Dizziness and Syncope

Abstract

Dizziness and syncope are common symptoms that have multiple differential diagnoses.

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FormalPara Key Points

• Dizziness and syncope are common symptoms that have multiple differential diagnoses.

• History and clinical examination are crucial to determine the aetiology of dizziness or syncope.

• Directed and focussed investigations are required to ascertain the diagnosis.

Introduction

Dizziness is a frequent but complex symptom that patients present with to the emergency department. The term “dizziness” is used by patients to describe a wide-ranging group of symptoms from the benign to the life threatening. Hence, the determination of aetiology and management requires precision.

The prevalence of dizziness and syncope among patients varies with age. Approximately 3 % of patients present with dizziness and the incidence of syncope vary from 1 to 5 %, with an increasing prevalence among patients aged greater than 50 years, along with more likelihood of dangerous causes [1, 3, 5].

Definitions

• (A) Syncope

  Syncope is defined as a transient loss of consciousness accompanied by loss of postural tone followed by recovery to a normal neurological state [4–6].

• (B) Dizziness

  Dizziness as a symptom is often vague and inexact. From a patient’s point of view, it can be difficult to explain and for a physician its analysis can be vexing.

Generally, the term dizziness is used to describe one or a combination of the following [7, 8, 10]:

• 1. Vertigo: An illusory rotatory or a spinning sensation

• 2. Light-headedness/presyncope: An impending sensation of faintness or feeling woozy

• 3. Imbalance/disequilibrium: A sensation of unsteadiness while walking or loss of posture

Pathophysiology

Syncope occurs due to cerebral or brainstem hypoperfusion resulting in the sequelae of loss of consciousness and loss of postural tone.

The perception of balance is maintained by sensory input from visual, proprioceptive and vestibular systems which are integrated via the cerebrum, cerebellum and brainstem to the subsequent motor outflow. Any disturbance in any of these systems or their connections can result in the symptom of dizziness or vertigo [3, 5, 7, 11].

Aetiology

The causes of dizziness and syncope are many (Table 56.1). The mechanisms through which they occur may overlap. Vestibular and otologic causes usually cause vertigo. Vertebrobasilar insufficiency and stroke like lateral medullary and anterior inferior cerebellar artery syndromes and cerebellar haemorrhage/infarction may present with vertigo, imbalance or even syncope at times. Cardiovascular causes usually cause symptoms as a result of decreased perfusion. Systemic causes and medications result in dizziness or syncope by a number of mechanisms, and there may be an overlap as with hypoglycaemia secondary to Addison’s disease or drugs. Medications and toxins will usually cause symptoms through various pathophysiological mechanisms but may precipitate other aetiologies, especially in the elderly [2–5, 10, 12].

Table 56.1 Causes of dizziness and/or syncope [2–5, 10, 12]

Clinical Features (Tables 56.2 and 56.3)

Table 56.2 Symptomology [3, 7, 9, 11]

Table 56.3 Examination of patients with dizziness or syncope [3–5, 7, 10, 11]

Physical examination remains the backbone of evaluation of dizziness and syncope. Patients may have returned to their presymptom state at the time of examination; therefore, a thorough examination is required to establish differentials.

Neuro-cardiogenic or vasovagal syncope is a type of situational syncope which can be precipitated by number of triggers. Emotion, pain and uneasy high-stress situations can be the inciting factor. There may be a prodrome of light-headedness, blurring of vision or diaphoresis. The event occurs when the patient is in upright posture, gradual in onset followed by a rapid recovery once the patient is supine. The pathogenesis is due to increased sympathetic outflow and sudden vagal modulation [4, 11].

Benign paroxysmal positional vertigo (BPPV) is the most common aetiology of vertigo. It occurs when otoconia (crystals of calcium carbonate) are dislodged from the utricle and drift into the semicircular canals, usually the posterior. The patient will experience vertigo when turning the head towards the affected side and it is usually episodic. It is diagnosed with Dix-Hallpike test which is done by placing the patient in a supine position with his head hanging off the edge of the examination table. The patient’s head is then turned to either side rapidly and held in that position and is observed for nystagmus which confirms BPPV. The nystagmus usually starts after a few seconds of latency and will reduce with repeat testing and time. In central causes, there will be no latency or reduction with time. Meniere’s disease is poorly understood pathophysiologically. Increased endolymph production resulting in elevated pressure is suspected. Episodes of rotational vertigo lasting for hours accompanied with nausea, vomiting, hearing loss and tinnitus can occur. Nystagmus will be present but it will not be related to position.

