Acute Vertigo

Harrison Lin

Rodney Omron

Dizziness is a common chief complaint in the emergency department (ED) that poses unique diagnostic challenges.¹ The feeling of “dizziness” can be described in many ways, many of which fall into the subcategory of a vestibular syndrome (VS). The patient’s description of dizziness as light-headedness versus spinning offers minimal benefit in diagnosing the underlying disease.¹

The differential diagnosis of dizziness in the ED is broad, with no single cause accounting for the majority of cases, so some rarely encountered diseases need to be considered in every dizzy patient. A systematic approach or direct feedback about every dizzy patient is critical to avoid misdiagnosis.²

Many of the most reliable diagnostic tools for dizziness, such as the Dix-Hallpike test for benign positional vertigo, are simple to perform bedside. By contrast, overreliance on advanced imaging without a systematic problem-based history and physical has been shown to increase length of stay, increase the cost of care, and falsely reassure providers that a life-threatening cause has been ruled out.

PATHOPHYSIOLOGY

See Figure 7.1 ³ and the section that follows.

Type	Prevalence	Pathophysiology
Benign paroxysmal positional vertigo (BPPV)	High	Caused by calcium carbonate debris that erodes or becomes dislodged from the macula epithelium within the utricle; 90% of BPPV is related to the posterior canal because it is closest to the utricle.⁴
Vestibular migraine (VM)	High	A key mechanism is the activation of the trigeminovascular system. The labyrinthine vessels are innervated by the trigeminal nerve terminals.⁵
Vestibular neuritis (VN)	Moderate	The most popular theory is that of a viral cause, but the evidence for it remains circumstantial. VN interferes with the vestibulo-ocular reflex, thus allowing the head impulse test to cause a catch-up saccade when present.¹
Ménière disease (MD)	Low	The prevalence of MD is 5-500 per 100 000 habitants, and familial MD is around 9% of cases. It is suspected from human temporal bone studies that MD is due to excessive accumulation of endolymph within the cochlear duct and the sacculus.⁵
Perilymphatic fistula	Low	Communication between the perilymph of the cochlea/vestibule and outside the inner ear is usually from the round or oval window. The etiology is trauma or congenital.
Labyrinthitis	Low	The etiology is viral, bacterial, or autoimmune causing dizziness and hearing loss.
Vestibular schwannoma	Low	It is the most common neoplasm of the cerebellopontine angle in adults. These tumors derive from myelinating Schwann cells of the vestibular division of the vestibulocochlear (eighth cranial) nerve.
Stroke	Low	A stroke occurs in 3.2% of all dizziness presentations to the ED. It is common from the anterior inferior cerebellar artery.¹

Approach/The Focused Exam

Triage-Titrate-Tests

The Triage-Titrate-Test (3-TTT) algorithm is a systematic way to approach the dizzy patient.

Triage: comprehensive review of systems to rule out stroke and to discover non-neurologic etiologies of dizziness.
TiTrATE: (Timing, Triggers, And Targeted History/Examination): Timing classifies symptoms into brief versus continuous. Triggers are aggravating factors (eg, vertigo with laying down). Targeted history/examination uses history elements (eg, trauma) to differentiate between the underlying causes of vertigo and lead to very specific physical examination maneuvers to better characterize the dizziness into peripheral versus central (see Table 7.1).
Tests: Ancillary tests such as labs and imaging are then ordered based on the history and examination.¹

Triage

Seeking associated factors and symptoms in addition to the chief complaint of dizziness is known as the Triage step in determining the underlying etiology. See Table 7.1 for other signs. Any one of the “deadly D” findings (dysarthria, dysphagia, dysphonia, dysmetria, and diplopia) should provoke a high suspicion of stroke. Also, any acute hearing loss, neck or head trauma, severe ataxia, or unilateral lean suggests a central cause.

Timing and Triggers

Symptoms should be classified as intermittent or persistent, each of which can further be divided into triggered or not triggered.

