Steven Go
EPIDEMIOLOGY
The estimated percentage of ED visits attributed to the complaint of “dizziness” is approximately 4%.
A cross-sectional analysis of older adolescents and adult visits to US ED’s found that the most common causes included otologic/vestibular (32.9%), cardiovascular (21.1%), respiratory (11.5%), neurologic (11.2%), metabolic (11.0%), injury/poisoning (10.6%), psychiatric (7.2%), digestive (7.0%), genitourinary (5.1%), and infectious (2.9%). “Dangerous” disorders were diagnosed in 15% and were especially common in patients >50 years of age.
PATHOPHYSIOLOGY
Vertigo results from the mismatch of the perception of movement by the visual, vestibular, and proprio-ceptive symptoms when none actually exists.
The visual system provides spatial orientation; the vestibular system provides the body’s orientation with respect to gravity, while the proprioceptive system helps relate body movements and indicates the position of the head relative to the body.
CLINICAL FEATURES
Vertigo presents as a sensation of movement when none exists. Patients often say that the “room is spinning,” but other descriptions may include rocking, tilting, somersaulting, and descending in an elevator.
Vertigo is classically separated into two general types: peripheral and central (Table 146-1).
Peripheral vertigo (involving vestibular apparatus and the eighth cranial nerve) usually has a sudden onset and intense symptoms.
Central vertigo (involving brain stem and cerebellum) can present abruptly or gradually, but usually has more ill-defined, less severe symptoms.
In general, causes of peripheral vertigo tend not to be life-threatening, whereas central vertigo are often more serious; however, this is not true in all cases and significant overlap of presentations can exist.
TABLE 146-1 Differentiating Peripheral from Central Vertigo
DIAGNOSIS AND DIFFERENTIAL
The etiology for vertigo is found in Table 146-2.
Initially, focus the history on whether true vertigo actually exists because it is often confused with “lightheadedness” or near syncope/syncope, which has its own differential and workup.
The initial episode should be described in detail by the patient, including speed of onset, severity, associated symptoms (especially involving loss of consciousness or the cranial nerves with special emphasis on aural symptoms), and temporal pattern (Table 146-3). Risk factors for stroke (age, hypertension, cardiovascular disease) and coagulopathy should be investigated.
Physical examination should include eye, ear, neurologic, and vestibular examinations, with particular focus on the cranial nerves and cerebellum.
Note the type (horizontal, vertical, rotatory) and direction of the fast component of any nystagmus. Isolated vertical nystagmus (without a rotary component) usually indicates a brain stem abnormality.
If benign paroxysmal positional vertigo (BPPV see below) is suspected, a Dix-Hallpike position test may be useful.
Based on history and physical examination, tentatively classify the vertigo as peripheral or central to help narrow the differential and direct the workup.
Suggested ancillary testing for various specific vertigo-associated conditions are summarized in Table 146-4.
In general, laboratory investigations are not indicated in true vertiginous patients unless a specific cause for central vertigo is being investigated.
With regards to imaging, obtain an emergent non-contrast head CT in elders, patients who have signs/symptoms of central vertigo (especially cranial nerve or cerebellar findings), hypertension, cardiovascular disease, other stroke risks, coagulopathy (eg, taking warfarin), headache, or for intractable or persistent (>72 hours) symptoms. If vertebrobasilar insufficiency
TABLE 146-2 An Etiologic Classification of Vertigo
TABLE 146-3 Temporal Patterns Seen in Vertigo
TABLE 146-4 Ancillary Testing of Vertigo and Dizziness
DISORDERS CAUSING PERIPHERAL VERTIGO
BPPV is thought to be caused by loose otoliths that enter the posterior semicircular canal and cause the inappropriate sensation of motion. BPPV occurs most often in women over age 50 years. Cranial nerve or central nervous system (CNS) findings are absent. Findings suggestive of BPPV are listed in Table 146-5.
The Dix-Hallpike position test can confirm BPPV. In this test, the patient begins seated with the head turned 45 degrees to the right. The patient is then rapidly lowered to a supine position with the head hanging over the edge of the bed an additional 30 to 45 degrees. Patients with BPPV will exhibit a shortlived nystagmus with the rapid component toward the affected ear. The patient is then returned to the sitting position and the maneuver is repeated with the head turned to the left. The side that is symptomatic serves as the starting point for the curative Epley maneuver.
Ménière disease is characterized by recurrent bouts of sudden onset of (usually) unilateral roaring tinnitus and a sense of fullness and diminished hearing in the affected ear. Because the diagnosis requires multiple episodes of attacks with progressive hearing loss, Ménière syndrome cannot be diagnosed on the first presentation of vertigo. It can be confirmed by glycerol testing and by vestibular-evoked myogenic potentials.
A perilymph fistula presents with sudden onset of vertigo during activities that can cause barotrauma such as flying, scuba diving, heavy lifting, and coughing. Infection can also cause a perilymph fistula, and the diagnosis is confirmed by nystagmus elicited by pneumatic otoscopy (Hennebert sign).
Vestibular neuronitis is characterized by the sudden onset of severe vertigo sometimes associated with unilateral tinnitus and hearing loss. It is thought to be viral in nature, lasts several days to weeks, and does not recur.