Vestibulitis typically presents with severe vertigo peaking in hours, plateauing over the next few days and may persist for weeks. Symptoms can worsen with change in position. Associated symptoms such as nausea and vomiting may be present but auditory symptoms are absent. When hearing loss is present, labyrinthitis is to be considered. Nystagmus will be spontaneous towards the affected side [3, 7, 10, 13].

Investigations

Studies estimate that physical examination and history are able to potentially diagnose 40 % of causes of syncope and dizziness. Therefore, investigating patients becomes imperative in most emergency rooms. Judicious and targeted investigations complimenting a thorough examination are essential for a quick diagnosis and to limit costs for a patient (Table 56.4).

Table 56.4 Directed investigations in patients with dizziness or syncope [4, 5, 7, 10, 11, 13]

When investigating patients in the emergency department, life-threatening causes need to be identified quickly. Without a supportive history or positive clinical examination, diagnostic tests can have a low yield. An ECG is still recommended though yield is low. It is used extensively in most risk stratification guidelines. ECG in addition to history and examination helps increase the yield of laboratory investigations in particular cardiac enzymes [4, 5].

Ultrasound has proven to be a very useful tool in identification of free fluid in trauma. Echocardiography is useful in patients with structural heart disease presenting with syncope or dizziness. Identification of impaired ejection fraction helps manage patients at serious risk. Other investigations help an emergency physician risk stratify the patient after a cause has been determined by a clinical examination or by radiological evaluation [5, 7].

Neuroimaging in patients with dizziness and syncope should be guided by clinical examination. During evaluation of a possible cerebellar stroke, imaging is vital. Though CT scan is the most frequently used modality due to its easy availability, it cannot be used conclusively to rule out certain pathologies. Physicians should recognize the limitations of CT in evaluation of acute strokes particularly in the posterior cranial fossa or brainstem. When available, MRI with diffusion weighted imaging should be performed as it provides a higher sensitivity than CT [7, 10, 11, 13].

Treatment and Disposition

Management of patients with dizziness and syncope will essentially be directed by the diagnosis. Treatment will also be dictated by the patient’s haemodynamic status. Primary stabilization of vital parameters with identification of risk factors will begin in the emergency department. Strokes, acute coronary syndromes, arrhythmias and suspected vascular emergencies will require intensive care management after stabilization in the emergency room. Unambiguous diagnoses will usually follow definitive management pathways [4, 7, 11].

Benign paroxysmal positional vertigo can be cured by Epley’s particle repositioning manoeuvre along with vestibular suppressants for acute symptoms of nausea and vomiting. Intravenous ondansetron is considered safe and effective for these symptoms. For patients presenting with severe vomiting, promethazine and benzodiazepines can be considered, but sedation is a frequent side effect. For other causes with acute symptoms, short-term therapy with these agents can be considered till definitive treatment for the cause is implemented [3, 7].

Patients in whom the diagnosis is elusive will require risk stratification and then appropriate disposition. A number of syncope risk stratification guidelines have been developed, but no set of rules have achieved complete validation to rely on. The focus of these rules is to admit high-risk patients and minimize admissions in low-risk patients. Currently, all rules either inadvertently miss risk stratifying some high-risk patients to reduce inpatient numbers or unnecessarily identify many patients as potential dangerous outcomes resulting in over admission. The various rules suggested are the San Francisco Syncope Rule (SFSR), the Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL) score, the European Guidelines in Syncope Study (EGSYS) score and the Risk Stratification of Syncope in the Emergency Department (ROSE) score. None of these rules have been completely validated. However, the common minimum criteria that have been present across all rules are the following:

• Older age

• History suggestive of structural heart disease or arrhythmias

• Unrelenting abnormal vitals

• Abnormal ECG [4–6, 11]

Patients who are discharged after evaluation for dizziness or syncope should be asymptomatic at discharge and advised follow up with appropriate departments.

Clinical pathway to manage dizziness and syncope