Intermittent = episodic vestibular syndrome (EVS)—seconds, minutes, or hours of vertigo. It usually has a duration of fewer than 30 seconds. Relapsing symptoms that last for weeks are not considered new onset and therefore fall in the chronic category.¹

Triggered = triggered episodic vestibular syndrome (t-EVS)
Not Triggered = spontaneous episodic vestibular

Persistent = acute vestibular syndrome (AVS)—continuous and persistent at rest. AVS can be further grouped into diseases triggered by a trauma or toxin (t-AVS) or spontaneously (s-AVS).¹

Triggered = triggered acute vestibular syndrome (t-AVS)
Not Triggered = spontaneous acute vestibular syndrome (s-AVS)

Intermittent and Triggered (t-EVS)

Intermittent and triggered (t-EVS) is vertigo that is brief, lasting seconds to minutes, and is triggered by something. The patient will say no to the question, “Are you dizzy right now without moving?” The trigger is often a change in head position but may also be a loud sound or valsalva.¹

Figure 7.1: The vestibular system comprises peripheral vestibular system, the ocular system, the brainstem, cerebellum, and cortex as well as postural muscles. A disruption of any part of this complex system causes dizziness. The peripheral vestibular system is composed of the utricle, the saccule, and the lateral, anterior, and posterior semicircular canals. The entire apparatus is encased by temporal bone. The macula and crista ampullaris are sensory neuroepithelia. Each contains rod-shaped sensory mechanoreceptors called hair cells. The utricle and saccule are structures that sense the position of the head, each contain macula. The exterior of the macula is coated with a gel-like membrane embedded with calcium carbonate particles called otoliths. Semicircular canals are oriented at right angles to each other. Endolymph flows through these canals, and at the end of each is a dilation called the ampulla, at the base of which is the crista ampullaris. The crista ampullaris is coated with the cupula, which is thicker than the gelatinous material on the macula and does not contain otoliths. (From Cohen BJ, Hull KL. Memmler’s Structure and Function of the Human Body. 12th ed. Wolters Kluwer; 2020. Figure 10.12.)

The most common causes of t-EVS are orthostatic hypotension and benign paroxysmal positional vertigo (BPPV) (Table 7.2). In cases where BPPV is suspected, the clinician should be looking for orthostatic hypotension in patients with positional triggers. Orthostatic hypotension (must have a change in blood pressure) should be distinguished from orthostatic dizziness (no change in blood pressure but a subjective feeling of light-headedness with standing), which may suggest decreased flow to the brain caused by a transient ischemic attack (TIA), cranial vascular stenosis, or intracranial hypotension.¹

TABLE 7.1 The Targeted History That Suggests a Cause for Acute Vertigo (Based on 3-TTT)

Dizzy + Other Symptoms (TRIAGE)	Intermittent and Spontaneous (s-EVS)	Intermittent and Triggered (t-EVS)	Persistent and Spontaneous (s-AVS)	Persistent and Triggered by Trauma or Toxin (t-AVS)
Altered mental status Loss of consciousness Neck pain Abdominal pain Dyspnea Palpitations New medications Fever Abnormal glucose	Vestibular migraine Ménière disease Panic attacks Vasovagal syncope Transient ischemic attack Subarachnoid hemorrhage Arrhythmia	Horizontal canal—benign paroxysmal positional vertigo Posterior canal—benign paroxysmal positional vertigo Posterior fossa tumor Orthostatic hypotension Transient ischemic attack/stroke Cranial vascular stenosis Intracranial hypotension Alcohol intoxication Myocardial infarct Unstable angina Pulmonary embolism Hypoglycemia Carbon monoxide poisoning Gastrointestinal/retroperitoneal bleed Dehydration Sepsis Adrenal insufficiency Diabetic ketoacidosis	Acute vestibular neuritis Multiple sclerosis Transient ischemic attack Stroke	Trauma Barotrauma Blast Whiplash Skull fracture concussion Vertebral artery dissection Direct vestibular nerve/labyrinthine concussion Mechanical disruption of the inner ear
				Toxin Aminoglycoside (gait unsteadiness, oscillopsia) Carbon monoxide poisoning
3-TTT, Triage-Titrate-Test; s-AVS, spontaneous acute vestibular syndrome; s-EVS, spontaneous episodic vestibular syndrome; t-AVS, triggered acute vestibular syndrome; t-EVS, triggered episodic vestibular syndrome.