Vestibular ganglionitis causes vertigo when a neuro-trophic virus such as varicella zoster reactivates. The most well-known variant, Ramsay Hunt syndrome (Herpes zoster oticus), is characterized by deafness, vertigo, and facial nerve palsy, associated with vesicles inside the external auditory canal.
Labyrinthitis, although commonly viral, also can be due to bacterial infection from otitis media, meningitis, and mastoiditis and presents with sudden vertigo with hearing loss and middle ear findings.
Ototoxicity may induce vertigo and hearing loss. Common offenders causing peripheral toxicity include salicylates, aminoglycosides, and cytotoxic agents. Anticonvulsants, antidepressants, neuroleptics, hydrocarbons, alcohol, and phencyclidine may cause centrally mediated vertigo.
Tumors of the eighth cranial nerve and cerebello-pontine angle, such as meningioma, acoustic neuroma, and acoustic schwannoma, also may present as vertigo with hearing loss. These tumors may be associated with ipsilateral facial weakness, impaired corneal reflexes, and cerebellar signs.
Vertigo may occur after a closed head injury (especially a basilar skull fracture) and tends to resolve over weeks. Vertigo can also occur as a complication of cochlear implantation surgery.
TABLE 146-5 Supportive Findings in Benign Paroxysmal Positional Vertigo
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Latency period of <30 s between the provocative head position and onset of nystagmus. |
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The intensity of nystagmus increases to a peak before slowly resolving. |
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Duration of vertigo and nystagmus ranges from 5-40 s. |
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If nystagmus is produced in one direction by placing the head down, then the nystagmus reverses direction when the head is returned to the sitting position. |
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Repeated head positioning causes both the vertigo and accompanying nystagmus to fatigue and subside. |
DISORDERS CAUSING CENTRAL VERTIGO
Cerebellar hemorrhage or infarction causes moderate vertigo and can be associated with nausea and vomiting. Cerebellar findings such as truncal ataxia, abnormal Romberg testing, and abnormal tandem gait are usually present. A sixth cranial nerve palsy or conjugate eye deviation away from the side of the hemorrhage can occur.
Lateral medullary infarction of the brain stem (Wallenberg syndrome) causes vertigo and ipsilateral facial numbness, loss of the corneal reflex, Horner syndrome, dysphagia, and dysphonia secondary to pharyngeal and laryngeal paralysis. Contralateral loss of pain and temperature sensation in the trunk and extremities also occurs. Sixth, seventh, and eighth cranial nerve findings can also occur.
VBI may result in sudden vertigo due to a brain stem transient ischemic attack that typically lasts minutes to up to 24 hours. Associated diplopia, dysphagia, dysarthria, blindness, and bilateral long tract signs (eg, clonus, muscle spasticity) and syncope may also be present. Unlike other causes of central vertigo, VBI may be induced by movement of the head due to decreased vertebral artery blood flow.
Veterbral artery dissection (VAD) can be caused by sudden rotation of the head (motor vehicle crash, chiropractic adjustments, sneezing) and presents with central vertigo. Associated symptoms may include vertigo, headache, and unilateral Horner syndrome.
Miscellaneous causes of central vertigo include multiple sclerosis, neoplasms, and basilar migraine.
OTHER CONDITIONS
Disequilibrium of aging is a condition that presents with vague dizziness and gait unsteadiness in the elderly. It is associated with age-related degradation of hearing, balance, proprioception, and vision. Symptoms are worsened by dim lighting, nighttime hours, unfamiliar surroundings, and the use of medications with anticholinergic effects and benzodiazepines.
Psychiatric dizziness presents as part of a known psychiatric disorder that is not associated with known vestibular disorders. This is often chronic and is frequently associated with anxiety disorders. This is a diagnosis of exclusion.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
In peripheral vertigo, first-line therapies include the antihistamines, such as diphenhydramine or meclizine, and antiemetics. Second-line drugs for treatment failures include antidopaminergic agents such as metoclopramide or promethazine. Transdermal scopolamine is not useful acutely due to its prolonged onset of action (4-8 hours), but may be used as a discharge medication. Benzodiazepines prevent the process of vestibular rehabilitation and should be used sparingly.
Antivertigo medications can have undesirable anticholinergic side effects such as drowsiness and urinary retention; therefore, these drugs should not be used in combination.
Treat patients with BPPV with the Epley maneuver to move the otoliths out of the semicircular canal; this may have curative effects in the ED. If the Epley maneuver is not completely successful, instruct the patient in vestibular rehabilitation exercises.
Treat Ramsay Hunt syndrome (Herpes zoster oticus) with antiviral therapy and symptomatic treatment within 72 hours of vesicle appearance.
Bacterial labyrinthitis requires appropriate antimicrobials and ENT consultation and admission.
Most patients with peripheral vertigo may be discharged home with follow-up for further testing to their PCP or ENT specialist. Patients with tumors should receive neurosurgical consultation. Admit patients with intractable symptoms.
Patients with central vertigo require imaging studies and specialty referral. Posterior fossa hemorrhage requires immediate neurosurgical consultation. Patients with tumors should also have urgent neurosurgical consultation. Emergent causes of central vertigo such as ischemic cerebrovascular incidents and VAD require neurologic consultation in the ED. Urgent causes such as suspected multiple sclerosis may be referred for outpatient neurologic consultation.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 164, “Vertigo and Dizziness, by Brian Goldman.