Evidence-Based Clinical Practice in Otolaryngology

Luke Rudmik

• Publisher: Elsevier
• Year: 2018
• ISBN:
  9780323544610
• Topic: Medicine
• Subtopic: Ear, Nose & Throat Medicine

Get a quick, expert overview of the many key facets of today's otolaryngology practice with this concise, practical resource. Dr. Luke Rudmik and a leading team of experts in the field address high-interest clinical topics in this fast-changing field.

• Presents an evidence-based, clinical approach to leading topics in otolaryngology.
• Covers key topics such as management of vertigo; management of adult sensorineural hearing loss; reflux in sinusitis; balloon catheter dilation in rhinology; epistaxis; functional rhinoplasty; sublingual immunotherapy for allergic rhinitis; pediatric obstructive sleep apnea; pediatric tonsillectomy; evaluation and management of unilateral vocal fold paralysis; management of hoarseness; endoscopic skull base resection for malignancy; management of glottic cancer; management of well-differentiated thyroid cancer; and management of the clinical node-negative neck in early stage oral cavity squamous cell carcinoma.
• Consolidates today's available information and experience in this challenging area into one convenient resource.

Chapter 1

Evidence-Based Practice

Management of Acute Vertigo

Euna Hwang, MD, FRCSC, and Darren Tse, BMBS, MRCS(Eng), FRCSC

Abstract

Vertigo is a specific symptom under the umbrella of dizziness. It is an illusion of motion in the absence of true motion. It can cause a great deal of debilitation and distress, especially when it is acute. The two most common diagnoses of acute vertigo in both primary care and subspecialty settings are benign paroxysmal positional vertigo (BPPV) and vestibular neuritis (VN). This article synthesizes the evidence for the management of these two peripheral vestibular disorders. BPPV is typically treated successfully by noninvasive and inexpensive particle-repositioning maneuvers. Surgery is also available for refractory cases. VN, an acute vestibular syndrome with prolonged and incapacitating vertigo, is managed with medications and vestibular rehabilitation therapy.

Keywords

Acute vestibular syndrome; Benign paroxysmal positional vertigo; Evidence-based otolaryngology; Peripheral vestibular disorder; Positional vertigo; Vertigo; Vestibular neuritis; Vestibular neuronitis

Vertigo is a form of dizziness. The American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) has defined vertigo as “an illusory sensation of motion of either the self or the surroundings in the absence of true motion” and “the sensation of motion when no motion is occurring relative to earth’s gravity.”^1,2 In other words, it is a symptom of perceived movement. Vertigo is caused by asymmetric inputs from the vestibular system following damage or perturbation to the peripheral vestibular apparatus (inner ear and vestibular nerve) or the central vestibular apparatus (brainstem and cerebellum). Vertigo is frequently experienced by the general population, accounting for a quarter of dizziness complaints, with a 12-month prevalence of 5% and an annual incidence of 1.4%.³ Vertigo can result in significant disability, including loss of work time and disruption of daily activities.⁴ As the prevalence of vertigo increases with age, it is also associated with an increased risk of fall and injury in the elderly population. This article focuses on the evidence-based practice in the management of the two most common diagnoses of acute vertigo: benign paroxysmal positional vertigo (BPPV) and vestibular neuritis (VN).^5,6

Benign Paroxysmal Positional Vertigo

Introduction

BPPV is a disorder of the inner ear in which episodic vertigo is elicited by changes in the head position relative to gravity.¹ Although these episodes of positional vertigo are rather short in duration, they can cause remarkable acute vertigo and persist for weeks to months, leading to distress and restricted movements and activities. BPPV had a lifetime prevalence of 2.4%, a 1-year prevalence of 1.6%, and a 1-year incidence of 0.6% in a population-based neurotologic survey. The 1-year prevalence of BPPV increased significantly with age, as it was seven times higher in the group aged above 60 years (3.4%), compared with the group aged 18–39 years (0.5%). The cumulative incidence of BPPV was near 10% by the age of 80 years.⁷ The peak age of onset appears to be in the sixth decade for idiopathic BPPV, and the mean age of onset is lower for secondary BPPV.⁸ About 17% of patients were found to have BPPV in one large dizziness clinic that evaluated more than 15,000 patients over almost 23 years.⁹ In addition to being reported as the most frequent cause of acute, recurrent vertigo, BPPV is typically treated successfully by noninvasive and inexpensive particle-repositioning maneuvers (PRMs).¹⁰ Hence, proper recognition and timely management of this peripheral vestibular disorder are paramount for adequate patient care in both primary care and subspecialty settings.

Pathophysiology

BPPV is generally accepted as the result of the abnormal presence of heavy calcium carbonate debris in a semicircular canal. These loose particles are otoconia (otoliths) that have been displaced from their original location in the utricle to a canal, where they provoke abnormal movement of the endolymph and cupula after reaching a critical mass when the head moves in the plane of the affected canal, resulting in abnormal nystagmus and vertigo. BPPV is thought to be caused by either canalithiasis (particles in a canal itself) or cupulolithiasis (particles adherent to the cupula of a canal) and can involve any of the three semicircular canals, whereas the superior (anterior) canal is rarely affected.^11,12 The underlying reasons for the dislodgement of otoliths from the vestibule remain unclear. Head trauma or whiplash injuries (15%), as well as other inner ear pathologies, such as Meniere disease (30%), VN (15%), otologic surgery, or sudden sensorineural hearing loss, are associated with secondary BPPV. The most common cause of secondary BPPV is head trauma. BPPV is primary or idiopathic in most cases (35%–70%).^8,9,12–16 The above-mentioned mechanism of canalithiasis leading to posterior canal BPPV and nystagmus was explained by Epley.^17,18 Free-floating particles have indeed been confirmed intraoperatively in patients with refractory posterior canal BPPV.^11,19,20 Lateral (horizontal) canal BPPV is also believed to be caused by the abnormal presence of debris in the lateral canal, which has not been demonstrated in vivo. Its pathophysiology is not as well understood as that of posterior canal BPPV, but the presence of particles in the lateral canal is supported by the phenomenon of canal conversion when a PRM to treat posterior canal BPPV results in lateral canal BPPV or vice versa.^1,21,22 Cupulolithiasis is thought to be more relevant in lateral canal BPPV than in posterior canal BPPV. The vertigo and nystagmus associated with the lateral canal variant are typically strong and last as long as the head is in the provocative position as debris adhere to the cupula.¹² The literature on superior canal BPPV is rather sparse because of its rarity from the anatomy of the superior canal that renders it difficult for debris to enter and stay. Its pathophysiology and findings are poorly understood and debated.^23–26

Posterior canal BPPV is the most common type, accounting for 60%–90% of BPPV diagnoses.^27–30 Lateral canal BPPV is present in 10%–20% of BPPV cases.³⁰ However, it may be underestimated in most reports as a large case series of 589 patients with BPPV revealed that lateral canal BPPV occurred in 40% of patients examined within 24 h of vertigo onset, as opposed to 26% when patients presented after 7 days of onset, which is consistent with the high natural remission rate of this type.^27,31 Superior canal BPPV is the rarest type with a reported frequency of 1%–2%.³⁰ Other infrequent variations comprise ipsilateral multicanal BPPV and bilateral multicanal BPPV.³²

Diagnosis

The diagnosis of BPPV is supported by a history of repeated episodes of positional vertigo that typically resolve within 1 min. They might be associated with nausea and vomiting. The transient vertigo is positional in that it is triggered by specific head movements, including looking up, bending forward, lying down from the sitti...