage, transient ischemic attack, subclavian steal syndrome, and complex migraine headache. Stroke and transient ischemic attacks generally cause focal neurologic deficits that do not recover rapidly or completely. Often, patients with cerebrovascular disease convey a history of nonsyncopal episodes featuring neurologic deficits. Syncope may be misconstrued as seizure because many patients with transient loss of consciousness have brief convulsive episodes, particularly if bystanders or objects keep them upright. Syncope can usually be differentiated from seizure by the brevity of the convulsions and the lack a true postictal phase.
●Psychiatric syncope – Anxiety and panic disorders can cause situational syncope. Emergency clinicians must be cautious when attributing syncope to psychiatric causes. Patients with hypoxia, inadequate cerebral perfusion, or other medical conditions may appear confused or anxious. Patients with psychiatric syncope are generally young, without cardiac disease, and complain of multiple episodes.
●Drug induced loss of consciousness – Drugs of abuse and alcohol may cause a transient loss of consciousness, but generally these patients manifest signs of toxicity, and do not spontaneously return to normal neurologic function immediately after regaining consciousness. Alcohol can also cause symptomatic orthostasis by impairing vasoconstriction [18].
●Metabolic – Metabolic causes of syncope include hypoglycemia and hypoxia.
